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PHAR 255 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What is the thyroid responsible for?

A

Synthesis, storage, and release of T3 and T4

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2
Q

What controls the synthesis and release of T3 and T4 ?

A

TSH –> thyroid stimulating hormone

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3
Q

what controls TSH?

A

thyrotropin-releasing hormone

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4
Q

What is required to create T3 and T4? (3)

A

Iodide, thyroglobulin, and Tyrosine

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5
Q

Process of creating T3? T4?

A

Iodide binds to tyrosine attached to thyroglobulin (Mono or diiodotyrosine)
MIT + DIT = T3
DIT + DIT = T4

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6
Q

Where is T4 converted to T3?

A

in peripheral tissue (kidney/liver)

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7
Q

ratio of T4:T3?

A

13:1

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8
Q

Actions of T3 and T4?

A

Heart: chronotropic and inotropic
ADipose tissue: catabolic
Muscle: catabolic
Bone: developmental
Nervous system: developmental
Gut: metabolic
Other: calorigenic

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9
Q

what % of T3 in circulation is directly from the thyroid?

A

20%

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10
Q

What % of T4 in circulation is directly from the thyroid?

A

100%

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11
Q

Which is more potent T3 or T4?

A

T3 ~ 4x more potent

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12
Q

what % of T4 is converted to inacive rT3?

A

45%

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13
Q

How is thyroid hormone regulated?

A

negative feedback loop

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14
Q

what promotes thyroid hormone release?

A

TSH
Low serum iodide

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15
Q

What inhibits thyroid hormone release?

A

high T3/T4 levels
Lithium
iodide excess

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16
Q

Male or female more prevalent for thyroid disease?

A

Female; 8/10 pts

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17
Q

what % of Canadians have over or under active thyroid glands? how many undiagnosed?

A

10%
>50%

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18
Q

What are the 4 common causes of hyperthyroidism?

A

Toxic diffuse goiter (graves disease)
Toxic multi-nodular goiter (plummers disease)
Acute phase thyroiditis
Toxic adenoma

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19
Q

Graves disease characteristics?

A

More common in younger, femal pts (20-50yrs old)
most common cause of hyperthyroidism
autoimmune disorder
immune system creates antibodies agaisnt TSH receptors
Can result in hyperplasia of thyroid gland, leading to a goiter

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20
Q

Plummers disease characteristics?

A

Most common in older females (>50)
Most common trigger for nodules to grow is Iodide deficiency
Develops slowly over years

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21
Q

Process of development of plummers disease?

A

Iodine deficiency –> less T4 production –> thyroid cells grow larger (multi-nodular goiter) –> TSH receptors mutate –> continually active

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22
Q

Acute phase thyroditis characteristics?

A

causes inflammation and damage to thyroid gland
damage = excess hormone release
eventually leads to hypothyroidism once stores are exhausted

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23
Q

Toxic adenoma characteristics?

A

benign tumours growing on thyroid gland
tumors become active like thyroid cells and secrete T3/T4 but do not respond to negative feedback loop

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24
Q

Hyperthyroidism non-specific symptoms?

A

Hand tremors
Diarrhea
Heat intolerance
wt loss
weakness
tachycardia
amenorrhea
HTN
anxiety
Afib
increased perspiration
palpitations
soft nails
emotional liabilty
insomnia
hair loss
apathy

