ENDOCRINOLOGY HB - KK (1).pdf disorders.

ENDOCRINOLOGY – 20HRS
Module competence
This module is designed to enable the leaner manage patients suffering from endocrine disorders
Module outcomeS
By the end of the module the leaner should be able to:-
•Review the anatomy and physiology of the endocrine system e.g regulation of blood glucose levels
using the negative feedback mechanism
•Manage patients with thyroid disorders using the nursing process e.g hypothyroidism (cretinism,
myoxedema), hyperthyroidism (thyrotoxicosis), goiter ( simple and malignant ) and neoplasms(
adenoma and carcinoma )
•Manage patients with pituitary disorders e.g acromegaly, dwarfism and simmond ’s disease.

•
Manage patients with parathyroid disorders using the nursing process e.g hyperparathoyidism,
hypercalcaemia, hypocalcaemia.
•
Manage patients with adrenal disorders using the nursing process e.g cushing’ s diseases , addison’ s disdease,
crohn’
s disease, congenital adrenal hyperplasia and pheochromocytoma.
•Discuss non- communicable disorders affecting the endocrine system e.g diabetes mellitus using the
following headings i.e
definition, epidemiology in the Kenyan scenario , mortality, socio-economic impact ,
classification, Risk factors ( modifiable and non modifiable ) path physiology, clinical features, diagnosis (
clinical features , laboratory investigations) , management :- hyperglycemia, hypoglycemia , health messages,
self management, areas of behavior change, nutrition therapy ( aims, assessment, importance ) physical activity,
prevention, complications ( acute and chronic ), diabetes in special groups i.e
(the pregnant womenand elderly)
Teacher strategies
Interactive lectures, group discussions, demonstration

MOLLY OCHAR RN,BScN

ADDISON’S DISEASE/ADRENAL GLAND
INSUFFICIENCY
Overview
This condition occurs if the adrenal gland does not make enough cortisol
and sometimes Aldosterone.
This disease may be a result of an auto immune reaction or an
infection which leads to hypofunction of the adrenal glands.
There is a decrease in adrenal steroids which are: glucocorticoids,
mineralocorticoids, and androgen.
It occurs in all age groups and both sexes,can be life threatening.

Causes
Autoimmune disease
Long lasting infections such TB and HIV can cause harm to the adrenal
glands.
Cancer cells that spread from other parts of the body
Bacterial infection to the gland.
Low levels of adrenocorticotropin hormones due to damage to the
pituitary or hypothalamus.
Prolonged use of steroids.

Pathophysiology

Signs and symptoms
Early signs:
Tiredness
Weakness
Loss of appetite
Weight loss
Dizziness when standing
Muscle aches
Nasuea, vomiting
Diarrhea
Patches of darkened skin or
unexplained tanning (bronzing)
Depression
Intolerance to heat or cold.
Craving for salty foods.
Late signs:
Sharp pain in the lower back,
abdomen, or legs
Dehydration
Hypotension
Loss of consciousness

Acute Adrenal Failure/Addisonian Crisis
Addisons disease can be accelerated by stress and infections leading to life threatening shock.

S/S
Sudden penetrating pain in: lower back, abdomen or legs
severe vomiting
Diarrhea followed by dehydration
Extreme weakness
Severe hypotension
Hypoglycemia
Vomiting
Diarrhoea
Coma (loss of consciousness)

Diagnosis
Blood tests to measure the level of hormones of cortisol and ACTH.
CT scan to measure the size of the A.gland.
MRI for pituitary or hypothalamic causes.
Management
Artificial cortisol hormone replacement therapy

Care of the patient with Addison’s Disease
ADL’s

Assessment

Dietary needs

Patient is total care during the
initial crisis
Assess turgor, mucous
membranes, orthostatic blood
pressures will signify need for
more fluids
Six small feeding, carbo’s, high
protein
Need to deal with stress

Nursing Diagnosis
Fluid and electrolyte imbalance related to lack of sodium and fluid loss
through the kidneys,sweatglands,GI tract for lack of aldosterone
Goal:patient maintains adequate fluid volume
Interventions:
Assess vital signs
Assess weight
Encourage oral fluids as the patient can tolerate,IVF
Administer replacement hormones
Imbalanced nutrition less than body requirements related to inadequate
intake evidenced by nausea,vomiting

Activity intolerance related to decreased production of glucose
Goal: patient maintains optimum nutritional status,maintains weight and
adequate dietary intake
Interventions:
high protein diet,low carbohydrate
Small frequent meals
Risk for decreased cardiac output low levels adrenal hormones
Goals: patient maintains adequate cardiac output evidenced by strong
peripheral pulses,normal vital signs,warm dry skin,alert and responsive.
Interventions
Administer IVF,artificial hormones

CUSHING’S SYNDROME
Def
The condition occurs when there is excessive production of cortisol

Causes
Prolonged use of corticosteroids which have the same effect as cortisol.
Pituitary gland tumor which leads to excessive production of ACTH which
in turn stimulates the adrenal gland to produce cortisol

Signs and Symptoms
Weight gain and fatty tissue deposits around the mid-section and upper
back,in the face (moon face) and between the shoulder (buffalo hump)
Pink or purple stretch marks on the skin of the abdomen,thighs,breast
and arms.
Thinning fragile skin that bruises easily.
Slow healing of cuts and infections.
Acne.
Severe fartigue
Muscle weakness

Depression, anxiety and irritability.
Loss of emotional control.
High blood pressure.
Bone loss leading to fractures over time.
Women with cushings syndrome may experience: thicker or more visible
body facial hair.
Irregular or absent menstrual periods.
Men with cushing syndrome may experience:
Decreased libido, decreased fertility, erectile dysfunction .

