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PH2501- pharmacology > 36-Thyroid gland: disorders and treatment > Flashcards

36-Thyroid gland: disorders and treatment Flashcards

1
Q

The thyroid gland

A

-Endocrine gland
-Synthesises, stores and secretes the thyroid hormones, T3 and T4
+T3= Tri-iodothyronine
+T4= Tetra-iodothyronine (thyroxine)
-Thyroid hormones increases basal metabolic rate
+Essential for growth and development: Cretinism= infant hypothyroidism
+Essential for healthy life

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2
Q

Essential stages of T3/T4 secretion

-See iodination (organification of tyrosine first

A

-Iodine uptake into cell
+Active transport by carrier
-Iodination of tyrosine residues on thyroglobulin (TG)
+By thyroperoxidase enzyme
+Called organic binding
-Formation of T3 and T4 from MIT and DIT
-Endocytosis of TG, enzymatic release of T3 and T4, secretion

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3
Q

Action of thyroid hormone

A

Affecting growth and development
-Direct and indirect action on cells
+Potentiates secretion and effects on growth hormone
-Needed for normal skeletal development and maturation of CNS
-Act by entering cell nucleus, T3 binds to receptor and switches it OFF
+Receptors normally STOPS transcription
+SO T3 causes increase mRNA and protein synthesis in cells
-NB because there work at the level of DNA it takes bit longer than receptor type responses

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4
Q

Transport and Action of thyroid hormones

A

-T3 and T4 transported bound to a protein carrier, TBG, little free
+TBG (thyroxine binding globulin)
-LARGE Pool T4, less active and mainly in circulation
-SMALL pool of T3, mainly intracellular
+T4 converted to T3 in target tissues, T3 is the active form

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5
Q

Metabolism

A
  • Deiodination
  • Deamination
  • Conjugation with glucuronic and sulphuric acids
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6
Q

When the system goes wrong

A

-Hypersecretion- Too much
-Hyposecretion- Too Little
-For each:
What might causes it?
What would happen to the body

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7
Q

Disorders of the thyroid function (hyperthyroidism- Graves disease)

A

Hyperthyroidism (Graves disease)
-Occurs in 2% of women, which is 10x incidence observed in men
-Autoimmune disease
+Abs directed against proteins on surface of follicular cells
-Causes overproduction of thyroid hormones
-Possible involvement of environmental or emtional trigger factors
NB- always check what other drugs patient is on e.g. amiodarone can cause hyper and hypothyroidism
-Historical treatment: rest and sedation: 50% mortality rate

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8
Q

Diagnosis

A

-Physcial examination
-Family history
-Blood tests
+Hormones (T3,4 increase)
+TSH levels (increase)
+Thyroid Abs
-Thyroid scan (iodine uptake radioactive)
-Goitre
-Exophthalmos- eyes popping out

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9
Q

Clinical features (of hyperthyroidism)

A

Result from generalised over activity of thyroid gland

  • Hot, flushed, heat intolerant
  • Enlarged thyroid gland (goitre)
  • Exophthalmos
  • Weight loss
  • Muscle weakness, tremor
  • Pulse rate increase, palpitations, sweating
  • Hair loss, menstrual changes
  • This can cause more serious diseases including AF
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10
Q

Treatment of hyperthyroid

1) Drug treatment (aim and major side effects)

A

Anti-thyroid drugs: Decrease T3/T4 secretion: used for
-Prompt control: relieve symptoms
-Mild hyperthyroidism
-Children or young adults
-Temporary treatment
-Treatmeant for 12-18 months
+Prolonged remission in 20-30% patients
-Allergic reactions 5%, rashes, fever, pains
-Neutrophils decreased, infection risk= death
-Agranulocytosis: rare, possible fatal
+Patient develops infection, sore throat, fever, mouth ulcers, brusing . get a blood test MUST WARN PATIENT

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11
Q

Anti-thyroid drugs 1.

