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Q5 GNMD > Thyroid disorders: Howell > Flashcards

Thyroid disorders: Howell Flashcards

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

A

15% of cases

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
Q

incidence and prognosis of anaplastic carcinoma

A

rare, older patients
80% die within a year

26
Q

sx of anaplastic carcinoma

A

rapid onset of mass, pain and hoarseness

27
Q

causes of hyperthyroidism

A

-graves disease
-toxic nodular goiter
-early thyroiditis
-cancer
-pituitary adenoma
-thyrotoxicosis factitia

28
Q

thyroid storm causes

A

untreated or inadequately treated hyperthyroidism
-borderline controlled but then trauma, surgery, infection etc happens and leads to this storm

29
Q

sx of thyroid storm

A

presents like excess hyperthyroidism

-sudden onset of fever
-marked weakness and muscle wasting
-extreme restlessness
-psychosis
-cv collapse, coma

30
Q

Graves diseases diagnostic criteria

A

hyperthyroidism with at least 1 of the following:

-goiter
-pretibial myxedema
-exopthalmus

31
Q

HLA associations to graves disease

A

HLAB8 and DR3D antigens

32
Q

pathophysiology of graves diasease

A

antibodies attach to TSH receptors and continually stimulate thyroid gland

33
Q

sx of graves disease

A

-wt loss, insomnia, tremors
-irritability, heat intolerance, diarrhea
-tachycardia, palpitation
-pretibial myxedema, goider
-exophalmus

34
Q

labs in graves disease

A
  • 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
Q

treatment for graves disease

A

-propanolol for sx
-PTU (propothiol uracil) : blocks increased thyroid hormone response

36
Q

how long after treatment of grave’s does it take for thyroid hormone levels to go back to normal

A

4-6 weeks
-40% of patients go into remission and can discontinue PTU after 1-2 years

37
Q

sx of toxic nodular goiter AKA plummers dz

A

-multiple or solitary nodules
-hot nodules: high RAI
-similar sx to graves except to ocular involvement, no pretibial myxedema, not autoimmune

38
Q

incidence of toxic nodular goiter

A

patients usually over 50 years old

39
Q

What type of hypothyroidism is hashimotos

A

primary hypothyroidism

40
Q

etiology of hashimotos

A

autoimmune condition where gland is unable to convert iodine into hormne

41
Q

2 major phenotypes of hashimotos

A
  1. goitrous
  2. atrophic: 10-20% haven anti-TSHr
    - both: lymphocytic infiltration of gland, follicular destruction : gih anti-TG and anti-TPO
42
Q

labs for hashimotos

A

-high TSH
-low t4
-initially high RAI uptake: temporary hyperthyroid state
-thyroid antibodies in 95% of cases

43
Q

Thyroid antibodies seen in hashimoto’s

A

-Anti-TSH
- anti-TG
-anti-TPO

44
Q

myxedema coma
incidence

A

severe, acute hypothyroid state
I: elderly during winter months

45
Q

sx of myxedema coma

A
  • profoud hypothermia
    -bradycardia
    -respiratory depression
    -slow deep tendon reflexes
46
Q

most common etiology of congenital hypothyroidism

A

65% of cases are due to thyroid gland dysgenesis

47
Q

clinical manifestation of congenital hypothyroidism

A
  • 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
Q

possible complications of congenital hypothyroidism

A

-CHD 4x more common in infants with congenital hypothyroidism

permanent neurologic damage if tx is delayed

49
Q
A

Q5 GNMD (15 decks)

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