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25
Graves specific symptoms?
exopthalmos (proptosis) --> eye protrusion Peri-orbital edema --> swelling around eye diplopia --> double vision diffuse goiter pre-tibial myxedema
26
Labs of serum TSH, Free T3, Free T4 in graves?
TSH decreased (below 0.1) T3 increased T4 normal to increased
27
Labs of serum TSH, Free T3, Free T4 in plummers?
TSH decreased (below 0.1) T3 increased T4 increased
28
What drug class may increased TSH secretion?
1st gen antipsycotics?
29
Drugs that can increase synthesis and release of T3/T4?
Amiodarone Iodine (chronic use)
30
What drugs can decrease thyroxin binding globulin?
Androgens (likely not clinically significant) Glucocorticoids (supraphysiological doses)
31
Anti-thyroid drugs?
Methimazole Propylthiouracil
32
Thioamide MOA?
interfere with thyroid peroxidase-mediated processes in T3/T4 production
33
What are the thioamides indicated for?
Graves Plummers pre-treatment before RAI
34
What does PTU do that MMI does not?
inhibits peripheral conversion of T4 to T3
35
Dosing for MMI?
MD: 5-15mg OD for all stages Intial doses: Mild = 10-15mg OD Moderate = 20-30mg OD Severe = 30-40mg OD
36
PTU dosing?
Intial dose of 300mg divided BID-TID MD of 100-150mg divided BID-TID
37
Thioamides onset? duration of therapy?
symptom improvement in 1-4 weeks, thyroid levels should normalize in 2-3months DoT: 12-18 months common, can tapper down to d/c to see if relapse occurs
38
Common SEs of thioamides?
GI upset rash arthalgia abnormal taste/smell usually go away within 4 weeks
39
Are SEs dose related in thioamides?
only for MMI not PTU
40
which thioamide has higher rates of SEs?
PTU
41
Serious SEs of thioamides?
Neutopenia/ agranulocytosis hepatotoxicity Vasculitis
42
What kind of hepatotoxicity is seen with MMI? PTU?
MMI --> reversible cholestatic jaundice PTU -->allergic type hepatocellular damage both can show increase in AST/ALT, concerned if >3x upper limit or an alcoholic
43
Do you regularly monitor WBCs in thioamide therapy to catch neutropenia/agranulocytosis?
No, not cost effective
44
Which thioamide are serious SEs more common in?
PTU
45
What can vasculitis lead to?
acute renal dysfunction arthritis skin ulcers/rashes respiratory problems
46
What do you tell a patient to watch for when starting thioamide therapy?
signs of infection headache malaise sore throat yellowing of skin (jaundice) fatigue weakness RUQ pain dark urine
47
DI's of thioamides?
Warfarin (decrease in INR) Digoxin (increased dig levels) MMI is a weak Cyp 2D6, 2C9 and 2E1 inhibtor
48
Monitoring of TSH, T3, and T4 for thioamides?
TSH T3 and T4 every 4-6 weeks until stable then every 2-3 months for 6-12 months, then 4-6months
49
How to monitor TSH when d/c thioamides?
at 3, 6, 12 months then annually
50
when is relapse most common?
in first 3 months of d/c
51
What will levels look like if relapse likely?
supressed TSH, normal T3/T4
52
What monitoring for thioamides? (not TSH, T3 T4)
CBCs, baseline and 1 week after starting LFTs baseline and 1 week later (watch AST/ALT)
53
Differences between MMT and PTU?
MMI quicker onset, less common SEs, better compliance (OD), cheaper, safer in 2nd and 3rd trimester
54
Drug used to control hyperthyroid symptoms?
beta-blockers
55
How does radioactive iodine work?
taken up by thyroid and causes tissue damage and ablation of gland, defintive treatment compared to thioamides
56
When is radioactive iodine used?
mild hyperthyroidism normal r slightly enlarged gland no exopthalmous
57
Downside of radioactive iodine?
permanent hypothyroidism can trigger thyroid storm/ thyrotoxicosis worsen exopthalmous
58
When is radioactive iodine contraindicated?
pregnancy and lactation sever hyperthyroidism exopthalmous
59
AE's of radioactive iodine?
intial hyperthyroidism exacerbation followed by hypothyroidism symptoms
60
How is radioactive iodine taken?
pre-treatment w/ thioamides 4-6w stop 3 days prior to RAI stop restart 3 days after RAI taper and d/c once thyroid hormone levels decline
61
Patient instructions for RAI?
Dont share anything w/ ppl avoid infants and young children and pregnant women (close contact) flush toilet 2x after peeing, wash hands well if neck pain or sore throat develops use acet if increased nervous, termors, palpitations call doc
62
THyroidectomy for?
pregnant who cant tolerate meds pts who wnat curative but not RAI pts with large goiters (RAI resistant)
63
Clinical importance of subclinical hyperthyroidism?
osteoporosis risk increase Cardiac abnormalities Increase in mortality
