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Unit 10 > Week 4: Endocrine 2 > Flashcards

Week 4: Endocrine 2 Flashcards

1
Q

What does the thyroid gland develop from?

A

The 1st and 2nd pharangeal pouches near the base of the tongue.

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2
Q

How do the thyroid gland and parathyroid gland contribute to calcium level regulation?

A

Parathyroid glands secrete parathyroid hormone - increases blood calcium ions, encourages release of calcium ions from the bone by stimulating osteoclasts
Thyroid gland parafollicular cells - secretes calcitonin, encourages movement of calcium ions from the plasma to the bone, inhibits osteoclasts and decrease renal calcium ion secretion

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3
Q

What are the main microscopic compoenents of the thyroid gland?

A

Follicular cells
Parafollicular cells
Colloid

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4
Q

What is colloid?

A

Found between follicular cells in the thyroid gland
Is mainly thyroglobulin and iodine - used in production of thyroid hormones

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5
Q

What are the different hormones secretes by the thyroid gland?

A

Thyroxin (t4) - 90%
Triiodothyronine (t3) - 9%
Reverse T3 - 1%
And parafollicular cells secrete calcitonin

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6
Q

What are the different types of T4?

A

Free - active form, able to enter tissue, 99% of T4
Bound - bound to thyroid binding globulin (TBG), often for storage in colloid, is inactive and unable to enter tissue

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7
Q

What enzyme converts T4 to T3?

A

Deiodinase enzyme

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8
Q

What are the effects of thyroid hormone on the cardiovascular system?

A

Promote normal cardiac output
Maintain heart rate and stroke volume

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9
Q

What are the effects of thyroid hormone of the neurological system?

A

Increase synapsis
Increase myelination
increase dendrites

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10
Q

What are the effects of thyroid hormone on the GIT?

A

Promote normal GIT motility and secretions

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11
Q

What are the effects of thyroid hormone of bones?

A

Maintain normal bone growth and maturation

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12
Q

What are the effects of thyroid hormone on skin?

A

Proliferation of skin cells
Hair and Nail growth
Skin hydration

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13
Q

What are the effects of thyroid hormone of metabolism?

A

Increased oxygen usage
Lipolysis
heat production
Glycolysis
LDL uptake
Increase BMR

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14
Q

What is the hypothalamic pituitary thyroid axis?

A

Stimulis to the hypothalamus causes it to release TRH.
THis travels to the anterior pituitary gland by the hypothalamic hypophysial vessels.
Stimulates thyrotropes to secrete TSH
TSH acts on the thyroid gland to secrete T3 and T4
T3 and T4 provide negative feedback to the hypothalamus and the pituitary gland to decrease TRH and TSH.
T3 and T4 travel and act on target tissue.

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15
Q

What part of thyroglobulin is iodinated?

A

Tyrosine residues - can gain one or two iodines.

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16
Q

What are the key processes in thyroid hormone production?

A

Trasnport of thyroglobulin and iodide into colloid
oxidation of iodide to iodine
Iodination of thyroglobulin
Coupling
Secretion of thyroid hormones

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17
Q

Describe how thyroid hormones are secreted from the colloid?

A

T3 and T4 are bound to thyroglobulin
Are endocytosed into the follicular cell
Exocytosed into the bloodstream - majority associated with thyroxine binding globulin in the blood stream now known as bound T3/4

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18
Q

Define hyperthyroidism

A

Overactive thyroid gland - specific disorder in which the thyroid gland produces an excess amount of thyroid hormone

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19
Q

Define thyrotoxicosis

A

Wider medical term used to describe when the body has an excess of thyroid hormones, due to any cause (including hyperthyroidism)

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20
Q

What are the common causes of primary hyperthyroidism?

A

Graves disease
Toxic adenoma
Toxic multinodular goiter

Also thyroid cancer and drugs (iodine excess)

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21
Q

What are the common causes of secondary hyperthyroidism?

A

Pituitary adenoma
Gestational thyrotoxicosis

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22
Q

How can you differentiate between primary and secondary hyperthyroidism on a thyroid function test?

A

Primary - low TSH and high T4/T3
Secondary - High TSh and high t4/t3

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23
Q

What are the symptoms of hyperthyroidism?

A

Memory tip: sweating
Sweating
Weight loss
Emotional lability (strong mood swings)
Appetite increased
Tremor and tachycardia
Intolerance of heat, irregular menstration, irritability
Nervousness
Goiter (enlarged gland) and GI problems

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24
Q

What is Graves disease?
Cause?

A

Also known as diffuse toxic goiter
Autoimmune disease of thyroid
Most common hyperthyroidism in the UK
Caused by increased levels of auto-antibodiy thryoid stimulating hormone receptor antibodies.

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25
Q

What are the key clinical features of Graves disease?

A

Normally age 20-40yrs
- thyroid eye disease/graves ophtlamopathy/exophthalmos
- thyroid acropachy - appears as clubbing or swelling of digits (increased bone formation)
- dermopathy - thickening of skin lower tibia and odema pre-tibia (overproliferation of skin cells)

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26
Q

What is graves opthalmopathy?

