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Unit 10 PBL cases > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

What is hyperthyroidism? e.g.

A

Set of disorders that results from increased synthesis of thyroid hormones
Examples:
- Grave’s disease
- Multinodular goiter (Plummer’s disease)
- Thyroiditis

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2
Q

What is the pathophysiology of Grave’s disease?

A

B cells produce autoantibodies against thyrotropin receptor
Serum IgG antibodies act like TSH and bind to TSH receptor in thyroid
Stimulate thyroid follicles to release more T3 and T4
Hormones enter bloodstream and bind to circulating plasma proteins, taken up by most cells
T4 converted to T3

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3
Q

What are the effects of T3?

A

Increases cardiac output
Stimulates bone resorption
Activates sympathetic NS

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4
Q

What are the effects of thyroid stimulating antibodies?

A

Thyroid hypertrophy
Hyperplasia
Fibroblast tissue around eyes and skin become stimulated

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5
Q

What are the symptoms of hyperthyroidism?

A

Anxiety and insomnia
Weight loss
Increased appetite
Diarrhoea/increased bowel frequency
Intolerance to heat/excessive sweating
Insomnia
Hair loss
Bulging eyes
Pretibial myxoedema

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6
Q

Why do the symptoms of hyperthyroidism occur? anxiety and insomnia, weight loss, increased appetite, diarrhoea

A
  • Anxiety and irritability
  • Weight loss: increased TH increases basal energy expenditure that decreases fat mass, speeds up metabolism
  • Increased appetite: compensatory response to increased energy expenditure
  • Diarrhoea/increased frequency of defecation: sympathetic hyperstimulation leads to decreased gut motility and diarrhoea
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7
Q

Why do the symptoms of hyperthyroidism occur? Intolerance to heat/excessive sweating, insomnia, hair loss, bulging eyes, pretibial myxoedema

A
  • Intolerance to heat/excessive sweating: increased metabolism produces more body heat > inability for thermoregulation
  • Insomnia: linked with sympathetic hyperstimulation which prevents sleep
  • Hair loss: T3 and T4 involved with hair maintenance
  • Bulging eyes: abnormal swelling of tissue in socket behind eye
  • Pretibial myxoedema: TSH antibodies activates fibroblasts, stimulates immune response
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8
Q

What are the risk factors for hyperthyroidism?

A

Family history
Sex: women 7-8x more common
Other autoimmune disorders: more likely to be diagnosed
Emotional/physical distress: high stress can trigger or exacerbate symptoms
Pregnancy: hormonal changes can trigger
Smoking: exacerbate symptoms

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9
Q

What are the symptoms of hypothyroidism?

A

Fatigue and depression
Sensitivity to cold
Constipation/diarrhoea
Weight gain
Muscle aches
Brain fog
Heavier menstrual flow
Thinning hair
Slowed heart rate

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10
Q

What causes the symptoms of hypothyroidism to occur? Fatigue and depression, sensitivity to cold, constipation, weight gain, muscle aches

A

Fatigue and depression: less TSH, less serotonin and noradrenalin
Sensitivity to cold: slower metabolism, less heat production
Constipation/diarrhoea: dysfunction in PNS and SNS, reduces gut motility
Weight gain: slowed metabolism, reduced basal energy expenditure - calorific surplus
Muscle aches: T4 deficiency, reduced mitochondrial oxidative capacity and cause abnormal glycogenolysis > atrophy of type 2 muscle fibres

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11
Q

What causes the symptoms of hypothyroidism to occur? Brain fog, heavier flows, thinning hair, slowed heart rate

A

Brain fog: TSH low, effects memory and focus
Heavier flows: low TSH, decreases progesterone, heavier bleeding
Thinning hair: T3 and T4 involved with hair maintenance
Slowed HR: reduced sympathetic stimulation, reduced catecholamine production and decreased parasympathetic stimulation > lower HR

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12
Q

What is the mechanism of thyroid hormone synthesis?

A

1) TSH from blood binds to TSH-R on BL memb of follicular cell
2) TSH increases Na/I cotransporter activity - increased I- in follicular cell
3) I- leaves enters colloid via pendrin. Cell also secretes Tg.
4) TPO in secretory vesicle oxidises I- to I - requires H202 from DUOX2
5) Iodination: TSH stimulates iodination of thyroglobulin MIT, DIT in colloid
6) Conjugation: TSH stimulates conjugated tyrosines (MIT, DIT) to form T3 and T4 linked to thyroglobulin
7) TSH stimulates endocytosis of iodinated Tg from colloid into cell
8) TSH stimulates proteolysis of iodinated thyroglobulin > T3, T4 in lumen of lysoendosome
9) TSH stimulates secretion of T3, T4 into blood by fac diff
10) TSH stimulates hyperplasia within thyroid gland

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13
Q

What receptors take up Thyroid hormones from the blood?

A

TR-alpha - predominantly in the brain
TR-beta - expressed in liver

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14
Q

What transports thyroid hormones around the blood?

A

Albumin
TBG
Transthyretin

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15
Q

How do thyroid hormones work?

