Thyroid Flashcards
What test best assesses thyroid function
TSH
What will happen to TSH in primary/secondary hyperthyroidism and primary/secondary hypothyroidism
Primary hyperT->TSH low, negative feedB
Secondary hyperT->+TSH= +T3/T4
Primary hyperT: +TSH->less negative feedB
Secondary hypoT: TSH low/normal with variabl response to TRH depending on site of lesion
When should free T3 be measured and why
If TSH suppressed and free T4 normal to rule out T3 toxicosis
When are thyroglobulin antibodies, TPO antibodies and TSH receptor inhibiting antibodies found
Hashimotos
When are Thyroid stimulating antibodies positive
Grave’s
What is the role of plasma thyroglobulin monitoring
Used to monitor residual thyroid activity post thyroidectomy
Normal/elevated suggest persistent, recurrent or metastatic disease
When might calcitonin be measured
If suspect medullar carcinoma / Men 2a or 2b symptoms
What is the role of thyroid USS
Size
Cystic vs solid nodule
FNAB
When is technitium scan done
Test of structure-> if nodule and hyperthyroid with low TSH
Differentiates between hot and cold nodules
When is radioactive iodine used
Test of function->order if thyrotoxic
Turnover of iodine
+uptake= overactive
-ve uptake->gland is leaking, exogenous hormone use, excess iodine (amiodarone/contrast dye)
When is FNA done
Differentiates between benign and malignant
When is RAIU increased
Graves
TMG
Toxic adenoma
When is RAIU decreased
Subacute thyroiditis
Recent iodine load
Exogenous iodine hormone
Define thyrotoxicosis
Clinical, physiological and biochemical findings in response to elevate thyroid hormone
Etiology of thyrotoxicosis
Hyperthyroidism:
Graves
MNG
Toxic adenoma
Thyroiditis:
Subacute
Silent
Postpartum
Extrathyroidal:
Endogenous->struma ovarii, teratoma, metastatic follicular
Exogenous
Excessive thyroid stimulation:
Pituitary thyrotroph
Pituitary thyroid hormone receptor resistance
+hCG (pregnancy, -ve TSH, +T4)
Drugs: Amiodarone Lithium Phenytoin Carbamazepine Rifampin
Clinical features of thyrotoxicosis
General: fatigue, heat intolerance, irritability, fine tremor
CVS: Tachy, AF, palpitations
GI: weight loss, diarrhea, +appetite, thirst, +frequency
Neurology: proximal myopathy, hypokalemic periodic paralysis
GU: oligomenorrhea, amenorrhea, decreased fertility
Dermatology: fine hair, moist, vitiligo, soft nails with onycholysis, palmar erythema. Acropachy and pretibial myxedema in Grave’s
MSK: decreased bone mass, muscle weak
Hematology: Graves->leukopenia, lymphocytosis, splenomegaly, lymphadenopathy
Eye: Graves->lid lar, retraction, proptosis, diplopia, decreased acuity, puffy, conjunctival injection
Overview management for thyrotoxicosis
Propylthiouracil/Carbimazole Propranolol Radioiodine Thyroidectomy Get help in pregnancy and infancy
Triad of Grave’s
Hyperthyroidism
Infiltrative opthalmopathy
Pretibial myxedema
Pathogenesis of Graves->pituitary, heart, liver, bone, genital, metabolic, white fat, CNS, muscle
Thyroid stimulating hormone receptor antibodies (TSI)->triggering->mimics TSH->+growth of thyroid gland
Pituitary->-ve expression of thyrotropic= Suppressed TSH
Heart->+ANP=+rate/contractility
Liver->+T1deiodinase, LDL receptors= +peripheral T3, -ve LDL
Bone->+psteocalcin, +ALP= +bone turnover
Genital->+SHBG, -ve testosterone, estrogen antagonism=-ve libido/erection, irregular menses
Metabolic->+FA oxidation, +Na/K ATPase= +thermogenesis
MSK->+SRCa2+ activated ATPase= proximal myopathy
Key factors in Grave’s
Risk factors Heat intolerance Sweating Weight loss Papitations Tremor TachyC Diffuse goitre Opthalmopathy
Investigations in Grave’s disease
TSH (suppressed) Free T4 (+, not in T3 toxicosis/subclinical) Free T3 T3RU, Free T4 index FBC (normocytic normochromic) UEC, Ca+ LFT+ Thyroid autoantibodies If opthalmopathy->visual acuity testing, eye movements
May consider: RAIU, TIS, T U/S (highly vascular, diffuse, enlarged)
Triggering events in Grave’s
Stress
Infection
Childbirth
What autoimmune conditions are associated with Grave’s
Vitiligo, T1DM, Addisons
What is the typical age of Grave’s patient
40-60 years
Initial management of Grave’s/hyperthyroidism
Carbimazole
Propranolol (usually only until rendered euthyroid)
