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NUR2226 > Week 7: Endocrine > Flashcards

Week 7: Endocrine Flashcards

1
Q

Name a disorder of the pancreas

A

Diabetes mellitus

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2
Q

Name a disorder of the adrenal glands

A

Cushing’s Syndrome

Adrenocorticol Insufficency

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3
Q

Name a disorder of the thyroid glands

A

Hypothyroidism

Hyperthyroidism

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4
Q

Describe the pancreas

A

The pancreas is a gland

A long shaped organ under the liver and stomach.

Works closely with the liver but is essentially an exocrine and endocrine organ.

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5
Q

Describe diabetes mellitus

A

a group of metabolic disorders in which there are abnormally high levels of blood glucose (a term used interchangeably with blood sugar) over a prolonged period of time.

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6
Q

What is DM characterised by?

A

An ineffective response to insulin at the target cells= known as insulin resistance

Insufficient or no release of insulin (hyposecretion of insulin) by the islets of langerhan cells in the pancreas

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7
Q

What is the function of the hormone insulin?

A

Secreted by Beta cells

I role is to shift glucose into cells where it can be used for energy.

Essentially, insulin enhances glucose absorption and is the body’s main fuel storage hormone.

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8
Q

Explain T1DM

A
  • an auto immune condition= the immune system is triggered to destroy all beta cells in the islet of langerhans
  • leads to absolute insulin deficiency
  • represents only 10% of call DM cases
  • onset is usually before 30 years old (common around puberty)
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9
Q

What causes T1DM?

A
  • exact cause unknown
  • strong link to genetics
  • strong link to some environmental factors such as exposure to viris or chronic illness.
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10
Q

Describe the onset of T1DM

A
  • long preclinical period
  • acute progression
  • abrupt onset of clinical manifestations
  • Hyperglycaemia will not occur until 80-90% of all beta cells in the islet of Langerhans have been destroyed. Therefore, there is a long time before clinical manifestations start to occur
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11
Q

Describe the prevention and cure for T1DM

A
  • No prevention

- No cure/life long disease

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12
Q

What are the characteristics of T1DM?

A
  • low to absent blood insulin levels
  • increased blood glucose levels
  • insulin sensitivity is normal to high
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13
Q

What is amylin and its relation to T1DM?

A

Amylin is co-released with insulin from the beta cells in the islet of Langerhans to suppress the release of glucagon from the alpha cells (glucagon is a hormone released to raise the blood glucose levels by breaking down glycogen)

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14
Q

Explain the pathophysiology of T1DM

A

→ glucose absorbed by the digestive tract

→ glucose enters the bloodstream

→ blood glucose levels increase

→ trigger signal sent to pancreas to release insulin and amylin

→ pancreas cannot produce any insulin because there are no Islet of Langerhans cells

→ no insulin or amylin released

→ excessive glucagon

→ blood glucose levels increase to dangerous levels

→ imbalanced homeostasis

→ metabolic alterations = hyperglycaemia and ketoanaemia

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15
Q

What are the clinical manifestations of T1DM?

A

Weight loss

Polyphagia (↑ hunger)

Polyuria (↑ urine production) → dehydration → hypovolaemia and hypotension

Polydipsia (↑ increased thirst)

Glycosuria (glucose in urine)

Lethargy

Impaired healing

Pruritus (itchy skin)

Blurred vision

Headaches

Mood swings

Leg cramps

Dizziness

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16
Q

Treatment and management of T1DM

A
  • People with T1DM will always need insulin = insulin dependent
  • Doses require frequent adjustments
  • Management plans are individualised according to factors such as age, weight, stability, comorbidities and usual exercise levels.
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17
Q

Explain T2DM

A
  • a life long and chronic health condition
  • T2DM=a silent but progressive disorder that develops over many years
  • Represents approximately 85-90% of all cases of DM
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18
Q

What is the cause to T2Dm and what are some risk factors?

