Week 6 Endocrine 2 Flashcards
Disorders of the thyroid, pituitary, and adrenal glands impact hormone regulation and overall health. Understanding common disorders associated with these glands is crucial for providing effective, person-centred care and support to patients.
The thyroid gland is situated
on the anterior surface of the trachea, just below the thyroid cartilage. The thyroid gland has two lobes that are connected by the isthmus and it has an average weight of approximately 34 grams. The size will vary over the lifespan and in relation to nutritional, environmental and genetic factors.
Alteration in the function of the thyroid gland are some of the most common endocrine disorders. Disorders of the thyroid gland include:
inflammation
hyperthyroidism
hypothyroidism
benign and malignant nodules
goitre
The thyroid gland produces two types of hormones
→ T3 (triiodothyronine) and T4 (thyroxine)
The thyroid-stimulating hormone (TSH) → regulates the systhesis and release
of T3 and T4 → secreted by the pituitary gland
Synthesis of T3 and T4 requires
iodine → we obtain iodine with the food we eat, for example, fish and other seafood, eggs, chicken, liver, milk, yoghurt
Thyroid Hormone Function
Thyroid hormones affect almost every cell in the body and are responsible for energy metabolism, growth and development.
Increases cellular metabolism → a strong and immediate, short-lived increase
Increases body temperature, heart rate & force of contraction, blood pressure, oxygen consumption and enhances oxygen delivery.
Regulates bone production → growth and development
If the release of T3 and T4 increases speeds up core bodily functions, what would a lack of T3 and T4 do?
Slow body activities down.
Hyperthyroidism
→ Overproduction and sustained synthesis of T3 and T4 (hyperactivity)
Hyperthyroidism
Aetiology and Cause
The most common cause of hyperthyroidism is Graves disease
An autoimmune disorder
→ The immune system produces antibodies that attack and stimulate the thyroid gland to produce and excrete excessive amounts of T3 and T4
Most common disorder of the thyroid for people in Australia
More common in women than men, aged 20-40
Mostly linked to hereditary factors
Other causes, thyroid cancer, excessive iodine intake, goitre
Hyperthyroidism
Diagnosis
Blood pathology → thyroid function test
→ decreased TSH & increased T4 will confirm diagnosis
Radioactive iodine uptake test
→ differentiates between types of hyperthyroidism
Comprehensive assessment with objective / subjective data collection and physical assessment
Hyperthyroidism
Clinical Manifestations
Most people with hyperthyroidism have an enlarged thyroid or a nodular thyroid.
Signs and symptoms reflect increased metabolism which speeds up bodily functions:
Cardiovascular: tachycardia, systolic hypertension, palpitations, bounding rapid heart rate, arrythmias, systolic murmurs, angina
Respiratory: tachypnoea, dyspnoea on mild exertion
Gastrointestinal: increased appetite, increased thirst, weight loss, increased peristalsis, increased bowel sounds, splenomegaly
Integumentary: thin brittle nails, alopecia, palmar erythema, excessive sweating, warm and moist skin, fine silky hair
Musculoskeletal: fatigue, muscle weakness, muscle wasting, peripheral oedema, osteoporosis
Nervous System: fine tremor, nervousness, anxiety, insomnia, mood changes, difficulty concentrating, fatigue, difficulty focusing eyes, depression
Reproductive: amenorrhea, changes in libido, impotence, fertility issues, gynaecomastia in men
Other: intolerance to heat, eyelid retraction, stare, exophthalmos, goitre, rapid speech
Hyperthyroidism
Treatment and Management
The goal of management is to block the adverse effects of excessive secretion of T3 and T4 and prevent complications. Choice of treatment depends on age, preferences, comorbidities and pregnancy.
Medication:
Anti-thyroid medications e.g. carbimazole or methimazole
→ reduces the synthesis of new T3 and T4
Takes weeks to stabilise hyperthyroidism due to existing stores of thyroid hormone within the gland.
