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Years 1+2 > S4C9 > Flashcards

S4C9 Flashcards

1
Q

What does the presence of TSH receptor autoantibodies and/or Thyroid peroxidase antibodies suggest?

A

an autoimmune thyroid disorder such as Graves or Hashimoto’s

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2
Q

What does the presence of thyroglobulin antibody indicate?

A

Thyroid cancer

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3
Q

What is BMI?

A

The body mass index (BMI) is a measure that uses your height and weight to work out if your weight is healthy.

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4
Q

What are the BMI ranges?

A

below 18.5 – you’re in the underweight range
between 18.5 and 24.9 – you’re in the healthy weight range
between 25 and 29.9 – you’re in the overweight range
between 30 and 39.9 – you’re in the obese range

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5
Q

What is the BMI formula?

A

The formula is BMI = kg/m2 where kg is a person’s weight in kilograms and m2 is their height in metres squared.

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6
Q

Explain the fight/flight response pathway.

A

Hypothalamus activates the sympathetic nervous system. This activates glands and smooth muscles. It also acitvates the adrenal medulla to release noradrenaline and adrenaline into the bloodstream.
At the same time, the hypothalamus also stimulates the anterior pituitary gland to release corticosteriod releasing factor. The pituitary gland the secretes ACTH, which arrives at the adrenal cortex to release ~30 hormones.
Overall Neural activity combines with hormones in the bloodstream to constitute the fight-or-flight response

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7
Q

What happens if there is a prolonged threat?

in regards to fight/flight

A

If threat continues, the hypothalamic-pituitary-adrenal axis activates.
Keeps the sympathetic nervous system active
Releases cortisol

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8
Q

What percentage of people have a long term anxiety problem in England?

A

17.6%

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9
Q

What is the recovery rate for someone with anxiety in England?

A

51%

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10
Q

Describe the Hypothalamus-Anterior pituitary-thyroid axis

A

The hypothalamus secretes TRH.
This stimulates the A Pituitary to secrete TSH
This activates the thyroid to produce T4 and T3.
T3 inhibits both the anterior pituitary and the hypothalamus secretions

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11
Q

Explain the synthesis of circulating hormone by the thyroid follicular cell

A

Na+ and I- are actively transported from the capillary in through basal membrane
TSH binds to a receptor on the basal membrane which activates cAMP
This causes Thyroglobulin and TPO biosynthesis and packaging.
They then move into the Colloid.
Iodine is transported into the colloid by pendrin
Iodine binds to Thyroglobulin
Then through organification it is turned into thyroglobulin containing thyroid hormone
Thyroglobulin gets degraded, leaving T4 and T3 to be secreted into the blood.

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12
Q

What is T4 broken down into?

A

Reverse T3

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13
Q

What is T3 broken down into?

A

T2

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14
Q

How much of each thyroid hormone is secreted?

A

80% T4

20% T3

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15
Q

How much of T4 is metabolised into T3?

A

40%

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16
Q

When treating someone, why do you give them T4 supplements instead of T3?

A

T4 lasts longer in body
T3 half-life is 1-3 days
T4 half-life is 5-7 days

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17
Q

What is the action of T3?

A

T3 binds to the Thyroid receptor attached to the retinoid X receptor
This affects gene expression
Meaning slow acting

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18
Q

Describe the epidemiology of hyperthyroidism

A

1% of the general population have overt hyperthyroidism
Sex women:men 5:1
Age range at presentation:
Graves disease: patients between 20–30 years
Toxic adenoma: patients between 30–50 years
Incidence of toxic multinodular goitre increases with age; peak incidence > 80 years of age

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19
Q

What are the different ways hyperthyroidism can occur?

A

Hyperfunctioning thyroid gland - overproduction of thyroid hormones by the thyroid gland
Destruction of the thyroid gland - release of preformed thyroid hormones secondary to inflammation/destruction of the thyroid gland
Exogenous hyperthyroidism - excessive intake of thyroid hormones
Exctopic hormone production

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20
Q

What are examples of hyperfunctioning hyperthyroidism?

A

Graves disease (60%-80% of cases)
Toxic multinodular goitre (15-20% of cases)
Toxic adenoma (3-5% of cases)
TSH-producing pituitary adenoma
β-hCG mediated hyperthyroidism - pregnancy 2.5%
Hashitoxicosis

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21
Q

What is the epidemiology of Graves?

A 
Major autoantigen is TSHR
0.8/1000 women per year over 20 years
<0.1/1000 per year over 20 years
20-40 y/o
More aggressive in children and males
0.2% in pregnancies
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22
Q

What can happen when pregnant with Graves?

A 
Spontaneous abortion
Premature labour
Small birth weight
	Congestive cardiac failure
Pre-eclampsia
1% generate fetal hyperthyroidism - placental crossing of TSHR stimulation Abs
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23
Q

What are the signs of fetal hyperthyroidism?

A

> 160bpm fetal
Goitre
Advanced neonatal bone age
craniosynotosis

24
Q

What is the pathophysiology of hyperthyroidism?