A
  • not exactly known
  • strong link to non-modifiable risk factors
    e. g. ethnic / cultural background (Aboriginal or Torres Strait Islander background, Pacific Islander, Indian subcontinent or Chinese cultural background)

genetics and family related risk factors

Modifiable risk factors include;

  • Hypertension
  • Dyslipidaemia
  • Obesity - especially high levels of abdominal obesity - where extra weight is carried around the waist.
  • Sedentary lifestyle - <2 ½ hours exercise per week
  • Poor diet - high fat, high caloried, high gylcaemic index foods
  • Smoking - increases risk of developing T2DM > 40%
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19
Q

Explain the onset of T2DM

A
  • Usually occurs with adults > 45 years of age, but now the diagnosis is more frequently occuring in the younger age groups including children and adolescents.
  • Progressive and long preclinical period of many years → clinical manifestations may never occur
  • By the time of diagnosis, >70% of Islet of Langerhans cells have died due to fatigue from overproduction of insulin
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20
Q

Explain so preventions and cures for for T2DM

A
  • healthy lifestyle choices
  • no prevention for genetically linked cases

Cures: nil/life long

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21
Q

What is T2Dm characterised by?

A

Normal to ↑ blood insulin levels → this will gradually deteriorate to low levels overtime

↑ blood glucose levels

↓ insulin sensitivity

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22
Q

Explain the pathophysiology of T2DM

A

Two issues lead to the pancreas losing the capacity to secrete enough insulin due to the gradual destruction of islet of Langerhans cells
1. insulin deficiency → relative shortage of insulin

  1. insulin resistance → ineffective response to insulin from target cells (loss of insulin sensitivity) → persistent hyperglycaemia

After oral intake
→ glucose absorbed by the digestive tract

→ glucose transported into the bloodstream

→ blood glucose levels ↑

→ target cells send a trigger signal to the pancreas to release insulin

→ Beta cells secrete insulin

→ target cells have developed in ineffective response to this insulin so send additional triggers for more insulin to be secreted

→ ↑ insulin secretion

→ hyperinsulinaemia

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23
Q

Why is chronic hyperglycemia an issue?

A

Chronic hyperglycaemia causes the Beta cells to become fatigued and they then gradually ↓ their response to the high levels of blood glucose

→ continuous ↓ in insulin production until almost completely diminished

→ Beta cells die from fatigue

→ severe lack of insulin

→ hyperglycaemia

→ body turns to lipids for fuel

→ ↑ lipid deposits in liver and skeleton

→ obesity

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24
Q

What are the clinical manifestations of T2DM?

A
  • often asymptomatic
  • often non-specific symptoms
  • Fatigue
  • Recurrent infections
  • Candida infections (fungal yeast infections)
  • Prolonged healing
  • Vision changes - blurred vision, cataracts, retinopathy
  • Paraesthesia - neuropathies from nerve degeneration and delayed conduction for example, peripheral neuropathy is altered sensation of the hands and feet

Some can experience the clinical manifestation associated with T1DM
polydipsia
polyuria
polyphagia

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25
Q

What is the treatment and management of T2DM?

A

First line management of T2DM is lifestyle changes

  • healthy diet - restrict calories, low fat, low glycaemic index foods
  • increase exercise
  • weight loss - improves glucose tolerance, insulin resistance decreases
  • cease smoking

Oral DM management agents - glucose lowering oral medications

50% of individuals with T2DM will require insulin within 10 years of diagnosis

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26
Q

What are the diagnostic levels for DM?

A

Fasting blood test= ≥ 7 mmol/L

Random BGL= ≥ 11.1mmol/L

Oral glucose tolerance test= ≥ 11.1mmol/L

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27
Q

What ais Hb1Ac?

A

As glucose circulates in the blood, some of it binds to haemoglobin which becomes haemoglobin A1c (HbA1c).

  • The amount of HbA1c formed is directly related to the amount of glucose in the blood.

Because red blood cells live for 3-4 months (90 - 120 days), HbA1c levels do not change quickly. Therefore the HbA1c level reflects the average amount of blood glucose during the last 2-3 months.
↑ blood glucose = ↑ HbA1c.

Therefore, uncontrolled DM → ↑ blood glucose levels → ↑ HbA1c levels.

What is the purpose of HbA1c?

  • Diagnosis of both T1DM and T2DM
  • To monitor progress
  • Aid treatment decisions.
    - If treatment plans have been changed or DM is considered unstable = Hb1Ac is tested every 3-4 months
    - IIf DM is stable = Hb1Ac is tested twice per year
28
Q

what is mmol/L

A

millimoles per liter of Blood glucose

29
Q

What are the ranges of BGL?

What is considered hypo and hyper?

A

Target ranges may differ depending on age, type of diabetes, duration of diabetes, the type of medication prescribed and co-morbidities.

Normal BGL= 4.0 – 8mmol/L
Hypo= <3.9mmol/L
Hyper= ≥ 14mmol / L

30
Q

How frequently should BGLs be tested?

