Thyroid disorders: Howell Flashcards

(49 cards)

1
Q

What type of myxedema can be found in hyperthyoridism

A

pretibial myxedema

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2
Q

what type of myxedema can be found in hypothyroidism ?

A

facial myxedema

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3
Q

causes of thyroid disorders

A

-high dose radiation
-cancer
-excessive intake of thyroid hormone or iodine
-pituitary adenoma (with increased TSH)
-pregnancy
-strum ovari: ovaries that have thyroid tissue

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4
Q

what is the most common causes of a goiter in the united states

A

hashimotos

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5
Q

what is the most common causes of a goiter worldwide

A

iodine deficiency

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6
Q

Pt presents with a painless, diffuse goiter.During PE thryoid gland feels rubbery and ntot hard .What is the cause of the goiter

A

hashimotos thyroiditis

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7
Q

pt presents with a painless, firm and nodular goiter. what is the most probable cause

A

cancer

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8
Q

pt presents with a diffuse enlargement of their thyroid. on PE it is tender to the touch. what is the most probable cause

A

de quervain’s thyroiditis

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9
Q

Sx of DeQuervains

A

-Diffuse enlargement of the thyroid gland
-slight fever, malaise, fatigue

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10
Q

Etiology of DeQuervains

A

viral etiology, high sedementation rate

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11
Q

labs in DeQuervains

A
  • low RAI utake
    -high T3 and T4
    -Low TSH
    -no antibodies
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12
Q

will you find antibodies associated with DeQuervains

A

no antibodies

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13
Q

prognosis for DeQuervains

A

usually resolves in a few weeks

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14
Q

Labs and sx in silent thyroditis

A

-high T4
-low RAI
- no pain and milder symptoms

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15
Q

when does silent thyroiditis usually occur? when does it resolve?

A

after pregnancy
usually resolves within 3 months without treatment

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16
Q

what is the most common type of thyroid cancer ?

A

papillary carcinoma

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17
Q

incidence of papillar carcinoma

A

70% of cases

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18
Q

sx of papillary carcinoma

A

-hoarseness of voices and dysphagia

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19
Q

what type of spread is papilalry carcinoma

A

lymphatogenous spread

common to find in cervical chain

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20
Q

Incidence of follicular carcinoma

21
Q

what type of spread is follicular carcinoma and where does it commonly spread to ?

A

hematogenous spread
common metastases to the bones, lungs, liver

22
Q

incidence of medullary carcinoma
sporadic vs familial

A

6-10% of cases
80% of cases are sporadic
20% are familial

23
Q

sx of medullary carcinoma

A

secretes calcitonin: decreases serum ca+

24
Q

what syndrome is associated with medullary carcinoma

A

MEN II (sipple’s syndrome)

multiple endocrine neoplasia II
also hyperparathyroidism and pheochromocytoma

25
incidence and prognosis of anaplastic carcinoma
rare, older patients 80% die within a year
26
sx of anaplastic carcinoma
rapid onset of mass, pain and hoarseness
27
causes of hyperthyroidism
-graves disease -toxic nodular goiter -early thyroiditis -cancer -pituitary adenoma -thyrotoxicosis factitia
28
thyroid storm causes
untreated or inadequately treated hyperthyroidism -borderline controlled but then trauma, surgery, infection etc happens and leads to this storm
29
sx of thyroid storm
presents like excess hyperthyroidism -sudden onset of fever -marked weakness and muscle wasting -extreme restlessness -psychosis -cv collapse, coma
30
Graves diseases diagnostic criteria
hyperthyroidism with at least 1 of the following: -goiter -pretibial myxedema -exopthalmus
31
HLA associations to graves disease
HLAB8 and DR3D antigens
32
pathophysiology of graves diasease
antibodies attach to TSH receptors and continually stimulate thyroid gland
33
sx of graves disease
-wt loss, insomnia, tremors -irritability, heat intolerance, diarrhea -tachycardia, palpitation -pretibial myxedema, goider -exophalmus
34
labs in graves disease
- TSH is the best initial test but is not be used to follow up treatment -follow up with T4 -RAI uptake : high. hot nodule -lows TSH bc free T3 downregulates TRH receptors in the pituitary` to decrease TSH release
35
treatment for graves disease
-propanolol for sx -PTU (propothiol uracil) : blocks increased thyroid hormone response
36
how long after treatment of grave's does it take for thyroid hormone levels to go back to normal
4-6 weeks -40% of patients go into remission and can discontinue PTU after 1-2 years
37
sx of toxic nodular goiter AKA plummers dz
-multiple or solitary nodules -hot nodules: high RAI -similar sx to graves except to ocular involvement, no pretibial myxedema, not autoimmune
38
incidence of toxic nodular goiter
patients usually over 50 years old
39
What type of hypothyroidism is hashimotos
primary hypothyroidism
40
etiology of hashimotos
autoimmune condition where gland is unable to convert iodine into hormne
41
2 major phenotypes of hashimotos
1. goitrous 2. atrophic: 10-20% haven anti-TSHr - both: lymphocytic infiltration of gland, follicular destruction : gih anti-TG and anti-TPO
42
labs for hashimotos
-high TSH -low t4 -initially high RAI uptake: temporary hyperthyroid state -thyroid antibodies in 95% of cases
43
Thyroid antibodies seen in hashimoto's
-Anti-TSH - anti-TG -anti-TPO
44
myxedema coma incidence
severe, acute hypothyroid state I: elderly during winter months
45
sx of myxedema coma
- profoud hypothermia -bradycardia -respiratory depression -slow deep tendon reflexes
46
most common etiology of congenital hypothyroidism
65% of cases are due to thyroid gland dysgenesis
47
clinical manifestation of congenital hypothyroidism
- prolonged jaundice -feeding problems -hypotonia -macroglossia -delayed bone maturation -umbilical hernia (developed over first few wks/months) -permanent neurologic damage if tx is delayed -CHD 4x more common in infants with congenital hypothyroidism
48
possible complications of congenital hypothyroidism
-CHD 4x more common in infants with congenital hypothyroidism permanent neurologic damage if tx is delayed
49