Brainscape's Knowledge GenomeTM

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


See full index

PHAR 255 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What is the general anatomy of the thyroid gland?

A

It is a butterfly-shaped endocrine gland in the front of the neck

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

What is the function of the thyroid?

A

Responsible for synthesis, storage and release of the two thyroid hormones (T3 and T4)

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

What is the most significant difference between T3 and T4?

A

T3 contains 3 iodines (more potent)

T4 contains 4 iodines (less potent)

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

What are the main cell types of the thyroid?

A
  • Colloid (storage for the building blocks (iodine, tyrosine, thyroglobulin) and finished product (T3 and T4)
  • Follicular cells (bring materials into and out of the colloid cells)
  • Parafollicular cells (responsible for Ca2+ balance via calcitonin (reduce Ca2+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the impact of thyroid resection on calcium levels?

A

No impact, despite loss parafollicular cells

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

What hormone controls T3 and T4 production?

A

It is controlled by TSH, which is controlled by thyrotropin-releasing hormone

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

What are the building blocks for T3 and T4?

A

MIT + DIT = T3

DIT + DIT = T4

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

What is the utility of T4 if it is less potent and more energetic?

A

It is a storage molecule and can allow for rapid changes in thyroid activity

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

What is the physiological ratio of T4:T3 (but normal can vary between people and different times)?

A

It is 13:1

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

What are the processes involved in thyroid introduction?

A
  1. Thyroglobulin synthesis
  2. Iodide trapping
  3. Oxidation of iodide
  4. Iodination of tyrosine
  5. Coupling of MIT and DIT
  6. Secretion of hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some actions of thyroid?

A
  • Heart (chronotropic and inotropic)
  • Adipose tissue (catabolic)
  • Muscle (catabolic, helps eventually build muscle)
  • Bone (development)
  • Nervous system (developmental)
  • Gut (metabolic)
  • Other tissues (calorigenic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the actions of T3 and T4?

A
  • Heart (chronotropic and inotropic)
  • Adipose tissues (catabolic)
  • Muscle (catabolic)
  • Bone (developmental)
  • Gut (metabolic)
  • Other tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What proportion of T4 is produced by the thyroid?

A

T4 in circulation is 100% from thyroid

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

What proportion of T3 is produced by the thyroid?

A

20% directly from thyroid (the rest is produced from conversion of T4 to T3)

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

What is the thyroid release feedback loop?

A

Low T3/T4 levels promote release of TSH, which promotes T3/T4

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

What inhibits TSH release?

A
  • High circulating T3/T4
  • Lithium
  • Iodide excess (inhibition of the organification of iodide)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the prevalence of thyroid disorders?

A

10% of Canadians have overactive or underactive thyroid glands (more than 50% are undiagnosed)

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

Do more men have thyroid disorders?

A

No, more than 80% with thyroid disease are women

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

What is hyperthyroidism?

A

Disease caused by excess synthesis and secretion of thyroid hormone

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

What are some causes of hyperthyroidism?

A

1, Toxic diffuse goiter (Graves disease)
2. Toxic multi-nodular goiter (Plummers disease)
3. Acute phase of thyroiditis
4. Toxic adenoma

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

What are some characteristics of toxic diffuse goiter (Graves disease)?

A

Auto-immune disorder (most common cause of hyperthyroidism, antibodies against the TSH receptor)

More common in younger, female patients

Hyperplasia of thyroid gland (leads to a goiter)

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

What are some characteristics of toxic multi-nodular goiter (Plummers disease)?

A

Common cause in older females

Second most common cause of hyperthyroidism

Triggered by iodine deficiency (reduced T4 production, )

Develops slowly over several years

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

What are the common cause of 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
24
Q

What are some common causes of toxic adenoma?

A
  • Benign tumours growinf on thyroid gland
  • Become active and act just like thyroid cells, secreting T3/T4?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the clinical presentation of hyperthyroidism?

A
  • 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
26
Q

What are some toxic diffuse goiter specific presentation?