Drugs which inhibit organic binding of iodine

A

The thiourelynes (thionamides)
-Carbimazole: precursor of methimazole which inhibits oxidation of iodide and coupling to tyrosine
+1st line in UK
+Thought to act by inhibiting the thyroperoxidase enzyme
-Propylthiouracil (PTU): also inhibits peripheral de-iodination of T4 to T3
+(T4 pro-hormones, less active, more abundant)
+In UK kept for people unable to take carbimazole

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12
Q

How is carbimazole used

A

-Give in high doses till euthyroid
-Reduce to maintenance dose
-Withdraw after 1-2 years and monitor
Clinical effect note:
-Rapid action to inhibit organic binding BUT large stores of T3 and T4 must be ‘Used up’ before therapeutic effects

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13
Q

Anti-thyroid drugs 2

A

-Drugs which reduce the uptake of iodine
+Thiocyanate
+Perchlorate
-Reduce uptake of iodine ion
+Seldom used today because of danger of aplastic anaemia (bone marrow damage reduces haemotopoietic stem cells)
-Sensible drug target … but side effects mean not clinically useful

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14
Q

Drugs used to relieve the symptoms of hyperthyroidism

A

Beta-blockers (BB)
-Propranolol, nadolol (less common)
-Used to reduce symptoms of overactivity of the sympathetic nervous system
+Reduces tumor, tachycardia, and the anxiety associated with the condition
+Not anti-thyroid
-Used in many patients prior to and during initiation of other treatments to reduce distress while waiting for therapeutic effects
NB- C/I in some patient.. asthmatics

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15
Q

Non-drug treatment of hyperthyroidism: radioactive iodine

A
  • 131-Iodine given as Aqueous solution or capsules
  • Taken up by active transport and concentrated in gland by I pump (this is specific because the thyroid is the only cells that take up iodine)
  • Local tissue destruction by X-ray and beta-particle emission
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16
Q

Normal follicle anatomy

A
  • Gland is made up of lots of little follicles
  • These contain the cells that are responsible for synthesising hormones
  • Colliod is a storage area in the middle which stores hormone
  • Lots of capillaries, lots of blood flow to take hormones and signals to and from
  • Hyperthyroidism (to high levels of hormone), the cells get bigger and swell so they pump out more hormone, they also have a smaller colloid so there is less storage- the swelling seen is known as a goitre
  • Hypothyroidism the cells become smaller meaning there ability to pump out hormone is reduced- the increased signal to produce more hormone with no results can cause the swelling fo the glands known as a goitre
17
Q

See iodination (organification of tyrosine first

A
  • 2 molecules of Tyrosine binds to thyroglobulin
  • Thyroid peroxidase places 2 iodide groups (on the aromatic ring) on each tyrosine forming diiodotyrosine (DIT)
  • Thyroid peroxidase takes Off one tyrosine the benzene group with -OH and 2 iodide groups come and and bind to the other tyrosine forming thyroxine
  • The reaction is known as iodination of tyrosine
  • You can also have the same process with just one iodide group this is monoiodotyrosine (MIT)
  • MIT+ DIT= T3
  • DIT+DIT= T4
18
Q

Synthesis and secretion of thyroid hormone

A

-Iodine active pump- brings iodine into the cell (if we block iodine pump no synthesis of thyroxine)
-T3 and T4 are produced
proteins are bound to it, and placed in thyroglobulin precursors in secretory vesicles
-Through pinocytosis occurs to bring more T3 and T4 in, proteolysis occurs to remove proteins from the hormones
-T3 and 4 are secreted into the blood

19
Q

Action of thyroid hormones: metabolism

A
  • Regulate metabolism in most tissue
  • Modulate effects of other hormones (glucagon)
  • T3 more potent than T4
  • Increase metabolism of carbohydrates, proteins and fat
  • Increase O2 use and heat production (due to increased metabolism in tissue)
  • Increased basal metabolic rate
20
Q

