HYPERTHYROIDISM,GRAVE’S

DISEASE,THYROTOXICOSIS
• Refer intro on the previous slides.
• RELEVANT TERMS:
• Toxic this, there is excessive secretion of
thyroxine. Common in women.
• If the disease commence a gland that was
previously normal, then it is referred to as
primary thyrotoxicosis or Grave’s disease.
• Non-toxic /simple goitre enlargement of the
thyroid is fairly common
 CAUSES OF HYPERTHYROIDISM

-autoimmunity
Grave,s disease most common cause of hyperthyroidism.
-diabetes mellitus, systemic erythematosus, rheumatoid
arthritis,pernicious anaemia or addison,s disease.
 PATHOPHYSIOLOGY
Hyperthyroidism results from autonomous
production of thyroid hormones ,independent
of TSH from the pituitary gland. The
hyperthyroidism of Grave's disease results
from an immunoglobulin that stimulates the
TSH receptor on the thyroid gland, resulting in
hypertrophy of the gland and overproduction
of thyroid hormones.
 Pathophysiology cont.
• This immunoglobulin, thyroid stimulating
immunoglobulin ,can be measured in the
patient,s serum as a marker of Grave,s disease
activity.
• Toxic solitary nodules and multinodular goitres
are benign tumours autonomously
overproducing thyroid hormone.The
underlying cause of these entities is unknown.
 HYPERTHYROIDISM cont.
• Excess thyroid hormone in the circulation
increases metabolic rate ,increases activity of
the sympathetic nervous system, and affects
fats and carbohydrate metabolism.
 CLINICAL FEATURES
• Enlargement of the gland
• Increased metabolic rate
• Heat production
• Oxygen consumption caused by overrall
increaesd in metabolism:heat
intolerance,increased body
temperature,,warm moist skin,increased
appetite,weight loss and muscle fatigue
 CLINICAL FEATURES cont.
• Nervousness, apprehension, emotional
instability and restlessness. Warm and moist
hands in contrast to cold moist extremities
associated with anxiety.
• Rapid pulse.
• Short of breath on exertion and palpitations as
a result of increased metabolic rate.
• exophthalmos
 Grave’s ophthalmopathy
• This may have an infiltrative or non-infiltrative
cause.Both types may be present in a patient.
• In infiltrative ophthalmopathy,the retrobulbar
connective tissue and extra ocular muscle volume
are expanded because of fluid retention resulting
from the accumulation glycosaminoglycans .The
increase in tissue mass forces the eye forward
(proptosis) up to the limits of the restraining action
of the extraocular ocular muscles(exophthalmos)
 Grave’s opthalmopathy cont
• The pressure in the retro bulbar space increases because
of the increased tissue and limited forward movement,
causing periorbital and lid oedema and pressure on the
optic nerve.
• Nonifiltrative changes occur as a result of thyrotoxicosis
and usually resolve when the hyperthyroidism is treated.
• Glycosaminoglycans and fluid accumulation also occur in
the connective tissue in other parts of the body – this
accumulation is seen in pretibial area-a condition called
myxoedema.
 Grave’s ophthamopathy CONT
SIGNS AND SYMPTOMS
• bright-eyed state resulting from retraction of upper
eye-lid.
• Lid-lag on downward gaze;upper lid lagging behind
globe movement .
• Lid movement is jerky and spasmodic
• Lid closure is problematic due proptosis.
• Periorbital oedema
• Sense of irritation and tearing
• Feeling of pressure behind eyes,blurred vision,diplopia
 THRYOID STORM
• This is a medical emergency in which a patient
develop severe manifestation of signs and
symptoms of hyperthyroidism.
• These include :elevated temperature ,increased
tachycardia, or onset of dysrhythmias ,blood
pressure and respiratory rate increase above base-
line, worsening tremors and restlessness,worsening
mental status (delirious or psychotic state) or coma
and sometimes abdominal pain.
 Thyroid storm
• This a rare manifestation of hyperthyroidism,
usually seen in individuals with Grave’s
disease.The symptoms result from severe
increase in metabolism and are usually
precipitated by a major stressor such as
infection,trauma,or surgery
 DIAGNOSIS
• AFTER comprehensive hx and physical
examination,TSH level should be tested.
