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Med 2 > Thyroid disorders, Parathyroid and Ca2+ > Flashcards

Thyroid disorders, Parathyroid and Ca2+ Flashcards

1
Q

What type of gland is thr thyroid gland?

A

Endocrine

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2
Q

What is the relevant anatomy of the thyroid gland?

A

Spans C5-T1
Two lobes joined by an isthmus - made of follicles which create and stories thyroid hormones.

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3
Q

What hormones are produced by the thyroid gland?

A

Tri-iodothyronine T3
Thyroxine T4

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4
Q

What is the differences/relationships between T3 and T4 as hormones?

A

T4 breaks down into T3
T3 is more active but has a shorter half life (1 day compared to 7 days)
This keep hormone levels more stable over time

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5
Q

What is the funcation of the thyroid gland?

A

Increase metabolic rate
Inc protein synthesis
Inc heart function
Inc heat production
Inc nervous system activity

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6
Q

What is the role of thyroid peroxidase in the production of thyroid hormones?

A

Iodine enters the colloid as iodide I- and is oxidised to iodine I+ by thyroid peroxidase.

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7
Q

Describe the histology of thyroid gland?

A

Follicular cells produce thyroid hormone - form rings (follicles) surrounding colloid
Between are parafollicular cells which produce calcitonin.
Also blood vessels

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8
Q

Give a basic description of how thyroid hormones are produced in the thyroid gland.

A

TSH stimulates hormone production
Follicular cells secrete thyroglobulin into the colloid
Iodide (I-) is secreted into colloid - is converted to iodine (I+) by TPO enzymes
Binds to thyroglobulin tyrosine rings to form iodinated thyroblobin - MIT or DIT,
MIT + DIT = T3 precurose
DIT and DIT = T4 precursor
Endocytosed into follicular cells
Fuses with lysosomes undergoes proteolysis to release T3 and T4 from thyroglobulin backbone
Secretes into blood-stream bound to TBG (this is inactive) - minority may be free T3 and T4 - this is active.

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9
Q

What is the role of thyroglobulin?

A

Is found in thyroid gland colloid
Secreted by follicular cells
Is a scaffold for thyroid hormone production

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10
Q

What is the role of calcitonin?

A

Secreted by para-follicular cells (C-cells) in thyroid gland
Regulates calcium metabolism
Decreases serum calcium levels by inhibiting osteoclast activity.

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11
Q

What type of recepotrs doe thyroid hormones act on?

A

Nuclear receptors

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12
Q

How does iodine deficiency affect the thyroid gland?

A

Hypothyroidism
Goiter

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13
Q

What is the hypothalamic pituuitary thyroid axis?

A

Hypo release TRH
Stimulates anterior pituitary to release TSH
Stimulates thyroid to release T£ and T4
Act in tissues
Act in brain to show negative feedback to the hypo and ant pituitary

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14
Q

What is meant by primary hypothyroidism?
What are the most common causes?

A

THyroid produces inadequate thyroid hormones

UK - autoimmune
Global - Iodine deficiency
Treatment of hyperthyroidism
Lithium/amiodarone

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15
Q

What is secondary hypothyroidism?
What are the most common causes?

A

Pituitary produced inadequate TSH

Tumours - pituitary adenoma
Surgery to pituitary
Radiotherapy
Sheehans syndrome
Trauma

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16
Q

How can thyroid function tests be used to differentiated between primary, secondary and subclinical thyroid disease?

A
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17
Q

What are the key symptoms of hypothyroidism?

A

MOMS SO TIRED

Memory loss
Obesity
Menorrhagia, malar flush, muscle aches
Sore muscles, skin dry
Slowness - physical (constipation, heart rate) and mental
Odema (fluid retention)
Tiredness (fatigue)
Intolerance to cold
Reduced heart rate and reflexes
Energy levels are low
Depression

Others - goiter, brittle nails, coarse hair, hair loss

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18
Q

What is hashimotos thyroiditis?

