Thyroid Flashcards Preview

Internal Medicine > Thyroid > Flashcards

Flashcards in Thyroid Deck (95):
1

What test best assesses thyroid function

TSH

2

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

3

When should free T3 be measured and why

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

4

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

Hashimotos

5

When are Thyroid stimulating antibodies positive

Grave's

6

What is the role of plasma thyroglobulin monitoring

Used to monitor residual thyroid activity post thyroidectomy
Normal/elevated suggest persistent, recurrent or metastatic disease

7

When might calcitonin be measured

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

8

What is the role of thyroid USS

Size
Cystic vs solid nodule
FNAB

9

When is technitium scan done

Test of structure-> if nodule and hyperthyroid with low TSH
Differentiates between hot and cold nodules

10

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)

11

When is FNA done

Differentiates between benign and malignant

12

When is RAIU increased

Graves
TMG
Toxic adenoma

13

When is RAIU decreased

Subacute thyroiditis
Recent iodine load
Exogenous iodine hormone

14

Define thyrotoxicosis

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

15

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

16

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

17

Overview management for thyrotoxicosis

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

18

Triad of Grave's

Hyperthyroidism
Infiltrative opthalmopathy
Pretibial myxedema

19

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

20

Key factors in Grave's

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

21

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)

22

Triggering events in Grave's

Stress
Infection
Childbirth

23

What autoimmune conditions are associated with Grave's

Vitiligo, T1DM, Addisons

24

What is the typical age of Grave's patient

40-60 years

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