Cushings Diagnosis
Physical examination for signs of cushings
B
lood test to measure the level of cortisol
CT scan and MRI to provide the image of the pituitatry and adrenal
glands.
Management
Aim of management is to lower the level of cortisol in the body by:
Reducing corticosteroid use.
If the cause is a tumour,surgery to remove the affected gland.
Anticortisol medications such as ketoconazole,mitotane (corticosteroid
inhibitor),metyrapone.
Radiation therapy to shrink pituitary or adrenal gland tumour.

Nursing Management

• Risk for injury related to weakness
• Risk for infection related to altered protein metabolism and inflammatory
response
• Self-care deficit related to weakness, fatigue, muscle wasting and altered sleep
patterns
• Impaired skin integrity related to oedema, impaired healing and thin and
fragile skin
• Disturbed body image related to altered physical appearance, impaired sexual
functioning, and decreased activity level
• Disturbed thought processes related to mood swings, irritability and
depression.

PHEOCHROMOCYTOMA
Def
They are a type of tumour of the adrenal glands that can release high levels
of epinephrine and norepinephrine.
The tumour grows in the adrenal medulla.

Adrenaline/Epinephrine controls bodily fxns eg heart rate, blood
circulation, breathing, digestion, sweating, urination and sexual arousal

Signs and symptoms
Headache,sweating and heart palpitations, high blood pressure,shortness
of breath.
Anxiety,nausea,tremors,weakness,abdominal pain and weight loss.
Diagnosis
History taking and physical examination
Blood tests to measure the level of adrenal medulla hormones
MRI or CT scan of the adrenal gland.

Management
Antihypertensives to control the blood pressure.
Surgery to remove the gland.
Chemotherapy or radiotherapy if surgery is not possible or if metastatic
Nursing management
Monitor vital signs especially blood pressure.
Administer antihypertensives medications as ordered.
Promote rest and decrease stressful stimuli.

Nursing Diagnosis
Risk for decreased cardiac output related increased levels of
vasoconstriction epinephrine and norepinephrine.
Activity intolerance reduced cardiac function abnormal heart rate,
increased blood pressure, verbal report of fatigue.
Acute pain.
Ineffective coping.
Deficient knowledge

Crohn’s Disease
Its an inflammatory bowel disease.
It causes inflammation of digestive tract which can lead to abdominal
pain, fatigue, weight loss and malnutrition.

Signs & Symptoms
Diarrhea, fever, Fatigue, Abdominal pain & cramping,. Blood in Stool,
Mouth sores, Reduced appetite and Weight loss, Pain or drainage near/
around the anus(fistula)

Other Signs & Symptoms
Inflammation of skin, eyes and joints
Inflammation of the liver or bile ducts
Delayed growth or sexual development in children

Causes
Exact cause is unknown.
Hereditary
Malfunctioning immune system

Complications
Bowel obstruction
Ulcers
Fistulas
Anal fissures
Malnutrition
Colon cancer

Diagnosis
Tests for anemia or infection.
Fecal occult blood test
Colonoscopy
Computerised Tomography(CT)
Magnetic Resonance Imaging(MRI)
Capsule Endoscopy

Treatment
There’s no cure currently & goal is to reduce the inflammation that triggers
s/s.
Anti-inflammatory drugs;-Corticosteroids i.e Prednisone, Methotrexate
Antibiotics I,e Ciprofloxacin, metronidazole
Anti-diarrheal i.e Loperamide
Pain relievers
Iron Supplements
Vit B12 shots
Calcium & Vit D supplements

Congenital Adrenal Hyperplasia
Read on this

Thank You

ENDOCRINOLOGY – 20HRS
Modul
e competence
This module is designed to enable the leaner manage patients suffering from
endocrine disorders
Module outcomeS
By the end of the module the leaner should be able to:-
1. Review the anatomy and physiology of the endocrine system e.g regulation of
blood glucose levels using the negative feedback mechanism
2. Manage patients with thyroid disorders using the nursing process e.g
hypothyroidism (cretinism, myoxedema), hyperthyroidism (thyrotoxicosis),
goiter ( simple and malignant ) and neoplasms( adenoma and carcinoma )
3. Manage patients with pituitary disorders e.g acromegaly, dwarfism and
simmond’s disease.
4. Manage patients with parathyroid disorders using the nursing process e.g
hyperparathoyidism, hypercalcaemia, hypocalcaemia.
5. Manage patients with adrenal disorders using the nursing process e.g
cushing’s diseases , addison’s disdease, crohn’s disease, congenital adrenal
hyperplasia and pheochromocytoma.
6. Discuss non- communicable disorders affecting the endocrine system e.g
diabetes mellitus using the following headings i.e definition, epidemiology
in the Kenyan scenario , mortality, socio-economic impact , classification,
Risk factors ( modifiable and non modifiable ) path physiology, clinical
features, diagnosis ( clinical features , laboratory investigations) ,
management :- hyperglycemia, hypoglycemia , health messages, self
management, areas of behavior change, nutrition therapy ( aims, assessment,
importance ) physical activity, prevention, complications ( acute and chronic
), diabetes in special groups i.e (the pregnant womenand elderly)
Teacher strategies
Interactive lectures, group discussions, demonstration