A

Autoimmune inflammation of the thyroid gland
Initially enlarged goiter followed by atrophy
Transient acute phase thyrotoxicosis then hypothyroidism.

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19
Q

What antibodies can be identified in Hashimoto’s thyroiditis?

A

Anti-thyroid peroxidase (Anti-TPO)
Anti-thyroglobulin (anti-Tg)

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20
Q

What are some risk factors for Hashimotos disease?

A

Female
Autoimmune disease - T1DM, addisons etc
Family history of thyroid or AI
Radiation exposure
Age - more common in older
Medication - lithium and amiodarone.

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21
Q

What condition can hashimotos thyroiditis put you at risk of?

A

MALT lymphoma

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22
Q

What is the goiter like in Hashimoto’s disease?

A

Firm and non tender

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23
Q

What is the treatment for hypothyroidism?

A

1st line = levothyroxine = synthetic T4
Metabolised to T3 in the body, dose is titrated based on TSH levels 4w initially then every 3 months

If suspect 2ndary cause urgent referral to endocrinology is required.

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24
Q

How can TSH levels be used to influence levothyroxine dose in hypothyroidism treatment?

A

TSH normal - remain same
TSH high - increase dose
TSH low - decrease dose

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25
Q

What are some complications of hypothyroidism?

A

Myxoedema coma
Dyslipidaemia
Metabolic syndrome
Coronary artery disease
Stroke
Heart failure
Neurologica/cognitive impairement
Adverse maternal/fetal outcomes

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26
Q

What is the key presentation of myxoedema coma?

A

Lethargy
Bradycardia
Hypothermia
Hyporeflexia
Hypoglycaemia
Seizures +/- coma

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27
Q

What is myxoedema coma?

A

Rare potentially fatal
Result of chronic untreated hypothyroidism
Normally in older patients who are undiagnosed or poor compliance
Can be triggered: infection, heart failure, stroke

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28
Q

What are the first line investigation for hypothyroidism?

A

TSH levels
Serum Free Thyroxine T4 levels

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29
Q

Define thyrotoxicosis

A

The clinical manifestation of excess circulating thyroid hormones

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30
Q

What is the difference between priamry and secondary hyperthyroidism?

A

Primary - thyroid gland cause
Secondary - pituitary/hypothalamus disorder

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31
Q

What are the most common causes of hyperthyroidism?

A

GIST

Graves disease
Inflammation (thyroiditis)
Solitary toxic nodule
Toxic multi-nodular goitre

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32
Q

How can TFT differentiate between primary, secondary and sub-clinical hyperthyroidism?

A
33
Q

What are the symptoms of hyperthyroidism?

A

SWEATING
Sweating/sexual dysfunction
Weight loss
Energy levels are high
Anxiety, arrhythmia
Tremor tachycardia and tiredness (fatigue)
Irritability and intolerance to heat and insomia
Neural - hyperreflexia
Goiter and GI (diahorrea, inc appatite)

34
Q

What is the most common cause of hyperthyroidism?

A

Autoimmune Graves disease

35
Q

What is graves disease?
Basic process?

A

Autoimmune - hyperthyroidism
TSH receptor antibodies - stimulate TSH receptors on thyroid resulting in over-production of thyroid hormones

36
Q

What antibodies are commonly found in graves disease?

A

TSH receptor antibodies
We may also find anti-TPO and and anti-TG

37
Q

What signs are specific to graves disease?

A

Diffuse goiter (no nodules)
Pertibial myxoedema (mucin deposits)
Thyroid acropathy (hand swelling and clubbing)
Graves orbitopathy (exopthalmos)

38
Q

What are the risk factors for graves disease?

A

FH - AI or graves
AI
Age - 30 to 50yrs
Female
Smoking - particularly for orbitopathy

39
Q

What is the course of disease in thyroiditis?

A

Initial hyperthyroidism then followed by hypothyroidism

40
Q

What antiabodies tends to be found in thyroiditis?

