Thyroid Flashcards
1
Q
thyroid pathway
A
- thyroid releaseing hormone is secreted by hypothalamus
- thyroid stimulating hormone released by anterior pituitary
- stimulates thyroid gland to release T4 and T3
- conjugated in liver then goes to circulatory system
- also circulates in intestine
- negative feedback on hypothalamus
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)
3
Q
where is T4 produce
A
only in the thyroid gland
4
Q
where is T3 porduced
A
20% in thyroid gland
deiodination of T4
5
Q
what is thyroglobulin
A
protein that both synthesizes and stores thyroid hormone
6
Q
what do you need iodin e for and where can you get it
A
synthesis of thyroid hormones
seafood, diary, iodinated salt
7
Q
which hormone has alonger half life
A
T4
8
Q
which hormone has a higher potency
A
T3
9
Q
what converts T4 to T3
A
5-deiodinase in the peripheray
10
Q
what is the purpose of binding proteins for thyroid hormone
A
ensure serum T4 and T3 remain in normal limits
11
Q
examples of binding proteins for thyrodi
A
thyroxine binding globulin
transthyretin
albumin
12
Q
4 types of thyroid disoreds
A
hypothyroidism and subclinical
hypethyroidism and subclinical
13
Q
two types of hypothyroidism
A
primary - autoimmune, congenital, iodine deficiency, infiltrative disease, latrogenic, drugs
central - problems with hypothalamus or pituitary
14
Q
drugs that cause hypothyroidism
A
lithium
amiodarone
interferon
tyrosine kinase inhibitors
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)
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
17
Q
lab values in primary hypo
A
tsh high
T4 T3 low
18
Q
subclinical hypo labs
A
tsh high
T3/4 normal
19
Q
hyperthyroidism labs
A
tsh low
T4/3 high
20
Q
subclinical hyperthyroidism labs
A
tsh low
T4/3 normal
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
22
Q
why do we rely on TSH for therapeutic endpoint
A
log linear feedback..?
most sensitive to changes
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
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
25
what is graves disease
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
26
what are some other hyperthyroid disorders
```
pituitary adenomas
toxic ademona
toxic multinodular goiter
painful subacute thyroidits
drugs
```
27
diference between grave and plummers disease
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?
28
diagnosis of graves
increased free T4
suppressed TSH
radioactive iodine uptake increase
thyroid related antibodies or biopsy
29
hyper GOT
min symptoms improve quality of life
min long term damage to organs
normalize free T4 and TSH
30
hyper effects on bones
lot of osteoclasts which release calcium into the bloodstream
31
4 treatemnt options for hyper
ablation with radioactive iodine or surgery
thionamides
non selective beta blocker
iodine
32
ablation first line for
graves, toxic nodule, multinodule goiter
33
concerns with ablation
leads to hypothyroidism
| will be asked to stop meds before to ensure radioactive iodine gets taken up
34
thionamide - methimaole
| MOA
inhibits synthesis by blocking oxidation of iodine in thyroid
doesnt inactivate circulatin T3 and T4
35
methimazole use
first line in graves
36
dosing of methimazole
daily due to long half life
37
AE o methimazole
```
rash, arthralgia, lupus like
fever agranulocytosis (**bone marrow stops working usually within 3months)
```
38
methimazole and propylthiouracil monitoring
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
efficacy of methimazole
slow onset to reduce symptoms 4-6mon
| TSH may remain low for months
40
thionamide - propylthiourical MOA
inhibits synthesis by blocking conversion of thyroxine to T3 in peripheral tissues
does not inactivate circulating
41
use of propylthiouracil
intolerant to MMZ *cant have agranulocytosis
| if pregnant use in first trimester
42
dosing of propylthiouracil
TID
43
AE of propylthiouracil
rash arthralgia, lupus
agranulocytosis early in therapy
**hepatotoxcity makes it second line
44
efficacy of propylthiouracil
slow onset in reducing symptoms 4-6 months
| remission rates: 20-30%
45
why dont we monitor liver function when on PTU
idiosyncratic