A

Bind to receptors
Activate transcription factors, lead to activation of certain genes and cell-specific responses

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16
Q

How are thyroid hormones excreted from the body?

A

Degraded by sulphation in the liver
Excreted in bile

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17
Q

What is the difference between the action of T3 and T4?

A

T3 has higher affinity to thyroid receptors
T4 is therefore relatively inactive
Deiodinases converts T4 into T3 (active) or rT3 (inactive)

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18
Q

What are the roles of thyroid hormone? 5

A

Metabolism:
Increase rate of hepatic gluconeogenic activity
Increase proteolysis and synthesis
Increase degradation of TAGs in adipose tissue, releasing FAs and glycerol
Thermogenesis: increases the expression of UCP1 in brown adipose tissue - increase heat generation
ANS: increase B adrenoreceptors for catecholamines - increase HR, BP, BR. Speed of reflexes and mental activity
CV: increases synthesis of cardiac muscle protein and CO
Bone: increases bone mineralisation

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19
Q

What is the HPT axis?

A

Hypothalamus: synthesises TRH which binds to TRH receptors on thyrotropic cell membranes in -
Anterior pituitary: (TRH stimulates) synthesises TSH, enters blood and binds to receptors on follicular cells in -
Thyroid gland: synthesis of T3 and T4
Control by negative feedback - high T3 and T4 > inhibit TRH and TSH production

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20
Q

What is tertiary hyperthyroidism and how can you diagnose it?

A

Excess TRH production from the hypothalamus

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21
Q

What is secondary hyperthyroidism?

A

Excess TSH - excess production
Excess T3 and T4 - due to raised TSH
Causes: TSH secreting tumour, TSH resistance to T3/4 negative feedback

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22
Q

What is primary hyperthyroidism? Causes

A

T3 and 4 high - excess production
Low TSH - negative feedback on pituitary or hypothalamus
Causes: Graves - 75%, toxic adenoma

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23
Q

How do T3 and T4 inhibit TRH and TSH synthesis?

A

T3 found in thyrotropes due to deiodination of T4, or entering from blood. Intracellular T3 decreases no. TRH receptors > indirect inhibition of T3/4 synthesis

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24
Q

What is the structure of the thyroid?

A

Left and right lobe
Joined by an isthmus

25
Q

What are anatomical relations of the thyroid?

A

Anteriorly are the infrahyoid muscles
Medially is the larynx, trachea and oesophagus
Laterally is the carotid sheath - common carotid A, internal jugular V, vagus N

26
Q

Where is the thyroid?

A

Anterior of neck
Spans C5-T1

27
Q

What is the arterial supply of the thyroid?

A

External carotid artery > superior thyroid artery > anterior (anterior surface) and posterior (lateral and medial surfaces)
Subclavian artery > thyrocervical trunk > inferior thyroid artery > superior and inferior (inferior and posterior surfaces)

28
Q

What is the venous drainage of the thyroid?

A

Superior, middle, inferior thyroid veins form venous plexus around thyroid gland
Superior and middle thyroid veins > internal jugular
Inferior thyroid vein > brachiocephalic vein

29
Q

What is the structure and location of the parathyroid?

A

Located posteriorly to the thyroid
Two superior parathyroid glands
Two inferior parathyroid glands

30
Q

What is the role of the parathyroid?

A

Production of the parathyroid hormone - PTH
Increases serum calcium by stimulation bone resorption through osteoclasts

31
Q

What is the arterial supply of the parathyroid?

A

Inferior thyroid artery

32
Q

What is the venous drainage of the parathyroid artery?

A

Superior, middle and inferior thyroid veins

33
Q

What are the histological structure of the thyroid?

A
  • Thyrocytes = follicular cells
  • Follicles are the structural unit - lined by single layer of follicular cells, and are filled with colloid
  • Colloid is composed of thyroglobulin (Tg) which can be taken up into follicular cells to produce T3 and T4
  • Large, pale-staining parafollicular cells/C cells - release calcitonin
  • CT septa divide gland into lobules
  • Vascular capillary network surrounds follicles
34
Q

What is is the repsonse to excercise in the CV system?

A
  • Increased HR
  • Increased stroke volume
  • Increased cardiac output
  • Redistribution of BF to active muscles
  • Vasodilation in working muscles, vasoconstriction in non-essential areas
35
Q

What are the physiological responses to excerise in the respiratory system?

A
  • Increased resp rate
  • Elevated tidal volume
  • Enhanced minute ventilation
  • Greater oxygen uptake
  • Increased CO2 removal
36
Q

What are the phsyiological repsonses to exercise in the muscular system?

A
  • Increased muscle fibre recruitment
  • Enhanced BF to active muscles
  • Improved O2 delivery and waste product removal
37
Q

What are the physiological responses to exercise in the metabolism?

A
  • Increased ATP production through aerobic and anaerobic pathways
  • Elevated glucose and fatty acid utilisation
  • Lactic acid accumulation in aerobic conditions
38
Q

What are the physiological repsonses to exercise in thermoregulatory repsonses and endocrine system?