A
  • Exophthalmos (or proptosis)
  • Peri-orbital edema
  • Diplopia (double vision)
  • Diffuse Goiter
  • Pre-tibial myxedema (rash on skin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the specific presentation of toxic multi-nodular goiter?

A
  • Same general hyperthyroidism symptoms
  • Individual thyroid nodules may be palpable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Review slide 22 for diagnostic lab tests

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

What drugs can induce hyperthyroidism?

A
  • 1st gen antipsychotics (Increases TSH secretion)
  • Amiodarone & iodine (Increases synthesis and release of T3/T4)
  • Androgens & Glucocorticoid (Decreases Thyroxin binding globulin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the treatment options for hyperthyroidism?

A

Drugs
- Thioamides
- Beta-blockers

Radioactive iodine (RAI)

Surgery (thyroidectomy)

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

What are the types of thioamides used in treatment of hyperthyroidism?

A
  • Methimazole (MMI)
  • Propylthiouracil (PTU)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are some specific indications for thioamides?

A
  • Toxic diffuse goiter
  • Toxic multi-nodular goiter
  • Pre-treatment before radioactive iodine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the goal of therapy for acheiving remission of hyperthyroidism with thioamides?

A
  • Relapses are common
  • About 30% remain in remission after 1-2 years of therapy with either drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the mechanism of action for thioamides?

A
  • They interfere with thyroid peroxidase-mediated processes in T3/T4 production
  • PTU also inhibits peripheral conversion of T4 to T3
35
Q

How are thioamides dosed?

A

It is an initial dose (lower maintenance doses)

Titrate dose if TSH and T4 does not improve in 4-6 weeks

Decrease dose gradually once euthyroid

Review slide 28

36
Q

Can thioamides be taken without food?

A

Take with or without food

37
Q

What is the onset of effect for thioamides?

A

Symptom improvement in 1-4 weeks

Euthyroid in 2 to 3 months

38
Q

How long does thioamide therapy for hyperthyroidism last?

A

12-18 months is common (taper to d/c to see if relapse occurs)

39
Q

What are some common side effects associated with thioamides?

A

Higher rates with PTU than MMI
- GI upset
- Rash
- Arthralgia
- Abnormal taste/smell

40
Q

What are some serious side effects associated with thioamide use?

A
  1. Agranulocytosis (0.3-0.4% of patients affected)
    - Fever, malaise, sore throat are the most common symptoms
    - WBC falls to less than 0.5 x 10^9
  2. Hepatoxicity (0.1-0.2%)
    - MMI (reversible cholestatic jaundice)
    - PTU (allergic type hepatocellular damage)
  3. Vasculitis (more common with PTU, like all side effects)
    - Damage to vascular tissue causing inflammation and destruction of blood vessels (acute renal dysfunction, arthritis, skin ulcers, respiratory problems)
41
Q

Review slide 34 for what to counsel patients on about thioamides

A
42
Q

What are some drug interactions associated with thioamides?

A

Warfarin (results in a decrease in INR, often resolved by adjusting warfarin dose)

Digoxin (Increase in digoxin levels)

Methimazole inhibits 2D6. 2C9, 2E1 (very weak interactions, clinically irrelevant)

43
Q

What are some monitoring tips for thioamides?

A

Assess TSH, T3, and T4 at 4-6 week intervals until stable, then every 2-3 months for 6-12 months, then every 4-6 months

CBC (baseline and 1 week later for agranulocytosis)

LFTs (baseline and 1 week later for signs of hepatotoxicity)

44
Q

What should be monitored when discontinuing thioamides?

A

TSH at 3, 6, 12, and annually

Relapse of hyperthyroidism after thioamide d/c is most likely in the first 3 months

45
Q

Review slide 38 on differences between thioamides (propylthiouracil and methimazole)

A
46
Q

What is the purpose of beta-blockers in hyperthyroidism treatment?

A

They reduce CV symptoms associated with hyperthyroidism
- Palpitations
- Tachycardia
- Tremors
- Anxiety
- Heat intolerance

47
Q

What beta-blockers are used in hyperthyroidism treatment?