64
Subclinical hyperthyroidism TSH T3/T4?
TSH: 0.1-0.3 free T3/T4 normal
65
Thyroid storm?
life threatening condition severe manifestation of hyperthyroidism can occur in untreated hyperthyroidism
66
Triggers of thyroid storm?
thyroid surgery or RAI trauma infection giving birth
67
What makes thyroid storm life threatening?
liver damage CV collapse Shock
68
Treatment of thyroid storm?
supportive care corect electrolytes treat arrythmias beta blockers to reduce symptoms anti-thyroid meds steroids to block T4 --> T3 conversion
69
causes of hypothyroidism? (7)
any defect on HPT axis: 1. chronic autoimmune thyroditis (hashimotos) 2. drug induced 3. latrogenic disease (thyroidectomy/RAI) 4. Post-partum thyroiditis 5. chronic iodine deficiency 6. central hypothyroidism 7. hypopituitarism
70
Most common hypothyroid cause?
Hashimoto's disease
71
Characteristics of Hashimoto's disease?
antibodies form and bind to TSH receptors and directly destroy thyroid cells Other antibodies that interfere w/ T3 and T4 production can form too
72
What drugs can cause hypothyroidism?
Lithium: blocks iodine transport into thyroid and prevents hormone release Amiodarone
73
Clinical presentation of hyothyroidism early disease?
wt gain fatigue sluggishness cold intolerance bradycardia constipation heavy menstration course,dry flakey skin brittle hair/hari loss slow and hoarse speech puffiness around eyes emotional liability impaired concentration +/- non-toxic goiter
74
Clinical presentation of advanced hypothyroidism?
Myxedema hypothermia confusion stupor/coma CO2 retention hypoglycemia hyponatremia
75
Lab tests of hypothyroidism?
subclinical hypothyroidism: TSH: increased (4.5-10) T3/T4: normal Hashimoto's: TSH: very increased (>10) T3: decreased T4: decreased (more than T3)
76
Drugs that can decrease TSH?
amiodarone, glucocorticoids, metformin
77
Drugs that decrease T4 to T3 conversion?
amiodarone beta blockers glucocorticoids
78
Drugs that decrease synthesis/release of T3/T4
amiodarone lithium iodine (acute use)
79
Drugs that increase T3/T4 metabolism?
carbamazepine phenobarbital phenytoin rifampin(iftaking levothyroxine)
80
Treatment of hypothyroidism?
Desicated thyroid (shit) liothyronine levothyroxine combined T3/T4
81
Why is desicated thyroid shit?
causes high peak T3, not well standardized batch to batch
82
Liothyroxine characteristics?
Contains T3, no effect on T4 short t1/2 causes wide fluctuations in serum levels expensive higher CV effects dose close to physiological ratio of T4:T3
83
Levothyroxine characteristics?
analogue of T4 1st line therapy t1/2 of 7 days conversion of T3 regulated by body
84
Levothyroxine dosing?
depends on age, wt, cardiac status, severity and duration of hypothyroidism average replacement dose: 1.6mcg/kg/d starting dose: 12.5mcg/d to mac wt based Empirically give 100mcg to healthy pts, 25-50 mcg if subclinical hypothyroidism
85
How to start levothyroxine?
start low and titrate up if: any CVD rhythm disorders > 50yrs Severe, long-standing hypothyroidism 12.5-25mcg and titrate up 12.5-25mcg every 4-6 weeks
86
How must levothyroxine be taken?
on empty stomach 30 min before meals or 1 hour after meal, best to take in morning
87
Levothyroxine SEs?
hyperthyroid symptoms cardiac risk increase aggravate exisitng CVD BMD reduction
88
Levothyroxine DI's?
absorption reduction: antacids, H2 blockers, PPIs, iron, Ca/mineral supplements, cholestyramine/colestipol Space these by 2-4hrs Raloxifene space 12hrs potent CYP inducers: cipro, phenytoin, carbamazepine, rifampin, pregnancy TCA's: increase risk of arrhythmias
89
Levothyroxine monitoring?
TSH: aim is low normal values, cant take 4-6 weeks to stabalize with each dosage change Free T4: normal to slightly elevated Free T3: normal Symptoms: improved in 2-3 weeks, maximum effect in 4-6 weeks once stable/symptom free monitor TSH every 6-12-24m
90
Treat subclinical hypothyroidism?
controversial; potentially clincially relevant if; - atherosclerosis - HF - MI - depression - low BMD - metabolic syndrome Treat if: - symptoms develop - pregnancy planning - HF - very young pt
91
What to consider if levothyroxine therapy fails?
decreased bioavailability: - poor adherence - malabsorption - improper admin Increased need: - recent wt gain - pregnant - new medicatons taht increased T3/T4 metabolism Other: - addisons disease - alterted HPT axis - insuffecient peripheral conversion of T4 to T3

PHAR 255 (14 decks)

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