Thyroid diseases Flashcards

1
Q

What are the most important causes of hypothyroidism?

A
  • IATROGENIC
  • autoimmune thyroiditis (Hashimoto)
  • congenital defect: agenesis, dyshormonogenesis
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2
Q

What are the types according to age?

A
  • Fetal or infantile: cretinism

- adulthood: hypothyroidism or myxedema

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3
Q

inadequate thyroid hormone production during fetal & neonatal development causes what disease?

A

cretinism

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4
Q

What are the types of cretinism?

A
  • iatrogenic
  • endemic: dietary iodine deficiency
  • sporadic: agenesis or dyshormonogenesis
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5
Q

What are the general clinical features of adult hypothyroidism?

A
tiredness 
weight gain
cold intolerance 
cold extremities 
periorbital puffiness 
goiter 
hyperlipidemia
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6
Q

What are the thyroid related congenital anomalies?

A
  • ectopic thyroid
  • dyshormonogenesis
  • thyroglossal cyst
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7
Q

What type of ectopic thyroid is present in the posterior third of the tongue?

A

Lingual thyroid

causing

  • dysphagia
  • speech impairment
  • respiratory obstruction
  • hemorrhage
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8
Q

What is an ectopic thyroid?

A
  • ectopic thyroid tissue may lie anywhere in the line of descent
  • could be the whole thyroid or just residual thyroid tissue
  • any disease that occurs in the thyroid could occur in ectopic goiter
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9
Q

What methods of investigation are used to confirm ectopic thyroid tissue?

A

radioisotope scan: shows uptake of iodine
CT scan: intrathoracic thyroid
ultrasound should be done to see if the thyroid is absent from its normal location

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10
Q

How should ectopic thyroid be treated?

A

surgical excision
L-thyroxine daily
radioisotope therapy for ablation

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11
Q

which congenital thyroid disorder is an autosomal recessive condition where there is either a deficiency of thyroid enzyme or inability to bind or retain iodine?

A

dyshormonogenesis

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12
Q

How should dyshormonogenesis be treated?

A

L-thyroxine

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13
Q

What is Pendered’s syndrome?

A
type of dyshormonogenesis 
abnormal thyroxin synthesis 
- goiter 
- +/- hypothyroidism 
- hearing loss
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14
Q

What is the cause of a thyroglossal cyst?

A

failure of obliteration of part of thyroglossal trunk

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15
Q

What is the most common area for a thyroglossal cyst to occur?

A

subhyoid area

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16
Q

What is the most specific diagnostic sign for a thyroglossal cyst?

A

MOVES UP WITH TONGUE PROTRUSION

moves up with deglutition

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17
Q

Which thyroid congenital anomaly may be accompanied by infection & fistula formation?

A

thyroglossal cyst

fistula is always acquired

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18
Q

What investigations should be used in assessment of thyroglossal cyst?

A
  • NECK US

- radio-isotope scanning

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19
Q

sistrunk operation is preformed to treat what?

A

thyroglossal cyst

  • removal of cyst, tract & body of hyoid bone
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20
Q

What is the classification of Goiter?

A

SIMPLE

  • diffuse
  • nodular

TOXIC

  • Grave’s
  • toxic nodule
  • toxic nodular goiter

NEOPLASTIC

  • Benign: follicular adenoma
  • Malignant

INFLAMMATORY

  • Autoimmune: Hashimoto
  • Granuloma: De-Quervain’s
  • Fibrosing: Riddle’s
  • Infective: very rare

MYXEDEMATOUS

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21
Q

What is most likely to be a malignancy in the thyroid?

A

solitary thyroid nodule

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22
Q

What is a dominant thyroid nodule?

A

by palpation you feel one nodule but on examination there are many impalpable small nodules

  • most likely benign
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23
Q

What are the causes of simple goiter?

A

PRIMARY IODINE DEFICIENCY

  • endemic areas (not enough iodine intake)
  • increased demand (puberty, pergnancy, & lactation)

SECONDARY IODINE DEFICIENCY
- drugs

DYSHORMONOGENESIS
- like Pendred’s syndrome (abnormal peroxidase enzyme)

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24
Q

which type of goiter is caused by an increased demand of T3 & T4 during pubertal age or pregnancy?

A

Physiological goiter (diffuse hyperplastic goiter)

its reversible if corrected early

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25
Q

What are the clinical signs of a physiological goiter?

A
  • symmetrical
  • diffuse
  • soft
  • smooth
  • Euthyroid
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26
Q

How should a physiological goiter be managed?