A

Choose propranolol (short-acting and easy to titrate) if no other compelling indication for a beta-blocker exists

48
Q

What is the role of radioactive iodine treatment in hyperthyroidism treatment?

A

Used commonly

radio-labelled iodine is taken up by the thyroid gland and causes tissue damage and ablation of gland

49
Q

What are the disadvantages of radioactive iodine therapy in hyperthyroidism therapy?

A
  • Permanent hypothyroidism
  • Can trigger thyroid storm/thyrotoxicosis
  • Worsen exopthalmous (protruding eyes)
50
Q

What are some contraindications for radioactive iodine therapy for hyperthyroidism?

A
  • Pregnant women/lactation
  • Severe hyperthyroidism/exopthalmous
51
Q

What happens to thyroid levels immediately after administration of radioactive iodine?

A

Initial hyperthyroidism exacerbation likely (controlled with thioamide pre-treatment and post-treatment)

52
Q

How is radioactive iodine therapy for hyperthyroidism initiated?

A

Pre-treatment with thioamides (used to achieve euthyroidism and prevent thyroiditis). Initiate 4-6 weeks before radioactive therapy, and stop 3 days before

Administer radioactive iodine therapy

Restart thioamides 3 days after administration of radioactive iodine therapy

Taper and discontinue once thyroid hormone levels decline

53
Q

What are some patient instructions following radioactive iodine therapy for hyperthyroidism?

A
  1. Do not kiss, exchange saliva, or share food or eating utensils for 5 days.
  2. Avoid close contact with infants, young children (under 8 years), and pregnant women for 5 days (patient can be in the same room though)
  3. No breast-feeding
  4. Flush toilet twice and wash hands thoroughly
  5. If sore throat or neck pain develops (take acet or aspirin)
  6. If increased nervousness, tremors, or palpitations, then call a physician (signs of hyperthyroidism after radioactive treatment)
54
Q

What is the role of surgery in hyperthyroidism treatment?

A

It is reserved for the following patient groups:
- Pregnant patients who cannot tolerate medication
- Patients who want curative therapy, but not RAI
- Patients with large goiters (resistant to RAI)

55
Q

What are some complications associated with surgical resection of the thyroid?

A
  • Hypoparathyroidism (Parathyroid is behind the thyroid, so it can be damaged during thyroid resection)
  • Vocal cord paralysis
  • Thyrotoxicosis
56
Q

Should thioamides be used to treat thyroiditis?

A

No, because thyroiditis is an acute condition and thioamides are used in more chronic presentations

57
Q

How is thyroiditis managed?

A
  • Self-limited
  • beta-blocker for symptom control
  • NSAIDs for pain
  • Steroids (for most severe cases)
58
Q

What is thyroid storm/thyrotoxicosis?

A

It is a rare, life-threatening condition that is characterized by severe manifestations of hyperthyroidism (liver damage, CV collapse, and shock)

59
Q

What causes thyroid storm/thyrotoxicosis?

A
  • Thyroid surgery or radioactive iodine therapy
  • Trauma
  • Infection
  • Giving birth
60
Q

What is the basic cause of hypothyroidism?

A

Results from a defect anywhere on the HPA axis

61
Q

What are the types of hypothyroidism?

A
  • Chronic autoimmune thyroiditis (Hashimoto’s)
  • Drug-induced
  • Iatrogenic disease (thyroidectomy/RAI)
  • Post-partum thyroiditis
  • Chronic iodine deficiency
  • Central hypothyroidism
  • Hypopituitarism
62
Q

What are some characteristics of chronic thyroiditis (Hashimoto’s)?

A
  • Most common cause of hypothyroidism
  • Autoimmune disorder where antibodies form and bind to TSH receptors and destroy thyroid cells
  • Other antibodies may form that can interfere with T3 and T4 production
63
Q

What are some drugs that can trigger hypothyroidism?

A
  • Lithium
  • Amiodarone
64
Q

What is the mechanism of action for lithium causing hypothyroidism?

A

Lithium blocks iodine transport into the thyroid and prevents hormone release

Monitor for hypothyroidism at 3 months, then every 6-12 months

65
Q

What is the mechanism of action for amiodarone causing hypothyroidism?