A

Disorders of the thyroid gland cause excess production of T3/T4
Compensatory decrease of TSH
Thyrotroph adenoma causes increased TSH levels and increased T3/T4 levels
Known as central hyperthyroidism
Excess intake/ectopic thyroid hormone production increases circulating T3/T4 levels
Compensatory decrease of TSH

25
Q

What are the effects of hyperthyroidism?

A

Generalised hypermetabolic state - increased substrate consumption
Hyperstimulation of the sympathetic nervous system
Thyroid hormone stimulates proliferation of beta-adrenergic receptors → induces a sympathomimetic effect
Cardiac effects
Caused by a direct effect of thyroid hormones on the cardiac myocytes and the hyperadrenergic state.

26
Q

What are the Basic clinical features of hyperthyroidism?

A

Heat intolerance, excessive sweating (moist, warm skin)
Weight loss despite increased appetite
Hyperdefecation (increased frequency of bowel movements)
Weakness, fatigue
Hyperreflexia
Eye issues
Goiter
Diffuse, smooth, nontender goiter; often audible bruit at the superior poles

27
Q

What are the eye-related symptoms of hyperthyroidism?

A

Lid lag
Sclera visible above the cornea when looking down; caused by adrenergic overactivity resulting in a spasm in the smooth muscle portion of the levator palpebrae superioris
lid retraction (“staring look”)
Sclera visible above the cornea when looking straight ahead.
Graves ophthalmopathy

28
Q

What is Graves opthalmopathy?

A

Manifests with bilateral exophthalmos, lid retraction, disturbances in ocular motility (causing diplopia), and conjunctival hyperaemia.
Inflammation of the extraocular muscles, causing increased retro-orbital pressure
Proptosis or optic nerve damage, diplopia, corneal ulceration
Usually associated with thyroid upset, but can be entirely separate
Higher frequency and worse outcome with cigarette smoking
Radioiodine aggravates
Treated with artificial tears, immunosuppression, debatable effects of radiotherapy
Ultimately ‘burns itself out’

29
Q

What are the cardiovascular symptoms of hyperthyroidism?

A

Tachycardia: seen in almost all cases of hyperthyroidism.
Palpitations, irregular pulse (due to atrial fibrillation/ectopic beats)
Hypertension with a widened pulse pressure
Cardiac failure: Elderly patients often present with features of cardiac failure (e.g., pedal edema, dyspnea on exertion).

30
Q

What are the musculoskeletal symptoms of hyperthyroidism?

A

Fine tremor of the outstretched fingers
Myopathy with muscle weakness, particularly in patients > 40 years of age
Osteopathy: osteoporosis , fractures (in the elderly)

31
Q

What are the Endocrinological symptoms of hyperthyroidism?

A

women: Oligo/amenorrhoea and anovulatory infertility
men: Gynecomastia, decreased libido, erectile dysfunction

32
Q

What are the Neuropsychiatric symptoms of hyperthyroidism?

A 
Anxiety
Agitation
Depression
Insomnia
Emotional instability
33
Q

Why use a thyroid ultrasonography?

A

Can diagnose the aetiology of hyperthyroidism (e.g. , diffuse enlargement, solitary/multiple nodules, increased vascularity of the gland)
Thyroid ultrasonography is particularly useful in evaluating hyperthyroidism in pregnant women since scintigraphy is contraindicated in this group of patients.

34
Q

What is a thyroid scintigraphy?

A

A nuclear medicine imaging technique, which demonstrates the structure and function of thyroid tissue based on its selective uptake of radioactive iodine (RAI)

35
Q

When would you use a thyroid scintigraphy?

A

Patients in whom the aetiology is uncertain or if physical examination suggest nodular thyroid disease
Identification of ectopic thyroid tissue
Evaluation of thyroglossal cyst

36
Q

When wouldn’t you use a thyroid scintigraphy?

A

pregnant or breast-feeding

37
Q

What are the most common findings when using a thyroid scintigraphy?

A

Graves disease: enlarged gland with diffusely increased RAI uptake
Toxic MNG: multiple nodular areas, both cold and hot, resulting in an overall heterogeneous appearance
Toxic adenoma: a hot nodule
Factitious hyperthyroidism: no uptake of RAI since there is no thyroid gland hyperfunction

38
Q

What can be given to treat the symptoms of hyperthyroidism?

A

Beta-blockers offer immediate control of symptoms
Improve tachycardia, hypertension, tremor and neuropsychiatric symptoms
Propranolol decreases peripheral conversion of T4 to T3 by inhibiting the 5’-monodeiodinase enzyme

39
Q

What different definitive therapies can be used o treat hyperthyroidism?

A

Anti-thyroid drugs
Radioactive iodine ablation
Surgery

40
Q

What are the indications of anti-thyroid drugs?

