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Unit 10 > Week 4: Endocrine 2 > Flashcards

Week 4: Endocrine 2 Flashcards

(69 cards)

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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
What are the key clinical features of Graves disease?
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)
26
What is graves opthalmopathy?
(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.
27
How common is graves opthalmopathy?
Affects 50% of patients with Graves, it is more commonly seen in smokers, follows separate time course to thyroid disease.
28
What are the symptoms of Graves opthalmopathy as it progresses?
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
What are the potential treatments for Graves opthalamopathy?
Lubrication - artificial tears Selenium - antioxidant effect IV methylprednisolone - suppress autoimmune reaction Orbital radiotherapy Surgery
30
What is toxic multinodular goitre/ Plummers disease?
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
What is toxic adenoma hyperthyroidism?
More common in young patients Functioning nodule secreting T3 and T4 Infiltrative ophthalmology is never present Almost always benign
32
What investigations will you do is suspected hyperthyroidism?
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
What are the different management lines from hyperthyroidism?
Pharamcological Radioactive iodine - destroys cells in the thyroid gland Surgery (hemithyroidectomy and thyroidectomy)
34
What are the pharmacological treatments for hyperthyroidism?
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
Potential complications of thyroidectomy?
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
What is thyroid storm?
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
What are the symptoms of thyroid storm?
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
What are the risk factors for thyroid storm?
Acute infection Recent surgery or RAI Withdrawl of antithyorid drugs
39
What is hypothyroidism? What re the different types?
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
How common is hypothyroidism?
1-4 per 100 people in the UK 10 times more common in females.
41
What are the common causes of primary hypothyroidism?
Hashimoto disease Thyroidectomy Iodine deficiency Drugs - lithium and iodine.
42
What are the common causes of secondary hypothyroidism?
Hypopituitarism Congenital
43
How can you distinguish between primary and secondary hypothyroidism on a thyroid function test?
primary - decreased T4/3, elevated TSH Secondary - decreased TSH, decreased T4/T3
44
What are the symptoms of hypothyroidism?
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
What are the common treatments of hypothyroidism?
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
What is myxoedema coma?
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
What are the treatments for myoxedema coma?
IV levothyroxine Electrolyte imbalances and hypothermia should also be addressed
48
What are the embryological origins of different components of the adrenal gland?
Cortex - from mesoderm Medulla - from neural crest cells
49
What are the different section of the adrenal gland?
Capsule Cortex - zona glomerulosa - zona fasciculata - zone reticularis Medulla
50
What is secretes by the renal medulla?
Catecholamines - noradrenaline and adrenaline
51
What hormones are secreted by the zona glomerulosa? (cortex)
Aldosterone and other mineralcorticoids
52
What hormones are secreted by the zona fasiculata? (cortex)
Mainly glucorticoids (cortisol) Some androgens
53
What hormones are secreted by the zona reticularis? (cortex)
Mainly androgens (testosterone and oesotrgen) Some glucorticoids.
54
What is the function of aldosterone?
Increase renal Na+ absorption Increase renal K+ secretion Increase H+ secretion
55
What is the function of cortisol (glucocorticoid)?
Stimulate gluconeogenesis Inhibit inflammatory responses Suppress immune response Enhance vascular responsiveness to catecholamines
56
What is the function of androgens?
Bone density Puberty Sexual function
57
What are the features of the Hypothalamic Pituitary Adrenal Axis?
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
What are the common causes of cushing syndrome?
Endocrine disorder - increased cortisol levels Ectopic ACTH secretion Adrenal cortisol excess Exogenous steroids Pituitary ACTH excess
59
What are the causes of Cushing disease?
Pituitary ACTH excess Form of Cushing syndrome
60
What are the symptoms of Cushing syndrome?
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
How do you investigate for cushing syndrome?
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
How do you treat cushings syndrome medically?
Adrenal enzyme inhibitor - metyrapone; 11beta-OH inhibtor - ketoconazole (anti-fungal) P450 enzyme inhibitor - Mitotane; inhibits side chain cleave and direct toxic effectt
63
How do you treat Cushing syndrome surgically?
Trans sphenoidal surgery Bilateral adrenalectomy Radiotherapy
64
What is Addisons disease an example of? On endocrine level
Primary Adrenal Insufficiency
65
What is Addisons disease?
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
What are the treatments for addison disease?
Replace the missing hormones
67
Who is Addisons disease most common in?
Women between 30 and 50yrs old
68
What are the common causes of secondary adrenal insufficiency?
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
What are the differentiating symptoms between primary and secondary adrenal insufficiency?
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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