Radioactive iodine therapy:
Radioactive iodine → absorbed by the thyroid
destroys thyroid cells → results in the decreased production of T3 and T4
Surgery:
One of six procedures may be undertaken
Partial thyroid lobectomy
Thyroid lobectomy
Thryoid lobectomy with isthmusectomy
Subtotal thyroidectomy
Total thyroidectomy
Radical total thyroidectomy
Radioactive iodine therapy:
Radioactive iodine → absorbed by the thyroid
destroys thyroid cells → results in the decreased production of T3 and T4
Administered orally as an outpatient procedure
6-8 weeks to stabilise hyperthyroidism
Not suitable for pregnant women as radioactive iodine crosses the placenta → affecting the development of the foetal thyroid gland.
It is not always possible to control how much of the thyroid gland is destroyed, so patients may go on to develop hypothyroidism as a result of treatment.
Partial thyroid lobectomy
removal of the upper or lower portion of one lobe
Thyroid lobectomy
- removal of one entire lobe
Thryoid lobectomy with isthmusectomy
- removal of one lobe and the isthmus
Subtotal thyroidectomy
- removal of one lobe, the isthmus and most of the other lobe
Total thyroidectomy
- removal of the entire gland
Radical total thyroidectomy
- removal of the entire gland and cervical lymphatic nodes.
Hyperthyroidism
Complications:
Thyrotoxicosis
Thyroid storm
Acute, severe, life-threatening emergency
Caused by excessive amounts of T3 and T4 released into circulation often as a result of excessive stressors, e.g. trauma, infection, surgery (thyroidectomy)
All same clinical manifestations of hyperthyroidism are present in severe form
→ severe tachycardia, heart failure, shock, hyperthermia, restlessness, irritability, seizures, vomiting, diarrhoea, delirum, coma and death
Treatment
→ Aim is to reduce circulating T3 & T4, manage symptoms and provide supportive therapy, e.g. fluid replacement, reducing temperature, respiratory support.
→ β-adrenergic blockers for symptomatic relief → block sympathetic nervous stimulation → decrease HR, decrease nervous systom responses
→ Most require nutirional support due to severe increase in metabilic rate → up to 6 meals a day plus high protein and carbohydrate snacks
Hypothyroidism
→ Underproduction and secretion of thyroxine with high levels of circulating TSH
→ Sometimes a person will have normal levels of thyroxine, with an abnormal level of TSH
Hypothyroidism
Types
Three types
Primary hypothyroidism
→ Hashimoto’s Disease
Secondary hypothyroidism
Transient hypothyroidism
Primary hypothyroidism
→ caused by Hashimoto’s disease with destruction of thyroid tissue through atrophy
Hashimoto’s Disease
→ an autoimmune disorder that creates antibodies which attack the thyroid gland
Secondary hypothyroidism
→ caused by pituitary gland disease with decreased TSH secretion
Transient hypothyroidism
→ related to subacute thyroiditis or discontinuance of thyroid replacement therapy
Hypothyroidism causes
Most common cause is the autoimmune disorder, Hashimoto’s Disease
The immune system produces antibodies that attack the thyroid gland (as if it is a bacteria or virus) → initial response is the increased secretion of T3 and T4 → temporary hyperthyrodism → also results in inflammation of the thyroid gland → overtime the ongoing inflammation prevents the thyroid gland from producing T3 and T4 → destruction of the thyroid gland → reduced excretion of T3 and T4
Other causes → insufficient dietary intake of iodine, treatment for hyperthyroidism such as removal of the thyroid gland or radiation treatment, medications such as lithium or amiodarone
Hypothyroidism
Aetiology
Insidious onset
More common in women aged 20-30 and older adults
Risk increased with pregnancy, bipolar, Downs syndrome, other autoimmune disorders e.g. type 1 diabetes, rheumatoid arthritis, MS
Hypothyroidism
Diagnosis
Blood pathology → thyroid function test → low plasma levels of free T4 and raised TSH level confirms hypothyroidism.
Comprehensive assessment with objective / subjective data collection and physical assessment
Hypothyroidism
Clinical Manifestations
Where overproduction of thyroid hormones result in increased metabolism, an underproduction results in decreased metabolism and decreased body activity. Some people will have hypothyroidism but remain asymptomatic. Usually, the first symptoms experienced will be weight gain and feeling overtired → easily overlooked and dismissed.