A

Patients with high likelihood of remission (e.g., small goitre, negative or low TRab titer, women)
Active Graves ophthalmopathy
Children age ≤ 5 years
Pregnancy
Thyroid storm
Patient preference
Patients who need rapid disease control before further treatment, e.g., achievement of euthyroid state prior to surgery.
Patients with an inability to follow radiation safety regulations

41
Q

What is the permanent remission rate after 1-2 years of treatment?

A

20-75%

42
Q

What is the drug of choice for hyperthyroidism when the patient is pregnant or in a thyroid storm?

A

Propylthiouracil

43
Q

What is radioactive iodine ablation?

A

The destruction of thyroid tissue using radioactive iodine (iodine 131) through a sodium/iodine symporter

44
Q

What are the indications for using RAIA?

A

High surgical risk; limited life-expectancy
Liver disease
Major adverse reaction to ATDs
Previous operations or radiation of the neck
No access to a high volume thyroid surgeon
Failure to achieve euthyroidism with ATDs
Patient preference
Patients with congestive heart failure, right heart failure, pulmonary hypertension, or periodic hypokalemic paralysis
Recommended especially for TMNG and TA patients with high nodular radioactive iodine uptake

45
Q

When shouldn’t you treat hyperthyroidism with RAIA?

A

Pregnant/breastfeeding
Children <5
Thyroid malignancy
Moderate to severe Grave ophthalmopathy

46
Q

What is the pre-treatment for RAIA?

A

Pre-treatment ATD: in patients who are at high risk for complications due to worsening of hyperthyroidism
4-6weeks before to rapidly achieve a euthyroid state
Must be discontinued 2-3 days before RAIA is begun to insure the tissue will take up the iodine
Young or middle-aged patients with mild to medium symptoms of hyperthyroidism, who undergo RAIA do not routinely require pre-treatment
Avoid excess iodine

47
Q

How does RAIA work?

A

Single oral dose of 131 Iodine
Isotope uptake by thyroid gland
Emission of β-radiation that slowly destroys the thyroid tissue

48
Q

What is the post-procedural care of RAIA?

A

Patients with Graves disease become hypothyroid after RAI ablation and require life-long thyroid hormone replacement.
Most patients with hyperthyroidism due to other conditions do not become hypothyroid, since only the hyperfunctioning tissue takes up RAI and is destroyed by RAIA.

49
Q

What are the indications for surgery?

A

Large goiters (≥ 80 g) or obstructive symptoms
Confirmed or suspected thyroid malignancy
Moderate to severe active Graves ophthalmopathy
Women planning to become pregnant in the next < 6 months
Large thyroid nodules
Patient preference
Access to a high-volume thyroid surgeon
Recommended especially for TMNG and TA patients with concomitant hyperparathyroidism, insufficient RAIA or retrosternal extension

50
Q

What are the contraindications for surgery?

A

Severe comorbidities that influence surgical risk

1st and 3rd trimester of pregnancy

51
Q

What are the precautions taken before a thyroidectomy?

A

ATD and beta blockers are given 4-8 weeks before - To reduce the risk of intraoperative risk of thyroid storm
Potassium iodide administered orally 10 days before - Inhibits release of T3/T4 and decrease thyroid blood flow, reducing intraoperative blood loss

52
Q

What is the post-procedural care for a thyroidectomy?

A

Management of calcium levels: measurement of serum calcium and intact parathyroid hormone levels
Transient hypoparathyroidism due to injury of the parathyroid gland is a common complication
Weaning of beta blockers

53
Q

What is a thyroid storm?

A

Thyrotoxic crisis

An acute exacerbation of hyperthyroidism, resulting in a life threatening hypermetabolic state

54
Q

What is the aetiology of a thyroid storm?

A

May occur spontaneously, but is often precipitated by on of the following:
A sudden surge in thyroid hormones
Stress-related catecholamine surge - worsened the pre-existing hyperadrenergic state of hyperthyroidism

55
Q

What are the clinical features of a thyroid storm?

A 
Hyperpyrexia w/ profuse sweating
Tachycardia
Hypertension
AF
Congestive cardiac failure
Severe nausea
Vomiting
Diarrhoea
Possibly jaundice
Severe agitation and anxiety
Delirium and psychoses
Seizures 
Coma
Low/ undetectable TSH
Elevated free T3/T4
56
Q

What are the treatments available for thyroid storm?

A

General measures:
Intensive care monitoring with fluid and electrolyte substitution
IV dextrose solutions are preferred to meet the high metabolic demand
Treatment of hyperthermia: ice packs, cooling blankets, and antipyretics (e.g., acetaminophen)

Treatment of underlying condition
Beta blockers should be promptly started (propranolol) - Control hyperadrenergic symptoms and inhibit peripheral conversion of T4 to T3
Antithyroid drugs
Potassium iodide/Lugol’s iodine - Inhibits further release of thyroid hormones from the glands
Glucocorticoids: IV hydrocortisone/dexamethasone
Inhibits peripheral conversion on T4 to T3 and prevents relative adrenal insuffiency in hyperthyroidism
Plasmapheresis: as a life-saving treatment, rarely needed
Eliminates the circulating thyroid hormones

Years 1+2 (21 decks)

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