DIltiazem (when CI to beta blockers)
When is dosing reassessed
Every 3-6 weeks
Is dosing initially based on TSH, or T3/T4 and why
TSH can be suppressed for months after hyperthyroidism is corrected
When is the maximum chance of remission for Grave’s
After 12-18 months of antithyroid medication
What are the options for subsequent therapy for hyperT
Continued antiT
Withdrawal
RI treatment
Thyroidectomy
When is surgery considered
Tracheal pbstruction/narrowing
Dysphagia
Stridor
Cosmetic
Preferred management in older people with large goitre
Antithyroid then RI
F/u after remission of hyperthyroidism
clinical and biochemical follow-up is at 1, 2, 3 and 6 months, then annually thereafter. The patient should be instructed to have prompt testing if any symptoms of recurrent hyperthyroidism develop.
Management of thyrotoxic storm
ABC 2 large bore cannula IVF NGT if vomiting Bloods for T3, T4, STH, cultures (if suspect infections) Monitor BP Sedate if necessary Propylthiouracil Lugol's solution Dexamethasone Propranolol Adjust fluids, cool with tepid sponging, paracetamol Get endocrinologist involved
Treatment of thyrotoxic storm overview
- Couteract peripheral effects
- Inhibit thyroid hormone synthesis
- Treat systemic complications
Block hormone synthesis and release
Decrease conversion of T4 to T3
Control tachyC and rate dependent HF
Restore hydration
Give sedation if necessary
S&S thyrotoxic storm
Severe hyperT \+Temperature Agitation Confusion Coma TachY AF, DV, goitre thyroid bruit Acute abdomen HF Cardiovascular collapse
Precipitants of thyrotoxic storm
Recent thyroid surgery, radioiodine, infection, MI, trauma
Investigations in thyrotoxic storm
TSH, T4, T3, cultures, cardiac enzymes
What is the effect of stable iodide (Lugols, potassium iodide)
Acutely inhibits iodide release from thyroid in Grave’s
Mechanism of action of carbimazole and propylthiouracil
Xiodination of thyroglobulin
Xconversion T4->T3
Side effects of thioreleyenes
Headache
Nausea
Rash
GIT disturbance
Most important->agranulocytosis. Monitor WCC if have sore throat/fever
Action of guanethidine eye drops
adrenergic antagonist= -ve sympathetic outflow
-ve exopthalmos
Indication, CI and mechanism for radioiodine
I: Mainly Relapse
CI: Pregnancy, thyroid eye disease as can worsen
M: Taken up as iodine->radiation destroys tissue
Important side effect of radioiodine
Hypothyroidism
Why is hypothyroidism +likely in Grave’s treated with radioiodine
++TSH= +iodine uptake
Indications, complications of surgery
Obstruction, thyrotoxic, failed medical, thyroid Ca, cosmesis, eye disease (radioiodine can make worse)
Complications: recurrent/superior laryngeal nerve injury, hypoparathyroidism, hoarseness, bleeding into neck->stridor
Definition of subacute thyroiditis
Acute inflammation->hyperthyroid stage->hypothyroidism->euthyroidism
Acute inflammation->release of steroid hormone, not +in production
Release of virus/thyroid antigen during infection->activation of cytotoxic T lymphocytes, damage to follicular cells
Subtype of subacute thyroiditis
Painful
Painless
Painful thyroiditis
DeQuervains
Epidemiology of DQ
+Female
40-50 yo
Presentation and progression of DQ
Post viral
Painful goiter, tender warm
Worse on movement
Investigations in subacute thyroiditis
thyroid-stimulating hormone (TSH)- suppressed
total T4, total T3, T3 resin uptake, free thyroxine index - ++
T3:T4 ratio- 15:1
radioactive iodine uptake- decreased
ESR- elevated
CRP- elevated
antithyroid antibodies (thyroid peroxidase antibodies)-normal
Why is propilthiouracil and carbimazole not useful in thyrotoxicosis associated w/ sbacute thyroiditis
The thyrotoxicosis associated is due to +release of thyroglobulin and not productio
Management of hyperthyroid stage of SAT
Supportive
Analgesia->ibuprofen, paracetamol + codeine
If pain not controlled by NSAIDs- prednisilone
Tachy/tremor->propranolol
If severe thyrotoxicosis- potassium iodide + prednisilone
Management of hypothyroid phase in SAT
Mild: observation and reassess
+/- Levothyroxine
Moderate: levothyroxine
Explanation for antithyroid
MOA: blocks thyroid hormone synthesis (propylthiouracil also blocks peripheral conversion)
Ind: Grave’s, thyroid storn, short term before surgery.
