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Thyroid Flashcards

1
Q

What test best assesses thyroid function

A

TSH

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2
Q

What will happen to TSH in primary/secondary hyperthyroidism and primary/secondary hypothyroidism

A

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

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3
Q

When should free T3 be measured and why

A

If TSH suppressed and free T4 normal to rule out T3 toxicosis

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4
Q

When are thyroglobulin antibodies, TPO antibodies and TSH receptor inhibiting antibodies found

A

Hashimotos

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5
Q

When are Thyroid stimulating antibodies positive

A

Grave’s

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6
Q

What is the role of plasma thyroglobulin monitoring

A

Used to monitor residual thyroid activity post thyroidectomy

Normal/elevated suggest persistent, recurrent or metastatic disease

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7
Q

When might calcitonin be measured

A

If suspect medullar carcinoma / Men 2a or 2b symptoms

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8
Q

What is the role of thyroid USS

A

Size
Cystic vs solid nodule
FNAB

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9
Q

When is technitium scan done

A

Test of structure-> if nodule and hyperthyroid with low TSH

Differentiates between hot and cold nodules

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10
Q

When is radioactive iodine used

A

Test of function->order if thyrotoxic
Turnover of iodine
+uptake= overactive
-ve uptake->gland is leaking, exogenous hormone use, excess iodine (amiodarone/contrast dye)

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11
Q

When is FNA done

A

Differentiates between benign and malignant

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12
Q

When is RAIU increased

A

Graves
TMG
Toxic adenoma

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13
Q

When is RAIU decreased

A

Subacute thyroiditis
Recent iodine load
Exogenous iodine hormone

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14
Q

Define thyrotoxicosis

A

Clinical, physiological and biochemical findings in response to elevate thyroid hormone

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15
Q

Etiology of thyrotoxicosis

A

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
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16
Q

Clinical features of thyrotoxicosis

A

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

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17
Q

Overview management for thyrotoxicosis

A 
Propylthiouracil/Carbimazole
Propranolol
Radioiodine
Thyroidectomy
Get help in pregnancy and infancy
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18
Q

Triad of Grave’s

A

Hyperthyroidism
Infiltrative opthalmopathy
Pretibial myxedema

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19
Q

Pathogenesis of Graves->pituitary, heart, liver, bone, genital, metabolic, white fat, CNS, muscle

A

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

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20
Q

Key factors in Grave’s

A 
Risk factors
Heat intolerance
Sweating
Weight loss
Papitations
Tremor
TachyC
Diffuse goitre
Opthalmopathy
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21
Q

Investigations in Grave’s disease

A 
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)