MOLLY OCHAR RN,BScN

Introduction
The nervous and endocrine systems control most functions in the
human body.
Endocrine dysfunction may result from deficient or excessive
hormone secretion, transport abnormalities, an inability of target
tissue to respond to a hormone or inappropriate stimulation of the
target tissue receptor.

The Hypothalamus
This is the mother gland and it controls the functions of most of the
other glands.
The disorders that can affect the hypothalamus are encephalitis,
head injury, tumours in the brain and haematomas.
Since it has many functions, the effects of disease on the
hypothalamus will be varied.
The effects include obesity, restlessness, disordered temperature
regulation, diabetes insipidus and precocious puberty.

If the posterior lobe of the pituitary is affected by either injury or
disease, it can result in diabetes insipidus, which manifests with
polyuria and polydipsia.
The management will involve either surgery or hormone therapy.
The most prominent disorders of the pituitary, however, are those
that affect the anterior pituitary.

Diabetes Inspidus
This is a general term for any condition that causes the body to make a lot
of urine.
Characterised by deficiency of ADH/ Vasopressin frm post . pituitary
The condition makes one extra thirsty making one pee a lot.
It is not related to blood sugar related Diabetes Mellitus, but does share
some of its signs and symptoms

Causes
Head trauma
Brain tumor
Surgical ablation of Pituitary Gland
Infections of CNS i.e Meningitis, Encephalitis, TB
Tumors eg Lymphoma of breast / Lungs, Metastatic disease
Failure of renal tubules to respond to ADH

Signs and Symptoms
Get really thirsty- Polydipsia
Pee a lot- polyuria even upto 20 litres per day.
Dehydration.
Unexplained weakness.
Lethargy.
Muscle pains.
Irritability.

Diagnosis
Analysis of urine samples.
Blood samples to see how the pituitary gland is working.(plasma levels of
ADH)
A fluid deprivation test, which shows how well the kidneys are working.
The test monitors the amount of urine made over the course of several
hours without drinking fluids.
MRI to check for problems with the pituitary gland.

Treatment

(synthetic ADH)Vasopressin and desmopressin can replace the missing
ADH.
Diuretics(Thiazides)- thiazides increases the concentration of the waste
products in the urine,which can have an effect of reducing the amount of
urine produced.
Anti-inflammatory i.e indomethacin,Ibuprofen and Aspirin
low sodium diet.

Syndrome of Inappropriate Secretion of
Anti-diuretic Hormone (SIADH)
Diabetes insipidus results from a lack or a deficiency of ADH.
The patient will present with polyuria and polydipsia, accompanied
by hemoconcentration.
It is managed by rehydration and electrolyte replacement.
On the other hand, SIADH is due to over-secretion of ADH and the
patient presents with hemodilution, and decreased urinary output.
These two conditions may be the result of an injury or infection to
the brain, pituitary and/or hypothalamus.

Hyperpituitarism
Hypopituitarism
Hyperaldosteronism

Hypopituitarism
This is a rare disorder that involves a decrease in one or more of the
anterior pituitary hormones.
Primary hypofunction may be as a result of autoimmune disorders,
infections, tumours, vascular diseases or destruction of the gland from
trauma, radiation or surgical procedures but the most common cause is
a tumour.
This is the result of a deficiency of growth hormone, which produces
retardation in children.
Males may have testicular atrophy.
Females will develop amenorrhoea.
Other effects include: decreased muscle strength, defective renal
function, altered thyroid metabolism and reduced basal metabolic rate.
Glucocorticoid and androgen abnormalities can occur.

Hyperpituitarism
This is the hyper-function of the pituitary.
It can result in:
Excess prolactin, which leads to amenorrhoea and inappropriate
secretion of breast milk.
In males it leads to impotence.
If it starts in childhood, hyperpituitarism can result in gigantism.
When it occurs in adulthood it leads to acromegaly.
In acromegaly individuals have enlarged hands, feet and lower jaw.
They also have coarse facial features and impaired glucose tolerance.
Cushing's syndrome is also one of the condition that result from
hyperpituitarism.

Hyperaldosteronism
Excessive aldosterone leads to hypernatraemia, hypertension and
headache.
The treatment of hyperaldosteronism involves surgery, potassium
supplements and sodium restriction.
Nursing care involves assessing the patient and instituting
interventions for hypokalaemia.
Maintenance therapy of the hormones may be given after
adrenalectomy, that is, the removal of the adrenal gland.