Prec: Propylthiouracil preferred in first trimester pregnancy. Carbimazole may be preferred in breastfeeding. Agranulocytosis- contraindicated
Adverse effects: usually in first 8 weeks. Itch, rash (use antihistamines), NV, leucopenia, gastric discomfort
Agranulocytosis- most commonly in first 3 months. Rapid onset.
Hepatotoxicity-> +LFTs usually resolves after 2 months with continued use.
Tell your doctor immediately is develop fever,, mouth ulcers, sore throat, rash, severe fatigue, nausea, abdominal pain or jaundice.
Types of painless subacute thyroiditis
Postpartum (5-10%)
Autoimmune
Lymphocytic
Progress of postpartum
Thyrotoxicosis at 2-3 mo
Hypothyroid phase 4-8 months
What can post partum thyroiditis be mistakenly diagnosed as
Postpartum depression
Prognosis of SAT
Full recovery in most
10% permanent hypothyroid
Main concern in simple non toxic goiter
Mass effects Dysphagia Tracheal deviation Pembertons sign Stridor
Epidemiology of simple goiter
Endemic->when 10% population has goiter
Sporadic in young femals
Goitrogenic foods
Etiology and pathogenesis of multinodular toxic goiter
Autonomous alterations in TSH++->recurrent hyperplasia and involution of follicular cells
+Size, number and colloid->rupture, hemorrhage, scarring and calcification
Endemic, sporadic, female, older age
Common presentation of MNG
Thyrotoxic features
Elderly with new onset AF
Investigations in T MNG
TSH-> suppressed Consider Free T4, T3- + I-123 thyroid scan and uptake- multiple hot and cold spots Tc99 scan Thyroid US Metabolic- possible hypercalcemia, LFTs FBC- anemia or leukocytosis. Baseline propr to starting antithyroid TPO- negative TSH antibodies- negative ECG- may show AF CT neck non-contrast- may delineate goiter
Management of T MNG in non-preg/non lactating, with/O mass effect/suspicion of Ca
Radioactive iodine therapy
Pre-treat with anti-thyroid->thiamazole
Second line->surgery
Management of TMNGwhen mass effect/suspicion of cancer
Surgery
Pre-treat with anti-thyroid-thiamazole
If +symptoms/CV risk->propranolol
Management of T MNG when pregnant/breastfeeding w/o mass/suspicion of Ca
Antithyroid drugs
?Surgery
If +symptoms, CV risk->propranolol
Management of thyroid eye disease
Get specialist input
Treat thyroid abnormalities
Advise to stop smoking as worsens
Artifical tears, sunglasss, avoid dust, elevate bed when sleeping
If more severe may need steroids
Sight-threatening->surgical decompression
Differential of diffuse goiter
Physiological
Grave’s
Hashimotos thyroiditis
Subacute thyroiditis
Differential of nodular goiter
Multinodular goiter
Adenoma
Carcinoma
Definition of hypothyroidism
Clinical syndrome caused by cellular responses to insufficient thyroid hormone
Symptoms
weakness lethargy cold sensitivity constipation weight gain depression menstrual irregularity myalgia dry or coarse skin eyelid oedema thick tongue facial oedema coarse hair bradycardia goitre
Signs
BRADYCARDIC Reflexes relax slowly Ataxia Dry skin/hair Yawning/drowsy/coma Cold hands Ascites/non-pitting edema/pericardial effusion/pleural effusion Round/puffy face Defeated demeanour Immobile +/- ileus CCF
Neuropathy, myopathy
Etiology
Autoimmune:
Primary atrophic thyroiditis
Hashimotos
Other: Post thyroidectomy/radioiodine Drug induced-goitrogens (iodine), PTU, MMI, lithium Infiltrative Iodine deficiency Congenital Neoplasia Subacute thyroiditis
Secondary hypothyroidism- pituitary
Tertiary- hypothalamus
Peripheral resistance- Refetoff syndrome
Hypothyroidism associations
Turners and Downs CF PBC Ovarian hyperstimulation POEM's syndrome Dyshormonogenesis
What is POEM’s syndrome
Polyneuropathy
Organomegaly
Endocrinopathy
m-protein bank
Pregnancy problems with hypthyroidism
Eclampsia Anemia Prematurity Low birthweight Stillbirth PPH
Subclinical hypothyroid investigation findings
+TSH, normal free T4
What is hashimoto’s
Chronic autoimmune thyroiditis
Two major forms of hashimoto’s
Goitrous
Atrophic
What is the difference between how goitrous and strophic hashimoto’s presents
Goitrous->goiter and euthyroid, then progresses to hypothyroidism
Atrophic presents with hypothyroidism from the start
What is the pathophysiology of Hashimoto’s
Defect in T suppressors lead to cell mediiated destruction of thyroid follicles.
