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PBL Y2 S4 > Case 9- Thyroid dysfunction > Flashcards

Case 9- Thyroid dysfunction Flashcards

1
Q

What are the 3 main functions of the thyroid gland?

A
  • Regulates basal metabolic rate (BMR)
  • Stimulates somatic and psychic growth
  • Role in calcium metabolism (with parathyroid gland)
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2
Q

What is the functional unit of the thyroid?

A

Thyroid follicles

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3
Q

What type of cells are follicular cells?

A

Simple cuboidal epithelial cells

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4
Q

How is are T3 and T4 synthesised?

A

1: PV nucleus in hypothalamus releases TRH
2: acts on thyrotrophs in AP to release TSH
3: Stimulates follicular cells to release thyroglobulin
4: Iodide moves into the FC with Na+ and then via pendrin proteins
5: iodide is oxidised to iodine via thyroid peroxidase (TPO)
6: TPO catalyses the iodination of tyrosine AA in thyroglobulin -> T3 and T4

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5
Q

How are T3 and T4 isolated and transported?

A

1: After synthesis = endocytosis of thyroglobulin with T3 and T4
2: lyosozyme enzymes split the thyroglobulin colloid to isolate T3 and T4
3: liver produces thyroxine-binding globulin (TBG), which binds to T3 and T4 to transport them in blood

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6
Q

What are the full names of T3 and T4? Which is the active form?

A

T4 (thyroxine) and T3 (triodothyronine)

T3= active form

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7
Q

How does T4 get converted into T3?

A

Crosses over the lipid bilayer to enter the cell, then 5’ deiodinase (also known as type 1 selenodeiodinase [D1]), enzyme removes iodine off T4 –> T3

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8
Q

How does thyroid hormone increase basal metabolic rate?

A

Retinoic acid and T3 bind to a transcription factor, activating it so it can stimulate genes. Overall result = protein synthesis of Na/K+ ATPase pumps. These pumps utilise ATP therefore leads to decreased cellular ATP, increased O2 usage = metabolic rate increases.

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9
Q

How does thyroid hormone cause increased BP?

A

Effects the heart - increases B1 adrenergic receptors (R for Adr/NA) so contractility, SV and Q goes up, acts on SAN/AVN to increase B1aR’s too, so HR increases [overall increases BP]

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10
Q

How does thyroid hormone affect the CNS?

A

Increases dendrites, myelination, synapses

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11
Q

How is the HPA axis altered in depression?

A
  • Increased corticotrophin-releasing hormone (CRH)
  • Enlarged pituitary and/or adrenal
  • Increased ACTH and/or cortisol during depressive periods
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12
Q

What is Cushing’s syndrome? What psychological symptoms may it present with?

A

Cortisol hypersecretion, often associated with depression and irritability. May also suffer:
- Fatigue
- Decreased libido
- Poor concentration
- Impaired memory and poor problem solving

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13
Q

What is Addison’s syndrome? What psychological symptoms may it present with?

A

Cortisol hyposecretion, often associated with lethargy and apathy. Other behaviours:
- Irritability
- Crying
- Insomnia/ impaired sleep
- Problems with memory and concentration
- Tachycardia

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14
Q

What are the differential diagnoses of Addison’s and Cushing’s syndrome?

A

Cushings - depression,
Addisons- anxiety, as the symptoms are non-specific and come and go (esp during periods of stress)

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15
Q

How can hyperthyroidism influence behavioural states?

A

Intense dysphoria, usually pronounced anxiety. May also include:
- Nervousness
- Emotional instability
- Restlessness
- Impaired concentration
- Insomnia and fatigue

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16
Q

How can hypothyroidism influence behavioural states?

A

Cognitive dysfunction = impaired memory, concentration, inattentiveness, slowness, poor problem solving

Mood= depressed mood, anxiety, irritability, confusion (if severe can = psychosis)

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17
Q

What is the 2-pattern response of stressors on endocrine response?