• Check free T4 level may be elevated.
• Ultrasound is used to define the size of the
gland.
• 24 hour radionactive iodine uptake test is
elevated in all cases of hyperthyroidism.
• Thyroid –binding globulin test.
 TREATMENT
• The two common antithyroid drugs are:
• 1.thionamides
• 2.propylthiouracil
• 3.methimazole(tapazole)
• 4.carbimazole and propylthiouracil taken for 1-2 years.
• These drugs block the synthesis of thyroid hormone
within the gland.
• The dosage of antithyroid drug is gradually tapered as
the patient becomes euthyroid and treatment is
generally maintained for 12 to 18 months.
 TREATMENT CONT.
• SIDE effects of antithyroid drugs include:
agranulocytosis, hence periodic monitoring of WBCs.
• Other forms of treatments include:
• Radiation :iodine-131 therapy of hyperthyroidism
• Surgery-partial thyroidectomy may be done if
radioactive iodine is contraindicated or antithyroid
drug therapy has failed.
• A complete thyroidectomy is done in the case of
cancer of the thyroid gland.
 NURSING INTERVENTION
• Risk for activity intolerance: the promotes a
balance of activity and rest.The first step is to
document baseline vital signs and vital signs in
response to activity and to monitor thee patient,s
response to and ability to tolerate activity.
Activity may be self limited because of fatigue.
• Provide period of uninterrupted rest in private
room with the means to control temperature; a
cool room is preferred by clients.
 NURSING INT.
• ANXIETY: the nurse provides information regarding the
physiologic reasons changes in appearance ,fatigue,
heat intolerance and sleep disturbance.Provide
symptomatic relief can decrease anxiety ,feelings of
frustration and powerlessness.
• The helps the patient identify coping strategies fo deal
with feelings.
• The nurse also helps the patient to explore relaxation
techniques to decrease anxiety.
• Protect the patient from stress producing visitors.
 NURSING INTERVENTION cont.
• Provide diet high in calories ,proteins,
carbohydrates with supplemental feedings
between meals and at bed time: vitamin
mineral supplements should be given as
prescribed.
• The should provide eye care in cases of
exomphthalmos: eye drops may be needed.
•
 CARE FOR THE PATIENT WITH THYROID
STORM
• Monitor patients V/S, intake output,neurologic
status and cardiovascular status every hour.
• Initiate IV line for medications and fluids.
• Administer increasing doses of oral
propylthiouracil as ordered (200 to 300mg orally.
• Administer iodide preparations as ordered; iv
sodium iodide given twice daily or oral
preparation is given.
 Care of the patient with thyroid storm
• Administer dexamethaxone 2 mg iv every 6 hours
because glucocorticoids inhibit the release of
thyroid hormones.
• Administer beta adrenergic blockers iv as ordered.
• Initiate measures to lower body temperature,
including external cooling devices ,cold baths,and
acetaminophen.Salicylates are contraindicated.
• Initiate support therapy such as oxygen
administration, and cardiac glycosides.
• Maintain a quiet ,calm ,cool, private
environment until the crisis is over.
• Maintain continuity of care.
• Decrease stressors by the use of patient
education, comfort measures or family
support.
 HYPOTHYRODISM
definition and aetiology
• Refers to low levels of thyroid hormone and encompasses:
• Congenital hypothyrodism(cretinism)
• Primary thyroid failure(e.g Hashimoto’s disease)
• Secondary thyroid failure (pituitary disease causing TSH
deficiency)
• Tertiary thyroid failure resulting from TRH deficiency
• External thyroid gland destruction( i.e after surgery , after
iodine therapy, from antithyroid drugs or medication side
effects.
• Miscellaneous (i.e envronmental iodine deficiency)
 HYPOTHYROIDISM CONT.
• Pathology: in primary autoimmune thyroid
failure,declining T4 production causes increased TSH
production with resultant hypertrophy of the
remaining functioning thyroid tissue.
• Progressive thyroid enlargement over time can ensue
with resulting clinical goitre.
• A goitre is an enlargement of the thyroid gland.If this
enlargement is not associated with hyperthyroidism or
hypothyroidism, cancer or inflammation, is referred to
as a simple goitre.