A
  • reassurance if Euthyroid
  • iodized salt
  • if there’s an abnormal enlargement of the thyroid that looks cosmetically displeasing L-thyroxine could be used to inhibit TSH
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27
Q

Which type of goiter is specifically endemic?

A
  • colloid goiter

- longstanding iodine deficiency

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28
Q

Which type of goiter will cause hyperinvolution of most acini when treated with iodine replacement?

A

colloid goiter

there will be accumulation of colloid in the gland causing its enlargement (only reversible in early stage)

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29
Q

What is the clinical appearance of a colloid goiter?

A
  • irregular enlarged soft gland
  • sometimes firm & rubbery
  • euthyroid
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30
Q

How should a colloid goiter be treated?

A

small gland: L-thyroxine to decrease TSH & colloid formation
large gland: subtotal thyroidectomy

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31
Q

What is the commonest disease of goiter & what is its cause?

A

Multinodular goiter
due to repeated episodes of stress —> persistent TSH stimulation —> diffuse hyperplasia of gland —> fluctuation of TSH level —> hyperinvolution —> inactive nodules & internodular tissue is active —> haemorrhage & necrosis —> inactive nodule formation —> MNG

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32
Q

MNG clinical picture?

A
  • slowly progressive enlarging neck swelling causing disfigurement
  • butterfly, globular or irregular shape
  • nodular surface
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33
Q

What are the complications of MNG?

A
  • secondary thyrotoxicosis (if there’s abnormal hyperactive function of internodular tissue)
  • follicular carcinoma
  • tracheal obstruction by compression (dyspnea & stridor)
  • cystic degeneration of nodule
  • hemorrhage in cyst –> stridor
  • retrosternal extension
  • cosmetic issue
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34
Q

What investigation should be done for MNG?

A
  • ULTRASOUND

- isotope scanning to differentiate between toxic

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35
Q

How should any simple goiter be treated?

A
  • in mild enlargement:
    consercative & follow up US every 6 months
  • large thyroid early in pathogenesis:
    give L-troxin to control TSH
  • late stage or complications:
    thyriodectomy - subtotal has a risk of recurrence
    - total no recurrence but life-long
    supplementation
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36
Q

What are the types of retrosternal goiter?

A
  • primary (intrathoracic): ectopic tissue in mediastinum
  • secondary: extension from enlarged thyroid from neck
  • plunging goitre: appear into neck by coughing or deglutition
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37
Q

What is the commonest type of a retrosternal goiter?

A

Secondary
(arises from lower pole of nodular goiter due to negative intrathoracic pressure it gets drawn into superior mediastinum)

38
Q

What is the clinical picture of a retrosternal goiter?

A
  • compression manifestation: on trachea, esophagus, carotid artery, IJN
  • hoarseness of voice
  • dilated veins over superior part of chest wall
  • Pemberton’s sign (RED FACE when hands are raised)
  • lower border of gland is not seen or felt
  • dull percussion over sternum
39
Q

What is the most beneficial method of investigation in retrosternal goiter?

A

CT

40
Q

What treatment should be done for a retrosternal goiter?

A
  • TOTAL THYROIDECTOMY
41
Q

What automimmune thyroid disease is caused by microsomal & thyroglobulin antibodies?

A

HASHIMOTO’S THYROIDITIS

42
Q

What is the pathogenesis of Hashimoto thyroiditis?

A

hyperplasia —> fibrosis

ASKANAZY CELLS are tyoical

43
Q

What is the clinical picture of Hashimoto thyroiditis?

A
  • HASHITOXICOSIS due to destruction of thyroid follicles THEN hypothyroidism
  • associated with other autoimmune diseases & hepatosplenomegaly
44
Q

What are the complication’s of Hashimoto thyroiditis?

A
  • Non-Hodgkin’s lymohoma

- hypothyroidism

45
Q

What investigation is most diagnostic test for Hashimoto?

A

thyroid antibody assay

46
Q

How should Hashimoto be treated?

A
  • L-thyroxine therapy

- if goitre is large and causing discomfort –> subtotal thyroidectomy

47
Q

Which thyroid disease is caused by a viral infection?

A
  • De-Quervain’s thyroiditis (mumps or coxsackie)
  • causes painful goiter
  • treated by steroids to decrease pain
48
Q

Which type of thyroiditis simulates malignancy?

A

Riedel’s Thyroiditis

  • collagen disorder
  • stony hard
  • FNA should be preformed to exclude malignancy
  • treat with isthectomy
49
Q

What are the types of toxic goiter?

