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Endocrine Week 1 > SG 1.1: Thyroid Disorder Cases > Flashcards

SG 1.1: Thyroid Disorder Cases Flashcards

1
Q

what are the 3 congenital thyroid disorders?

A
  1. thyroglossal duct cyst
  2. lingual thyroid
  3. congenital hypothyroidism
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2
Q

what is the most common cause of preventable intellectual disability?

A

congenital hypothyroidism

check TSH on a newborn in the first week of life! if TSH is elevated, immediately give TG

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3
Q

how does the thyroid develop?

A

it starts at the base of the tongue, travels down the thyrroglossal duct to the anterior neck and if the duct persists then the patient gets a cystic dilation

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4
Q

what is athyroglossal duct cyst? how does it present?

A

cystic dilation of thyrglossal duct remnant

presents as anterior neck mass in the middle

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5
Q

how does congenital hypothyroidism present?

A
  1. floppy baby
  2. difficult to arouse
  3. hypotonic
  4. large anterior fontanelle
  5. umbilical hernia
  6. slowing mental activity
  7. myxedema –> puffy, non pitting edema
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6
Q

what developmental issues does hypothyroidism cause? what are its 5 signs?

A

creationism

  1. mental retardation
  2. short stature, abnormal skeleton
  3. coarse facial features
  4. big tongue
  5. umbilical hernia
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7
Q

how does hypothyroidism cause cretinism?

A
  1. hypothyroidism in early pregnancy
  2. thyroid agenesis
  3. dyshormogenetic goiter; patient unable to make thyroid hormone
  4. iodine deficiency
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8
Q

what is the most common enzyme deficiency causing dyshormonogenetic goiter?

A

thyroid perodidase deficiency

this is the enzyme that is hormone that iodinates TG to form T4 and T3

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9
Q

what are the 4 thyroid disorders to remember?

A
  1. hyperthyroidism: Graves, thyroid storm, multi nodular/toxic goiter
  2. hypothyroidism: hypothyroid myxedema, Hashimoto thyroiditis
  3. subacute deQuervain granulomatous thyroiditis
  4. Reidel fibrosing thyroiditis
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10
Q

why do you get increased BMR and SNS activation in hyperthyroidism?

A

BMR increased Na/K ATPase with the generation of heat

sympathetic drive increases due to increased B1 adrenergic receptor activity

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11
Q

why do you get increased BMR and SNS activation in hyperthyroidism?

A

BMR increased because metabolism of thyroid hormones involves Na/K ATPase with the generation of heat

sympathetic drive increases due to increased B1 adrenergic receptor activity

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12
Q

why do you have heat intolerance and sweating in hyperthyroidism?

A

increased Na/K ATPase uses lots of ATP

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13
Q

how does hyperthyroidism effect calcium levels?

A

hypercalcemia from bone resorption which can lead to osteoporosis

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14
Q

how does hyperthyroidism affect cholesterol level and sugar levels?

A

hypocholesterolemia

hyperglycemia due to thyroid causing gluconeogeneis sand glycogenolysis

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15
Q

what is a multinodular goiter?

A

enlarged thyroid with multiple nodules

due to relative iodine deficiency like food that stops iodine absoprtion

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16
Q

what is a toxic goiter?

A

multinodular goiter that has a region that becomes overactive

it secretes excess thyroid hormone

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17
Q

what is a thyroid storm and how does it present?

A

exacerbation of hyperthyroidism resulting in elevated catecholamines and massive hormone elevation

presents as:

  1. arrhythmias
  2. hyperthermia
  3. vomiting
  4. hypovolemic shock
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18
Q

how do you treat a thyroid storm?

A
  1. B blockers
  2. PTU
  3. steroids
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19
Q

what does PTU do in addition to blocking peroxidase?

A

inhibits peripheral conversion from T4 to T3

T3 is the active form

20
Q

how does Graves disease lead to hyperthyroidism?

A

autoantibody IgG that stimulates the TSH receptor and increases thyroid release

21
Q

who gets graves disease?

A

women of childbearing age

22
Q

what are the 3 signs of Graves disease?

