8 Thyroid Disorders Flashcards
Q: What shape is the thyroid gland? Texture? from outside? How many parts are there to it? Name them.
A: shield shaped
soft and covered by cartilage
can feel thyroid cartilage= palpable
4
- pyramidal lobe
- left lobe
- right lobe
- isthmus
Q: What can occur during thyroid operations? why? What else can be damaged? result?
A: bleeding, it’s close to lots of blood vessels
left recurrent larynheal nerve
voice change
Q: What is visible from a side view of the thyroid? (3)
A: -superior parathyroid gland
- inferior parathyroid gland
- recurrent (inferior) laryngeal nerve running behind it = one of many important nerves that run along side thyroid
Q: Draw a thyroid gland outline and label. (3) Which lobe is largest?
A: REFER
pyramidal lobe
isthmus
parathyroid glands
RIGHT
Q: What is the foramen caccum? (2)
A: dimple at back of tongue (dissappearing thyroglossal duct)
Q: What’s the weight of an adult thyroid?
A: 20g
Q: When does the thyroid start developing? From? How? (3) Wrong?
A: 7 weeks in utero (once it has reached the correct place)
from base of tongue= midline outpouching of floor of pharynx
- > outpouching forms a duct that elongates down= thyroglossal duct
- > migrates down into neck until in correct place to grow (7 weeks = in correct position)
- > divides into 2 lobes
if grows in wrong place= get lump
Q: What can happen if parathyroid glands grow in the wrong place?
A: can cause calcium problems
Q: What is the thyroglossal duct? function?
A: cord connecting thyroid to back of tongue
no function
Q: What are the 3 possible problems with thyroid development?
A: Agenesis (complete absence)
Incomplete descent (ie base of tongue to trachea)= incorrect place
thyroglossal cyst (Segment of duct persists and presents as a lump years later)
Q: What is a lingual thyroid? Treatment? Downside?
A: where it didn’t move at all and has grown at the back of the tongue
remove
-would need to be on thyroid hormone replacement for life
Q: What is thyroxine essential for? Proof? Where does it occur?
A: normal brain development
neonates with thyroxine deficiency in utero have irreversible brain damage = cretin
countries with high iodine deficiency
Q: What is a cretin? Feature? What happens when baby cretin is given thyroxine?
A: An individual with irreversible brain damage caused by lack of thyroxine
short
- tongue back in mouth
- more alert
Q: How can cretinism be prevented? When?
A: Given thyroxine immediately if the TSH is found to be high
All babies have a heel prick for a blood test for thyroid function (measuring TSH) at the same time as the Guthrie test (for phenylketonuria) at 5-10 days of age
Q: What is the site of thyroxine synthesis? Summarise. (3) Diagram. Active forms and inactive form?
A: thyroid follicular cell
- pituitary gland makes TSH
- stimulates iodine uptake from said cells ^
- events occur to produce thyroid hormone-> T3 and T4
REFER- 6 arrows
T3 and 4 are in the active form while thyroxine is inactive
Q: Describe thyroid gland thyroxine storage.
A: have enough stored in colloid to last a month -> released as you need it (TSH controls)
Q: Give an example of a thyroid hormone. Role. (2)
A: T4 goes into circulation and controls things like basal metabolic rate and body temperature
Q: Compare thyroglobulin and thyroxine binding globulin. Which can be measured?
A: Thyroglobulin is not thyroxine binding globulin
Thyroxine binding globulin bonds 75% of thyroxine in the circulation whereas thyroglobulin is INSIDE the thyroid gland only
TBG
Q: Which cells have a receptor for thyroid hormones? What are the overarching roles of thyroid hormones? (3)
A: all
regulate growth, development, metabolic rate
Q: What percentage of the population is affected by thyroid disease? Male:female? Overacitve:underactive?
A: 5%
1: 4 (more common in females)
1: 1
Q: What is primary hypothyroidism also called? What type of disease is it? Cause? (2) Result? (2) How do you clinically diagnose?
A: myxoedema
Primary thyroid failure
Autoimmune damage to the thyroid (or operation)
- Thyroxine levels decline (causes below)
- TSH levels climb
Measure TSH
Q: Draw the HPT axis.
A: hypothalamo-pituitary-thyroid axis
REFER
H produces TRH (thyrotrophin RH)
thyrotrophs in pituitary produce thyrotrophin/TSH (thyroid stimulated hormone)
cause T3 and T4 release from the thyroid
negative feedback to the pituitary and hypothalamus
Q: What are the features of primary hypothyroidism? (8)
A: -Deepening voice
- Depression
- tiredness
- Cold intolerance
- Weight gain with reduced appetite
- Constipation
- Bradycardia
- Eventual myxoedema coma
Q: Why is treatment of primary hypothyroidism essential? (3)
A: -Otherwise patients will die
- They will perform poorly
- Cholesterol goes up - causing death from heart attacks and strokes
Q: What is the treatment of primary hypothyroidism? (2)
A: Simply replace thyroxine - usually one tablet (100 micrograms on average) daily
Monitor the TSH and adjust dose until TSH is normal
Q: What’s the quantitative result of an overactive thyroid? (2) Name? (2)
A: Make too much thyroxine
TSH levels fall to zero
(thyrotoxicosis or hyperthyroidism)
Q: What are the metabolic effects of an overactive thyroid? (5)
A: Raised basal metabolic rate
Raised temperature
Burn up calories and lose weight
Increased heart rate= dangerous
Every cell in the body speeds up
Q: What are the sympomatic features of hyperthyroidism? (9)
A: Myopathy
Mood swings
Feeling hot in all weather
Diarrhoea
Increased appetite but weight loss
Tremor of hands= adrenaline making them over anxious
Palpitations
Sore eyes
goitre=swelling of the neck resulting from enlargement of the thyroid gland
Q: What are the causes of hyperthyroidism? (1)
A: Graves’ disease, where the whole gland is smoothly enlarged and the whole gland is overactive
Q: What is Graves disease? What does it involve? What does it cause? (4) Don’t confuse?
A: Autoimmune
Antibodies bind to and stimulate the TSH receptor in the thyroid
- goitre (smooth)
- hyperthyroidism
- Other antibodies bind to muscles behind the eye and cause exophthalmos
- Other antibodies stimulate growth/swelling of the shins and cause PRETIBIAL MYXOEDEMA (hypertrophy in front of tibia)
Not to be confused with myxoedema= hypothyroidism
