Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PHAR255 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Describe the thyroid gland.

A

butterfly-shaped endocrine gland in front of neck
responsible for synthesis, storage, and release of T3 and T4

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

Describe thyroid gland physiology.

A

synthesis and secretion of T3 and T4 controlled by thyroid stimulating hormone (TSH), which is controlled by thyrotropin releasing hormone
creation of T3 and T4 require iodide, thyroglobulin, and tyrosine
1) iodide binds with tyrosine attached to thyroglobulin=MIT or DIT
2) MIT + DIT = T3 or DIT + DIT = T4
3) then secreted into circulation
4) some T4 converted to T3 in peripheral tissue (13:1)

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

What are the actions of T3 and T4?

A

heart: chronotropic and ionotropic
adipose tissue: catabolic
muscle: catabolic
bone: developmental
nervous system: developmental
gut: metabolic
other tissues: calorigenic

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

Describe some relevant points about circulating T3 and T4.

A

T4 in circulation is 100% from thyroid
T3 in circulation is 20% directly from thyroid
T3 is ~4x more potent than T4
45% of T4 is converted to inactive rT3
the rest of T4 and T3 circulate in active free form or protein-bound inactive form

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

Describe the thyroid hormone release process.

A

regulated by a negative feedback loop
hormone release promoted by:
-TSH (release stimulated by low T3/T4)
-low serum iodide
hormone release inhibited by:
-high circulating T3/T4
-lithium
-iodide excess

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

What is hyperthyroidism?

A

disease caused by excess synthesis and secretion of thyroid hormone
-several causes possible
-causes a constellation of symptoms

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

What are the common causes of hyperthyroidism?

A

toxic diffuse goiter (Graves)
toxic multi-nodular goiter (Plummers)
acute phase of thyroiditis
toxic adenoma

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

Describe Graves disease.

A

more common in younger, female patients (age 20-50)
most common cause of hyperthyroidism
autoimmune disorder
-immune system creates antibodies against TSH receptor
can result in hyperplasia of thyroid gland=causes goiter

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

Describe Plummers disease.

A

most common in older, female patients (>50)
second most common cause of hyperthyroidism
iodine deficiency most common trigger for nodules to grow (but can be many others)
develops slowly over several years

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

Describe acute phase of thyroiditis.

A

causes inflammation and damage to the thyroid gland
damage causes excess hormone to be released
eventually leads to hypothyroidism once T3/T4 stores exhausted

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

Describe toxic adenoma.

A

benign tumours growing on thyroid gland
become active and act just like thyroid cells, secreting T3/T4 but not responding to negative feedback

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

What are some symptoms of hyperthyroidism?

A

all body systems overstimulated, non-specific
tremor in hands
diarrhea
heat intolerance
unintentional weight loss
weakness
tachycardia
amenorrhea

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

What are some symptoms that are specific to toxic diffuse goiter?

A

exophthalmos
peri-orbital edema
diplopia
diffuse goiter
pre-tibial myxedema

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

What are symptoms specific to toxic multi-nodular goiter?

A

individual thyroid nodules may be palpable
same general hyperthyroidism symptoms

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

How is hyperthyroidism diagnosed?

A

based on clinical symptoms and lab tests
-low TSH, elevated T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an example of a drug which can influence lab tests for hyperthyroidism?

A

amiodarone
-increases synthesis and release of T3/T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the anti-thyroid (thioamides) drugs?

A

methimazole
propythiouracil

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

What are the indications for the anti-thyroid (thioamides) drugs?

A

toxic diffuse goiter
toxic multi-nodular goiter
pre-treatment before RAI

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

What are the goals of therapy with thioamides?

A

achieve remission
-relapses are common
-about 30% remain in remission after 1-2 yrs of therapy with either drug

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

What is the MOA of the thioamides?

A

interferes with thyroid peroxidase-mediated processes in T3/T4 production
-PTU also inhibits peripheral conversion of T4-T3

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

In general, how are the thioamides dosed and titrated?

A

high initial dose–>lower maintenance doses
titrating dose if TSH and T4 does not improve in 4-6wks
decrease dose gradually once euthyroid
PTU dosing is same regardless of severity, MMI doses differ based on severity

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

How should thioamides be taken?

A

take with or without food
Terrys Tips:
-if convenience a priority, give both as a single daily dose
-if lowered nausea more important, give divided doses

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

What is the onset for thioamides?

A

symptom improvement in 1-4 weeks
euthyroid in 2-3 months

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

What is the duration of therapy for thioamides?