When there is low or no production of all of the pituitary hormones, the
condition is called pan hypopituitarism.
This is a chronic deficiency of function of the pituitary gland that leads to
atrophy of many of the viscera including the heart, liver spleen,kidneys,
thyroid, adrenals and gonads.
A destructive or atrophic lesion affecting the pituitary glands with loss of
hormones leads to atrophy of the thyroid, adrenal glands and in turn
brings atrophic changes to their target organs and the viscera. The
decrease in size of the endocrine glands may be extreme.

SIMMOND’S DISEASE/ PANHYPOPITUITARISM

Signs and Symptoms
Insufficient level of gonadotropins can cause:
In women: missed menstrual cycles,infertility ,osteoporosis,vaginal dryness,loss or reduction in female
characteristics.
In men: impotence,reduced size of testes,decreased production of sperms, infertility ,reduced muscle
mass,loss or reduction in men characteristics e.g. beard growth.
Insufficient levels of growth hormone can cause:
In children: stunted growth,dwarfism.
In adults: weakness,overweight, reduced cardiac output,low blood sugar levels and reduced exercise
tolerance.
Insufficient levels of thyroid stimulating hormones can lead to:
Hypothyroidism.
Insufficient corticotrophic levels can lead to:
Underactive adrenal gland,which causes low blood pressure,hypoglycaemia,fatigue,weight loss,vomiting.
Excessive prolactin levels can cause:
In women: missed period,infertility and milk secretion.
In men: reduced facial and body hair, small testes.

Causes
This condition is most often caused by damage to the pituitary gland.
In adults it is usually a result of pituitary surgery.
In children may be caused by: infection,stroke,tumor of pituitary.

Diagnosis
MRI scan
Blood tests to measure target hormones levels

Management
The goal is to restore normal blood hormone levels of the thyroid, adrenal,
oestrogen or testosterone and sometimes growth hormone.
Treatment options include:
Hormone replacement therapy based on what types of hormones are
missing.
Tumor removal done if the causeof damage is a tumor.
Radiation therapy: done if the cause of the damage is a cancer or tumor.

ACROMEGALY
Chronic metabolic disorder in which there is too much
growth hormone and the body tissue gradually enlarge.
The following changes take place in the body:
Enlargement of the hands, feet, nose, lips and ears, heart,
kidney, skull
Protruding brow and lower jaw, gaps between lower teeth
Headaches and visual disturbances.

Pathophysiology
Acromegaly is characterised by hypersecretion of growth
hormone (GH), which is caused by the existence of a
secreting pituitary tumor.
Pituitary tumors are benign adenomas and can be classified
according to size (microadenomas being less than 10mm in
diameter and macroadenomas being greater than 10mm in
diameter). In either situation, hypersecretion of GH in turn
causes subsequent hepatic stimulation of insulin-like
growth factor-1.

Acromegaly Causes
Overproduction of growth hormones is caused by a benign
tumor of the pituitary gland
Tumors produce excess growth hormones and, as they
expand, compress surrounding brain tissues, such as the
optic nerves

Symptoms of acromegaly
Body odor
Carpal tunnel syndrome
Decrease muscle strength
(weakness)
Easy fatigue
Enlarged feet
Enlarged hands
Weight gain

Enlarged glands in the skin
(sebaceous glands)
Enlarge jaw and tongue
Excessive height
Swelling of bony areas
around the joint

Excessive sweating
Headache
Hoarseness
Joint pain
Limited joint movement
Sleep apnea

Widely spaced teeth
Excess hair growth in
females
Thickening of skin, skin
tags

Investigation
Visual field tests
Assessment of other pituitary hormones: prolactin, adrenal,
thyroid and gonadal hormones.
MRI scan of pituitary and hypothalamus: more sensitive
than CT scan.
CT scan: for lung, pancreatic, adrenal or ovarian tumors that
may secrete ectopic growth hormone or GHRH.
Total body scintigraphy with radio-labelled octreoScan
(somatostatin) to aid localization of the tumour.
Cardiac assessment: electrocardiogram, echocardiogram.

Acromegaly Treatment
Surgery, drug therapy or radiation therapy to remove or
destroy the tumor.

Complications
Arthritis
Cardiovascular disease
Colonic polyps
Glucose intolerance or diabetes
High blood pressure
Sleep apnea
Spinal cord compression
Uterine fibroids
Vision abnormalities

Dwarfism Description
Also known as growth hormone deficiency and
hyposecretion of growth hormone.
A person of short stature less than 4’ 10”
Disproportionate body parts
Pituitary dwarfism

Dwarfism Causes
Acondroplasia
A genetic condition that causes growth factors not to be
registered by the bones.
Human growth hormone (HGH) deficiency
Many reasons for this including genetics, stress and
malnutrition.

Types of dwarfism
Acondroplasia
Dystrophic dysplasia

Characteristic of Acondroplasia
People this type have an average size trunk, short arms and
legs with a slightly enlarged head and prominent forehead.
Most of the people with this type are born to average sized
parents
The average adult height is about 4 feet tall.