A

(TRAb)TSH receptor antibodies bind to TSH receptor antigen. TSH receptor antigen on thyroid gland is thought to be similar to proteins found on orbital fibroblast, allow cross reactivity.
Activate T cell when exposed to antigen to secrete cytokines.
Activate fibroblast GAG deposition leading to increasing tissue around the back of the eye, GAG also cause swelling by trapping water, causing the eye to buldge forward.
In some cases there is also an increase in adipose tissue around the back of the eye.

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27
Q

How common is graves opthalmopathy?

A

Affects 50% of patients with Graves, it is more commonly seen in smokers, follows separate time course to thyroid disease.

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28
Q

What are the symptoms of Graves opthalmopathy as it progresses?

A

NO SPECS
N; no signs/symptoms
O: only occular irritation
S: soft tissue involvement (conjunctival odema or infection)
P: proptosis
E: extraocular muscle involvement
C: corenal exposure and ulceration
S: sight loss (as compressed nerve)

29
Q

What are the potential treatments for Graves opthalamopathy?

A

Lubrication - artificial tears
Selenium - antioxidant effect
IV methylprednisolone - suppress autoimmune reaction
Orbital radiotherapy
Surgery

30
Q

What is toxic multinodular goitre/ Plummers disease?

A

Second most common type of hyerthyroidism in the UK
Most common in the middle aged or eldery
Long standing goitre
Iodine deficiency
Opthalmopathy is extremely rare
Lorge nodular goitre - may extend retrostrenal
may be present for many years

31
Q

What is toxic adenoma hyperthyroidism?

A

More common in young patients
Functioning nodule secreting T3 and T4
Infiltrative ophthalmology is never present
Almost always benign

32
Q

What investigations will you do is suspected hyperthyroidism?

A

Serum TSH and T4/T3 to confirms and determine if primary or secondary
Test for autoimmune cause:
TSHR-ab in graves disease and others
Thyroid stimulating immunoglobulin in graves disease
Thyroid peroxidase antibodies (inhibitory) found in Hashimoto autoimmune disease

33
Q

What are the different management lines from hyperthyroidism?

A

Pharamcological
Radioactive iodine - destroys cells in the thyroid gland
Surgery (hemithyroidectomy and thyroidectomy)

34
Q

What are the pharmacological treatments for hyperthyroidism?

A

Thioamides - inhibit TPO - such as carbimazole or propylthiouracil
Beta blockers - reduce cardiovascular complications
Calcium ion channel blockers - given if can not tolerate beta blockers

35
Q

Potential complications of thyroidectomy?

A

Hoarsness of voice - potential paralysis of vocal cords - if damage to recurrent laryngeal nerves
Transient hypocalcemia - due to damage leading to transient low activity of parathyroid glands.

36
Q

What is thyroid storm?

A

Also known as thyrotoxic crisis
Is an acute life-threatening complication of hyperthyroidism
Rare but potentially life-threatening
Rapid and high spike in thyroid hormones
Diagnositic criteria is at least 1 CNS complication and two other symptoms

37
Q

What are the symptoms of thyroid storm?

A

CNS manifestations - restlessness,delirium, psychocis and coma
Fever - 38 degrees or higher
Tachycardia 130bpm or higher and atrial fibrillation
Chronic heart failure (pulmonary odema and cardiogenic shock)
GIT manifestation (nausea, vomiting and diarrhea)

38
Q

What are the risk factors for thyroid storm?

A

Acute infection
Recent surgery or RAI
Withdrawl of antithyorid drugs

39
Q

What is hypothyroidism?
What re the different types?

A

An endocrine condition caused by a deficiency in thyroid hormone
Primary - thyroid gland too little TH
Secondary - pituitary too little TSH
Tertiary - hypothalamus too little TRH

40
Q

How common is hypothyroidism?

A

1-4 per 100 people in the UK
10 times more common in females.

41
Q

What are the common causes of primary hypothyroidism?

A

Hashimoto disease
Thyroidectomy
Iodine deficiency
Drugs - lithium and iodine.

42
Q

What are the common causes of secondary hypothyroidism?

A

Hypopituitarism
Congenital

43
Q

How can you distinguish between primary and secondary hypothyroidism on a thyroid function test?

A

primary - decreased T4/3, elevated TSH
Secondary - decreased TSH, decreased T4/T3

44
Q

What are the symptoms of hypothyroidism?

A

MOMS SO TIRED
memorly loss
Obesity
Malat flush/menorrhagia
Slowness (mentally and physically)
Skin and hair dryness
Onest gradual
Tiredness
Intolerance to cold
Raised BP
Energy level falls
Depression/ delayed relaxation of reflexes

45
Q

What are the common treatments of hypothyroidism?

A

Replacement of thyroxine
a) levothyroxine - synthetic T4 - typically start at 1.6mcg/kg with a TSH target of 0.4-4.5mU/L
Doste is triturated up and down by 25mcg as needed, TSH levels are checked every 2-3 months then yearly once stabilises

46
Q

What is myxoedema coma?

A

Severe complication of untreated and severe hypothyroidism
Rare and life-threatening
Patients are hypoglycemia, hypothermic, hyponatremia, hypoxia and hypercabia, bradycardia and demonstrate cognitive decline
Symptoms include: hair loss, receeding hair line, dry skin, corse skin and thin brittle nails and nonpittingodema (commonly seen in the feet)

47
Q

What are the treatments for myoxedema coma?

A

IV levothyroxine
Electrolyte imbalances and hypothermia should also be addressed

48
Q

What are the embryological origins of different components of the adrenal gland?

A

Cortex - from mesoderm
Medulla - from neural crest cells

49
Q

What are the different section of the adrenal gland?

A

Capsule
Cortex
- zona glomerulosa
- zona fasciculata
- zone reticularis
Medulla

50
Q

What is secretes by the renal medulla?

A

Catecholamines
- noradrenaline and adrenaline

51
Q

What hormones are secreted by the zona glomerulosa? (cortex)

A

Aldosterone and other mineralcorticoids

52
Q

What hormones are secreted by the zona fasiculata? (cortex)

A

Mainly glucorticoids (cortisol)
Some androgens

53
Q

What hormones are secreted by the zona reticularis? (cortex)

A

Mainly androgens (testosterone and oesotrgen)
Some glucorticoids.

54
Q

What is the function of aldosterone?

A

Increase renal Na+ absorption
Increase renal K+ secretion
Increase H+ secretion

55
Q

What is the function of cortisol (glucocorticoid)?

A

Stimulate gluconeogenesis
Inhibit inflammatory responses
Suppress immune response
Enhance vascular responsiveness to catecholamines

56
Q

What is the function of androgens?

A

Bone density
Puberty
Sexual function

57
Q

What are the features of the Hypothalamic Pituitary Adrenal Axis?

A

Hypothalamus releases CRH travels down the hypothalmic-hypophyseal portal vessels binds to receptors on corticotrophes in the anterior pituitary gland
Cortictrophes secretes ACTH which travels in the blood to the adrenal cortex and causes cortisol secretion.

58
Q

What are the common causes of cushing syndrome?

A

Endocrine disorder - increased cortisol levels

Ectopic ACTH secretion
Adrenal cortisol excess
Exogenous steroids
Pituitary ACTH excess

59
Q

What are the causes of Cushing disease?

A

Pituitary ACTH excess

Form of Cushing syndrome

60
Q

What are the symptoms of Cushing syndrome?

A

MOON FACIES
menstrual disorders and moon faces
Osteopenia or osteoporosis
Obesity
Neurosis (depression of psychosis)
face
Altered muscle physiology
Supra-clavicular and dorsa-cervical fat (buffalo hump)
Infection
Elevated blood pressure
Skin (easy bruising)

61
Q

How do you investigate for cushing syndrome?

A

Test 24 hour free cortisol or on low dose dexamethasone suprresion
Measure cortisol levels: is between 3.5-44ug/d in free and below 2ug on dexamethsone is considered normal
Is abdnormal - then investigate for cause of decrease
Is ACTH is decreased - adrenal tumour
If ACTH increased - pituitary or ectopic

62
Q

How do you treat cushings syndrome medically?

A

Adrenal enzyme inhibitor
- metyrapone; 11beta-OH inhibtor
- ketoconazole (anti-fungal) P450 enzyme inhibitor
- Mitotane; inhibits side chain cleave and direct toxic effectt

63
Q

How do you treat Cushing syndrome surgically?

A

Trans sphenoidal surgery
Bilateral adrenalectomy
Radiotherapy

64
Q

What is Addisons disease an example of?
On endocrine level

A

Primary Adrenal Insufficiency

65
Q

What is Addisons disease?

A

Autoimmune destruction of adrenal cortex
Causes loss of
Glucocorticoids = hypoglycemia, anorexia, weight loss, nausea and vomiting
Mineralcorticoids = hyperkalemia, metabolic acidosis, hypotension
Adrenal androgens = decreased pubic and axillary hair and decreased libido

Key features = bronze pigmentation of skin due to increase ACTH stimulating melanocyte stimulating hormone

66
Q

What are the treatments for addison disease?

A

Replace the missing hormones

67
Q

Who is Addisons disease most common in?

A

Women between 30 and 50yrs old

68
Q

What are the common causes of secondary adrenal insufficiency?

A

Disorder of the adrenal gland - decreased levels of ACTH leading to decreased production of glucocorticoids and androgens from adrenal gland (although adrenal gland is structurally intact)

Bening pituitary tumour
inflammation
Previous pituitary surgery
People who take corticosteroids to treat other conditions, or when stop taking altogether rather than tapering off

69
Q

What are the differentiating symptoms between primary and secondary adrenal insufficiency?

A

Secondary - don’t have hyperpigmentation, less likley to be severely dehydrated and more likely to have hypoglycemia.

Unit 10 (37 decks)

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