A

Anti-TPO
Anti-Tg

41
Q

What are the different causes of thyroiditis?

A

Hashimoto’s thyroiditis
De Quervains - subacute - associated with fever
Post partum - painless 2-6month after delivery/miscarriage
Drug induced

42
Q

What is De Quervains thyroiditis?
What is its disease progression?

A

Sub acute thyroiditis
Triggered by a viral infection (2 to 8 weeks before)
1. Thyrotoxicosis - goiter, flu like illness, raised inflammatory markers
2. Hypothyroidism (10% remain here)
3. Return to normal

43
Q

What is the management for De Quervains thyroiditis?

A

Self limiting
Conservative - beta blockers and NSAIDS

44
Q

Give an overview of solitary toxic nodules as a cause of hyperthyroidism?

A

Single abnormal thyroid nodule releases excessive thyroid hormone
Usually benign adenomas
Treatment with beta-blockers +/- surgical removal

45
Q

How does toxic multinodular goiter present as a cause of hyperthyroidism?

A

Aka Plummers disease
Most common in over 50yrs
Multiple autonomously acting thyroid nodules.
Palpate within a goiter

46
Q

What are some common side effects of anti-thyroid medication?

A

Carbimazole - pancreatitis
PTU - severe liver reactions
Both - agronulocytosis - can present with severe infections (norm sore throat in exams)

47
Q

How is hyperthyroidism initially managed?

A

Specialist endocrinologist
1st line = carbimazole (TPO inhibitor)
2nd line = propylthiouracil (TPO inhibitor)
Usually normalised within 4-8 weeks

48
Q

How is hyperthyroidism long term management treatment organised?

A

Maintenance carbimazole
Titration-block - titrate dose (decrease) to maintain normal levels
Block and replace - higher dose to stop all production with give levothyroxine

49
Q

How does radioactive iodine treat thyroid disease?

A

Treats hyperthryoidism
Drank
Taken up by thyroid - destroyes proportion of cells
Decrease hormone production
Remission may take 6months - after which thyroid tends to be underactive (require levothyroxine)

50
Q

What warnings must be given for the use of radioactive iodine in treatment of hyperthyroidism?

A

Not be pregnant now or in 6 months
Men must not conceive in next 4 months
Limit contact with vulnerable - children and pregnant women

51
Q

What is the use of beta-blockers in hyperthyroidism?

A

Propanolol
Combat adrenaline-related symptoms
Non-selective
Useful in patients with thyroid storm

52
Q

What different types of surgery can be used in the treatment of hyperthyroidism?

A

Total thyroidectomy
Partial thyroidectomy
Thyroid nodulectomy

53
Q

What are some common complications of hyperthryoidism?

A

Thyrotoxicosis crisis
Graves orbitopathy
Compression symptoms (dysphagia, breathlessness, hoarse voice)
Atrial fibrillation
Heart Failure

54
Q

How can a pituitary adenoma present indirectly?

A

Bitemporal hemianopia (peripheral vision loss) - pressure on optic chiasm
Loss of visual acuity (optic nerve)

55
Q

What can trigger a thyrotoxic crisis?

A

Thyroid strom - life threatning hyper
Infection, trauma, pregnancy, surgery, stroke, undiagnosed, stopped antithyroid medication

56
Q

How does thyrotoxic crisis present?

A

Fever
Tachycardia/arrhythmia
Agitation/delirium
Hypertension
Hyperthermia
Heart Failure
Jaundice
Coma

57
Q

What is the management for thyrotoxic crisis?

A

Emergency admission
Fluid resuscitation
Betal blockers
Steroids
Anti-arrhythmic medications
Anti-thyroid medications

58
Q

What investigations should be done for thyroid disease?

A

Bedside = ECG
Bloods - TFT, FBC, HbA1c, lipid profile, CRP/ESR, U&Es, LFTs, bone profile
Auto- antiTPO, Anti-Tg, TSH receptor
Imaging - US thyroid and FNA, radioactive iodine uptake scan

59
Q

What can different findings on a radio-active iodine uptake scan of a thyroid intake pathology?