 HYPOTHYROIDISM
• Endemic goitre refers to a goitre that occurs in
a certain geographic area , and from a
common cause, such as iodine deficiency
• Goitrogenic factors include :iodine deficiency,
foods such as (cabbage ,turnips,
soybeans),lithium, intrinsic abnormality in
thyroid hormone synthesis.
 HYPOTHYROIDISM
THYROIDITIS
• This may be classified as acute , subacute or
chronic. Hashimoto disease is the most
common cause of chronic thyroiditis. Most
patients have thyroid enlargement owing in
part to the trophic effects of the compensatory
increase in TSH.
• Secondary and tertiary hypthyroidism is
associated with low levels of TSH such that
thyroid growth is not stimulated .
 THYROIDITIS
• The tissues are infiltrated with lymphocytes
and varying degrees of fibrosis. There is
progressive glandular destruction which results
in an initial decline in T4 levels and subsequent
elevation of TSH.
• T3 levels fall into the subnormal range after T4
levels.Thyroid autoantibodies and
antithyroglobulin are present in more than
90% of patients with Hashimoto’s disease.
 THYROIDITIS
• Acute thyroiditis:-is a bacterial infection of the
thyroid.
• Causative agents are:pyogenic bacteria,miliary
tuberculosis,fungi,pneumocystitis carinii.
• Symptoms:fever and tender thyroid mass.It is rare
in developed countries.
• Subacute:is of unknown aetiology,but possible
autoimmune factor.
• Symptoms: non-tender enlarged thyroid gland.
 THYROIDITIS
• Self-limiting form of hyperthyroidism followed
• Hypothyroidism
• Symptomatic treatment during hyperthyroid
phase consists of beta-blockers but
antithyroid medications.
• Post partum thyroiditis-occurs within a few
months within a few months after delivery in
1%-5% of pregnancies.
 THYROIDITIS
• Silent or painless thyroiditis: nontender
thyroiditis associated with the presence of
thyroid antibodies .Goitre may or may not be
present. Permanent hypthyroidism may result.
• Chronic thyroiditis-autoimmune process
characterized by lymphocytic infiltration of the
thyroid ,inflammation ,and fibrosis.May
present with a large goitre.
CLINICAL FEATURES OF HYPOTHYROIDISM
• dull mental processes
• Apathy
• Lethargy
• Intolerance
• Anorexia
• Cold intolerance
• Decrease body temperature/subnormal body
temperature.
• Cool dry skin
• Decrease appetite
 Clinical features CONT.
• Myxoedema-facial oedema,periorbital
oedema,enlarged tongue,deepened or horse
voice.
• Fatigue
• Anaemia.
• Constipation
• Dry, brittle hair
• Pale,dry, coarse skin
 Clinical features
• Enlarged tongue:drooling
• Decreased BMR
• Decreased
thyroxine(T4),triiodothyronine(T3) ,T3 resin
uptake and radioactive iodine uptake.
• Deecreased libido
• Hoarseness
• Thinning of lateral eyebrows
 MYXOEDEMA
• This form of severe hypothyroidism,that is
characterized by swelling of the affected areas
,especially face,back and lower extremities
.Dermatlogical changes also occurs as well .
• Myxoedema occurs in Grave,s disease and
Hashimoto thyroiditis.The condition occurs in
aadults.
 MYXOEDMA COMA
• This is the most severe form hypothyroidism
and ultimately can occur in any patient with
untreated ,prolonged hypothyroidism,
representing a potentially fatal endocrine
emergency; precipitated by a severe
physiologic stress, sedatives ,opioids, exposure
to cold, surgery, infections and trauma.
 Myxoedema coma
• symptoms
• Patients present with the symptoms of hypothyroidism
are comatose.
• Hypothermic
• Hypercapnea
• Hypoxia
• Cardiomegaly
• Hypotension,bradycardia,arrythmias
• Seizures,tremors,ataxia,slow mentation,delusions and
psychosis
 DIAGNOSIS HYPOTHYROIDISM
• Free T4 index and serum TSH assay.
• Thyroid antibody test
• Fine needle aspiration biopsy
• Thyroid Cancer test.
 TREATMENT
• Apart from the unusual situations of iodine
deficiency and goitrogenic drugs ,most goitres
are of unknown aetiology ,manifesting as
euthyroid Hashimoto’s disease.