A

Thermoregulatory:
- Elevated body temperature due to increased metabolic activity
- Enhanced sweating for heat digestion
- Redistribution of BF to help regulate temperature
Endocrine:
- Release of adrenaline and noradrenaline from adrenal glands
- Elevated cortisol levels to mobilise energy stores
- Increased growth hormone secretion to support tissue repair

39
Q

What are the physiological responses to exercise in the NS and renal system?

A

NS:
- Activation of motor neurons to initiate muscle contraction
- Enhanced coordination and proprioception
- Release of endorphins, lead to reduced perception of pain
Renal system:
- Decreased urine production due to redirected BF
- Increased reabsorption of water and electrolytes

40
Q

What are the physiological responses to exercise in the GI system and immune system?

A

GI:
- Reduced BF to digestuive organs
- Suppressed appetite during and immediately after exercise
Immune:
- Short term enhancement of immune function
- Possible temporary suppression with extreme, prolonged exercise

41
Q

What is propranolol used for?

A

Slows down heart rate
Usually used for hypertension
Can also help with physical symptoms of anxiety

42
Q

What is the mechanism of action of propranolol?

A

Binds to beta 1 and 2 receptors of the cardiac myocytes
Prevents binding of adrenaline and noradrenaline
Leads to less conversion of ATP to cAMP which decreases calcium accumulation in cell
Less calcium in cell mean less calcium binds to troponin C and less contractility occurs

43
Q

What type of drug is propranolol?

A

Non-selective beta adrenergic antagonist

44
Q

Side effects of propranolol

A

Abdominal discomfort
Depression
Diarrhoea

45
Q

What is carbimazole used for?

A

Used to treat hyperthyroidism

46
Q

What kind of drug is carbimazole?

A

Antithyroid agent

47
Q

What is the mechanism of carbimazole?

A

Carbimazole enters body, converted into methimazole which inhibits function of TPO - which is responsible for iodination and coupling reactions of the thyroid gland to produce T3 and T4
Reduced T3 and T4 production, and levels in blood

48
Q

What are the side effects of carbimazole?

A

Very rare: bone marrow disorders, haemolytic anaemia

49
Q

What are the alternative treatments to carbimazole?

A

Radioiodine: Sodium iodide orally is rapidly absorbed and distributed within ECF and then into the thyroid gland. Iodide concentrated in the thyroid follicle via Na/I symporter and subsequently oxidised to iodine
Emit beta particles which penetrate and destroy the follicular cells from inside
Cells undergo pyknosis and necrosis > fibrosis of gland

50
Q

What is the effect of radioiodine therapy, and how is it monitored and treated?

A

Hypothyroidism: important to have regular blood tests strating from 4-6 weeks after treatment and then every 3 months after that until stable
Treated early with levothyroxine

51
Q

How does levothyroxine work?

A

Synthetic T4 hormone as a chiral compound that converts to T3
Diffuses into cell nucleus and binds to thyroid hormone receptor attached to DNA > thyroid response element > activates gene transcription > mRNA and protein synthesis > cause metabolic effects

52
Q

What are the treatment options for hyperthyroidism?

A

Symptomatic therapy: medicine to alleviate symptoms, not part of long term management
Anti-thyroid drugs: control hyperthyroidism by inhibiting production of thyroid hormones
Radioactive iodine therapy: given orally, damages thyroid tissue
Surgery: total thyroidectomy or lobectomy
Lifestyle: avoiding iodine and stress can help control symptoms

53
Q

What are the pros and cons of antithyroid medication?

A

Pro:
- Non-invasive treatment
- Reversible
- Symptom relief
- Preservation of thyroid function
Cons:
- Relapse once stopped
- Duration of treatment
- Side effects
- Not a permanent solution

54
Q

What are the pros and cons of radioiodine therapy?

A

Pros:
- Effective treatment
- Non-invasive
- Convenience
- Low risk of relapse
Cons:
- Permanent hyperthyroidism
- Delayed onset of action
- Side effects
- Need for precautions

55
Q

What are the pros and cons of thyroidectomy?

A

Pros:
- Permanent resolution
- Quick symptom relief
- Less radiation exposure
- No need for lifelong monitoring
Cons:
- Surgical risks
- Permanent hypothyroidism
- Hospitalising
- Scar

56
Q

What is the normal proportion of T3 to T4?

A

Thyroid releases more T4 than T3 20:1
T4 is therefore a better marker of thyroid function

57
Q

What is the triage system?

A

Clinical process of prioritising patients
Completed before full assessment to support effective management of demand and flow, by identifying time critical requirements for patients

58
Q

What are the aspects needed for communicating with a patient according to the NHS?

A

Patient-centered
Shared decision making
Safety reassurance
Deliberate language - no jargon
The whole patient journey - clear on next steps
Contact point - easy access to further info
Communications method - make sure they have a way of getting in contact
Cancellation policy
Interim information and services

59
Q

What is the effect of good doctor-patient relationship?

A

Adherence to treatment
Patient returning
Patients disclose more information
Fewer repeat consultations
More satisfied
Better mental health

Unit 10 PBL cases (6 decks)

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