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Block 2 FCM > Grave's Disease > Flashcards

Grave's Disease Flashcards

1
Q

What lab panel result is consistent with hyperthyroidism?

A

Depressed TSH, elevated FT3 and FT4

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2
Q

What exam finding is specific for Grave’s disease?

A

Pretibial Myxedema

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3
Q

Where on the thyroid would you see radio iodine uptake during scintigraphy?

A

Diffuse uptake bilaterally

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4
Q

First line treatment for Grave’s disease in pregnancy?

A

PTU

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5
Q

MOST COMMON FORM OF HYPERTHYROIDISM in US

A

Grave’s disease

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6
Q

Dopamine and somatostatin can both put negative feedback on the TRH to inhibit ______.

A

pituitary gland.

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7
Q

TRH is released from hypothalamus and causes release of ____ to stimulate thyroid gland.

A

TSH

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8
Q

There are receptors on the thyroid gland to receive the TSH, which then produce T3 and T4 which goes to surrounding tissues and then there is again another feedback loop, T3 and T4 will act as ________ on hypothalamus and pituitary gland to try and keep everything in homeostasis.

A

inhibitors

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9
Q

What is hyperthyroidism?

A

abnormally elevated levels of thyroid hormone (T3 and T4)

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10
Q

What can Hyperthyroidism lead to?

A

thyrotoxicosis (hypermetabolic condition)

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11
Q

what is thyrotoxicosis?

A

disturbances of the normal homeostatic mechanism (at the level of the pituitary gland, the thyroid gland, or in the periphery) increasing basal metabolic rate

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12
Q
  • Binding of TSH to receptors on the thyroid gland leads to the release of ___.
A

T4, T3

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13
Q

Elevated levels of these hormones act on the hypothalamus to decrease TRH secretion and thus the synthesis of TSH

A

T4, T3

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14
Q

> 99.9% of T4 and T3 in the peripheral circulation is active or inactive?

A

inactive- it is bound to plasma proteins,

very few is free

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15
Q

Is Free T3 or T4 more biologically active?

A

T3

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16
Q

the body’s sensitivity is increased to catecholamines when there is elevated ___ count

A

T3

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17
Q

These are Essential to proper development and differentiation of all cells of the human body. They Regulate protein, fat, and carbohydrate metabolism, affecting how human cells use energetic compounds. They also Stimulate vitamin metabolism

A

thyroid hormones

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18
Q

T3/T4 synthesis requires ___.

A

iodine

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19
Q

Lack of dietary iodide causes ___.

A

goiter

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20
Q

what happens when iodide is introduces to a person with goiter?

A

thyrotoxicosis. Can act as a immune stimulator, triggering autoimmune disease.

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21
Q

In hyperthyroidism, what are levels of T3, T4, and TSH

A

high T3 and T4 and low TSH

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22
Q

what is grave’s disease also known as?

A

Diffuse Toxic Goiter

“Basedow Disease”- europe

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23
Q

is grave’s an autoimmune disorder?

A

yes

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24
Q
  • Thyroid –stimulating immunoglobulins (TSI) or TSH receptor antibodies bind to TSH receptor sites on thyroid cell membranes – this will stimulate gland to hypersynthesize hormones- when they bind to them they tell the thyroid to produce _____.
A

T3 and T4

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25
Q

Circulating auto-antibodies against the thyrotropin (TSH) receptors results in?

A

continuous stimulation of the thyroid gland

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26
Q

Grave’s Auto-Antibodies

A

thyroid-stimulating immunoglobulin (TSI), thyroid-stimulating antibody (TSab),
or TSH-receptor antibody (TRab)

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27
Q

what Stimulate iodine uptake, protein synthesis, and thyroid gland growth?

A

Grave’s Auto-Antibodies

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28
Q

Pituitary thyrotropin secretion is suppressed due to increased _____ (negative feedback)

A

thyroid hormones

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29
Q

what Causes 60-80% of cases of thyrotoxicosis in the US

A

Grave’s

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30
Q

occurence rate of graves in US

A

30/100k

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31
Q

Grave’s Peak occurrence in people aged ____.

A

20-40 years

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32
Q

Lower rates of Grave’s in ___.

A

African Americans

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33
Q

is there a higher male or female ratio in Grave’s disease?

A

higher female.

m:f= 1:5-10

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34
Q

Graves ophthalmopathy is more common in women or men?

A

women

35
Q

presentation of grave’s in younger patients?