Cardiovascular: bradycardia, decreased force of contractions, hypotension, cardiac hypertrophy, distant heart sounds, anaemia, heart failure, angina
Respiratory: bradypnoea, dyspnoea, decreased breathing capacity
Gastrointestinal: decreased appetite, weight gain and difficulty losing weight, constipation, nausea and vomiting, distended abdomen, enlarged tongue
Integumentary: dry, itchy, coarse skin, dry and sparse hair, and diffuse alopecia, decreased sweating, poor mucosa turgor
Musculoskeletal: fatigue, muscle weakness, muscular aches and arthralgia, altered sensation hands/feets (paraesthesia), delayed tendon reflexes, peripheral oedema, cool extremities
Nervous System: apathy, fatigue, poor memory and difficulty concentrating, slow mental processes, slow slurred speech
Reproductive: menorrhagia then later, amenorrhea, decreased libido, infertility
Other: cold intolerance, dysphonia, myxoedema (puffy face, hands and feet)
Hypothyroidism
Treatment and Management:
Medication
Treatment is through oral replacement therapy of thryoid hormones → levothyroxine.
→ Low-dose synthetic thyroxine (25-50mcg daily) initially
→ Gradually increasing in increments on a monthly basis until the serum TSH level is normal.
Hypothyroidism
Complications
Myxoedema coma
→ An extreme and decompensated form of hypothyroidism
→ Nervous system clinical manifestations, such as mental sluggishness, drowsiness and lethargy, may progressively result in severe alterations in consciousness and coma
→ Life-threatening medical emergency
→ More common in older aged adults
→ Can be precipitated by infection, medications, trauma and exposure to cold temperatures
→ Clinical manifestations → cardiovascular collapse, hypothermia, hypotension, hypoventilation, hyponatraemia, hypoglycaemia and lactic acidosis
Treatment → support of vital functions and intravenous thyroid hormone replacement
The pituitary gland is
pea-sized, weighs approximately 500mg, located at the base of the brain, behind the nose, and is attached to the inferior aspect of the hypothalamus.
The pituitary gland has two lobes:
the anterior and the posterior lobes.
The hypothalamus is
responsible for secreting several hormones to influence numerous glands, affect a variety of bodily functions and to maintain homeostasis. It forms the structural and functional basis of the endocrine system.
The posterior lobe of the pituitary gland takes messages from the brain, via the hypothalamus, to produce adequate hormones that affect many parts of the body, including stimulating other hormones. It is therefore often referred to as the ‘Master Gland’.
The pituitary gland produces:
Growth hormone
Prolactin
Adrenocorticotrophic hormone (ACTH) → targets cells in the adrenal gland
TSH → targets cells in the thyroid gland
Follicle stimulating hormone (FSH) → targets cells in the ovaries
Luteinising hormone (LH) → targets cells in the ovaries
Growth hormone
→ important for growth, development of muscles and bones, cellular growth and division → acromegaly is a disorder that occurs when the pituitary gland produces too much growth hormones
Pituitary Gland
Disorders
Due to it’s overarching affect on other glands, disorders of the pituitary gland can result in a vast range of clinical manifestations and these can be very challenging to diagnose.
They share these traits:
→ The pituitary gland may increase or decrease the production and secretion of multiple hormones simultaneously.
→ Hormone imbalances can result in extreme signs and symptoms, some of which mimic other diseases → misdiagnosis
→ Pituitary disorders have an insidious onset → delayed diagnosis
Pituitary disorders are often caused by a pituitary tumor → underproduction or overproduction of a range of hormones.
→ Most pituitary tumors are benign.
When a tumor grows on or near the pituitary gland, the tumor can:
→ Change hormone production, leading to symptoms such as weight gain, stunted or excessive growth, hypertension, decreased libido and fluctuations in mood.
→ Press against the pituitary gland, optic nerves or brain tissue, causing visual impairment or headaches.
Anti Diuretic Hormone (ADH) is produced by
It’s primary function is
ADH is produced by the hypothalamus and stored and released by the pituitary gland.
It’s primary function is to control how the body stores and releases water.
Diabetes Insipidus
Secreted when plasma osmolarity rises → main function is to decrease the amount of water lost from the kidneys.