• Suppression therapy:in this thyroid hormone is
exogenously suppplied.
• Replacement therapy: for hypothyroidism is
daily oral levothyroxine. Dose is according to
body weight.
 TREATMENT
• Hypothyroidism is treated favourably in
uncomplicated cases with thyroxine .In cases where
there are complications, such as ischaemic heart
disease ,tri-iodothyronine,T3 may be given.T3 acts
very rapidly ,but the effect is sustained for a shorter
period than thyroxine.The dosage at the beginning is
usually very small and gradually increased.
• The pulse is checked frequently and maintenance
dose is established .Drug therapy is usually
replacement of naturally occurring hormones.
 TREATMENT OF HYPOTHYROIDISM
cont.
• Adverse effects are almost entirely related to
under-replacement, producing symptoms of
hypothyroidism remaining ,or over-
replacement ,producing symptoms of
hyperthyroidism. Allergic reactions are rare.
 Care of patient in myxoedema coma.
• Supportive care:oxygen and intubation and
mechanical ventilatory support.
• Correction of hypothermia.
• Correction of electrolyte and glucose abnormalities.
• Administration of vasopressors
• Administration of antibiotics
• Administration of hydrocortisone.
• Specific therapy is the adminstration of IV
thyroxine.
 NURSING CARE
• Monitor vital signs and record
• The nurse should teach patient and family
about the condition and be patient with client
when he/she is lethargic.
• Teach patient and family to be alert for signs of
complications such as: angina pectoris, cardiac
failure, myxoedema coma(weakness ,syncope,
slow pulse rate, subnormal temperature, slow
respirations and lethargy).
 Nursing care
• Advise patient to seek medical supervision on regular
basis and when sign of illnes develop.
• Explain the importance of hormone replacement therapy
throughout life.

• Review the signs of hypothyroidism and hyperthyroidism

• Explain that increase sensitivity to narcotic analgesics
and tranquillizers necessitate dosage adjustments.OTC
should be avoided unless approved by a physician.
 NURSING CARE
• Skin care :A minimum of soap is used on the patient skin
and oily lotions and creams are applied to relieve skin
dryness.
• Diet :it should be low in calories to decrease or to
maintain body weight; low in fat and cholesterol because
of accompanying increase in serum cholesterol; high in
fibre with increase fluid intake to promote bowel function.
• Elimination; laxatives or enemas may be necessary to
maintain adequate bowel elimination.Or the diet should
contain roughage.
 NURSING CARE cont.
• Teach patient to take in adequate fluids to
maintain hydration and to avoid constipation.
• The patient must learn self management in
relation to drug therapy and symptom control.
• PATEIENT TEACHING is according to the
identified needs, the severity of the
symptoms, the impact of the disorder on the
patient life and functioning.
 HYPERSECRETION OF CORTISOL
CUSHING,S SYNDROME
• This is as a result of excess secretion of aldosterone
(hyperaldosteronism) arising from adrenal disorders.
CAUSES
-primary Hyperfunction of one or both of the adrenal cortices as a
result of a disorder.

-pathological hypersecretion of ACTH by the anterior pituitary gland

Primary hyperactivity of the adrenal cortex caused by neoplasm
such as an adenoma/phaeochromocytoma but may also occur as
a result of hyperplasia.
-common cause is excessive administration of ACTH.
 False-positive elevation of cortisol
• Acute/chronic illness:acute stressors may
result in high cortisol levels.
• Obesity:this results in high levels of urinary
17-hydroxycorticosteroids and 17-ketogenic
steroids
• pregnancy,oestrogen therapy and
contraceptives –these can increase serum
cortisol and give abnormal results.
 False-positive elevation of cortisol
• Alcoholism: alcoholic may have clinical and
diagnostic characteristic of Cushing’s syndrome,but
abstinence from alcohol reverse these signs.
• Depression:endogenous depression results in
increased cortisol levels, loss of diurnal
rhythms,increased urine free cortisol etc.However,
such patients have increased cortisol in response to
insulin-induced hypoglycemia,where as cushing
syndrome patients donot.
 pathophysiology
• There is loss of diurnal variation in cortisol secretion.