Characteristic of dystrophic dysplasia
Short limbs
Cleft palate
Club feet
Ears with cauliflower appearance

Diagnosis
•Dwarfism is often diagnosed in childhood on the basis of
visible symptoms
•A physical examination can usually suffice to diagnose
certain types of dwarfism
•Genetic testing and diagnostic imaging.

Dwarfism Treatment
Hormone therapy if growth hormone deficiency.
PT and braces if the condition causes pain.

Prevention
Genetic testing
Growth hormone deficiency may be remedied via injections
of human growth hormone (HGH) during early life.

Definition
Abnormally large growth due to an excess of growth
hormone during childhood, before the bone growth plates
have closed

Causes
Non-cancerous (benign ) tumor of the pituitary gland (most common
cause).
•Commedy complex
•McCune Albright Syndrome
•Multiple endocrine neoplasia type 1 (MEN-1)
•Neurofibromatosis

Sign and symptoms
Delayed puberty
Double vision or difficulty with side (peripheral) vision
Frontal bossing and a prominent jaw
Headache
Increased sweating
Irregular periods (menstruation)
Large hands and feet with thick fingers and toes
Release of breast milk
Thickening of the facial features
Weakness

Exams and Tests
CT or MRI scan of the head showing pituitary tumor
Failure to suppress serum growth hormone (GH) levels after
an oral glucose challenge (maximum 75g)
High prolactin levels
Increased insulin growth factor-1 levels
Damage to the pituitary leading to decreased levels of
cortisol, estradiol (girls), testosterone (boys) and thyroid
hormone.

Treatment
Medications may be used to reduce GH release, block the
effects of GH, or prevent growth in stature. They include:
Dopamine agonists, such as bromocriptine mesylate and
cabergoline which release growth hormone release.
GH antagonist, pegvisomant which blocks the effects of GH
Sex hormone therapy, such as estrogen and testosterone,
which may inhibit the growth of long bones
Somatostatin analogs, such asoctreotide and long acting
lanreotide which reduce GH release

•Radiation of the pituitary gland to regulate GH.
•Surgery to remove pituitary tumour, which is the treatment
of choice for well-defined pituitary tumours.

Complications
•Delayed puberty
•Difficulty functioning in everyday life due to large size and
unusual features
•Diminished vision or total vision loss
•Embarrassment, isolation, difficulties with relationship and
other social problems.
•Hypothyroidism
•Severe chronic headaches
•Sleep apnea

MOLLY OCHAR RN,BScN

Introduction
The thyroid gland is a butterfly-shaped organ located in the lower neck
anterior to the trachea.
It consists of two lateral lobes connected by an isthmus. The gland is
about 5 cm long and 3 cm wide and weighs about 30 g.
The blood flow to the thyroid is very high, about five times the blood
flow to the liver. This reflects the high metabolic
activity of the thyroid gland.

The thyroid gland produces three hormones:
1.thyroxine (T4),
2.triiodothyronine (T3),
3.and calcitonin.
Thyroxine and triiodothyronine are referred to collectively
as thyroid hormone.

FUNCTION OF THYROXINE AND
TRIIODOTHYRONINE
The primary function of the thyroid hormone is to control the
cellular metabolic activity.
T4, a relatively weak hormone, maintains body metabolism in a steady
state.
T3 is about five times as potent as T4 and has a more rapid metabolic
action.
These hormones
Accelerate metabolic processes by increasing the level of specific
enzymes that contribute to oxygen consumption and altering the
responsiveness of tissues to other hormones.
Influence cell replication and are important in brain development.
Its necessary for normal growth.
Through their widespread effects on cellular metabolism, influence
every major organ system.

Hypothyroidism
Hypothyroidism results from suboptimal levels of
thyroid hormone.
Thyroid deficiency can affect all body functions and
can range from mild, subclinical forms to myxedema,
an advanced form.

Causes

Hashimoto’s thyroiditis (autoimmune) the thyroid gland is
enlarged and has decreased ability to make thyroid hormones.
The body’s immune system inappropriately attacks the thyroid.
Lymphocytic thyroiditis.(if the inflammation is caused by WBC
lymphocyte)
Thyroid destruction from radioactive iodine or surgery i.e
treatment of head and neck cancers, lymphoma
Atrophy of thyroid gland with aging
Medications Lithium, Iodine compounds,Antithyroid
medications.
Infiltrative diseases of the thyroid (amyloidosis, scleroderma)
Severe iodine deficiency and Iodine excess.

Signs & Symptoms
Increased cholesterol levels.
Depression.
Fatigue.
Brittle nails
Hair loss.
Memory loss.
Dry skin.
Constipation.
Numbness and tingling of fingers
Cold intolerance
Hoarseness
Excessive sleepiness.
Vague aches and pains.
Swelling of the legs
As dx progresses: Eye puffiness, Slowing of HR, Hypothermia, Heart failure

Complications
myxedima coma
enlarged heart (cardiomyopathy),
accumulation of fluid around the lungs (pleural
effusion)
accumulation of fluid around the heart. (pericardial
effusion)

Diagnosis
Blood tests-thyroid hormones decreased.
Patients clinical history, thyroid scan.
If pituitary or hypothalamic cause suspected ,MRI of
the brain

Management
Thyroid hormone replacement using Synthetic
Levothyroxine

Myxedema Coma
This is a loss of brain function as a result of severe long
standing low level thyroid hormone in the blood. It is
considered a life threatening complication of
hypothyroidism.though it’s a very rare condition.