Decreased ADH → excess water is lost from the body through urine → triggers increased intake water → diabetes inspidus (DI).
There are two main types of diabetes inspidus (DI):
1) Neurogenic DI (or central DI)
2) Nephrongenic DI
Neurogenic DI (or central DI)
→ caused by brain tumours, head trauma or brain surgery → damages the posterior pituitary gland.
Nephrongenic DI
→ inability of the renal tubules to sense the presence of ADH → can be hereditary or result from renal failure.
diabetes inspidus results in:
Increased urinary output → as much as 20L per day
Increased thirst (polydipsia) and dehydration
Hypernatraemia and hyperosmolarity → evidenced by a low specific gravity on urinalysis.
If caused by trauma → symptoms of DI generally appear within 3-6 days and may be short-lived resolved early (e.g. raised ICP) → may also be chronic.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
The syndrome of inappropriate anti-diuretic hormone hypersecretion (SIADH), is a condition in which the pituitary gland produces too much arginine vasopressin.
SIADH → aldosterone is supressed → increases renal excretion of sodium → retention of fluid within the cells.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Patients present with:
Water retention
Hyponatraemia
Decreased urinary output with concentrated urine
Hyper-osmolality
Neurological manifestations such as headaches or confusion
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
CAUSES:
A malignant tumour (e.g. carcinoma of the lung or pancreas)
Pituitary surgery
Head injury
Medications
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
DIAGNOSIS:
Diagnosis is made by excluding other causes of hyponatraemia → delayed treatment.
Thorough patient history and physical examination of hypovolaemia (decreased skin turgor, dry mucous membraines, tachycardia) or hypervolaemia (ascites or oedema), urine output and osmolality are essential.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
TREATMENT:
Goal of teatment is to treat the underlying cause, e.g. if due to medication, discontinuing the medication will often resolve hyponatraemia.
Fluid restriction - based on urine output
If symptoms are severe → furosemide and intravenous hypertonic (3%) saline → decreases the circulatory volume and prevents sodium excretion
Demecloyclcline (tetracycline antibiotic) with the side effect of inducing excessive urination and inhibiting vasopressin action may be beneficial in chronic situations and helps maintain an adequate fluid balance
Vasopressin antagonists may be prescribed
Monitoring of sodium levels and correction of hyonatraemia must be undertaken with caution in order to prevent cerebral osmotic demylination.
Adrenal Gland
There are two, small, highly vascularised pyramid-shaped adrenal glands located close to the upper pole of each kidney, behind the peritoneum. Each gland has two distinct portions: the inner medulla and the outer cortex. Both portions have different structures and hormonal functions
Adrenal Cortex
Weighs 80% of the adrenal gland
Outer part of the adrenal gland
Has 3 different zones
Cells are stimulated by the adrenocorticotrophic hormone (ACTH) from the pituitary gland
Secretes several hormones including steroid hormones
*Cortisol → glucocorticoid → needed to maintain life and protect the body from stress → has metabolic, anti-inflammatory and growth-suppressing effe cts → will also increase BGL → named for their effects on glucose metabolism
*Aldosterone → mineralocorticoid → targets the kidneys to retain water and sodium in the blood → essential for water and electrolyte balance
*Androgens → sex hormones → oestrogen and testosterone → gonadcorticoids
Cholesterol is a precursor for steroid hormone synthesis
Adrenal Medulla
Weighs 20% of the adrenal gland
Inner part of the adrenal gland
Secretes catecholamines → adrenaline, noradrenaline and dopamine → all considered neurotransmitters because when they are secreted by the adrenal medulla, they are released straight into circulation → flight or fight response
Cushing’s syndrome
→ Hyperactivity of the adrenal cortex → overproduction of corticosteroids, in particular, glucocorticoids
Cushing’s syndrome
Aetiology
A chronic disorder
More common in women than men
Usually diagnosed between 20 and 40 years, although it can occur at any age.