Control of thyroid hormone secretion

HPT AXIS

A
  • HPT (hypothalamus, anterior pituitary, Thyroid gland) axis
  • Other brain centres (e.g. cold outside)- must increase metabolism therefore increase thyroid hormone
  • Hypothalamus release TRH (thyrotropin releasing hormone) to act on the anterior pituitary
  • Anterior pituitary releases TSH (thyroid stimulating hormone) which acts on thyroid gland
  • Thyroid gland then releases thyroid hormone into target cells throughout the body
  • Thyroid hormone gives negative feedback to the pituitary and hypothalamus to inhibit them to prevent over secretion
21
Q

Radioactive iodine

A
  • Slow progressive effect, difficult to control
  • May produce hypothyroidism due to more destruction (need replacement therapy)
  • 1st line treatment
  • Or after failure of anti-thyroid drugs
  • Or after failure of thyroidectomy
  • Or a standard procedure for some thyroid cancers
22
Q

Non drug treatment of hyperthyroidism: Surgery

A

-Thyroidectomy
+For patients where 131-I and drugs have failed
+Patients with large goitre: cosmetic effects, swallowing or breathing difficulties
-Ideally: sub-total thyroidectomy leaving patient with enough gland to be euthyroid
+BUT possibility of recurrent thyrotoxicosis or developing hypothyroidism is great
-Hypothyroidism: Need thyroid replacement therapy

23
Q

Aim of all of these treatments

A
  • Patient is euthyroid- normal hormone levels

- BUT what if they become hypothyroid

24
Q

Hypothyroidism (symptoms and potential causes)

A

-Syndrome cause by deficiency of thyroid hormones
+weakness, fatigue, cold intolerance
+Weight gain, skin thickness
+Intellectual deterioration, mental and physical lethargy
+Goitre (increased TSH)
-Possible causes
+Congenital
+Autoimmune disease: Abs to thyroglobulin
+Inflammation of thyroid (hashimotos thyroiditis)
+Dietary iodine deficiency

25
Q

Names for types of hypothyroidism

A

-Hashimotos thyroiditis (Auto-immune)
+Inflammatio, fibrosis and decreased function of thyroid gland. goitre evident
-Myxoedema
+Hypothyroidism developing in adult life
+Adult onset slow and insidious, confused with normal ageing process. increase in women
+In rare cases, becomes medical emergency, requires treatment by T3
-Cretinism: affects children from birth
+Mental retardation, pot belly, dwarfism
+Prevented by rapid treatment with T4 at birth
(Maternal I deficiency and congenital dysfunction in hormone biosynthesis)

26
Q

Thyroid replacement therapy

A

-Thyroxine used to replace deficiency
-Aim of therapy
+replace thyroid hormone function
+Normal physical and mental development
=Reduced goitre (Suppress raised TSH levels
-optimum dose determined individually
+Single dose before breakfast
+Empty stomach, 30 mins before food
+Counsel re drug interactions which can impair absorption or metabolism
+Antacids, Fe drugs affecting CYP450 enzymes MUST MONITOR

27
Q

Thyroid replacement therapy

A

-Life long therapy, monitor effects
-Signs of overdose
+Tremor, agitation, weakness
-Insomnia
-Weightloss, flushing
-Arrhythmias, anginal pain
-Diarrhoea
NON compliance leading to increased doses
-Check TSH levels if raised then not taking tablets

28
Q

Drugs for thyroid replacement therapy

A

-Levothyroxine
+treatment of choice for maintenance
+Once daily dose
-Liothyronine
+similar action but more rapidly metabolised
+May be used in severe hypothyroid states
+Used IV as part of supportive treatment of thyroid coma

29
Q

Monitoring of replacement therapy

A

-Monitor TSH levels
+Within 8 weeks of starting levothyroxine
+After a dose change
+Annually once established

30
Q

Organification (iodination of tyrosine)

A
  • 2 Tyrosine molecules binds to thyroglobulin
  • Thyroid peroxidase that places iodine onto the tyrosines
  • Thyroidperoxidase then combines the 2 tyrosines to form thyroxine leaving (H2)C=

PH2501- pharmacology (47 decks)

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