A

as per facility policy

  • 4x daily
  • 4-6 hourly if patient is on continuous feeds
  • hourly if on continous insulin infusion until 3 consecutive stable readings are obtained. then check every 2/24
  • 10-15mins during hypogylcemia
31
Q

When must ketones be checked?

A

Blood ketones must be checked if:

  • T1DM is suspected
  • Diabetic Ketoacidosis (DKA) is suspected
  • Hyperglycaemia (>14mmol/L) is persistent (either T1DM or T2DM and insulin deficient)
32
Q

Explain the glycemic index

A

The glycemic index or GI ranks carbohydrates according to their effect on blood glucose levels. The lower the GI, the slower the rise in blood glucose levels will be when the food is consumed. The effect may differ from person to person.

  • reccomended that diabetucs have moderate carbs but lots of high fibre and low GI foods for stable BGLs

Some research has shown that by eating a diet with a lower GI, people with diabetes can reduce their average blood glucose levels. This is important in reducing the risk of developing diabetes-related complications.

33
Q

What are the management goals for DM?

A
  • restore normal blood glucose levels = euglycaemia

- correct related metabolic disorders

34
Q

Explain a nursing assessment on a patient with diabetes

A

Primary assessment
If not already performed = airway, breathing, circulation, disability (mental status assessment)

Secondary Assessment
General appearance = looks well/unwell, discomfort, skin colour = pallor, flushed face
Full set of vital signs
BGL - including ketones if BGL level is high
Hydration assessment - oral mucosa, skin turgor

Focused Assessment - for example, respiratory assessment if the patient is hyperglycaemic
Inspection, auscultation, palpation and percussion
Smell the patient’s breath - is it sweet / acetone smelling?

Additional Assessment Essentials
Urine assessment = urinalysis, colour, sediment, odour
Fluid balance = input and output
Weight
Skin integumentary assessment = look for wounds and breaks in the skin, infections, dry skin, discolouration including erythema, bruising and document all findings
Falls risk assessment = people with peripheral neuropathy will have increased risk of falls

35
Q

What are some nursing care considerations for someone with DM?

A

Start discharge planning early and adhere to Organisation guidelines -

  • when to take BGL
  • care of wounds
  • National Standard documents
  • falls risk assessment
  • skin integrity assessments
  • fluid balance chart

Follow Medical advice regarding medication
Escalate care promptly if there are any concerns or patient deterioration

36
Q

Explain some key points of promotion and prevention for DM

A 
Identify and monitor patients at high-risk of instability or complications, e.g.
- pre - post operative stages
- critically unwell
- with infections
- who are stressed
have poor understanding of their condition
- that can not self manage appropriately
- with chronic complications of DM

Ensure

  • adequate and targeted education
  • your patient can self-care to actively manage their diabetes
  • your patient can adjust their lifestyle choices to maximise blood glucose stability

Routinely monitor and reassess patients, e.g., BGL as per Organisation regime and intake and output

Undertake patient assessments each shift

37
Q

What pre opertaive cautions need to be taken for a patient with DM?

A

a patient with DM can potentially have blood glucose instability due to factors such as the fasting requirements

Nursing management can be complex
- pay particular attention to medicaion administration and timing of this

38
Q

Explain so interprofessional year considerations that may need to occur to ensure a holistic and effective care of someone with DM

A

Nursing team

  • accurate documentation
  • ISBAR handover
  • discuss concerns and progress

Diabetes educator
- to ensure comprehensive patient education and ongoing care direction remains person-centered

Liaise with treating medical team (documentation and verbal discussion)

  • how often to perform BGLs
  • dose adjustments of medications
  • results of diagnostics e.g. urinalysis
  • fluid maintenance
  • red flags with assessment: changes to urinalysis, abnormal vital signs, abnormal BGLs, MET call criteria
  • referrals to Specialist care, e.g., Endocrinologist
  • summaries to General Practitioner

Pharmacist
- education on current medication management

Allied health

  • Occupational Therapist= falls prevention
  • Podiatrist= essential for ongoing foot care and prevention of diabetic foot disease

Physiotherapist / Exercise Physiologist

Dietician

  • nutritional needs - balanced diet = low sugar, low glycaemic index, low fat
  • electrolyte balances
  • fluid balance

Social worker

  • anxiety
  • family support
  • home support

Wound nurse
- management of wound and guidance on appropriate dressings

39
Q

Define hypoglycemia

A

Hypoglycaemia refers to low blood glucose levels.