A

12-18 months is common
may taper to d/c and see if relapse occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the common side effects of the thioamides?
*dose related for MMI, but not PTU* *most of these AEs will improve over 4 weeks* GI upset rash arthralgia abnormal taste/smell
26
Which thioamide is more likely to produce the common adverse effects such as GI upset, arthralgia, etc?
PTU
27
What are the serious adverse effects of the thioamides?
neutropenia/agranulocytosis hepatotoxicity vasculitis
28
Describe neutropenia/agranulocytosis as serious adverse effects of the thioamides.
small decline is neutrophils is common agranulocytosis is rare (more common with PTU) usually occurs within the first 90 days WBC falls to < 0.5 x 10 to the 9 fever, malaise, sore throat most common symptoms abrupt onset *regular monitoring is not cost effective*
29
Describe hepatotoxicity as a serious adverse effect of thioamides.
rare (more common with PTU) MMI can cause reversible cholestatic jaundice PTU can cause allergic hepatocellular damage resolves once drug d/c but can result in death both can increase AST/ALT, concern if > 3x ULN or alcoholic
30
Describe vasculitis as a serious adverse effect of thioamides.
more common with PTU auto-immune process damages vascular tissue causing inflammation and destruction of blood vessels leads to: -acute renal dysfunction -arthritis -skin ulcers/rashes -respiratory problems
31
What are the drug interactions of the thioamides?
warfarin: decrease in INR digoxin: increase in levels methimazole weakly inhibits 2D6, 2C9, and 2E1
32
How can we monitor the thioamides for effectiveness?
1-4 weeks for symptom improvement assess TSH, T3 and T4 at 4-6 wk intervals until stable; then q2-3 months for 6-12 months, then q4-6 months if d/c, watch for relapse: -TSH at 3 mo --> 6 mo --> 12 mo --> annually -relapse most likely within first 3 months
33
How can we monitor the thioamides for safety?
CBCs: baseline and 1 week later LFTs: baseline and 1 week later -watch for AST/ALT > 3x ULN, and signs of hepatotoxicity
34
What is the use of beta-blockers in hyperthyroidism?
reduces symptoms of hyperthyroidism (mainly CV) -palpitations, tachycardia, tremor, anxiety, heat intolerance
35
Which beta-blockers are used in hyperthyroidism?
most are effective Terrys Tips: -choose propranolol if no compelling indication for a BB -short acting and easy to titrate/withdraw
36
What is the use of radioactive iodine for hyperthyroidism?
definitive treatment compared to thioamides -causes tissue damage and ablation of gland -used commonly
37
When is radioactive iodine given for hyperthyroidism?
mild hyperthyroidism normal or only slightly enlarged gland no exophthalmos
38
What are the downsides/complications of radioactive iodine?
permanent hypothyroidism can trigger thyroid storm/thyrotoxicosis worsen exophthalmos
39
What are the contraindications to radioactive iodine?
pregnancy/lactation severe hyperthyroidism/exophthalmos
40
What are the adverse effects of radioactive iodine?
initial hyperthyroidism exacerbation likely followed by hypothyroidism symptoms
41
Why do we pre-treat with thioamides prior to radioactive iodine?
to achieve euthyroid status and avoid thyroiditis recommended for all, but must pre-treat: -elderly patients, cardiac disease or severe hyperthyroidism
42
How do we initiate and stop treatment with thioamides prior to radioactive iodine?
initiate 4-6 weeks before RAI stop three days prior to RAI restart three days after RAI taper and d/c once thyroid hormone levels decline
43
When do we use thyroidectomy for hyperthyroidism?
pregnant pts who cant tolerate medication patients who want "curative" therapy but not RAI patients with large goiters
44
What are the complications of thyroidectomy?
hypoparathyroidism vocal cord paralysis thyrotoxicosis
45
What is subclinical hyperthyroidism?
TSH of 0.1-0.3, normal FT3/FT4, asymptomatic
46
Why is subclinical hyperthyroidism important?
osteoporosis risk increases cardiac abnormalities increase in mortality
47
What is the treatment for subclinical hyperthyroidism?
if at risk for complications: -strongly consider treatment or check levels again in 3 mo if at low risk for complications: -recheck levels in 4-6 mo unless TSH < 0.1
48
What is the management of thyroiditis?
self-limiting beta-blockers for symptom control NSAIDs for pain course of steroids for severe cases
49
What are the causes of hypothyroidism?