A

1: stress promotes adaptive changes in the endocrine system to help the person deal with the threat, i.e. mobilisation of fuel, increased resistance to infection
2: prolonged/ repeated stress= adaptive changes such as enlarged adrenal glands

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18
Q

What is an allostatic load? What can it lead to?

A

Cumulative burden of chronic stress and life events
Prolonged stress can lead to dysregulation of endocrine function.

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19
Q

What is thyrotoxicosis and what can it be caused by?

A

Excess circulating thyroid hormone. Causes:
- Pharmacological: i.e. taking too much thyroid hormone
- Transient: viral infection (e.g. coxsackie), inflammation of the thyroid (transient wave of overactivity then leads to underactivity)

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20
Q

What can cause hyperthyroidism?

A
  • Graves disease
  • Toxic nodule - single or multiple, benign follicular adenomas
  • TSH-secreting pituitary adenoma: rare tumour secreting high TSH so T3/T4 are elevated. Doesnt respond to the negative feedback loops
  • Pituitary thyroid hormone resistance syndrome: genetic mutations in beta gene, usually euthyroid but thyrotoxic symptoms
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21
Q

What are some symptoms of hyperthyroidism?

A
  • Irritability, nervousness
  • Hyperactivity
  • Heat intolerance & sweating
  • Weight loss
  • Increased appetite
  • Dyspnoea
  • Palpitations
  • Diarrhoea
  • Hair loss
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22
Q

How does hyperthyroidism lead to heat intolerance and sweating?

A

Thyroid hormone causes vasodilation of blood vessels to lose excess heat from the high metabolism, also Adr/NA stimulate sweat glands to produce more sweat for evaporative cooling

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23
Q

How does hyperthyroidism lead to dyspnoea?

A

tracheal compression from a large goitre

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24
Q

What finding may be present in a patient with hyperthyroidism for:
- Percussion
- Auscultation

A
  • Percussion of the sternum may = dull, indicates the thyroid may have extended below and behind (retrosternal goitre)
  • Auscultation: bruit (constant noise), i.e. increased BF to the thyroid gland
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25
Q

What might the results of thyroid function tests be for a patient with hyperthyroidism? i.e. overt primary, subclinical primary, and secondary

A

Overt = T3 and T4 high, TSH low
Subclinical = T3 and T4 normal, TSH low - indicates the thyroid hormones have been compensated for
Secondary = T3 and T4 high, TSH high

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26
Q

What is a differential for hyperthyroidism? What would indicate this?

A

Grave’s disease = thyroid auto-antibodies (for TSH receptor), positive clinical picture and TFTs, positive family history

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27
Q

What 3 investigations may be done if you suspect hyperthyroidism? What might they show?

A
  • Ultrasound of the neck: may show increased inflammation or increased vasculature (accounting for the bruit), can show if there’s nodules or not
  • Radioiodine uptake scan: also shows if there’s nodules
  • 24hr urinary iodine excretion: can confirm if its due to excessive iodine intake
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28
Q

What are some risk factors for Grave’s disease?

A
  • Female sex: 10x more likely
  • Family history
  • Smoking
  • Low iodine intake: may cause MNG or SNG
  • Autoimmune disease
  • People with psychiatric disorders?
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29
Q

Whilst waiting for an endocrinologist’s referral, what may you prescribe to a patient with suspected hyperthyroidism?

A

Beta blockers for adrenergic symptoms (i.e. palpitations, tremor, tachycardia, anxiety)

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30
Q

What would you treat hyperthyroidism with?

A

Anti-thyroid drugs: thionamides, such as carbimazole (1st line) or propylthioruacil (2nd line)

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31
Q

What is carbimazole contraindicated in?

A

Pregnancy - use PTU

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32
Q

What is the MOA of thionamides?

A

Act as a preferred substrate for iodination by TPO - the key step in thyroid hormone production

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33
Q

After euthyroidism is achieved, what two drug regimens may be used?

A
  • Titration-block regimen: dose is adjusted depending on free T4 levels - titrate to lowest dose possible to maintain euthyroid state
  • Block and replace: give thionamide and then when free T4 is normal, add levothyroxine
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34
Q

What is radioactive iodine treatment?
What patients might this be used for?

A

Induces damage of DNA leading to death of thyroid cells = decreases thyroid function and/or reduction in thyroid size.
- First line definitive treatment for Grave’s and toxic MNG

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35
Q

Who is radioactive iodine treatment contraindicated in?

A

People with Grave’s and has active or severe orbitopathy
Patients with Grave’s but are pregnant

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36
Q

What are some complications of untreated hyperthyroidism?

A
  • Graves orbitopathy
  • Thyrotoxic crisis (thyroid storm) - leads to fever, tachycardia, hyperthermia
  • Compression symptoms - dysphagia or breathlessness
  • Cardiac problems
  • Osteoporosis
  • Psychosis
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37
Q

Where is hyperthyroidism more prevalent?

A

In iodine-deficient areas, such as Denmark

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38
Q

What is Grave’s disease?

A

Systemic autoimmune disorder - characterised by TSH-receptor auto- antibodies, leading to thyroid hyperplasia and excessive secretion of thyroid hormone. Has waves of inflammatory stimulation

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39
Q

Who is at increased risk for Grave’s disease?

A
  • Women
  • People with a personal or family history of autoimmune disorders (i.e. T1DM, Addison’s vitiligo, pernicious anaemia, myasthenia gravis, coeliac disease)
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40
Q

Other than the typical hyperthyroidism symptoms, what signs may be present in Graves disease?

A
  • Orbitopathy: bulging of the eyes forwards
  • Pretibial myoxedema: thickening of the skin
  • Vitiligo: white patches
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41
Q

What is Grave’s orbitopathy?

A

Inflammation of extra-ocular muscles, causing increased retro-orbital pressure leading to proptosis = eye(s) pushed forward.

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42
Q

When would you be concerned about a patient with Graves Orbitopathy?

A

If the eyes don’t get pushed forward, the pressure can damage the optic nerve, leading to inability of the eyes to function (= diplopia, corneal ulceration, blindness).

43
Q

How might you treat Grave’s disease?

A
  • Carbimazole
  • Carbimazole + thyroxine (block and replace)
  • Beta-blockers - symptom relief
44
Q

How might Grave’s disease be affected by pregnancy?

A
  • Exacerbated early in pregnancy, as hCG stimulates the thyroid so low TSH is normal (reduces it further)
  • Ameloriated later in pregnancy
45
Q

Why is radioiodine treatment for Grave’s contraindicated in pregnancy?

A

Fetal thyroid is present at 8-10 weeks - risk of damaging it

46
Q

What is the half life of T3 and T4 in circulation?

A

T3= 1-3 days
T4= 5-7 days

47
Q

How might TFT results differ for overt, subclinical and secondary hypothyroidism?

A

Overt: high TSH but low free T4
Subclinical: high TSH but normal T4 and T3
Secondary: inappropriately low or normal TSH, but free T4 is low

48
Q

What can cause primary hypothyroidism?

A
  • Drugs, such as amiodarone and lithium
  • Iodine deficiency
  • Autoimmune thyroiditis (Hashimoto’s)
  • Post-ablative surgery or therapy
  • Transient thyroiditis
  • Genetics
49
Q

What can cause secondary hypothyroidism?

A

Pituitary or hypothalamic disorder

50
Q

What is the most common cause of primary hypothyroidism in the UK?

A

Hashiomoto disease

51
Q

Which genes may be implicated in hypothyroidism? What do they lead to?

A
  • TTF1, PAX8 = gland never forms properly
  • Pendren syndrome = can’t handle degradation of thyroglobulin and subsequent release of T3 and T4
52
Q

What causes pernicious anaemia?