Occurs when there is too much insulin in proportion to available blood glucose and blood glucose levels drop to less than 4 mmols/L

40
Q

What causes hypoglycemia

A
  • Imbalance between blood glucose and insulin. For example - mismatched food intake with diabetic medications
  • Reduced food intake
  • poor timing intake of food
  • Increased exercise
  • Dehydration
  • Illness
  • Stress
  • Medications / Drugs
  • Surgery
41
Q

What are some clinical manifestations of Dm?

A
  • Confusion
  • altered conscious state
  • combative and agitated state
  • difficulty speaking
  • visual disturbances
  • seizures
  • coma
  • death
42
Q

Explain the management of hypoglycemia

A
  • escalate the care e.g. a MET (Medical Emergency Team) call or notifying the nurse in charge depending on the level of blood glucose.
  • can be quickly reversed wit effective treatment
  • If the blood glucose level is less than 4.0 mmol/L, immediately begin treatment for hypoglycaemia.
  • If the blood glucose is 4.0mmol/L or greater, investigate other possible causes of the signs and symptoms.
  • note that each hospital will have their own protocol to identify the management of hypoglycaemia.
43
Q

Explain the management of hypoglycemia in a conscious patient

A

Refer to the national Insulin chart for protocol or hospital policy.

  • Administration of 15–20 grams of quick-acting carbohydrate (e.g. 150 mL of soft drink, 8–10 jelly beans, 1 tablespoon of syrup or honey, 4 teaspoons of jam, 120 mL juice, commercial glucose [per label instructions])
  • Check blood glucose levels after 15 minutes
  • Repetition of quick-acting carbohydrate administration after 15 minutes if no improvement in blood glucose
  • Administration of additional food of longer-acting carbohydrate (e.g. slice of bread, dry biscuits) after symptoms subside
  • Immediate notification of healthcare provider or emergency service (if patient outside hospital) if symptoms do not subside after two to three administrations of quick-acting carbohydrate
44
Q

Explain the management of hypoglycemia in a worsening or unconscious patient

A
  • Subcutaneous or intramuscular injection of 1 mg glucagon
  • Intravenous administration of 50 mL 50% glucose
  • Determine cause of hypoglycaemia (after correction of condition)
45
Q

Briefly explain diabetic ketoacidosis

A

Occurs by sever hyperglycaemia and ketoanaemia, acidosis and sever dehydration.

  • increased metabolism of fat + proteins because body cant metabolism glucose for energy.
  • fat releases chemical by product called ketones
  • pH drops
  • ketoacidosis
  • buffering system triggered to compensate for imbalance
  • resp compensation

Symptom include;

  • deep rapid resp rate
  • fruity breath
  • ketonaturia
  • diabetic coma
  • death
46
Q

Briefly explain hyperosmolar hyperglycaemic state (HSS)

A
  • Patients with T2DM can become severely hyperglycaemic with high osmolarity as a direct result of a physiological stress such as an acute infection or, for example, an episode of dehydration. With HHS, there are no blood ketones present, so the patient will not exhibit signs of acidosis.

Associated symptoms are usually subtle and occur over a period many weeks which contributes to ongoing osmotic dehydration. This results extreme dehydration, lethargy and confusion eventually leading to seizures, altered conscious state, coma and death.

47
Q

What can hyperglycaemia over long periods of time cause?

A 
Complications with;
- nervous system 
- sensory issues 
- Cardio vascular issues 
- msk issues 
skin issues 
immune issues
48
Q

Explain diabetic foot disease

A

DFUs can be defined as;

  • ulceration
  • infection
  • ischaemia
  • neuro-arthropathy of the foot in people with diabetes and who have developed peripheral neuropathy, peripheral arterial disease or have a history of previous foot disease.

Peripheral neuropathy
- results in paraesthesia of hands and feet.

loss of protective sensation (e.g. standing on something but not realising its sharp)= leads to increased risk of infection
- this leads to the development of foot ulcers

Diabetic foot ulcers (DFUs) result in poor patient outcomes, posing a major burden on quality of life, significant risks to morbidity and mortality, and increased healthcare costs.

49
Q

How are DFUs classified?

A

SINBAD

Site 
Ischemia 
Neuropathy 
Bacterial infection 
Depth
50
Q

What are some key points of education for a patient with a DFU?