Causes
History of hypothyroidism
Thyroid surgery.
Radioactive iodine treatment for thyroid disease.
Pituitary or hypothalamic disease

Signs & Symptoms
The body temperature is abnormally low. (26.6 c)
Severe mental changes including hallucinations,
disorientation, seizures and deep coma.
Oedema all over the body with swollen eyes and thickening
of the tongue.
Sparse, dry hair and loss of the eyebrows.
Difficulty in breathing.
Pleural and pericardial effusion.
The heart may slow down and its ability to pump blood
forward can be impaired.
The GIT does not function well and may be paralyzed.

Diagnosis
Blood test T3,T4 and TSH levels.
Management
Maintaining Vital functions i.e Assisted ventilation to
combat hypoventilation.
Warming them to raise the body temperature to normal.
Start antibiotics until it is certain that infection is not
present.
Thyroid hormone replacement.
If hypoglycemia is evident, concentrated glucose may be
prescribed to provide glucose without precipitating fluid
overload.

Nursing management
Nursing Diagnosis: Activity intolerance related to fatigue and depressed
cognitive process
Goal: Increased participation in activities and increased independence
Nursing Diagnosis: Risk for imbalanced body temperature
Goal: Maintenance of normal body temperature

Nursing interventions Rationale Expected Outcomes
1. Provide extra layer of
clothing or extra
blanket.
2. Avoid and discourage
use of external heat
source (eg, heating pads,
electric or
warming blankets).
3. Monitor patient’s
body temperature and
report decreases from
patient’s baseline
value.
4. Protect from exposure
to cold and drafts.

1. Minimizes heat loss
2. Reduces risk of
peripheral vasodilation
and vascular collapse
3. Detects decreased
body temperature and
onset of myxedema
coma
4. Increases patient’s
level of comfort and
decreases further heat
loss
Experiences relief of
discomfort and cold
intolerance
• Maintains baseline body
temperature
• Reports adequate
feeling of warmth and
lack of chilling
• Uses extra layer of
clothing or extra
blanket
• Explains rationale for
avoiding external
heat source

Cretinism/Congenital
hypothyroidism
This is under activity of the thyroid gland at birth
which results in growth retardation, developmental
delay and other abnormal features. Can be due to
deficiency of iodine in the mother’s diet during
pregnancy.

Causes
Missing or poorly developed thyroid gland.
A pituitary that does not stimulate the thyroid gland.
Thyroid hormones that are poorly formed or do not
work.
Medications the mother took during pregnancy.
Lack of iodine in the mother’s diet during pregnancy.

S&S
Puffy face
Thick tongue that sticks out.
Constipation
Dry, brittle hair.
Lack of muscle tone.
Jaundice
Poor feeding.
Short height.
Sleepiness.

Diagnosis
Physical examination may show the above symptoms.
Thyroid ultrasound scan.
X-ray of the long bones.
Management
Newborns should be screened for hypothyroidism as
early diagnosis is very important.
Artificial thyroid hormone replacement helps to
ensure thyroid hormone levels are in a normal range.

Nursing Management
Nursing Diagnosis: Activity intolerance related to fatigue and depressed
cognitive process
Goal: Increased participation in activities and increased independence
Outcome:
Participates in self-care activities
• Reports decreased level of fatigue
• Participates in activities and events in environment
Interventions
Promote independence in self-careactivities.
a. Space activities to promote rest andexercise as tolerated.
b. Assist with self-care activities whenpatient is fatigued
Rationale
Encouragement needed in fatigued, oftendepressed patient
a. Encourages activities while allowingtime for adequate rest
b. Permits patient to participate to the extent possible in self-care activities

Thyrotoxicosis/Hyperthyroidism
Second most prevalent endocrine disorder, after
diabetes mellitus.
This is a condition in which the thyroid over produces
hormones
Graves’ disease, the most common type of
hyperthyroidism, results from an excessive output of
thyroid hormones caused by abnormal stimulation of
the thyroid gland by circulating immunoglobulins.
It affects women eight times more frequently than
men, with onset usually between the second and
fourth decades (Tierney et al., 2001).

Causes
Graves’ disease an autoimmune disorder causes antibodies to
stimulate the thyroid to secrete too much hormone.The body’s
immune system mistakenly attacks and damages the thyroid.
Excess iodine in the blood.
Thyroiditis.Which can result in extra thyroid hormones being
produced.
Lumps (nodules) on the thyroid –
this results in extra thyroid
tissue, which can mean extra thyroid hormones are produced.
Tumours of ovaries and testes.
Benign tumours of the thyroid and pituitary Gland.
Large amounts of thyroid hormone replacement taken through
dietary supplements or medication.