A

Autoimmune destruction of the parietal cell, loss of intrinsic factor secretion and consequently vitamin B12 defiency

53
Q

What are some signs and symptoms of hypothyroidism?

A
  • Fatigue and lethargy
  • Cold intolerance
  • Weight gain: eating the same but metabolism is slowed (low levels of lipolysis in adipose tissue)
  • Constipation
  • Depression
  • Mentally slowed, dull: lack of synpases/ myelination/ dendrities in CNS
  • Dry, brittle thinning hair
  • Hoarse voice – more advanced
54
Q

How can you distinguish primary and secondary hypothyroidism from the signs/symptoms?

A

Secondary would have the same symptoms as primary hypo, but would may also have:
- Recurrent headaches
- Diplopia and/or visual field defects

Also, abnormal pituitary hormone production can lead to sex hormone dysfunction (atrophic breasts, galactorrhoea, amenorrhoea, erectile dysfunction).

55
Q

What might you look at in the blood when assessing a patient for hypothyroidism?

A
  • Thyroid function test
  • Mixed dyslipidaemia: reduced LDL uptake from the liver
  • Normochromic normocytic anaemia or macrocytosis (latter= B12 deficiency)
56
Q

How else might you investigate for hypothyroidism?

A

Detailed family history - likely autoimmune cause
Drug history

57
Q

What are some potential complications of untreated hypothyroidism?

A
  • Cardiovascular: HF, stroke, CHD
  • Reproductive: infertility, miscarriage, stillbirth, pre-eclampsia
  • Neuro: impaired concentration, memory, decreased vision and hearing
  • Myxyoedema coma: fatal but rare = bradycardia, lethargy, seizures
58
Q

How would you manage/treat a patient with overt hypothyroidism? Why?

A

Levothyroxine - give life-long at usually 100 mcg/d. Repeat blood tests after 4-6 weeks!
Patient has low T3 and T4 so there’s low negative feedback at the pituitary = high TSH. As you restore T3 and T4, TSH returns to normal range.

59
Q

How would you manage/treat a patient with normal T3 and T4 but high TSH (compensated response)?

A
  • If seen with symptoms = give levothyroxine to see if you can normalise TSH levels and symptoms improve
  • If no symptoms = may repeat the test
60
Q

If the T3, T4 and TSH were all low, what should be considered?

A

Pituitary disease
sick euthyroid syndrome

61
Q

What are the 3 zones of the adrenal cortex? What does the zonation depend on?

A

Zonation depends on the enzymes within it
- Zona glomerulosa: cells in outer most part, produce mineralocoticoids
- Zona fasiculata: main producers of cortisol (glucocorticoids)
- Zona reticularis: responsible for producing sex steroid precursors

62
Q

What enzymes are responsible for conversion of cortisol to cortisone and vice versa (in peripheral tissues)?

A

HSD11B1: Cortisone –> cortisol
HSD11B2: Cortisol –> cortisone

63
Q

What enzyme is present in the zona glomerulosa and is responsible for production of progesterone from pregnenolone?

A

3B-hydroxysteroid dehydrogenase (type 2)
i.e. HSD3B2

64
Q

Which adrenal zones does the HPA axis regulate?

A

Zone fascicularis and zona reticularis

65
Q

What syndromes may occur if there was hormone excess in the zona glomerulosa or zona fasciculata?

A

Glomerulosa: Conns syndrome (mineralocortoid excess)
Fasiculata: Cushing’s (glucocorticoid excess)

66
Q

What is Cushing’s syndrome?

A

Excessive, inappropriate endogenous cortisol secretion characterised by:
- Features of glucocorticoid excess
- Loss of circadian rhythm to control secretion
- Disruption of negative feedback loop

67
Q

What signs/ symptoms may be present in Cushing’s syndrome?

A
  • Rounded face with purplish discoloration
  • Fat deposition on back of neck
  • Central obesity- buffalo hump
  • Weight gain
  • Hypertension
  • Easy bruising
  • Proximal myopathy: may find it difficult to stand up out of the chair
  • Purplish stretch marks on abdomen
68
Q

How might Cushing’s syndrome be diagnosed?

A
  • Assess cortisol levels over 24hr, would see a loss of circadian rhythm (usually falls at night and increases in the morning)
  • Dexamethasone suppression test: then reassess cortisol response in morning (24h monitoring)
  • Exclude pseudo-Cushings, i.e. from alcohol or depression
69
Q

What findings would indicate Cushing’s syndrome from a dexamethasone suppression test?

A

Cortisol should be supressed due to the negative feedback with dexamethasone [should be <50nmol/L]
therefore, if >50nmol/L = diagnose with excess

70
Q

What are some causes of Cushing’s syndrome?

A
  • Taking endogenous cortisone, i.e. prednisolone in asthma or RA
  • Ectopic ACTH-secreting tumour: in the lung, i.e. late stage lung cancer
  • Corticotroph tumour (Cushing’s disease): secretes excess ACTH
  • Adrenocortical tumour: in the adrenal gland itself
71
Q

How can you distinguish whether Cushing’s syndrome is caused by an adrenal tumour?

A

Due to negative feedback, adrenal tumour would have very low ACTH

72
Q

What tests might you do to distinguish ACTH-dependent causes of Cushing’s syndrom?

A
  • low dose dexamethasone suppression test
  • Inferior petrosal sinus sampling
  • high dose dexamethasone suppression test = localises Cushing’s
73
Q

Explain how inferior petrosal sinus sampling would indicate the cause of Cushing’s

A

Canulate veins/ sinuses going into the pituitary, then compare ACTH from here to blood in the periphery (can do baseline test or give CRH)

  • If levels of ACTH are high in a sinus then indicates tumour in the gland
74
Q

Explain how the high dose dexamethasone suppression test would indicate the cause of Cushing’s

A
  • If cortisol is driven by ACTH then the pituitary tumour will retain some elements of negative feedback, so cortisol should fall after high doses of dexamethasone supplementation
  • Ectopic ACTH will not have the negative feedback so cortisol will stay high
75
Q

What drugs may be given to treat Cushing’s?

A

Can block production of cortisol, i.e. metyrapone, ketoconazole, mitotane.

76
Q

How might you treat a pituitary tumour causing Cushing’s?

A
  • Trans-sphenoidal hypophysectomy: through the nose, can remove some bone and take away the tumour from pituitary gland.
  • Radiotherapy
    However, 20-50% may not be permenantly cured, and may require bilateral adrenalectomy. would need to replace hormones
77
Q

What is Addison’s disease?

A

Primary hypoaldosteronism = reduction in all steroids (glucocorticoids and/or mineralocorticoids) that are normally secreted by the 3 layers of adrenal cortex. Usually reduction in cortisol, aldosterone and DHEA.

78
Q

Other than Addison’s disease, what can cause of hypoadrenalism?

A
  • Autoimmune disorders, i.e. T1DM, thyroid disease, PA, vitiligo
  • Tuberculosis / AIDS
  • Metastatic tumour
  • Lymphoma
  • Intra-adrenal haemorrhage or infarction
79
Q

What are some symptoms of hypoadrenalism?

A

-Weakness and tiredness
- Nausea and vomiting, GI disturbance
- Postural hypotension: take BP lying down and standing up – will see it drop when they stand up
- Abdominal pain
- Weight loss
- Hypoglycaemia
- Hypotensive, hyperkalaemia patient (think primary hypoadrenalism!!)

80
Q

What 2 signs strongly indicate primary hypoadrenalism?

A

Hypotension and hyperkalaemia

81
Q

What test may you do if you suspect a patient has hypoadrenalism? What is a diagnostic result?

A

Short synacthen test: give ACTH IV or IM and measure cortisol 30 minutes later.
If cortisol <400 nmol/L = inadequate

82
Q

How do you treat hypoaldosteronism?