A
  • Importance of appropriate footwear and foot care
  • Establish a regular self-monitoring schedule (including visual checks)
  • Develop an action plan to respond to early problems (for example, skin breakdown).
  • Importance of annual foot screens to assess their risk of foot ulceration
  • When to return for further footwear advice if their foot risk status increases should be emphasised
51
Q

What are the 6 key elements for prevention of DFP

A
  1. Assess all people with diabetes and determine their risk of developing foot complications
  2. Perform regular focused assessments on the feet of high-risk people
  3. Education of the patient and their support persons
  4. Routine wearing of appropriate footwear, including well fitting shoes and socks
  5. Treatment of pre-ulcerative signs
  6. Early referrals to the interprofessional team
52
Q

What should the focus of care be for someone with DFU?

A
  • Relief of pressure and protection of the ulcer
  • Restoration of skin perfusion
  • Treatment of infection
  • Metabolic control and treatment of co-morbidity
  • Local wound care
  • Education for patient and their support persons
53
Q

What factors should be considered when choosing a dressing for a DFU?

A
  1. Type of dressing required to promote wound healing
  2. Dressing should be comfortable - to prevent increased pain or discomfort
  3. Infection management as required
  4. Frequency of dressing change
  5. If the person is managing their wound at home - access to dressings may influence choice of dressing
54
Q

Describe the adrenal gland and its function

A
  • small glands found at the top of each kidney
  • vital role in several key body functions such as metabolism, stress response, sex function, immune response and blood pressure regulation.
55
Q

Describe Cushing syndrome

A

A group of manifestations caused by the chronic exposure of excessive circulating levels of the hormone cortisol (hypercortisolism)

56
Q

What can cause Cushing syndrome?

A
  • exogenous cortisole (medicine)
    e. g. use of steriod medication to treat stuff like asthma and rheumatoid arthritis
  • Adrenal tumours (cells of the adrenal cortex divide rapidly and secrete excess cortisole)
  • pituitary adenoma (benine tumor)= this is crushing disease= secretes to much adrenocortiotropic hormone which over stimulates adrenal glands and causes the increased release of cortisole
  • lung cancer
  • pancreatic cancer
  • Long term administration of exogenous steroids
    - such as prednisolone resulting in a ‘cushingoid appearance’ = reversible once steroids treatment is ceased BUT this must be done gradually or it can result in acute adrenal insufficiency

Gradual withdrawal from high dose steroid therapy is necessary as it allows the anterior pituitary gland the opportunity to secrete increasing amounts of adrenocorticotropic hormone (ACTH), which stimulates the adrenal glands to secrete cortisol.

57
Q

What are the symptoms of cushing syndrome?

A

Any condition that causes the increased levels of cortisol

Can be
Exogenous= drug related
Endogenous= adrenal tumor or excess ACTH (this is called crushing disease) or from an ectopic site

  • directly related to the effcts of excess cortisole on its target tissues
    e.g
  • muscle waisting and thinning
  • easy bruising
  • abdominal striae
  • truncal obesity ‘- buffalo hump (hump of fat on shoulder)
  • full moon shaped face
    Hyperglycemia- can lead DM, hypertension, CVD
  • increased chnace of infection
58
Q

How is cushing syndrome diagnosed?

A
  • Cortisol levels
  • Dexamethasone suppression test
  • Saliva swab for cortisol levels
  • 24-hour urine collection testing for elevated levels of few cortisol, normal levels is 80-120mcg/24 hours

Can get false positive results with individuals who drink large amounts of alcohol daily or who take certain medications such as phenytoin or rifampicin

  • measuring free cortisone in a 24hr urine sample
  • blood or saliva late an night check if there is a normal daily rise and fall in cortisole
  • Dexamethasone supression test= low does of this exogenous steroid that supressess ACTH production which should cause decreased cortisole levels
    - if this is positive the exact cause of exogenous cortisole must be found
  • ACTH plasma levels acn be checked
    Low ACRH plasma= adrenal adenomoas + carcinomas
    High ACTH plasma= crushing disease + ectopic acth production
    - injection of dexamethasone to see if ectopic sites respone

Imaging

  • MRI of pituitary gland
  • CT of adrenal
  • CT of chest, abdomen, pelvis if there seems to be an etopic site of ACTH production
59
Q

Explain the treatment of Cushing syndrome syndrome

A

Goal= treat the underlying cause

If due to exogenous medis
- slowly redunong the med and getting rid of it (avoiding withdrawals)

If due to pituitary adenoma
- surgical removal of adenoma may be neccessary

Adrenal steroid inhibitors
- in eptopic or spreach adrenal carcinomas.