no biomarkers effectively assess risk
sudden, unpredictable
46
why should patients report pharyngitis
agraunlocytosis is a possibility
47
beta blocker MOA
beta adrenergic manifestation of hyperthyroidism
48
use of beta blockers
for severe symptoms while awaiting onset of thiourias
49
beta blocker of choice
non selective
| propranolol becuase it can inhibit some peripheral conversion
50
efficacy of beta blockers
no efect on the underlying disease
can block T4 peripherally
acute role in thyroid storm
51
iodine MOA
inhibits release of stored thyroid hormone
| helps decrease the vascularity and size before surgery
52
why mix iodine with juice
tastes terrible
53
AE of iodine
hypersensitivity, metallic taste, sore in mouth
54
what should you not take before ablation
iodine may reduce the uptake of radioactive iodine
55
efficacy of iodine
effective for 7-14 days used a week before surgery
| role in stopping thyroiditis mediated release of stored hormone and in thyroid storm
56
what are some problems with not treating subclinical hyper
if >60 - afib
| post menopause - decrease bone density
57
if subclinically is untreated screen _____
annually
58
causes of thyriod storm
trauma, infection, antithyroid agent withdrawal, severe throiditis, post ablative therapy
59
presentation of thyroid storm
fever, tachycardia, vomit, dehydration, coma, tachypnea, delirium
60
treatment of thyroid storm
```
large dose PTU preferred bc peripheral effects and short half life
iodine
beta blocker
steroid
antipyretic
```
61
why dont you use nsaids in thyroid strom
cause displacement of protein bound thyroid increasing release
62
treatment options for hypo
desiccated thyroid
liothyronine
levothyroxine
63
levothyroxine MOA
synthetic T4 supplement
64
why is levothyroxine the DOC
easier to titrate
| allow body to fine tune itself by converting exogenous T4 to T3
65
dosing for levothyroxine and what to do in elderly and CVD
1.6mcg/kg/day using IBW
| decrease the dose in elderly and CVD
66
AE usually from overtreatment are
same as hyper
67
efficacy of levothyroxine
clinical remission
| labs normal
68
how to take levothyroxine
empty stomach
69
disadvantage of liothyronine
```
short half life
rapid absorption causes high peak right after dose
increased CV
difficult dose titration
increased cost
```
70
desiccated thyroid disadvantages
```
natural product with varying potencies
allergic reaction
rapid absorption
difficult dose titration
avoid
```
71
are eltroxin and synthroid interchangeable
no
72
monitoring TSH in hypo therapy
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
why do you initally monitor T4 when treating hypo
TSH may remain abnormal for months
74
adults under 50 with severe hypothyroidism monitoring
2-4 weeks
75
when would you caution using TSH alone as a marker
on dopaminergic agents, somatostatin analogs
| CS
76
what should you counsel a patient on for levo
```
indication
how it works and when
beenfits and side effects
follow up
what to do if dose missed
monitor
```
77
how long should you increase levo dose for in pregnnacy
week 16-20
78
monitoring in pregnancy
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
how much should you adjust LT4 by in pregnancy
25-50mcg
80
when should LT4 be reduced to the preconception dose
after delivery,
| test TSH 6 weeks postpartum
81
when do we treat subclinical hypothyroidism
TSH 4.5-10 and
symptoms of hypothyroid
antithyroid peroxidase antibodies present
history of CVD, HF, risk factors
82
causes of myxedema coma
trauma, infection, HF, meds
83
presentation of myxedema coma
coma not required and uncommon
altered mental state
diastolic hypertension
hypothermai, hypoventilation
84
myxedema coma treatment
thyroid hormone replacement IV
antiobiotc therapy to preven sepsis
steroid to suppres inflammation
85
differences between nodules and goiter
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
primary causes of hypothyroidism
hashimoto thyroiditis
latrogenic - surgery, radiation, drugs
iodine deficiency
87
secondary causes of hypothyroidism
pituitary disease
| hypothalamic disease
88
drugs that cause hypothyroidism
amiodarone, lithium, sulfonylureas