A

Diffuse high uptake = graves
Focal high uptake - toxic multinodular goitre and adenomas
Cold areas = thyroid cancer

60
Q

What are some red flags for a neck lump?

A

Hard, fixed mass
Age >35yrs
Mucosal lesion in head/neck
Persistent hoarsness/dysphagia
Trismus (spasm of jaw muscles)
Unilater ear pain

61
Q

What is the role of the parathyroid gland?

A

Chief cells produce PTH in response to hypocalcemia.

62
Q

How does parathyroid hormone increase blood calcium?

A
  1. Increase osteoclast activity - re-absoring Ca2+ from bones
  2. Increase Ca2+ reabsoprtion in kidneys (less urinated out)
  3. Increase VitD activity - increase Ca2+ absorption from intestines
63
Q

What is the relationship between calcium and phosphate in the body?

A

Inversely related
As calcium levels rise, phosphate will fall
Phosphate binds to calcium reducing available free calcium within the bloodstream

64
Q

What are the common causes of primary, secondary and tertiary hyperparathyroidism?

A

Primary - tumour
Secondary - Low VitD/CKD
Tertiary - hyperplasia (secondary to secondary)

65
Q

How can blood tests differentiate between primary, secondary and tertiary hyperparathyroidism?

A

Primary - high PTH and high calcium
Secondary - high PTH, low/normal calcium
Tertiary - high PTH and high Calcium

66
Q

What is the treatment for primary hyperparathyroidism?

A

Surgical removal

67
Q

What is the treatment for secondary hyperparathryoidism?

A

Correct low VitD ?CKD

68
Q

What is the treatment for tertiary hyperparathyroidism?

A

Partial surgical removal

69
Q

Explain the process behind tertiary hyperparathyroidism

A
  1. Prolonged secondary hyperparathyroidism
    2.Hyperplasia of the parathyroid glands = higher baseline PTH
  2. secondary hyperparathyroidism is treated and baseline PTH remains inappropriately high.
  3. causinghypercalcemia.
  4. Treatment is surgically removing part of the parathyroid tissue to return PTH to normal.
70
Q

What are the main causes of hypercalcemia?

A

Primary hyperparathyroidism
Malignancy

71
Q

What are the main symptoms of hypercalcemia?

A

Stones - kideny stones
Bones - bone pain
Moans - fatigue, depression, psychosis
Groans - constipation, nausea, vomitting

72
Q

What change in calcium levels can indicate malignancy?

A

Severe or sudden raise
Requires emergency treatment

73
Q

How common in hypercalcemia of malignancy?

A

20% of all cancer patients
Most associated with multiple myeloma

74
Q

What are the mechanisms by which hypercalcemia of malignancy occur?

A
  1. Excessive secretion of PTH related protein
  2. Bony mets and osteoclast activating factors
  3. Production of 1,25dihydroxy Vit D (calcitriol)
75
Q

What is the treatment for hypercalcemia of malignancy?

A

IV saline (to restore intra-vascular volume)
Followed by IV bisphopshonates +/- calcitonin

76
Q

What are the most common causes of hyperparathyroidism?

A

Damage to parathyroid gland during surgery
Autoimmune disease
Hypomagnaseamia (reversible)
Radio-active iodine treatment for hyperthryoidism (rare)

77
Q

What are the signs and symptoms of hypocalcemia?

A

Praseathesia and muscle cramps
Tetany (increase muscle spasm)
Crampy abdominal pain
Emergencies - seziures, prolonged QT interval, laryngospasm

78
Q

What signs can be induced during examination to show hypocalcemia?

A

Trousseaus signs - carpopedal spasm induced by pressure applied by arm by inflated bp cuff
Chvosteks sign - twitching of facial muscles in response to tapping over the facial nerve.

Med 2 (4 decks)

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