S&S
Excessively high metabolic rate. (hypermetabolic state):
a rapid heart rate,elevated blood pressure and hand tremors.
Shortness of breath, dizziness, Loss of consciusness
Excessive sweating and develop low tolerance for heat.
Frequent bowel movements, weight loss, irregular
menstrual cycles
Thyroid gland can swell into a goitre.
Eyes appear quite prominent which is a sign of
exophthalmos, a condition that is related to Graves’s
disease.
Skin has a Salmon colour, warm, soft & moist

Other S&S
Increased appetite.
Nervousness.
Restlessness.
Inability to concentrate.
Weakness.
Irregular heartbeat.
Difficulty sleeping.
Fine brittle hair.
Itching.
Hair loss.
Nausea and vomiting.
Breast development in men.

Diagnosis
History and physical examination which will reveal common
signs of hyperthyroidism.
Cholesterol test: low levels is a sign of an elevated metabolic rate,
the body is burning through cholesterol quickly.
T4,free T4,T3 measures how much thyroid hormone is in the
blood.
TSH level is abnormally low is the first sign of hyperthyroidism.
Thyroid scan and uptake allows to see if the thyroid is overactive.
Ultrasound: measures the size of the entire thyroid gland, as well
as any masses within it.
CT scan or MRI scans can show if a pituitary tumour is present
that is causing the condition.

Management
Anti-thyroid medications such as methimazole stop
the thyroid from making hormones.
Radioactive iodine effectively destroys the cells that
produce hormones.
Surgery: a section or all of your thyroid gland may be
surgically removed. You will then have to take thyroid
hormone supplements to prevent hypothyroidism.
Beta blockers such as propranolol can help control
rapid pulse, sweating, anxiety and high blood
pressure.

Nursing diagnosis
Imbalanced nutrition, less than body requirements,
related to exaggerated metabolic rate, excessive
appetite, and increased gastrointestinal activity
• Ineffective coping related to irritability, hyper-
excitability, apprehension, and emotional instability
• Low self-esteem related to changes in appearance,
excessive appetite, and weight loss
• Altered body temperature

Thyroiditis
Inflammation of the thyroid gland, can be acute,
subacute, or chronic. Each type of thyroiditis is
characterized by inflammation, fibrosis, or
lymphocytic infiltration of the thyroid gland.

1.Acute Thyroiditis
Acute thyroiditis is a rare disorder caused by infection of the thyroid gland by
bacteria, fungi, mycobacteria, or parasites. Staphylococcus aureus and other
staphylococci are the most common causes.
S&S
anterior neck pain and swelling,
fever,
dysphagia,
dysphonia.
Pharyngitis or pharyngeal ,
erythema (redness), and
tenderness of the thyroid gland.

Treatment
Antimicrobial agents and fluid replacement. Surgical incision and drainage may
be needed if an abscess is present.

2.Subacute Thyroiditis
The condition presents as a painful swelling in the anterior neck that
lasts 1 to 2 months and then disappears spontaneously without residual
effect. It often follows a respiratory infection.
S&S
The thyroid enlarges and may be painful.
Skin is reddened and warm.
Difficulty in swallowing.
 Irritability, nervousness, insomnia,
weight loss—

manifestations of hyperthyroidism
Treatment
NSAIDS to relieve neck pain
Beta-blocking agents (eg, propranolol [Inderal])may be used to control
symptoms of hyperthyroidism

3.Chronic Thyroiditis(Hashimoto’s
dx)
or chronic lymphocytic thyroiditis; its diagnosis is based on
the histologic appearance of the inflamed gland. In
contrast to acute thyroiditis, the chronic forms are usually
not accompanied by pain,pressure symptoms, or fever, and
thyroid activity is usually normal or low rather than
increased.
If untreated it leads to hypothyroidism.
Treatment
Rx aim is to reduce the size of the thyroid gland and prevent
hypothyroidism
Thyroid hormone Therapy.
Surgery

Thyroid Storm(Thyroid crisis,
Thyrotoxicosis)
Thyroid storm (thyrotoxic crisis) is a form of severe
hyperthyroidism,usually of abrupt onset.
Untreated it is almost always fatal, but with proper
treatment the mortality rate is reduced substantially.
The patient with thyroid storm or crisis is critically ill
and requires astute observation, aggressive and
supportive nursing care during and after the acute
stage of illness.

Clinical manifestations
High fever (hyperpyrexia) above 38.5°C (101.3°F)
• Extreme tachycardia (more than 130 beats/min)
 GI symptoms(weight loss, diarrhea, abdominal pain
Cardiovascular symptoms (edema, chest pain,
dyspnea,palpitations)
• Altered neurologic or mental state, which frequently
appears as delirium psychosis, somnolence, or coma

Causes
 injury,
infection,
thyroid and nonthyroid surgery,
 tooth extraction,
insulin reaction, diabetic acidosis,
pregnancy,
digitalis intoxication,
abrupt withdrawal of antithyroid medications,
extreme emotional stress,
or vigorous palpation of the thyroid.

Management
A hypothermia mattress or blanket, ice packs, a cool environment,
hydrocortisone, and acetaminophen (Tylenol). Salicylates(eg, aspirin)
are not used because they displace thyroid hormone from binding
proteins and worsen the hypermetabolism.
Humidified oxygen is administered to improve tissue oxygenation and
meet the high metabolic demands. Arterial blood gas levels or pulse
oximetry may be used to monitor respiratory status.
Intravenous fluids containing dextrose are administered to replace liver
glycogen stores that have been decreased in the hyperthyroid patient.
PTU or methimazole is administered to impede formation of thyroid
hormone and block conversion of T4 to T3, the more active form of
thyroid hormone.
Hydrocortisone is prescribed to treat shock or adrenal insufficiency.
 Iodine is administered to decrease output of T4 from the thyroid
gland.

Goitre
Enlargement of the thyroid gland
Nodular Goitre
Some thyroid glands are nodular because of areas of hyperplasia
(overgrowth).
No symptoms may arise as a result of this condition,these nodules
slowly increase in size with some descending into the thorax, where
they cause local pressure symptoms.
Some nodules become malignant, and some are associated with a
hyperthyroid state. Thus, the patient with many thyroid nodules may
eventually require surgery.
Endemic (Iodine deficient) goitre
Iodine deficiency is the main cause of goiters. Iodine is essential to
helping your thyroid to produce thyroid hormones. When you don’t
have enough iodine, the thyroid works extra hard to make the thyroid
hormone, causing the gland to grow larger.

Causes
Iodine deficiency.
Grave’s disease (autoimmune disease)occurs when the thyroid produces more
thyroid hormone than normal which is known as hyperthyroidism.
Hashimoto’s disease: destruction of the thyroid. in this situation the thyroid
does not produce enough thyroid hormone, causing hypothyroidism. The low
thyroid hormone causes the pituitary gland to make more thyroid stimulating
hormone (TSH), which causes the thyroid to swell.
Hashimoto’s thyroiditis (autoimmune) the thyroid gland is enlarged and has
decreased ability to make thyroid hormones. The body’s immune system
inappropriately attacks the thyroid.
Inflammation: some people develop thyroiditis, an inflammation of the
thyroid that can cause goitre.
Thyroid Nodules: solid or fluid containing cysts may appear on the thyroid and
cause it to swell. These nodules are often non-cancerous.
Thyroid cancer: cancer may affect the thyroid, which causes swelling on one
side of the gland.
Pregnancy: being pregnant can sometimes cause the thyroid to become larger.

Signs & Symptoms
Noticeable swelling in the neck
Difficulty in swallowing or breathing because the
enlarged thyroid gland causes compression of the
surrounding structures.
A tight feeling around the neck.
Coughing.
Hoarseness in the voice.
Dizziness when raising the arm above the head

Diagnosis
Physical examination neck swelling.
Blood tests detect changes in hormone levels and an
increased production of antibodies, which are
produced in response to an infection or injury.
Thyroid scan U/S: which show the size and condition
of the thyroid.
Biopsy

Management
Observation: if the goiter is small and doesn’t cause problems,
and the thyroid is functioning normally,wait and see approach.
If hypothyroidism give artificial thyroid hormone
replacent,enable the pituitary gland to make less TSH,which
should result in stabilization of the gland. Often decreasing the
size of the gland.
Corticosteroids reduce inflammation if the cause was thyroiditis.
Radioactive iodine for hyperthyroidism. It is taken orally and
reaches the thyroid gland through the blood stream,destroying
thyroid cells which results in diminished size of the thyroid.
Surgery for removal of the thyroid if it grow too large or doesn’t
respond to medication therapy.

Thyroid Cancer
It occurs in the cells of the thyroid gland(Butterfly shaped gland at
the base of neck, just below the Adam’s apple)

Types of Thyroid Cancer
Papillary T.C- Most common and least aggressive Asymptomatic
nodule in a normal gland Starts in childhood or early adult life,
remains localized Metastasizes along the lymphatics if untreated
More aggressive in the elderly
Follicular adenocarcinoma
Medullary
Anaplastic
Thyroid lymphoma

Causes
The exact cause is unknown, though there are factors
that may be associated with an increased risk of
developing cancer:
Thyroid conditions such as thyroiditis and goitre.
Radiation exposure to the neck.
Diets low in iodine
Poorly controlled diabetes.
Acromegaly
Obesity
Genetic predisposition (family history of cancer)

Signs &Symptoms
A lump that can be felt through the skin on your neck
Changes to voice…hoarseness
Difficulty in swallowing.
Pain in neck and throat
Swollen neck lymph nodes

Diagnosis
Ultrasound
Fine needle aspiration biopsy
Management
Most thyroid cancers require surgery to remove the
tumour.
Lobectomy: the thyroid has two lobes joined in the middle
with a fibrous tissue bridge called isthmus. If the tumour is
just confined to a small area, the surgeon may just remove
the affected lobe.
Total thyroidectomy: to completely remove the thyroid
gland and hopefully ensure that the cancer will not recur.
Lymph node resection: thyroid cancer can spread to local
lymph nodes, and these nodes often are removed.