Morning serum cortisol level may be high and the
evening serum cortisol may show a decline on the
normal scale.
• Excess glucocorticoids can occur as a result of
disorders at different levels of the hypothalamic-
pituitary-adrenal axis.The most common cause of
non-iatrogenic cusging’s syndrome is pituitary
adenoma, in which excess ACTH production results
in excess glucocorticoid production.
 pathophysiology
• PRIMARY adrenal neoplasm or hyperplasia
with ectopic ACTH or CRH .This condition is
more common in women than in men.
 CLINICAL FEATURES
• Weakness
• Decreased libido
• Mood swings to psychosis
• Obese trunk because of increased deposition of fat on the trunk with
relatively thin legs.
• Hypertension
• Moon face
• Buffalo hump
• Acne
• Increased susceptibility to infection
• Hirsutism
• Ecchmotic areas
 CLINICAL FEATURES
• Purple striae on the breast and abdomen
• Amenorrhoea
• Hyperglycemia
• Hypokalemia
• Elevated plasma cortisol
• Elevated ketosteroids.
• osteoporosis
 DIAGNOSIS
• Magnetic resonance imaging.
• 24 hour urine free cortisol
• CT scan of the adrenal gland
• Chest x-ray
• Abdominal scan
 MEDICAL TREATMENT
• This is reserved for those patients who fail
surgical intervention.That is when surgical
therapy is not feasible or the effects of
radiotherapy are still pending.
• All these therapies revolves around inhibition of
cortisol production.
• Medications used include:ketoconazole,
metyrapone, aminoglutethemide and
mitotane.Others are:cyproheptedine(periactin)
 SURGICAL TREATMENT.
• IF LESION on pituitary is causing
hypersecretion of ACTH, a hypophysectomy or
irradiation of the pituitary may be done.
• Surgical excision of adrenal
tumours( adrenalectomy) is done.
•
 NURSING CARE
• Assessment:vital signs ,weight and blood glucose
level should be checked to establish a baseline.
• Protect the client from infection; the nurse
ensures monitoring of patient’s WBCs, checks
the mouth,skin and lungs for early signs of
infection. Patients exposure to pathogens must
be minimized. Visitors and staff with RTIs are
limited. Invasive procedures are avoided and
aseptic techniques is used if necessary.
 Nsg CARE cont.
• The patient is at risk of injury (fracture) because of
decreased bone mass so injury should be avoided.
• The nurse should help patient in identifying
sources of trauma and ways to avoid them.
• The nurse should instruct the patient on diet and
supplementation.She should encourage diet rich
in nutrient dense foods such as fruits,
vegetables,whole grains and legumes to improve
and maintain nutritional status.
 Nsg Care CONT.
• Patient should be given high protein diet and
potassium supplements.
• The nurse should help the patient deal with
disturbed body image, sexuality and self-
concept.
 ADDISON’S DISEASE
ADRENAL INSUFFICIENCY
• This is adrenal cortex hyposecretion of cortisol that
results in cortisol deficiency.
• This is due to alteration in any step in the
hypthalamic-pituitary-adrenal axis(CRH deficiency,
ACTH deficiency, or primary adrenal disease).
• Dysfunction may be temporary(transient ACTH
deficiency after removal of an ACTH producing
pituitary adenoma) or permanent(adrenal
suppression resulting from chronic glucocorticoid
therapy)
 Aetiology cont.
• Permanent adrenal insufficiency most
commonly as a result of acute autoimmune
destruction(addison’s disease) of the adrenal
glands.
• Tuberculosis of the adrenal gland accounts for
adrenal failure and so do metastatic
cancer,adrenal haemorhage,surgical removal
AIDS,fungal infections,congenital adrenal
hyperplasia etc.
 PATHOPHYSIOLOGY
• The major distinguishing feature between
primary and secondary adrenal insufficiency
lies with the degree of skin pigmentation and
mineralocorticoid deficiency.
• Patient with primary adrenal failure have a
large compensatory increase in ACTH and
concurrent increase in melanocyte-stimulating
hormone with resultant increase in skin
pigmentation.
 Pathophysiology CONT.
• IN CONTRAST pallor is present in secondary
adrenal failure where ACTH secretion is low.