A

Hydrocortisone lifelong: 10mg on waking, 5mg mid afternoon. Double in significant illness (e.g. ‘flu’). Patient should also have a steroid alert bracelet and card.

83
Q

Other than hydrocortisone, what else might you treat a patient with Addison’s disease with?

A

A mineralocorticoid replacement – fludrocortisone (100 mcg). Helps sustain BP and potassium levels.

84
Q

What is Conns syndrome? What zone is affected?

A

Primary mineralocorticoid (i.e. aldosterone) excess = over production in zona glomerulosa

85
Q

What are some symptoms of Conns syndrome?

A

Hypokalaemia, weakness and lethargy. Headaches due to hypertension

86
Q

What can cause hypokalaemia?

A

➢ Vomiting: metabolic alkalosis
➢ Diarrhoea: fluid loss from the bowel
➢ Insulin therapy
➢ Diuretic use
➢ Rare causes = renal tubular acidosis and Barter syndrome

87
Q

What is the typical presentation of Conns syndrome?

A

young person, severe HTN, high sodium, low potassium

88
Q

How would you treat Conns syndrome?

A

If unilateral cause= remove adrenal gland
If bilateral tumour = Spironolactone and eplerenone

89
Q

What is the MOA of spironolactone and eplerenone?

A

Aldosterone acts on the mineralocorticoid receptor (MR) in the DCT. Spironolactone and eplerenone are MR antagonists, so block aldosterone effect

90
Q

What is a phaemochromocytoma?

A

Tumour in the adrenal medulla, where you make catecholamines

91
Q

What is the classic triad of symptoms of phaemochromocytoma?

A
  1. Hypertension
  2. Throbbing, bilateral headaches
  3. Palpitation
92
Q

What is the MOA of hydrocortisone?

A

binds to glucocorticoid receptor, leading to downstream effects such as inhibition of inflammatory transcription factors and promotes anti-inflammatory genes.

93
Q

What is the MOA of fludrocortisone?

A

inactive pro-drug. Synthetic adrenal steroid with high mineralocorticoid activity. It acts on the kidneys to increase Na+ resorption and K+ excretion.

94
Q

What is sensitivity?

A

measure of the probability of correctly diagnosing a condition
= True positives / number of those with the disease
i.e. TP / TP + FN

95
Q

What is specificity?

A

measure of the probability of correctly identifying a non-diseased person
= True negatives/ those without the disease
i.e. TN / TN + FP

96
Q

On a frequency polygon, what happens if the axis of cut off goes to the left? I.e. the cut off value for the disease gets lower

A

= less FN but also less TP

97
Q

On a frequency polygon, what happens if the axis of cut off goes to the right? I.e. the cut off value for the disease gets higher

A

More TP but more FP

98
Q

What is positive predictive value (PPV)?

A

probability disease is present when the test is positive
TP / TP + FP

99
Q

What is Negative predictive value (PPV)?

A

probability disease is not present when the test is negative
TN / TN + FN

100
Q

What is false negative rate? How can it be calculated?

A

Divide number of false negatives by (true positive + false negative)

Also equal to 1- sensitivity

101
Q

What is false positive rate and how can it be calculated?

A

divide number of false positives by (FP + TN)

Also equal to 1-specificity

102
Q

What curve is used to determine accuracy of tests? What does it assess?

A

ROC curve = Plot sensitivity (y axis) against 1-specificity (x axis)
Looks at the ability of the test to detect true positive, compared with the proportion of false positives detected

103
Q

What is determined as a good plot line on an ROC curve?

A

As close to 1 as possible

104
Q

What are the five main factors to consider when considering the most appropriate diagnostic test and cut off point?

A
  • Serious of the disease – if fatal then want most number of TP
  • Prevalence of disorder
  • Cost of the test
  • Invasiveness of procedure, usually more accurate but not well tolerated
  • Stress on those who are false positive

PBL Y2 S4 (9 decks)

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