  • Surgery is required to treat tumours
  • Radiotherapy can also be considered
  • Gradual tapering of dose and discontinuation of exogenous steroids
60
Q

Explain Adrenocorticol insufficiency

A
  • the hyposecretion of hormones of the adrenal or pituitary gland
  • either primary insufficiency = addisons disease
  • secondary insufficiency
61
Q

Explain primary adrenal insufficiency including the cause

A

aka Addisons disease
- Occurs from a disorder of the adrenal gland where they can no longer secrete the adrenal hormones

Cause:

  • 80% of cases caused by an autoimmune response = adrenal tissue destroyed by antibodies
  • 20% of cases caused by conditions of physical stress such as tuberculosis, trauma, surgery or cancer
62
Q

Explain secondary adrenal insufficiency including the cause

A

Occurs because the pituitary gland does not make enough adrenocorticotrophic hormone (ACTH) which results in deficiency of corticosteroids

  • More common than primary insufficiency

May be caused by

  • Pituitary disease, OR
  • Suppression due to exogenous corticosteroid administration
63
Q

Explain the complications of adrenal insufficiency aka Addison’s crisis

A

Addison’s crisis

  • Life-threatening complication secondary to critically low blood cortisol levels
  • Results when normal glucocorticoid medications are suddenly withheld, OR
  • During acute episode physiological changes such as vomiting, diarrhoea, infection, trauma, stress, surgery
  • Early intervention essential in preventing critical deterioration

Symptoms are usually severe and include:

  • mental status changes, such as confusion, fear, restlessness, agitation, delirium
  • visual and auditory hallucinations
  • loss of consciousness
  • high fever
  • sudden pain in the lower back, abdomen, or legs
  • death
64
Q

What are some symptoms of Addison’s disease?

A
  • Hyperpigmentation
  • hypotension
  • weakness
  • weight loss
  • nausea
  • vomiting
  • constipation
  • abdominal pain
  • vitiligo

Adrenal crisis

  • fever
  • syncope
  • convulsions
  • hypoglycemia
  • hyponatremia
  • sever vomiting and diarrhea
65
Q

How is Addisons disease diagnosed?

A

Grouping of subjective and objective data obtained from key clinical manifestations and physical assessment

  • ACTH stimulation test = cortisol levels in the blood and/or urine after a dose of a synthetic stimulating hormone ACTH is administered
  • Serum cortisol levels = will be decreased
  • Serum ACTH levels
  • Electrolytes = hyponatraemia, hyperkalaemia
  • Glucose levels = -Hypoglycaemia
  • 24-hour urine collection testing for decreased cortisol levels, normal level is 80-120mcg/24 hours

CT or MRI of pituitary or adrenal galnd

66
Q

What is the treatment and management of adrenocortical insufficiency?

A

Primary goal= to normalise hormone secretion with treatment focusing on the management of the underlying cause.

First line management is hormone replacement:

    - Daily glucocorticoid replacement therapy such as hydrocortisone / prednisolone = higher doses will be needed when stressed or unwell to prevent Addison's Crisis
    - Daily mineralocorticoid in the morning such as fludrocortisone

If unwell, the patient will require admission for the following until electrolyte imbalances are resolved, blood pressure has normalised and the patient stabilised.

    - high-doses of hydrocortisone
    - shock therapy
    - fluid replacement with normal saline and 5% dextrose
67
Q

Describe the thyroid gland

A

a butterfly shaped gland that sits at the front of the neck, below the prominence of the thyroid cartilage; sometimes called the Adam’s apple.

uses iodine from the diet to make two main hormones that regulate vital bodily functions such as metabolism, energy, growth and development. These hormones are:
Triiodthyronine (T3)
Thyroxine (T4)

The hypothalamus and the pituitary gland (in the brain) communicate with the thyroid gland to maintain T3 and T4 balance.

The hypothalamus produces thyroid releasing hormone (TRH) that signals the pituitary to tell the thyroid gland to produce more or less of T3 and T4 by either increasing or decreasing the release of a hormone called thyroid stimulating hormone (TSH).

When T3 and T4 levels are low in the blood, the pituitary gland releases more TSH to tell the thyroid gland to produce more thyroid hormones.
If T3 and T4 levels are high, the pituitary gland releases less TSH to the thyroid gland to slow production of these hormones.

NUR2226 (9 decks)

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