Cushing’s syndrome
Cause:
Several causes
Iatrogenic → long-term use of exogenous glucocorticoid → commonly used in inflammatory conditions such as asthma, rheumatoid arthritis and lupus erythematosus
Pituitary adenoma (Cushing’s disease) → hypersecretion of ACTH → 80% of cases
Ectopic tumours → ACTH secreting tumours e.g. small cell lung cancer, pancreatic tumour
Adrenal causes → excessive production of cortisol → benign or malignant tumour.
Cushing’s syndrome
Clinical Manifestations:
Can be seen in all body systems and are related to hypersecretion of corticosteroids:
→ Rapid weight gain, particularly of the trunk and face
→ Hirtuism (facial hair growth) → especially in women
→ An irregular or absent menstrual cycle, testicular atrophy
→ Muscle wasting and weakness
→ Fat pads along the collar bone
→ Hyperhidrosis (excessive sweating)
→ Thinning of the skin
→ Mood swings, irritability, anxiety, depression
→ The appearance of purple lines over the abdomen, thighs or buttocks (as a result of weakening and rupture of the deeper layers of skin).
Cushing’s syndrome
Diagnosis:
Plasma cortisol & ACTH levels
24-hour urine collection → elevated free cortisol
Imaging → CT, MRI, x-ray
Cushing’s syndrome
Treatment & Management:
Goal of treatment is to regain balanced hormone levels
Treatment depends on underlying cause
→ If a tumour → surgical removal of the tumour or the adrenal gland. Usually only one adrenal gland is removed; however in the presence of an adrenocorticotropic hormone-producing tumour, bilateral adrenalectomy may be performed.
→ Radiation therapy
Medication
→ Hormone replacement
→ Suppress the synthesis or secretion of cortisol from the adrenal gland
→ Where the cuase is induced iatrogenic Cushing’s syndrome, the reduction or ceasing of medication will resolve the symptoms → should only be under the medical supervision → sudden withdrawal of medication may cause adrenal supression → life-threating Addisonian crisis.
→ Symptom management
Adrenocortical Insufficiency
→ Hypoactivity of the adrenal cortex
Adrenocortical Insufficiency
Aetiology and Cause
The most common cause is Addison’s disease (primary cause)
Results from complete destruction or dysfunction of the adrenal cortex
→ The adrenal cortex no longer produces aldoserone, glucocorticoids or adrenal androgens
A chronic disorder
Linked to an autoimmune response
→ Antibodies attack the adrenal tissue → dysfunction, destruction
Often associated with other disorders of the endocrine system
Affects >2500 Australians
→ Most common in people <60 years of age, affecting both males and females equally
Secondary cause is reduced ACTH secretion
→ Corticosteroids and androgens are reduced
→ Mineralocorticoids remain within normal limits
→ Caused by pituitary disease
Adrenocortical Insufficiency
Risk factors include:
Adrenal haemorrhage
Bacterial or fungal infections e.g. tuberculosis
AIDS
Removal of both adrenal glands
Cancers or tumours affecting both adrenal glands
Adrenocortical Insufficiency
Clinical Manifestations
Lethargy
Muscle weakness
Weight loss
Hypotension
Hypoglycaemia
Hyponatraemia
Hyperkalemia
Hyperpigmentation
Adrenocortical Insufficiency
Treatment and Management
→ Usually requires the use of long-term medications to relieve the clinical manifestations:
Glucocorticoid (prednisolone)
→ Also effective in treating many other diseases and disorders
→ Indication → primary and secondary adrenal insufficiency
→ Dose → 15-25mg daily
→ Action → replacement of cortisol
Precaution
→ Long-term use often leads to serious complications and adverse reactions → not recommended for minor chronic conditions
→ Should not be ceased abruptly
→ Needs to be taken early in the morning and with food
Nursing Management
Providing nursing care of a patient experencing an endocrine disorder requires:
Collection of data
→ Targeted health history questions
→ Subjective data collection
→ Objective data collection (Eg Head to toe assessment, Vital signs)
→ Past history → surgery, pregnancies
→ Medications
→ Other information gathering (Medical notes, Family / carer information)
Risk assessments
→ Skin integrity
→ Falls risk
→ Risk for pressure areas
→ Psychosocial status
→ Nutritional assessment (hydration assessment)
Diagnostics
→ You will be required to have an understanding of the normal ranges for blood results. If you are not familiar of the normal ranges, you should know where to find the normal ranges, e.g. pathology resources (Thyroid function test, Glucose levels, HbA1c, Liver function test, Full blood count, Urea, electrolyte and creatinine)
→ ECG
→ Ward urinalysis test or urine studies
→ BHCG
→ Weight and height
Preparation and care related to interventions
→ Surgical care
→ Radiation
Supportive care
→ Emotional support
→ Education
→ Reassurance
Nursing referrals
→ Nurses can initiate referrals within the interprofessionl team (Diabetes educator, Support groups, Dietician)
Patient education is vital in the management of endocrine disorders, and can include:
Education on condition
Why replacement therapy must be lifelong
Replacement therapy dosages and appropriate timing of dose
The importance of not missing a dose
Symptomatic relief can be prolonged
There is a potential for overreplacement which can lead to hyperactivity of a gland
How to recognise signs and symptoms → symptom management
Concomittent drug use
Many hormone replacements can interact with several other medications.