A

Can cause hyperthyroidism (5-25%)

Increased risk if history of thyroid dysfunction

Monitor every month for 3 months, then every 3 months for 6 months, then every 6-12 months

66
Q

What is the clinical presentation of hypothyroidism?

A

PNS-like activity

  • Slow harse speech
  • Puffiness around eyes
  • Emotional lability
  • Impaired concentration
  • Hypothermia
  • Confusion
  • Hypoglycemia
67
Q

Review slide 55 for lab results that are significant to diagnosing hypothyroidism?

A
68
Q

What substance is elevated in hypothyroidism patients?

A

TSH

69
Q

Review slide 56 for a series of drugs that can affect levels of hormones and substances that are used to diagnose hypothyroidism

A
70
Q

What are some treatment options for hypothyroidism?

A

Replacement of thyroid hormone is necessary. The following are options to resolve the deficiency of thyroid hormones:

  • Desiccated thyroid
  • Liothyronine
  • Levothyroxine
  • Combined T3/T4
71
Q

What are some characteristics of desiccated thyroid?

A
  • First agent available
  • Prepared from thyroid glands of animals
  • Contains T3 and T4
  • Causes high peak T3 (and shorter half-life)
  • Not well standardized batch to batch
72
Q

What are some characteristics of Liothyronine?

A
  • Contains T3, no effect on T4
  • Short half-life (causes wide flucuations in serum levels)
  • Costly
  • Higher incidence of cardiac adverse effects
  • Try to dose close to physiological ratio of T4:T3 (13:1)
73
Q

What are some characteristics of Levothyroxine?

A
  • Analogue of T4
  • Standard 1st therapy
  • Half life of 7 days (potential for weekly dosing)
  • Conversion to T3 regulated by body
74
Q

How is levothyroxine dosed?

A

Depends on age, weight, cardiac stus, severity, and duration of hypothyroidism (ensure titration is gradual and safe)

Average replacement dose is 1.6mcg/kg/day (100mcg is given empirically to young, healthy patients)

Starting dose: (12.5mcg/day to max weight based dose)

75
Q

What are some populations that we should be more careful with initiating levothyroxine?

A

Start low (12.5-25mcg) and titrate up by 12.5-25mcg every 4-6 weeks

  • Any CVD
  • Rhythm disorders
  • More than 50 years old
  • Severe, long-standing hypothyroidism
76
Q

What are some administration instructions for levothyroxine?

A

Administer on empty stomach, 30 minutes before meals or 1 hours after

Best to take in the morning and stagger from other drugs

77
Q

What are some side effects associated with levothyroxine?

A
  • Hyperthyroidism symptoms (nervousness, hyperactivity, mood swings)
  • Cardiac risk increase
  • Aggravate existing CVD
  • BMD reduction
78
Q

What are some drug interactions associated with levothyroxine?

A

Drugs that reduce absorption of levothyroxine:
- Antacids
- Iron
- Ca2+/mineral supplements
- Cholestyramine

79
Q

What are some drug interactions associated with levothyroxine?

A

Potent CYP inducers increase thyroid hormone metabolism:
- Ciprofloxacin
- Phenytoin
- Carbamazepine
- Rifampin
- Pregnancy of arrhythmias

80
Q

What are some monitoring parameters for levothyroxine?

A

TSH (aim for low normal value, 2.5mIU/L). Any lower increases risk for cardiac toxicity

Levels can take 4-6 weeks to stabilize with each dose (then monitor TSH every 6-12 months)

Symptom improvement in 2-3 weeks, with max effect in 4-6 weeks

81
Q

Is subclinical hypothyroid treated in most cases?

A

No, it is not treated often (only treated if patient develops symptoms, planning pregnancy, heart failure, or a very young patient)

82
Q

What are some reasons for levothyroxine treatment failure?

A
  • Decreased bioavailability (poor adherance, malabsorption)
  • Increased need (recent weight gain, pregnancy, new meds that increase metabolism)
  • Other conditions (Addison’s disease, altered HPA)
83
Q
A

PHAR 255 (15 decks)

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