B cells->autoantibodies against thyroglobulin, thyroid peroxidase, TSH receptor and Na/I symporter
Risk factors for Hashimoto’s
Female
Genetic susceptibility (Down’s, Turner’s)
Family/personal history of autoimmune disease
Smoking
High iodine intake
Stress and infection
Investigations in Hashimoto’s
High TSH Low T4 Thyroid peroxidase and thyroglobulin antibodies \+LDL Anemia
What is myxedema coma
Severe form, untreated hypothyroidism
Presentation of myxedema coma
Impaired consciousness Hypoventilation Hypothermia Hyponatremia Hypotension Hypoglycemia Bradycardia Generalised edema
What is myxedema coma complicated by
Trauma Sepsis Cold exposure Administration of hypnotics/narcotic Stressful events
Why hyponatremia in myxedema
Low activity of Na/K ATPase->impaired sodium/water reabsorption
Treatment of myxedema coma
ABCs, ICU
Baseline cortisol then Hydrocortisone
Thyroxine
Supportive: mechanical ventilation, fluids, vasopressor, rewarming, dextrose
ECG monitoring
Look for underlying cause and treat->infection, MI etc
Must have IV therapy b/c impaired GI motility
Investigations in myxedema
\+TSH Low T4, T3 UEC: hyponatremia \+Serum creatinine (reduced renal excretion) ABG Cultures->look for sepsis \+Creatinine kinase Glucose->hypoglycemia CBC->look for infection
CXR: Cardiomegaly, pericardial effusion, congestive heart failure, and/or pleural effusion are observed.
What is sick euthyroid syndrome
Transient change in thyroid hormones amoungst patients with serious illness, trauma or stress
No intrinsic thyroid/pituitary disease
Low T3, Low TSH, (if severe low T4)
With recovery TSH may overshoot and become high
Mechanisms of SES
Inhibition of thyroid-releasing hormone and thyroid-stimulating hormone secretion
Abnormal thyroid binding to thyroid binding proteins
Decrease in thyroid binding globulin
Commonest cause of thyroid mass
Colloid mass
Thyroid adenoma or hyperplastic nodule
Less common cause of thyroid mass
Non-toxic multinodular goitre Toxic adenoma, single Toxic multinodular goitre Differentiated thyroid cancer (papillary, follicular) Medullary thyroid cancer Anaplastic thyroid cancer Lymphoma Simple epithelial-lined thyroid cyst Thyroglossal duct cyst Acute suppurative thyroiditis Subacute granulomatous thyroiditis Chronic lymphocytic (Hashimoto's) thyroiditis Painless lymphocytic thyroiditis Graves' disease Enlarged parathyroid gland(s): benign Parathyroid carcinoma Metastasis from non-thyroidal malignancies
Counselling the use of levothyroxine
Synthetic version of normal hormone
Give to bring levels up to normal
Once daily before breakfast
Tablet form
Take for life
Start test dose then review in 2-3 weeks
TSH test every 2-3 months until stable
When TSH level stable, check annually
Side effects rare when thyroxine levels stable
May have hyperthyroid symptoms-vomiting, diarrhea, HA, palpitations, heat intolerance
Safe in pregnancy- may need to increase dose