Some examples include:
Anticoagulants → increases the risk of bleeding
Thyroxine, oral hypoglycaemia agents and insulin → interferes with action and stimulates hepatic gluconeogenesis and glycogenolysis
Aspirin and levothyroxine can increase the risk of bleeding
Blood glucose levels must be closely monitored when patients are receiving this medication because it can result in glucocorticoid induced diabetes and hyperglycaemia.
Levothyroxine
Endogenous insulin
Prednisolone
Sulfonylureas
Prednisolone
Your patient has developed peripheral neuropathy, a chronic complication of diabetes mellitus. Considering this diagnosis, which of the following nursing management strategies would you ensure that you implement?
Stool chart
Fluid balance chart
Neurovascular assessment
Falls risk assessment
Falls risk assessment
Exophthalmos (bulging of the eyes) is a classic sign of this endocrine disorder.
Cushing’s syndrome
Hyperthyroidism
Addison’s disease
Hypothyroidsim
Hyperthyroidism
Patients diagnosed with this condition have excessive levels of adrenocorticotropic hormone (ACTH) or corticosteroids which can cause hypoglycaemia and pronounced changes in physical appearance.
Cushing’s syndrome
Addison’s disease
Hashimoto’s disease
SIADH
Cushing’s syndrome
Your patient is soon to return to the ward after having a thyroidectomy performed. You know that you will need to perform routine post-op vital signs and regular wound assessments. Considering the type of surgery that was performed, what other essential assessment will you need to complete due to potential swelling, at the same time as when you are reassessing the patient’s vital signs?
Hide answer choices
Neurological assessment
Falls risk assessment
Secondary assessment
Airway and breathing assessment
Airway and breathing assessment
Long-term corticosteroid use can lead to Cushing’s syndrome. Which of the following statements is true?
It can also occur from overproduction of cortisol by the adrenal glands.
It is also known as hypocortisolism and is due to abnormally high levels of the hormone cortisol.
It is genetic and characterised by weight loss, lethargy and brittle bones
It is caused by an under-production of insulin from the pancreas
It can also occur from overproduction of cortisol by the adrenal glands.
A patient has been diagnosed with Hashimoto’s disease. An important nursing intervention when
caring for this patient is:
Pain assessment chart
Neurological observation chart
Skin integrity chart
Wound assessment chart
Skin integrity chart
A patient with Grave’s disease develops the following: heart rate 160 per minute, temperature 40.2⁰C,
severe vomiting and seizures. These are classic clinical manifestations of:
Addison’s crisis
Thyrotoxicosis
Diabetic ketoacidosis
Myxoedema coma
Thyrotoxicosis
This drug is used to treat hyperthyroidism. Adverse effects include the potential to cause birth defects
if used in the first trimester of pregnancy.
Levothyroxine
Prednisolone
Sulfonylureas
Carbimazole
Carbimazole
Hydrocortisone is used to treat Addison’s disease. Which of the following is an important nursing consideration when educating the patient on safe use of this drug?
This medication is best taken on an empty stomach.
This medication should not be ceased abruptly.
This medication has no serious complications.
This medication is best taken to management minor conditions.
This medication should not be ceased abruptly.