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22
Q

Triggering events in Grave’s

A

Stress
Infection
Childbirth

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23
Q

What autoimmune conditions are associated with Grave’s

A

Vitiligo, T1DM, Addisons

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24
Q

What is the typical age of Grave’s patient

A

40-60 years

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25
Initial management of Grave's/hyperthyroidism
Carbimazole Propranolol (usually only until rendered euthyroid) DIltiazem (when CI to beta blockers)
26
When is dosing reassessed
Every 3-6 weeks
27
Is dosing initially based on TSH, or T3/T4 and why
TSH can be suppressed for months after hyperthyroidism is corrected
28
When is the maximum chance of remission for Grave's
After 12-18 months of antithyroid medication
29
What are the options for subsequent therapy for hyperT
Continued antiT Withdrawal RI treatment Thyroidectomy
30
When is surgery considered
Tracheal pbstruction/narrowing Dysphagia Stridor Cosmetic
31
Preferred management in older people with large goitre
Antithyroid then RI
32
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.
33
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 ```
34
Treatment of thyrotoxic storm overview
1. Couteract peripheral effects 2. Inhibit thyroid hormone synthesis 3. 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
35
S&S thyrotoxic storm
``` Severe hyperT +Temperature Agitation Confusion Coma TachY AF, DV, goitre thyroid bruit Acute abdomen HF Cardiovascular collapse ```
36
Precipitants of thyrotoxic storm
Recent thyroid surgery, radioiodine, infection, MI, trauma
37
Investigations in thyrotoxic storm
TSH, T4, T3, cultures, cardiac enzymes
38
What is the effect of stable iodide (Lugols, potassium iodide)
Acutely inhibits iodide release from thyroid in Grave's
39
Mechanism of action of carbimazole and propylthiouracil
Xiodination of thyroglobulin | Xconversion T4->T3
40
Side effects of thioreleyenes
Headache Nausea Rash GIT disturbance Most important->agranulocytosis. Monitor WCC if have sore throat/fever
41
Action of guanethidine eye drops
adrenergic antagonist= -ve sympathetic outflow | -ve exopthalmos
42
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
43
Important side effect of radioiodine
Hypothyroidism
44
Why is hypothyroidism +likely in Grave's treated with radioiodine
++TSH= +iodine uptake
45
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
46
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
47
Subtype of subacute thyroiditis
Painful | Painless
48
Painful thyroiditis
DeQuervains
49
Epidemiology of DQ
+Female | 40-50 yo
50
Presentation and progression of DQ
Post viral Painful goiter, tender warm Worse on movement
51
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
52
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
53
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
54
Management of hypothyroid phase in SAT
Mild: observation and reassess +/- Levothyroxine Moderate: levothyroxine
55
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.
56
Types of painless subacute thyroiditis
Postpartum (5-10%) Autoimmune Lymphocytic
57
Progress of postpartum
Thyrotoxicosis at 2-3 mo | Hypothyroid phase 4-8 months
58
What can post partum thyroiditis be mistakenly diagnosed as
Postpartum depression
59
Prognosis of SAT
Full recovery in most | 10% permanent hypothyroid
60
Main concern in simple non toxic goiter
``` Mass effects Dysphagia Tracheal deviation Pembertons sign Stridor ```
61
Epidemiology of simple goiter
Endemic->when 10% population has goiter Sporadic in young femals Goitrogenic foods
62
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
63
Common presentation of MNG
Thyrotoxic features | Elderly with new onset AF
64
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 ```
65
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
66
Management of TMNGwhen mass effect/suspicion of cancer
Surgery Pre-treat with anti-thyroid-thiamazole If +symptoms/CV risk->propranolol
67
Management of T MNG when pregnant/breastfeeding w/o mass/suspicion of Ca
Antithyroid drugs ?Surgery If +symptoms, CV risk->propranolol
68
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
69
Differential of diffuse goiter
Physiological Grave's Hashimotos thyroiditis Subacute thyroiditis
70
Differential of nodular goiter
Multinodular goiter Adenoma Carcinoma
71
Definition of hypothyroidism
Clinical syndrome caused by cellular responses to insufficient thyroid hormone
72
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 ```
73
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
74
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
75
Hypothyroidism associations
``` Turners and Downs CF PBC Ovarian hyperstimulation POEM's syndrome Dyshormonogenesis ```
76
What is POEM's syndrome
Polyneuropathy Organomegaly Endocrinopathy m-protein bank
77
Pregnancy problems with hypthyroidism
``` Eclampsia Anemia Prematurity Low birthweight Stillbirth PPH ```
78
Subclinical hypothyroid investigation findings
+TSH, normal free T4
79
What is hashimoto's
Chronic autoimmune thyroiditis
80
Two major forms of hashimoto's
Goitrous | Atrophic
81
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
82
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
83
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
84
Investigations in Hashimoto's
``` High TSH Low T4 Thyroid peroxidase and thyroglobulin antibodies +LDL Anemia ```
85
What is myxedema coma
Severe form, untreated hypothyroidism
86
Presentation of myxedema coma
``` Impaired consciousness Hypoventilation Hypothermia Hyponatremia Hypotension Hypoglycemia Bradycardia Generalised edema ```
87
What is myxedema coma complicated by
``` Trauma Sepsis Cold exposure Administration of hypnotics/narcotic Stressful events ```
88
Why hyponatremia in myxedema
Low activity of Na/K ATPase->impaired sodium/water reabsorption
89
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
90
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.
91
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
92
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
93
Commonest cause of thyroid mass
Colloid mass | Thyroid adenoma or hyperplastic nodule
94
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 ```
95
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

MI Internal Medicine (67 decks)

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