results from a defect anywhere on the HPT axis -chronic autoimmune thyroiditis (Hashimotos) -drug induced -iatrogenic disease -post-partum thyroiditis -chronic iodine deficiency -central hypothyroidism -hypopituitarism
50
Describe Hashimotos.
most common cause of hypothyroidism autoimmune disorder where antibodies form antibodies bind to TSH receptors which directly destroy thyroid cells other antibodies may form that interfere with production of T3 and T4
51
What are some drug-induced causes of hypothyroidism?
lithium amiodarone
52
Describe lithium as a drug-induced cause of hypothyroidism.
blocks iodine transport into the thyroid & prevents hormone release may cause subclinical or over hypothyroidism patients with a history of thyroid dysfunction at risk, elderly monitor at 3mo, then q6-12mo
53
Describe amiodarone as a drug-induced cause of hypothyroidism.
can cause hyper or hypothyroidism increased risk if history of thyroid dysfunction monitor q1mo x 3mo, then q3mo x 6mo, then q6-12mo
54
What are some symptoms of hypothyroidism?
weight gain fatigue cold intolerance bradycardia constipation
55
What are the expected labs for Hashimotos?
elevated TSH low T3 and T4
56
Which drugs can influence lab results for hypothyroidism?
amiodarone -decreases TSH -decreases synthesis/release of T3/T4 lithium -decreases synthesis/release of T3/T4
57
What are the options for therapy of hypothyroidism?
desiccated thyroid liothyronine levothyroxine
58
Describe desiccated thyroid.
first agent available prepared from thyroid glands of animals contains T3 and T4 causes high peak T3 not well standardized batch to batch
59
What are the limitations of desiccated thyroid?
4:1 ratio (much more potent) short t1/2
60
Describe liothyronine.
contains T3, no effect on T4 short t1/2 (causes wide fluctuations in serum levels) costly higher incidence of cardiac adverse effects try to dose close to physiologic ratio of T4:T3
61
When can liothyronine be considered?
people uncontrolled on levothyroxine
62
Describe levothyroxine.
analogue of T4 standard 1st therapy t1/2 of 7 days conversion to T3 regulated by body
63
What should be considered when determining an initial dose of levothyroxine?
age weight cardiac status severity and duration of hypothyroidism *higher baseline TSH usually predicts higher T4 dose*
64
What is the average dose of levothyroxine?
1.6mcg/kg/d
65
What is the starting dose range for levothyroxine?
12.5mcg/day to max wt. based if subclinical, 25-50mcg empirically *often give 100mcg empirically to young, healthy patients*
66
When do we recommend starting low and titrating up for levothyroxine?
any CVD rhythm disorders > 50 years old severe, long-standing hypothyroidism *start low (12.5-25mcg) and titrate up by 12.5-25mcg q4-6 weeks*
67
How should levothyroxine be administered?
administer on empty stomach, 30 min before meals or 1 hour after, QAM best
68
What are the side effects of levothyroxine?
hyperthyroidism symptoms cardiac risk increase aggravate existing CVD BMD reduction
69
What are drug interactions of levothyroxine?
absorption reduction -antacids/H2 blockers/PPIs -iron -calcium/mineral supplements -cholestyramine/colestipol *space levothyroxine 2-4 hours away from these meds (raloxifene space by 12h)* potent CYP inducers increases thyroid hormone metabolism -ciprofloxacin -phenytoin -carbamezepine -rifampin -pregnancy TCAs: increased risk of arrhythmia
70
How should levothyroxine be monitored?
TSH-->aim for low normal value (~2.5mlU/L) -lower values can increase risk of cardiac toxicity -may take 4-6 wks to stabilize with each dose change free T4-->normal to slightly elevated free T3-->normal symptoms-->improvement in 2-3 wks, maximum effect in 4-6 wks once stable and symptom free, monitor TSH q6-12-24mo
71
What is subclinical hypothyroidism?
TSH of 4.5-10mlU/L, normal T3/T4, "asymptomatic"
72
What does subclinical hypothyroidism increase the risk for?
atherosclerosis heart failure MI depression low BMD metabolic syndrome
73
When do we treat subclinical hypothyroidism?
if patients develop symptoms, planning pregnancy, HF, very young
74
What should we do if levothyroxine treatment fails?
consider: decreased F: -poor adherence -malabsorption -improper administration increased need: -recent weight gain -pregnancy -new meds that increase metabolism of T3/T4 other conditions: -Addisons -altered HPT axis -insufficient conversion of T4 to T3

PHAR255 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions