Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical 2.0 winter > Thyroid > Flashcards

Thyroid Flashcards

1
Q

thyroid pathway

A
  1. thyroid releaseing hormone is secreted by hypothalamus
  2. thyroid stimulating hormone released by anterior pituitary
  3. stimulates thyroid gland to release T4 and T3
  4. conjugated in liver then goes to circulatory system
  5. also circulates in intestine
  6. negative feedback on hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are thyroid hormones used for in the body

A

important for normal growth and development (cognition) in children
maintain metabolic stability in adults
regulate normal growth and maturation
thermoregulation
cognitive and peripheral nervous function
cardiac function (highT4 increase CO HP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

where is T4 produce

A

only in the thyroid gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

where is T3 porduced

A

20% in thyroid gland

deiodination of T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is thyroglobulin

A

protein that both synthesizes and stores thyroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what do you need iodin e for and where can you get it

A

synthesis of thyroid hormones

seafood, diary, iodinated salt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

which hormone has alonger half life

A

T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which hormone has a higher potency

A

T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what converts T4 to T3

A

5-deiodinase in the peripheray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the purpose of binding proteins for thyroid hormone

A

ensure serum T4 and T3 remain in normal limits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

examples of binding proteins for thyrodi

A

thyroxine binding globulin
transthyretin
albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

4 types of thyroid disoreds

A

hypothyroidism and subclinical

hypethyroidism and subclinical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

two types of hypothyroidism

A

primary - autoimmune, congenital, iodine deficiency, infiltrative disease, latrogenic, drugs
central - problems with hypothalamus or pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

drugs that cause hypothyroidism

A

lithium
amiodarone
interferon
tyrosine kinase inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

signs of hypothyroidism

A 
weak 
poor concentration
paresthesia
impaired hearing 
hoarse voice
bradycardia
dyspnea
weight gain 
constipation
cold intolerance
menorrhagia(heavy period) 
dry skin 
puffy hands, face, feet
muscle cramps
alopecia (lose hair)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

signs of hyperthyroidism

A 
hyperactive 
irritable 
tremor
fatigue 
goiter 
lid retraction 
ophthalmopathy 
tachycardia
weight loss increased appetite
heat intolerance
diarrhea
polyuria
light periods
loss of libido 
warm moist skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

lab values in primary hypo

A

tsh high

T4 T3 low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

subclinical hypo labs

A

tsh high

T3/4 normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

hyperthyroidism labs

A

tsh low

T4/3 high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

subclinical hyperthyroidism labs

A

tsh low

T4/3 normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why dont we use free T3 as a marker

A

not directly related to thyroid function because only20% made by the thyroid the rest is through conversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

why do we rely on TSH for therapeutic endpoint

A

log linear feedback..?

most sensitive to changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

goals of therapy

A

achieve euthyroid state and manage symptoms
recognize which patients with goiter or thyroid nodules require treatment
ensure appropriate management of hypo and hyper in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

risk factors for thyroid diease

A 
personal or strong family history of thyroid diseae
diagnosis of autimmune disease
past history of neck irradiation
drug therapies lithium and amiodarone
women over 50 
elderly 
women pregnant or post partum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is graves disease

A

autoimmune disease
thyroid stimulating antibodies trick the thyrotopin receptor on the surface of thyroid cell into thinking its TSH
activate the enzyme adenylate cyclase the same as TSH resulting in hormone synthesis and release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are some other hyperthyroid disorders

A 
pituitary adenomas
toxic ademona
toxic multinodular goiter
painful subacute thyroidits
drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

diference between grave and plummers disease

A

graves in females and peak 40-60, plummers over 50 and young?
graves has exophthalmos and redness over both shins, plummer no extrathyroidal symptoms
graves has strong familial disposition, plummers long standing history of goiter
plummers only a mild increase in T4 and T3
iodine uptake is diffuse in graves?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

diagnosis of graves

A

increased free T4
suppressed TSH
radioactive iodine uptake increase
thyroid related antibodies or biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

hyper GOT

A

min symptoms improve quality of life
min long term damage to organs
normalize free T4 and TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

hyper effects on bones

A

lot of osteoclasts which release calcium into the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

4 treatemnt options for hyper

A

ablation with radioactive iodine or surgery
thionamides
non selective beta blocker
iodine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

ablation first line for

A

graves, toxic nodule, multinodule goiter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

concerns with ablation

A

leads to hypothyroidism

will be asked to stop meds before to ensure radioactive iodine gets taken up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

thionamide - methimaole

MOA

A

inhibits synthesis by blocking oxidation of iodine in thyroid
doesnt inactivate circulatin T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

methimazole use

A

first line in graves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

dosing of methimazole

A

daily due to long half life

37
Q

AE o methimazole

A 
rash, arthralgia, lupus like
fever agranulocytosis (**bone marrow stops working usually within 3months)
38
Q

methimazole and propylthiouracil monitoring

A

baseline CBC
TSH and fT4 every 4-6 weeks till stable
symptom improvement in a couple days, 3-4 weeks to see significant
4-12 weeks till euthyroid adjust maintenance dose then
daily for hepatotoxicity, baseline LFT

39
Q

efficacy of methimazole

A

slow onset to reduce symptoms 4-6mon

TSH may remain low for months

40
Q

thionamide - propylthiourical MOA

A

inhibits synthesis by blocking conversion of thyroxine to T3 in peripheral tissues
does not inactivate circulating

41
Q

use of propylthiouracil

A

intolerant to MMZ *cant have agranulocytosis

if pregnant use in first trimester

42
Q

dosing of propylthiouracil

A

TID

43
Q

AE of propylthiouracil

A

rash arthralgia, lupus
agranulocytosis early in therapy
**hepatotoxcity makes it second line

44
Q

efficacy of propylthiouracil

A

slow onset in reducing symptoms 4-6 months

remission rates: 20-30%

45
Q

why dont we monitor liver function when on PTU

A

idiosyncratic
no biomarkers effectively assess risk
sudden, unpredictable

46
Q

why should patients report pharyngitis

A

agraunlocytosis is a possibility

47
Q

beta blocker MOA

A

beta adrenergic manifestation of hyperthyroidism

48
Q

use of beta blockers

A

for severe symptoms while awaiting onset of thiourias

49
Q

beta blocker of choice

A

non selective

propranolol becuase it can inhibit some peripheral conversion

50
Q

efficacy of beta blockers

A

no efect on the underlying disease
can block T4 peripherally
acute role in thyroid storm

51
Q

iodine MOA

A

inhibits release of stored thyroid hormone

helps decrease the vascularity and size before surgery

52
Q

why mix iodine with juice

A

tastes terrible

53
Q

AE of iodine

A

hypersensitivity, metallic taste, sore in mouth

54
Q

what should you not take before ablation

A

iodine may reduce the uptake of radioactive iodine

55
Q

efficacy of iodine

A

effective for 7-14 days used a week before surgery

role in stopping thyroiditis mediated release of stored hormone and in thyroid storm

56
Q

what are some problems with not treating subclinical hyper

A

if >60 - afib

post menopause - decrease bone density

57
Q

if subclinically is untreated screen _____

A

annually

58
Q

causes of thyriod storm

A

trauma, infection, antithyroid agent withdrawal, severe throiditis, post ablative therapy

59
Q

presentation of thyroid storm

A

fever, tachycardia, vomit, dehydration, coma, tachypnea, delirium

60
Q

treatment of thyroid storm

A 
large dose PTU preferred bc peripheral effects and short half life
iodine
beta blocker
steroid 
antipyretic
61
Q

why dont you use nsaids in thyroid strom

A

cause displacement of protein bound thyroid increasing release

62
Q

treatment options for hypo

A

desiccated thyroid
liothyronine
levothyroxine

63
Q

levothyroxine MOA

A

synthetic T4 supplement

64
Q

why is levothyroxine the DOC

A

easier to titrate

allow body to fine tune itself by converting exogenous T4 to T3

65
Q

dosing for levothyroxine and what to do in elderly and CVD

A

1.6mcg/kg/day using IBW

decrease the dose in elderly and CVD

66
Q

AE usually from overtreatment are

A

same as hyper

67
Q

efficacy of levothyroxine

A

clinical remission

labs normal

68
Q

how to take levothyroxine

A

empty stomach

69
Q

disadvantage of liothyronine

A 
short half life 
rapid absorption causes high peak right after dose
increased CV
difficult dose titration 
increased cost
70
Q

desiccated thyroid disadvantages

A 
natural product with varying potencies 
allergic reaction 
rapid absorption 
difficult dose titration
avoid
71
Q

are eltroxin and synthroid interchangeable

A

no

72
Q

monitoring TSH in hypo therapy

A

baseline, 4-8 weeks until normal, then 6-12months
if change dose 6-8 weeks
clinical improvement in 2 weeks
complete recovery in several months

73
Q

why do you initally monitor T4 when treating hypo

A

TSH may remain abnormal for months

74
Q

adults under 50 with severe hypothyroidism monitoring

A

2-4 weeks

75
Q

when would you caution using TSH alone as a marker

A

on dopaminergic agents, somatostatin analogs

CS

76
Q

what should you counsel a patient on for levo

A 
indication 
how it works and when 
beenfits and side effects
follow up 
what to do if dose missed
monitor
77
Q

how long should you increase levo dose for in pregnnacy

A

week 16-20

78
Q

monitoring in pregnancy

A

TSH more accurate, total T4 instead of free

every 4 weeks during first half of pregnancy then one additional time between week 26-32

79
Q

how much should you adjust LT4 by in pregnancy

A

25-50mcg

80
Q

when should LT4 be reduced to the preconception dose

A

after delivery,

test TSH 6 weeks postpartum

81
Q

when do we treat subclinical hypothyroidism

A

TSH 4.5-10 and
symptoms of hypothyroid
antithyroid peroxidase antibodies present
history of CVD, HF, risk factors

82
Q

causes of myxedema coma

A

trauma, infection, HF, meds

83
Q

presentation of myxedema coma

A

coma not required and uncommon
altered mental state
diastolic hypertension
hypothermai, hypoventilation

84
Q

myxedema coma treatment

A

thyroid hormone replacement IV
antiobiotc therapy to preven sepsis
steroid to suppres inflammation

85
Q

differences between nodules and goiter

A

nodule is a growth within the thyroid gland large enough to be felt
goiter involves the entire thyroid gland where the gland is enlarged, can be uninodular and multinodular

86
Q

primary causes of hypothyroidism

A

hashimoto thyroiditis
latrogenic - surgery, radiation, drugs
iodine deficiency

87
Q

secondary causes of hypothyroidism

A

pituitary disease

hypothalamic disease

88
Q

drugs that cause hypothyroidism

A

amiodarone, lithium, sulfonylureas

Clinical 2.0 winter (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions