Thyroid Flashcards
(28 cards)
1
Q
Factors contributing to low TSH
A
- Glucocorticoids
- Dopamine
2
Q
Factors contributing to low T3
A
- High cortisol levels
- Circulating inhibitors of deiodinase activity e.g. free fatty acids
- Drugs which inhibit deiodinase - propranolol, amiodarone
- Cytokines
3
Q
Factors contributing to low T4
A
- Reduced hormone binding protein
- Reduced binding to binding proteins
4
Q
Drugs that cause hyperthyroidism
A
- Interleukin 2
- Amiodarone
- Interferon alpha
- Iodine
5
Q
Drugs that cause low TBG
A
- Danazol
- Androgens
- Danazol
- Glucocorticoid
6
Q
Drugs that cause high TBG
A
- Estrogens
- Tamoxifen
- Raloxifen
- Methadone
7
Q
What is the most specific test for Grave’s disease
A
TSH receptor antibody
8
Q
Role of colestyramine in thyroid storm
A
- Increases T4 clearance
- Dexamethaone and PTU prevent conversion of T4 → T3
9
Q
Alemtuzumab and autoimmune thyroid disease
A
- Seen in nearly half of patients on alemtuzumab
- Grave’s disease (75%)
- Subacute painless thyroiditis
- Hashimoto’s thyroiditis
- Thyroid receptor antibodies - TRAB
- Mainly stimulating - hence hyperthyroidism, can also be blocking (can also alternate leading to alternating thyroid status)
- Treatment → high rate of remission either spontaneously or with treatment
- Anti-thyroid drugs first line
- Spontaneous hypothyroidism can occur too
10
Q
Autoimmune manifestations of Alemtuzumab
A
- Grave’s disease
- ITP
- Haemolytic anaemia
- Anti-GBM glomerulonephritis
Notes on alemtuzumab:
- Humanised anti-CD52 monoclonal antibody
- Depletes autoreactive lymphocytes → immune suppression, followed by immune reconstitution → B cell mediated autoimmunity
11
Q
Role of biotin in interpreting thyroid function tests:
A
- Need to stop and reassess thyroid function in 3-4 weeks
- TSH/Thyrotropin assay → excess biotin occupies streptavidin binding sites → low thyrotropin signal antibody detected yielding a falsely low thyrotropin level and falsely elevated T4 level
12
Q
Effect of biotin on blood tests
A
- TSH/T4 - hyperthyroid (falsely)
- Falsely elevated vitamin D
- Falsely low troponin
13
Q
Effects of amiodarone on thyroid function
A
- Both hypothyroidism and hyperthyroidism
- Inhibits 5’-monodeiodination of T4-T3, decreasing T3 production (spurious result)
- Direct toxic effect on thyroid follicular cells (destructive thyroiditis - type 2 AIT)
- Beta blockade - masks symptoms of thyrotoxicosis
14
Q
Distinguishing between AIT Type I and Type II
A
Type I
- More common in early phase post amiodarone commencement
- Autoantibodies may be positive
- Normal vascularity on doppler ultrasound
- Slow response to carbimazole/steroids
Type II
- More common
- More common in late phase or following discontinuation
- Vascularity reduced on Doppler ultrasound
- Rapid response to steroid
15
Q
Effect of CTLA4 inhibitors and immune checkpoint inhibitors on thyroid function
A
- CTLA4 inhibitors (ipilimumab) - hypophysitis, central hypothyroidism
- PD-1 inhibitors (pembrolizumab, nivolumab) → primary hypo- or hyperthyroidism
- Stopping immune checkpoint inhibitors generally not required
- Thyroid function improves in nearly half of people if stopped
16
Q
Effect of lithium on thyroid function (and other endocrinopathies)
A
- Hypothyroidism (goitre)
- Parathyroid hyperplasia (hypercalcaemia)
- Nephrogenic diabetes insipidus
- Not related to therapeutic range
- Predisposing factors:
- Female
- >40 years of age
- Presence of TPO antibodies
- Duration of use
17
Q
Causes of primary hyperthyroidism
A
- Grave’s disease
- Toxic multinodular goitre
- Toxic adenoma
- Thyroiditis (early stages)
- Drugs - biotin, amiodarone, immune checkpoint inhibitors, alemtuzumab
- Excess iodine, thyroxine
- Pregnancy related - hyperemesis gravidarum, hydatidiform mole
18
Q
Features suggesting Grave’s disease
A
- More common in females (8:1)
- Peak onset 40-60 years
- Pathognomic signs - diffuse goitre, thyroid eye disease (bilateral proptosis, lid retraction, scleral injection, periorbital oedema), pretibial myxoedema, clubbing
- Thyroid uptake scan → uniform normal or diffuse high uptake
- Antibodies - TSH-R Ab positive, TPO Ab often mildly positive
19
Q
Features of toxic multinodular goitre
A
- More common in women
- 50+ years
- Nodularity present for years
- Normal or elevated multifocal uptake with suppression of surrounding thyroid on thyroid uptake scan
- TSH-R Ab negative, TPO Ab low titre or absent
20
Q
Features of toxic adenoma
A
- Female > male
- 30-50 years
- Slow growing, solitary thyroid nodule
- Thyroid uptake scan → elevated focal uptake with suppression of surrounding thyroid
- TSH-R Ab negative
- TPO Ab low titre or absent
21
Q
MEN 1 Features
A
- Pituitary adenomas
- Parathyroid tumour
- Pancreatic adenomas
22
Q
MEN 2A Features
A
- Phaechromocytoma
- Medullary thyroid cancer
- Parathyroid adenomas
23
Q
MEN 2B Features
A
- Phaechromocytomas
- Medullary thyroid cancers
- Mucosal neuromas
- Marfanoid habitus
24
Q
Causes of subclinical hypothyroidism
A
Transient
- Non-thyroidal illness recovery
- Poor adherence with thyroxine
- Malabsorption of thyroxine
- Drugs (amiodarone, lithium)
Persistent
- Physiological - aging (TSH <7- 10)
- Obesity (TSH <7-10)
- Assay interference
- TSH or TRH resistance (rare)
- Adrenal insufficiency
25
Absolute indication for treating subclinical hypothyroidism
* Pregnancy
26
What is the first line agent for treating hyperthyroidism in pregnancy after the first trimester
* Carbimazole
Generally use Proplythiouracil in first trimester
27
Causes of normal T4/T3, low TSH
* Subclinical hyperthyroidism
* Recent treatment of hyperthyroidism
* Drugs (steroids, dopamine)
* Assay interference
28
Significance of subclinical hyperthyroidism and when to treat
* Progression to overt hyperthyroidism can occur → especially when TSH \<0.1
* Can be A/W cardiovascular disease (AF, CHF, CAD), bone loss, fractures, dementia → particularly in \> 65 years with severe disease
* Data lacking re when to treat - but generally in \>65 years, and post-menopausal women, especially when TSH \<0.1