A
  • diffuse toxic goiter (Grave’s disease, Primary
    thyrotoxicosis)
  • toxic multinodular goiter (secondary thyrotoxicosis)
    (Plummer’s disease)
  • toxic nodules (autonomous nodule)
50
Q

What disease is caused by an automimmune disorder with increased levels of TSI, Ts Ab, & LATS?

A

Grave’s disease

51
Q

what does the Exophthalmos producing substance cause?

A

Grave’s opthalmopathy

52
Q

What is the characteristic triad of Grave’s disease?

A
  • toxic manifestation
  • diffuse vascular fleshy symmetrical goiter
  • eye signs & pretibial myxoedema
53
Q

long standing simple nodular goiter that is causing hyperthyroidism will lead to?

A

toxic nodular goiter

  • nodules are inactive & internodular thyroid tissue is overactive
  • usually in middle aged or elderly
54
Q

a completely healthy thyroid gland with a single nodule that is over active is called?

A

autonomous nodule

- autonomous hypertrophy & hyperplasia at nodule

55
Q

What effects will an autonomous nodule have on TSH?

A

high levels of circulating thyroid hormone will SUPPRESS TSH secretion —> normal thyroid tissue will be inactive

56
Q

What is your diagnosis for a patient that is presenting with toxic & autoimmune manifestation?

A

Graves

57
Q

What age group is Grave’s disease more common in?

A

younger age group

58
Q

What age group is secondary thyrotoxicosis more common in?

A

older age group

59
Q

What are the metabolic changes that will occur in a patient developing a toxic goiter?

A
  • sympathetic over activity
    dyspnea, palpitation, tiredness, sweating, heat intolerance, nervousness, flushed face, warm moist extremities
  • increased catabolism (increased appetite & decreased weight)
  • fatigue & muscle weakness
  • fine tremors
  • exaggerated reflexes
60
Q

What are the effects of toxic goiter on the cardiovascular system?

A
  • palpitations even at rest
  • shortness of breath at rest
  • angina
  • thyrotoxic arrhythmia stages
    • multiple extrasystoles
    • paroxysmal atrial tachycardia
    • paroxysmal atrial fibrillations
    • persistent atrial fibrillation not responsive to digoxin
61
Q

What is the difference between true & false exophthalmos?

A

TRUE FALSE
- actual protrusion of - retraction of upper eyelid
eyeball (only in - hypercontraction of Muller’s
autoimmune) muscle caused by sympathetic
hyperactivity

62
Q

What other systemic effects could toxic goiter have on the patient?

A
  • oligo- or amenorrhea
  • urinary frequency
  • hair loss
  • pruritus & palmar erythema
  • ostemyletia
  • generalized bone aches due to osteoporosis
63
Q

what is pretibial myxoedema?

A
  • bilateral, symmetrical, shiny, yellowish thickened dry skin with coarse hair in feet & ankles
  • due to deposition of myxomatous tissue in skin & subcutaneous plane under the effect of LATS
  • only in Grave’s disease (like acropathy (clubbing))
64
Q

compare between primary & secondary thyrotoxicosis

A

GRAVE’S SECONDARY
- younger - older
- acute - gradual
- remission & exacerbation - progressive
- mainly toxic manifestations - neck swelling followed
by toxic manifestations
- neurological - cardiovascular
- true & false exophthalmos - only false
- may have other autoimmune - no
manifestations
- diffuse enlargement - NODULAR enlargement
- mild enlargement - large
- thrill & bruit - no

65
Q

What investigations should be done in suspected toxic goiter?

A

THYROID FUNCTION TEST

  • increased TH3 & TH4
  • suppressed TSH

AUTOANTIBODY TITER
- only in Grave’s

NECK US

ISOTOPE SCANNING
- differentiate between primary toxic & secondary

66
Q

How should Grave’s disease be treated?

A

MEDICAL TREATMENT

  • antithyroid drugs
  • beta blockers
  • Lugol’s iodine
  • tranquilizers

IF MEDICAL TREATMENT DOESN’T WORK FOR 18 MONTHS
- if patient is <45 years old SURGERY
if patient is >45 years old RADIOACTIVE IODINE

67
Q

How should secondary thyrotoxicosis be treated?

A

SURGERY

prepare patient with medical treatment before surgery to avoid thyrotoxic crises

68
Q

How should a toxic nodule be treated?

A
  • if patient is <45 SURGERY

- if patient is >45 RADIOIODINE

69
Q

What are the contraindications for medical treatment?

A
  • toxic autonomous nodule
  • retrosternal goiter
  • lactation & pregnancy
70
Q

What is the commonest used antithyroid drug?