A
  1. goiter
  2. exophthalmos
  3. pretibial myxedema
23
Q

in Graves disease why do you get a goiter?

A

antibodies stimulate TSH receptor which increases thyroid hormone production resulting in thyroid hyperplasia

24
Q

what is the histology seen in Grave’s disease?

A

hyperplasia

large follicular areas with lots of colloid

25
Q

what is the blood test done for Graves disease?

A
  1. increased free T4

2. TSH drops

26
Q

how do you treat Graves?

A
  1. B blockers
  2. PTU/MTU
  3. radioactive ablation
27
Q

what is used to treat accidental exposure to I-131 to prevent cell damage?

A

potassium iodine

it competitively binds to sodium-iodine symporter to prevent radioactive iodine into the follicular cells

28
Q

how does thionamide work? what pathway does it involve?

A

it blocks peroxidase which is a catalyst in oxidation, organification and coupling

  1. follicular cell makes tyrosine into thyroglobulin
  2. thyroglobulin is pushed into the lumen
  3. oxidation: follicular cell takes iodine from blood into the lumen, oxidize into diatomic iodine
  4. organification: thyroglobulin and I2 becomes thyroglobulin with monoiodotyrosine (MIT) or diiodotyrosine (DIT)
  5. coupling: makes TG with T3 (MIT+DIT) or T4 (DIT + DIT)
29
Q

what disease does hypothyroidism cause in older children or adults? what symptoms?

A
  1. weight gain despite normal intake
  2. slow mental activity
  3. muscle weakness
  4. cold intolerance and decreased sweating
30
Q

hypothyroidism myxedema affects what parts of the body?

A
  1. larynx (deep voice)
  2. tongue
  3. subcutaneous tissues
31
Q

how does hypothyroidism affect cholesterols levels?

A

high cholesterol levels

32
Q

what are the 4 causes for hypothyroidism myxedema?

A
  1. Hashimoto thyroiditis
  2. iodine defieicny
  3. drugs
  4. iatrogenic (thyroid ablation)
33
Q

what is the best screening test for primary hypothyroidism?

A

TSH

TSH increases first, then T4 drops, then T3 drops

TSH does not go up in central hypothyroidism but that form is uncommong

34
Q

what is the 1st manifestation of hypothyroidism? what test is needed to confirm?

A

hypothyroid myopathy (muscle weakness) causing high creatine kinase

confirm with TSH test

35
Q

what is Hashimoto thyroiditis? what gene is related to it?

A

autoimmune destruction

associated with HLA-DR5

36
Q

how does Hashimoto thyroiditis feel?

A

painless

just a bunch of hyperthyroidism symptoms

37
Q

how does Hashimoto thyroiditis progress?

A

starts as hyperthyroidism because thyroid hormone can leak out while the thyroid is being damaged

then they become hypothyroidism with low T4 and high TSH

38
Q

what antibodies are seen in Hashimoto?

A
  1. antimicrosomal (TPO) antibodies

2. antithyroglobulin antibody

39
Q

what test is used to confirm Hashimoto?

A

thyroid peroxidase antibody

but Hashimoto is a clinical diagnosis; this just confirms it

40
Q

what histology is associated with hashimoto thyroiditis?

A
  1. chronic inflammation with germinal centers

2. Hurthle cells

41
Q

patient with long standing Hashimoto with thyroid gland progressively increasing in size. what is the differential?

A

B cell lymphoma

this is because there’s germinal centers formed from B cells surrounding T cells in Hashimoto’s

B cells from marginal zones

42
Q

what is deQuervain’s granulomatosis?

A

self limiting

painful thyroid with transient hyperthyroidism

hypothesized that it’s caused by viruses

43
Q

what is the ESR with patient with granulomatous thyroiditis?

A

high ESR and CRP

low radio iodine uptake

44
Q

what is the hisotology associated with subacute granulomatosis?

A

inflammatory infiltrate with giant cells

45
Q

what is Reidel fibrosing thyroiditis?

A

chronic thyroid inflammation with extensive fibrosis

hypothyroidism

hard as wood non-tender thrhoid

fibrosis may extend to local structures

Endocrine Week 1 (11 decks)

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