• Patients with primary adrenal insufficiency are
mineralocorticoid deficient, in
contrast,patients with secondary adrenal
insufficiency are not mineralocorticoid
deficient and therefore donot exhibit
electrolyte disturbances or hypotension.
 pathophysiology
• There water retention in secondary adrenal
insufficiency because of increased ADH
secretion, a mild decreased in serum sodium.
• Patients with primary adrenal insufficiency
,there is excretion of sodium with
characteristic hyponatremia,hypokalemia and
hypotension ,progressive dehydration can lead
adrenal crisis (addisonian crisis) with
shock,,renal failure and death.
 CLINICAL MANIFESTATIONS
• Decreased gluconeogenesis and glycogenesis:
• Hypoglycemia,inability to tolerate prolonged
fast,weakness,light headedness and fatigue.
• ACTH levels increase as a result diminished
negative feedback on secretion of ACTH which
stimulates melonocyte –stimulating hormone
as a result generalized hyperpigmentation
occurs.
 Clinical manif. Cont.
• Hypovolemic shock characterized by
hypovolaemia,hypotension and tarchycardia.This is
as a result of diminished activity of catecholamines.
• Dercreased glucocorticoid deficiency may lead to
dysphoria,apathy or depression .
• Dehydration,hypovolaemia,hyponatremia,hyperkale
mia,muscle weakness,fatigue,postural hypotension
and hypovolaemic shock as a result of aldasterone
deficiency.
 Clinical manif.
• Decreased weight,increased BUN,increased
BUN,increased haematocrit,decreased skin
turgor.
• Vomiting
• diarrhoea
• Anorexia
• decreased serum cortisol level
• Increased plasma ACTH
 DIAGNOSIS
• History
• 24-HOUR urine specimen for lab analysis of
17-hydroxycorticosteroids and 17-ketosteroids
• Lab check of electrolytes levels.
• Skin pigmentation
 TREATMENT
• This done by maintenance dose of corticosteroid
preparations.These are replaced by oral
administration of cortisol preparation
(hydrocortisone) 2 -3 times daily.
• Fludrocortisone(synthetic aldosterone) is given orally
daily because of the deficiency of
mineralocorticoid(aldosterone).
• The patient with secondary adrenocortical
insufficiency does not require the aldosterone
replacement.
 NURSING CARE
• OBSERAVTION:monitor vital signs ,weigh
patient daily,institute intake and output chart.
• Monitor blood glucose and electrolyte levels.
• The nurse should observe for potential
adverse effects of the drug.If the patient
receives doses slightly in excess of normal
amounts will lead to certain changes, especial
with prolong administration.
 Nursing care
• Constant observation for side effects such as
restlessness, insomnia, euphoria,mood swings.
• Protect patient from infection because he/she is
susceptible to infection , as a result of the drug
ability to suppress lymphocytes and antibody
production.
• Patient and family should avoid contact with
those infected as patient is put in a private room.
 Nursing care
• Diet : the nurse should emphasize on high protein,high
carbohydrate diet with the amount of sodium
recommended by the doctor as the needs additional
sodium.However,patients with secondary adrenal
insufficiency donot require additonal salt.
• Administer steroid with milk or antacid to limit ulcerogenic
factor of the drug.
• Fluids: the nurse encourages fluids and continually
monitors the patient hydration status. Daily intake of about
2 L/day is recommended .Vomiting is prevented by
administration of an anti-emetic.
 Nursing care
• Activity: the importance of regular and adequate
hours of rest, stopping activities short of fatigue and
avoiding exposure to cold is stressed.He/she should
be fed and bath by the nurse.i.e absolute rest is
recommended to avoid energy expenditure and
hypotension.
• Patient should aware of lifelong replacement
therapy.
• The nurse should instruct the patient to wear
medical alert band.
 Nursing care
• Individual coping: the patient and family should
understand that stressful situation or illness
demands more corticoids.To prevent a serious
crisis or acute corticoid insufficiency,prompt
medical attention is necessary with any
disorder of respiratory infection,vomiting
,diarrhoea, fainting or sudden weakness.The
role of worry and emotional situations in
precipitating crisis is emphsized.
 Question
• What is addisonian crisis ?how is it managed?