A

CARBIMAZOLE

  • blocks oxidation of inorganic iodine with tyrosine
  • suppresses autoimmune process in Grave’s
  • up to 60mg/day should be given initially
  • taken for a maximum of 1 & a half year
71
Q

Which antithyroid drug could be used in pregnancy?

A

Propyl thiouracil

  • blocks peripheral conversion of T4 & T3
  • decreases autoantibody levels
  • could be used in children with hyperthyroidism as well
  • could lead to neonatal goiter
  • 100 - 200mb every 8hours till euthyroid then maintenance done of 50mg/day
72
Q

What are the drugs used to prep patient for thyroidectomy?

A

PROPRANOLOL (inderal) + carbimazol until Euthyroid

  • reduces cardiac problems
  • blocks peripheral conversion of T3 & T4

LUGOL’S IODINE

  • decreases vascularity of gland making it firm and easier to handle during surgery
  • 10 days prior to surgery 10-30 drops/day
73
Q

What are the disadvantages of medical treatment?

A
  • prolonged course of treatment
  • can’t predict remission or relapse
  • relapse rate is 40%
  • size of swelling may not regress
74
Q

What are the indications of surgical treatment?

A
  • failure of drug treatment in primary thyrotoxicosis in young patients
  • autonomous toxic nodule in <45 years
  • nodular toxic goiter
  • retrosternal toxic goiter
75
Q

What are the disadvantages of surgical treatment?

A
  • recurrent thyrotoxicosis: subtotal thyroidectomy
  • thyroid insufficiency
  • complications of surgery
76
Q

What are the indications of radioiodine therapy?

A
  • primary thyrotoxicosis after 45 years of age
  • autonomous toxic nodule
  • recurrent thyrotoxicosis
  • refusal of surgery
77
Q

What are the contraindications of radioiodine therapy?

A
  • <45 years old
  • pregnancy & lactation
  • secondary thyrotoxicosis (extensive fibrosis)
  • iodine allergy
78
Q

What are the complications of radioiodine therapy?

A
  • myxoedema (IN GRAVE’S cause all glands are hyperactive)
  • genetic mutation, leukemia, carcinoma
  • isolation
  • takes 3 months to get full response then patient has to take antithyroid drugs
79
Q

What is the first line of treatment in a toxic thyroid in pegnancy?

A

propyl thiouracil + inderal (propranolol)

ONLY IN 2nd trimester surgery is allowed

80
Q

What is the first line treatment of toxic thyroid in children, and what is absolutely contraindicated?

A

First line = carbimazole + inderal until puberty if there’s no regression then subtotal thyroidectomy

Contraindicated = radioiodine

81
Q

secondary thyrotoxicosis causing thyrocardia should be treated with?

A
  • control symptoms first & stabilize patient

- subtotal thyroidectomy

82
Q

how should recurrent thyrotoxicosis after surgery be treated?

A
  • <45 yrs surgery

- >45 yrs radioiodine

83
Q

how should a thyrotoxicosis patient with recent onset of proptosis be treated?

A

AVOID early thyroidectomy cause it could lead to malignant exophthalmos
- medical treatment until exophthalmos is static for 6 months then total thyroidectomy

84
Q

What is the difference between proptosis & exophthalmos?

A

PROPTOSIS: protrusion of eyeball due to any disease
EXOPHTHALMOS: protrusion of eyeball due to thyroid disease

85
Q

What is malignant exophthalmos?

A

exophthalmos + complications

86
Q

What is the pathogenesis of exophthalmous?

A

infiltration of retrobulbar tissues with fluid & round cells causing edema of retrobulbar contents mainly in GRAVES

87
Q

How can we clinically differentiate between true & false exophthalmos?

A
  • Nafziger’s test: tilting patient’s head while standing behind patient
  • Frazer’s test: look at patient from the side
88
Q

What is the first eye sign to appear?

A
STELLWAG'S SIGN
starring look (infrequent blinking)
89
Q

What is the second eye sign to appear?

A

DALRYMPLE’S SIGN
upper eye lid retraction
rim of upper sclera can be seen

90
Q

What is the 3rd eye sign to appear?

A

VON GRAEFE’S SIGN lid lag

inability of eyelid to keep pace with eyeball during examination

91
Q

What is Joffroy’s sign?

A

absence of wrinkling on forehead when patient looks up

only in true exophthalmous

92
Q

Lack of convergence of eyeball is called?

A

Moebius sign: due to lymphocytic infiltration of inferior oblique & rectus muscles in primary toxicosis