A

Younger patients tend to exhibit symptoms of sympathetic activation (eg, anxiety, hyperactivity, tremor)

36
Q

presentation of grave’s in older patients?

A

Older patients have more cardiovascular symptoms (eg, dyspnea, atrial fibrillation) and unexplained weight loss, fewer presenting signs, don’t present with as many signs as younger patients do

37
Q

________ suggests Graves disease

A

Ophthalmopathy suggests Graves disease

38
Q

Symptoms (ROS) in Grave’s

A
  • Gen: Fatigue, general weakness
  • Derm: warm moist skin, sweating, pretibial myxedema (very specific for Grave’s)
  • Neuro: tremors, prox muscle weakness
  • CV: palpitations, CP, edema, DOE
  • Resp: Dyspnea
  • GI: increased motility (Bowel Movements)
  • OPH: tearing, Gritty Foreign Body sensation, photophobia, eye pain, protruding eye, diplopia (issues with tracking), visual loss
  • Renal: polyuria, polydipsia
  • Metabolic: heat intolerance, weight loss, poor glycemic control
  • GU: irregular menses, decreases flow, amenorrhea, gynecomastia, impotence
  • PSYCH: restless, anxiety, irritable, insomnia
39
Q

Physical Exam findings for Grave’s

A
  • Irregular heart rhythm, tachycardic, tachypnea, murmur
  • Hyperactive BS, hand tremor, ↑DTR, prox muscle weakness, warm, moist skin, alopecia, edema, acropachy (clubbing of fingers and fatty deposits between joints- unique to grave’s), restless, anxious,
40
Q

Symptoms/signs Unique to Grave’s?

A

Ophthalmopathy and dermopathy:

- Pretibial myxedema, proptosis, lid lag/retraction, EOM changes, periorbital edema, visual loss, chemosis, injections

41
Q

what % of grave’s patients have proptosis/eye changes

A

30%

42
Q

How is thyroid gland in patient with Grave’s?

A
  • Thyroid gland is diffusely enlarged and smooth (should feel both lobes equally, not focused in isthmus it should be all over), thyroid bruits
43
Q

will there be thyroid nodules in persons with gRAVE’S?

A

There can be, +/- thyroid nodules

44
Q

% of Grave’s patient have at least mild ophthalmopathy

A

50%

45
Q

Thyrotropin receptors are very expressive in _____.

A

fat and connective tissue

46
Q
A

chemosis (inflammation of mucosal layer in skin), injection, lid retraction, diplopia, proptosis, acropachy

47
Q

2 phases in ophthalmopathy for Grave’s

A

Inflammatory and fibrotic

48
Q

first phase in ophthalmopathy for Grave’s

A

Inflammatory: deposition of glycosaminoglycan (polysaccharide) in muscles, periorbital edema, pain

49
Q

second phase in ophthalmopathy for Grave’s

A

Fibrotic: diplopia, further lid retraction- when lid starts retracting you see more of eye and it becomes even more pronounced

50
Q

what increases risk of getting ophthalmopathy with grave’s?

A

Higher risk in smoker receiving radioactive iodine

51
Q

Symptomatic ophthalmopathy pts require ______.

A

full retinal/fundoscopic exam

52
Q

Work up for Grave’s

A
  • Thyroid function tests (first step is to do a thyroid panel)
  • ↓TSH
  • ↑T3, T4
  • TSI autoantibodies positive in up to 80% Grave’s (diagnostic)
  • Anti–thyroid peroxidase (anti-TPO) antibody not diagnostic but present in 85% of patients with Grave’s
  • Baseline LFTs for anti-thyroid Rx (methinazole can be liver toxic)
  • HgA1c
53
Q

If the etiology of thyrotoxicosis is not clear after physical examination and other laboratory tests, it can be confirmed by ____

A

Radioactive Iodine Scanning

54
Q

what is Iodine Uptake?

A
  • the degree and pattern of isotope uptake indicates the type of thyroid disorder
55
Q

Radiology report for Radioactive Iodine Scanning in pt with Grave’s

A

“normoechogenic and large glands with increased radioresistance”- fancy talk for large on both sides

56
Q

What will iodine uptake look like in patients with Grave’s disease?

A

Diffuse enlargement of both thyroid lobes, with uniform uptake of isotope and elevated radioactive iodine uptake

57
Q

first treatment for grave’s

A

Radioactive Iodine

58
Q

Indications for Radioactive Iodine treatment for Grave’s

A

large diffuse gland, multiple thyrotoxicosis symptoms, elevated thyroxine (T4), titres of TSI

59
Q

what medication should be withheld before doing Radioactive Iodine treatment for Grave’s?

A

o Withhold anti-thyroid drugs prior to tx (preferably two days- best results for two weeks) can require higher doses of RI if on anti-thyroids

60
Q

Radioactive Iodine treatment will cause what long term?

A

Hypothyroidism within 2-3months- requires lifelong replacement

61
Q

Concerns with Radioactive Iodine?

A
  • can spark thyroid storm especially in the elderly- this can be mitigated by pretreating with anti-thyroid meds PTU/Methimazole.
62
Q

Contra Indication with Radioactive Iodine?

A

pregnancy, breast feeding, and recent lactation ,Children under 5- increases risk of thyroid cancer, severe ophthalmopathy

63
Q

Can Radioactive Iodine exacerbate pre-existing ophthalmopathy?

A

yes

64
Q

Do Anti-thyroid drugs/thyroidectomy influence course of ophthalmopathy?

A

no

65
Q

Ablation of ____ may help in long term treatment of ophthalmopathy

A

thyroid

66
Q

]Correction of ______ is treatment for ophthalmopathy

A

hyper/hypothyroidism

67
Q

ophthalmopathy treatment

A

Mild-Moderate Dz: local tx- eye patches, sunglasses, elevating head at night, artificial tears and ointments. If that not helpful: high dose steroids, orbital radiotherapy or orbital decompression

68
Q

how to treat Severe or progressing ophthalmopathy?

A
  • high dose steroids (40mg/d) continued until evidence of improvement. Tapered over 1-3 months.
69
Q

You can do Surgical decompression for ____ reduction for disfigurement (generally to be done during the fibrotic phase when patient is euthyroid).

A

proptosis

70
Q

Pretibial Myxedema Treatment

A
  • Tx: topical steroids with occlusive dressing (saran wrap) 3-10 weeks
  • Severe: high burst PO steroids
71
Q

How does Pretibial Myxedema present?

A
  • Elevated firm, non-pitting thickening of lower legs bilaterally
72
Q

percentage of Grave’s patients with Pretibial Myxedema ?

A
  • Observed in 5-10% pts

- Tend to be same patient w/ophthalmopathy

73
Q

Is thyroidectomy recommended 1st line therapy for Grave’s?

A

no

74
Q

When can Thyroidectomy

be a treatment option for Grave’s?

A 
o	Non-compliance or intolerant of anti-thyroid medication
o	Moderate to severe ophthalmopathy
o	Large Goiters/Compressive symptoms
o	Refusal or CI to Radioiodine therapy
o	Questionable thyroid carcinoma
o	Permanent cure 
o	Severe hyperthyroid in children
75
Q

consults for Grave’s

A 
-	Refer to Endocrinologist
o	Pregnancy
o	Newborns
o	Not responsive to usual therapy
-	Refer to Ophthalmologist
o	Proptosis
o	Follow up visual acuities, prevention, eye muscle functions
-	Refer to Dermatology 
o	myxedema not responsive to topical steroids
76
Q

2016 Guidelines

for Grave’s

A
  • Beta blockers for symptomatic thyrotoxicosis (HR >90)
  • Overt Grave’s: RI therapy, anti-thyroid medications, surgery
  • Methimazole used for 12-18 months, d/c if T4 & TR Abys are normal
  • Children (<5) with Grave’s: avoid RI (risk of thyroid CA later). Can use methimazole, thyroidectomy
77
Q

Anti-thyroid medications

A

Methimazole, Propylthiouracil (PTU)

78
Q

what antithyroid do you use during first trimester?

A

Propylthiouracil (PTU)

79
Q

what antithyroid is usually reserved for use in thyroid storm?

A

Propylthiouracil (PTU)

80
Q

which antithyroid is more potent and longer-acting

A

Methimazole

81
Q

Prognosis for Grave’s untreated?

A

severe thyrotoxicosis (thyroid storm)- potentially fatal

82
Q

chronic complication of Grave’s

A

o Weight loss, muscle atrophy, bone resorption
o Psychocognitive complications
o Ophthalmologic complications (blindness)
o Osteoporosis
o Cardiac Hypertrophy
o Arrhythmias
Atrial fibrillation/flutter

83
Q

usual prognosis after Grave’s treatment

A

hypothyroid after treatment (require replacement)

Block 2 FCM (21 decks)

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