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BMS200 > week 4, lecture 3 > Flashcards

week 4, lecture 3 Flashcards

1
Q

what are the 2 types of autoimmune hypothyroid syndromes

A
  • Hashimoto’s thyroiditis
  • Subacutethyroiditis
    (DeQuervain thyroiditis)
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2
Q

what deficiency can cause hypothryoid

A

iodine

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3
Q

causes of hypothyroidism or reduced thyroid function

A

▪ Autoimmune hypothyroid syndromes:
* Hashimoto’s thyroiditis * Subacutethyroiditis
(DeQuervain thyroiditis)
▪ Iodine deficiency & non-toxic goiter
▪Lesscommoncauses: congenital hypothyroidism, hypopituitarism, hypothalamic disease, infiltrative disorders
▪ Iatrogenic (i.e. treatment for hyperthyroidism)

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4
Q

what is thyrotoxicosis

A

increase levels of hormones

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5
Q

toxic vs non toxic thyroid diseases

A

toxic= produces t3, t4

non toxic- doesnt produce t3,t4

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6
Q

hyperthyroidism and thyrotoxicosis conditions

A

▪ Graves disease

▪ Toxic multi-nodular goitre,
toxic nodules

▪Thyroidneoplasms
* Follicularandpapillary adenomas and adenocarcinomas
* Medullaryandanaplastic carcinomas

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7
Q

what is one of the most common endocrine diseases

A

hashimotos thyroiditis

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8
Q

is Hashimoto more women or men

A

women 4/1000

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9
Q

findings in hasimoto

A

-lymph infiltration (follicle atrophy, lose colloid)
- mild fibrosis

-can progress to atrophic thyroiditis (more fibrosis, follicles gone)

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10
Q

genes and suspectibility for hasimottos

A

HLA haplotypes, polymorphism in CTLA4

  • Association between T1DM, Addison’s disease ,pernicious
    anemia, vitiligo
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11
Q

T cells in hasimotots

A

▪ Damage to T-cells thought to be mediated primarily by cytotoxic T-cells
* Localproductionofinflammatorycytokinesmaycontribute (TNF, IL-1, IFN-gamma)
* Althoughanti-thyroidantibodiesareproduced,theylikelyare not as important in damaging the follicular cells
▪ Antibodies are diagnostically useful, though – anti-TPO and anti-thyroglobulin antibodies mainly
▪ Can also have antibodies that block the TSH receptor (not stimulate it)

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12
Q

hasimotos; which mechanism is more prominent antibodies causing opsonization and killing thyroid or T cells binding and killing thyroid cells directly

A

T cells binding and killing thyroid cells directly

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13
Q

clinical features of hasimotos

A

think bad metabolism

fatigue, cold intolerance, slow mental and physical

goitre

skin (increase CT) ; macroglossia, hoarseness, facial puffiness, periorbital edema

myxedema- thick skin but no pitting

coarse hair lose 1/3 outer eyebrow

bradycardia, hypotension

hypoventilation

amenorrhea

constipation, weight gain, poor appetite

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14
Q

what is skin finding in hasimotos

A

myxedema

thicken but no pitting edema

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15
Q

what is the thyrotoxic phase in hashimotos

A

early phase where excessive thyroid hormone is released due to autoimmune destruction of the gland

then progress to hypothyroidism as the
gland is further compromised

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16
Q

what is subacute thyroiditis * AKA de Quervain’s thyroiditis, granulomatous thyroiditis, viral thyroiditis…

what’s the casues

A

viruses

mumps, coxsackie, influenza, adenoviruses, and echoviruses, SARS-CoV-2

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17
Q

early to late stages of subacute thyroiditis

A

▪ Early stages: patchy, inflammatory infiltrate, multi-nucleate
giant cells (derived from macrophages)

▪ Initially neutrophilic → lymphocytic infiltration

▪ Usually the inflammation subsides → resolution of symptoms, lab abnormalities… however long-term hypothyroidism in some (15%)

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18
Q

what happens to giant cells in subacute thyroiditis

A

multi-nuclei

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19
Q

features of subacute thyroiditis

A

bad neck pain, tender, fever (mimics pharyngitis)

signs of hypothryoid or thyrotoxicosis

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20
Q

subacute thyroiditis time course of ESR UT4 and TSH

A

ESR high in thyrotoxic beginning phase and then decreases

T4 high at beginning and has negative feedback on TSH making it low

then when T4 goes down TSH will then compensated and go up and try to make more T4

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21
Q

who does silent thyroiditis usually occur in

A

people with underlying autoimmune thyroid disease

  • Occurs in up to 5% of women 3-6 months after pregnancy (TPO antibodies before deliver) or women pregnant with T1DM is 3x common
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22
Q

time course of silent thyroiditis

A

▪ Brief period of (usually) mild thyrotoxicosis (2-4 weeks)

▪ Mild (usually) hypothyroidism for 4-12 weeks

▪ Resolution – most resolve, but some will, over time, develop permanent hypothyroidism (follow-up recommended)

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23
Q

symptoms in silent thyroiditis

A
  • Goitre is painless, no fever, no ESR elevations

▪ The “silent” refers to the lack of thyroid pain

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24
Q

why can there be a gaiter in both thyrotoxic and hypothryoid state

A

thyrotoxic because lots of hormone is being made and store making the gland bigger

hypothryoid because not making enough hormone initially but TSH will compensate and come in an overstimulate to make more t3/t4 and enlarge it

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25
Q

what conditions have noticeable gaiters

A

▪ Autoimmune conditions: Hashimoto’s thyroiditis,
Graves’ disease
▪ Nodular thyroid diseases & iodine deficiency ▪ Thyroid neoplasms

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26
Q

what is a diffuse non-toxic gaiter

A

*englarged, no nodules, no thyrotoxicosis (no high levels of t3,t4)

Diffuse enlargement of the thyroid, no nodules, no thyrotoxicosis (hence non-toxic) – also known as simple goiter

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27
Q

what is the main cause of diffuse-non toxic gaiter

A

Usually caused by iodine deficiency worldwide

▪ Can occur with sufficient iodine – in this case cause is unknown
(idiopathic)

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28
Q

what is the mechanism of iodine deficiency that causes a diffuse non-toxic gaiter

A

Iodine deficiency→decreased ability to iodinate thyroglobulin→modestly decreased thyroid hormone production→increased TSH from pituitary→stimulation of colloid production

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29
Q

t3,t4 and TSH findings in diffuse non toxic goiter (iodine deficient- cant make t3t4)

what about follicles and colloid

A

▪ Often TSH is only mildly increased or normal, but total T4 is decreased
▪ Follicles that are uniformly enlarged with lots of colloid

  • Sometimes a simple goiter can cause compression of underlying structures (thoracic outlet, trachea)
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30
Q

non-toxic multinodular goiter- what does the thyroid look like

A
  • Nodules tend to be widely variable in size, with a wide range of histologies:

▪ Cystic areas filled with colloid, or hypercellular, hyperplastic regions with less colloid
▪ Fibrosis is common

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31
Q

what is euthryoid

A

preservation of thyroid function

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32
Q

non toxic- gaiters -what is the thyroid functioning like?

A

commonly preserved (euthyroid) but could be hypothyroid (i.e. if large iodine deficient)

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33
Q

mass effects of non-toxic gaiters

A

▪ Simple goiters can be quite large, but unusual for them to cause significant compressive effects
* compressive effects can be exacerbated by raising the arms when a substernal goiter is present
* Esophageal compression (dysphagia) or tracheal compression can also occur

34
Q

what happens to MIT,DIT, T3, T4 in hypothryoid

A

MIT and DIT ratios increase

T3 and T4 are low but the proportion of T3 secreted is relatively higher than T3

((T3 is the more active form of thyroid hormone, so this shift may be a way to maximize the effects of the limited hormone production.))

35
Q

what does low t3 and low t4 have on feedback in hypothyroid

A

Low T3 & T4→Increased TRH→Increased TSH secretion & development of a goiter

36
Q

what is cretinism in hypothyroid

A

mental and physical developmental delays due to the lack of thyroid hormones during critical periods of growth.

37
Q

what is myxoedema coma caused from

A

Complication of long-term hypothyroidism PLUS another precipitating factor:
▪ Infection (pneumonia, UTI/urosepsis, sepsis in general)

▪ Burns, severely impaired pulmonary function, GI hemorrhage,
stroke, trauma, surgery
▪ Hypoglycemia, hypothermia
▪ Lots of medications

38
Q

myxoedema coma= x + y

A

long term hypothyroid complication + infection

39
Q

myxoedema coma; who’s effected

A

very rare and serious but old and women>

40
Q

myxoedema coma clinical features

A

hypotension –> shock

increased diastolic BP

dysrhythmia

bradycardia

neurologic slow, psychosis

hypoventilation

obstructive sleep apnea

ileus, nausea, vomit,

hyponatremia (low sodium effects mental status)

41
Q

signs and symptoms of thyrotoxicossis

A

hyperactive, irritable, dysphoria, heat intolerance, sweating, palpitations, weak, fatigue, weight loss, diarrhea

tachycardia, tremor, goiter, warm skin, muscle weak, lid retraction

42
Q

what is the most common cause of thyrotoxicosis (increase thyroid hormones)

A

graves disease

43
Q

what happens in grave disease

A

TSH receptor-stimulating immunoglobulins (TSIs) stimulate the TSH receptor and are not responsive to negative feedback from increases in thyroid hormone production

44
Q

graves disease vs hashimoto

A

graves; make too much thyroid hormone

Hashimoto thyroiditis can cause your thyroid to not make enough thyroid hormone.

45
Q

what is stimulating TSH receptor in graves disease to make extra hormones

A

TSH receptor-stimulating immunoglobulins (TSIs)

46
Q

genes that could be causing graves disease

A
  • Immune factors: polymorphisms in immunoregulatory genes
    ▪ CTLA-4, PTPN22, CD25 (alpha-chain of high-affinity IL-2 receptor)
47
Q

risk factors for grave disease

A

genes

stress, smoking

sudden increases in iodine intake

48
Q

opthalmopathy in graves disease

A

▪ Orbital tissues express the TSH-R → autoimmune attack →
increased fibrosis

▪ As well, some pro-inflammatory cytokines increase activation of fibroblast and GAG secretion (extraocular muscles swell)

▪ There may also be aberrant IGF-1 signaling involved

Begins as eye grittiness ,excess tearing, and lid retraction

49
Q

clinical features of graves disease

A

opthalmopathy

thyroid dermopathy (rare) – skin plaques that are red and finger clubbing

50
Q

graves symptoms

A

general thyrotoxicosis PLUS opthalmopathy and dermopathy

but the general symtpoms are: hyperactive, palpitations, heat intolerance, tachycardia, tremor, goiter, etcc

51
Q

toxic multi nodular goiter what can happen to the nodules? (makes it different that non-toxic MNG)

A

some of the nodules in toxic MNG become autonomous (operate independently of TSH and produce TH)
▪ Nodules can be monoclonal or polyclonal

52
Q

clinical features of toxic multinodular goitre

A

mild hyperthyroid (or subclinical)

TSH abnormal (low) , T4 normal, T3 slightly higher

53
Q

toxic multinodular goitre findings in tsh t3 t4

A

TSH abnormal (low) , T4 normal, T3 slightly higher

54
Q

symptoms in toxic multinodular goitre

A

▪ Atrial fibrillation +/- palpitations, tachycardia
▪ Nervousness, tremor, weight loss
▪ Could be a history of recent iodine supplementation

55
Q

toxic adenoma– what is the mutation

A

Uncommon disorder where a single nodule has gained an activating mutation of the TSH-R

TSH can make t3, t4

56
Q

toxic adenoma

A

mutate TSH-R

TSH-r –> alpha GPCR —> adenylyl cyclase –> cAMP –> increase cell growth, differentiate, increase hormone synthesis

mild thyrotoxicosis

can cause toxic MNG

57
Q

thyroid storm (emergency)

A

exacerbation of hyperthyroid (usually after acute illness)

  • Stroke, infection, trauma, diabetic ketoacidosis, surgery (especially thyroid surgery), radioioidine therapy for hyperthyroidism
58
Q

what is thyroid storm

A

Due to rapid release/increase in thyroid hormone levels

59
Q

causes of thyroid storm?

A

▪ May be due to magnified, “overactivation” of the sympathetic
nervous system
▪ May also be due to increased global oxygen (and therefore blood flow) requirements

60
Q

features of thyroid stomr

A

hyperthermia (fever)
diaphoresis (sweating)
tachycardia
impaire consciousness
GI; nausea, ab pain, diarrhea
–>also signs and symptoms of thryotoxicosis

61
Q

congenital hypothyroid- can it be transient or permanent

A

both, permanent more common

  • Neonatal hypothyroidism may be transient, due to maternal factors that cross the placenta
  • However, permanent hypothyroidism is more common and occurs in the majority of newborns with congenital hypothyroidism

▪ Lifelong thyroid hormone support

62
Q

causes of congenital hypothyroid

A

▪ Gland dysgenesis (doesnt develop properly), TSH-R antibody from mother

▪ Mutations: central hypothyroidism (secondary or tertiary), gland dysgenesis, abnormal TH synthesis

  • Transplacental TH (thyroid hormone) support to treat if discovered in utero
63
Q

clinical features of congenital hypothyroidism

A

▪ feeding problems, hypotonia, enlarged tongue
▪ delayed bone maturation and growth, umbilical hernia, prolonged jaundice
▪ Importantly, permanent neurologic damage results if treatment is delayed.
▪ Typical features of adult hypothyroidism may also be present.
▪ Other congenital malformations, especially cardiac, are four times more common in congenital hypothyroidism

64
Q

non maliganant neoplasm (adenomas) vs malignant

A

follicular adenoma

▪ Papillary carcinoma (70 – 80%)
▪ Follicular carcinoma (5 – 10%)
▪ Medullary carcinoma (derived from calcitonin-secreting C-cells) ▪ Anaplastic carcinoma

65
Q

most common adenoma

A

follicular adenoma (usually dont secrete thyroid hormone)

66
Q

most common malignant neoplasm/ carcinoma

A

papillary carcinoma

67
Q

hyperplasia vs neoplasia

A

▪ Hyperplasia is responsible for the development of MNGs (multinodular goiter), for
example
* Growthisstimulatedbysomesortofstimulus/signal
▪ Neoplasias grow despite the absence of external stimuli/signals

68
Q

most common thyroid cancer

A

papillary

69
Q

papillar adenoma

A

good survival rate
most dont metasize but if do go to lung or bone

▪ Cells with large, clear nuclei that are arranged in
papillary or follicular structures (many subtypes)
▪ Most are well-differentiated, but some have an increased risk of metastasis, which is magnified when they have the capability to invade vessels (angioinvasion)
* Typical sites of metastasis: bone and lung
▪ Most are identified in earlier stages and have a very
good survival (minimal impact on mortality) * Only about 1% present with stage IV cancer

70
Q

most common cause of follicular carcinoma

A

iodine deficient

71
Q

how to know if non malignant adenoma or follicular carcinmoa

A

carcinoma invades capsule, vessels

72
Q

what is good treatment to follicular or papillary carcinoma

A

TSH suppression therapy

via giving T3 and T4 to have negative feedback

73
Q

how to get rid of well-differentiated thyroid cancer

A

give t3t4

or give radioactive iodide

74
Q

anapaestic thyroid cancer

A

Rare, but extremely aggressive due to its rapid
metastases

  • Don’t take up iodine well or respond to TSH (in treatment options)
75
Q

Medullary thyroid carcinoma;;
what cells are secreting things?

A

Derived from C-cells, secretes high levels of calcitonin

76
Q

genetic factors in thyroid cancer

A

TSH-R mutations at G alpha subunit

RTK, RAS, MAPK pathway

p53, beta catedin

Some thyroid nodules have activating mutations of the TSH receptor and the GSα subunit.
* 70% of PTCs show activation of the RET-RAS-BRAF signalling pathway
▪ Receptor tyrosine kinase = RET (specific gene = RET/PTC)
▪ RAS mutations, which stimulate the MAPK signalling cascade, are found in around 20-30% of thyroid neoplasms
* Poorly differentiated cancers also involve mutations in the RET-RAS-BRAF pathway…
▪ However p53 mutations are much more common in these malignancies
▪ Often mutations in the beta-catenin gene (CTNNB1) are present as well

77
Q

risk factors for thyroid cancers

A

radiation

▪ Radioactive isotope uptake during nuclear waste release
into the atmosphere (radioactive iodine) ▪ Generalized radiation
* Sometimes radiation to ablate hyperthyroidism can increase risk of later cancer development
* Children seem more vulnerable to harm through radiation

78
Q

what is propylthiouracil (PTU)- anti thyroid drug inhibit

A
  1. ▪ Inhibits thyroid peroxidase (major effect)
  2. ▪ Also inhibits de-iodination of T4 – T3 in the thyroid (minor effect)
  3. stops t3/t4 production
  4. stops t4 from being converted into active t3
79
Q

what is methimazole anti thyroid drug inhibit

A

▪ Inhibits the activity of thyroid peroxidase, no effect on deiodinases

▪ May also reduce inflammatory mediators within the thyroid (IL-2, ICAM-1, anti-thyrotropin receptor antibodies)

80
Q

which drug is better; propylthiouracil PTU or methimazole

A
  • To note, methimazole often chosen over PTU due to liver toxicity of PTU
81
Q

what is levothryoxine? what to use in?

A

synthetic t4

hypothryoidism

82
Q

what is radioactive iodine for

A

– used for well-differentiated thyroid cancers
▪ Uptake destroys the thyroid gland
▪ Can be used for Graves’ disease if resistant to other anti- thyroid medications

BMS200 (43 decks)

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