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PATHO/PHARM II > Conditions Effecting the Endocrine System and Pharmacology > Flashcards

Conditions Effecting the Endocrine System and Pharmacology Flashcards

Exam 3

1
Q

A&P of thyroid gland:

Where is the thyroid located?

A

Located at the base of the neck below the larynx

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2
Q

A&P of thyroid gland:

What does the thyroid wrap around?

A

Wraps around the trachea

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3
Q

A&P of thyroid gland:

What does the thyroid consist of?

A

Consists of two lobes, one on either side of the trachea, connected by a thin band of tissue

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4
Q

A&P of thyroid gland:

What does the thyroid regulate?

A

Regulates metabolic rate, heart and digestive function, muscle control, and bone maintenance

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5
Q

A&P of thyroid gland:

What does the thyroid contain?

A

A vascular gland, containing several functional units (follicles) that secretes hormones:

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6
Q

A&P of thyroid gland:

What hormones does the thyroid secrete?

A

Thyroxine (T4) and Triiodothyronine (T3)

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7
Q

A&P of thyroid gland:

Thyroxine (T4) and Triiodothyronine (T3): What do they stimulate?

A

Stimulates cell growth and tissue differentiation

Stimulate energy use

Stimulate the heart – increased rate/force of ctx

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8
Q

A&P of thyroid gland:

How does the Thyroxine (T4) and Triiodothyronine (T3) stimulate energy use?

A

Raises BMR, heat production, oxygen consumption

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9
Q

A&P of thyroid gland:

What does Thyroxine (T4) and Triiodothyronine (T3) do to the heart when it stimulates the heart?

A

– increased rate/force of ctx  better CO, increased O2 demand

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10
Q

A&P of thyroid gland:

What percent of circulating hormones are Thyroxine (T4) and Triiodothyronine (T3)?

A

95% of circulating thyroid hormones

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11
Q

A&P of thyroid gland:

What are Thyroxine (T4) and Triiodothyronine (T3) needed for?

A

Needed for normal brain & nervous system development

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12
Q

A&P of thyroid gland:

What is the process in which T3 and T4 are made?

A

Hypothalamus stimulates pituitary gland to produce the thyroid-stimulating hormone (TSH), which stimulates T3 and T4.

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13
Q

Regulation of Hormone Release :

Hormones are released in response to what?

A

In response to an alteration in the cellular environment

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14
Q

Regulation of Hormone Release :

Hormones are released to maintain what?

A

To maintain a regulated level of certain substances or other hormones

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15
Q

Regulation of Hormone Release:

What are hormones regulated by?

A

Hormones are regulated by chemical, endocrine, or neural factors

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16
Q

Regulation of Hormone Release:

Where are hormones released and distributed?

A

Hormones are released into the circulatory system by endocrine glands and distributed throughout body

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17
Q

Regulation of Thyroid Hormone Release (2 of 2):

Positive feedback: What is it?

A

Response to stimulus increases synthesis and secretion of hormone

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18
Q

Regulation of Thyroid Hormone Release (2 of 2):

Example of Positive feedback with thyroid hormone?

A

Thyrotropin-releasing hormone (TRH) released from the hypothalamus in response to low thyroid levels

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19
Q

Regulation of Thyroid Hormone Release (2 of 2):

Where does secretion of thyroid hormone occur?

A

Stimulates secretion of thyroid stimulating hormone (TSH) from anterior pituitary

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20
Q

Regulation of Thyroid Hormone Release (2 of 2):

Positive Feedback: What kind of hormone is secreted?

A

stimulates secretion of Thyroid Hormone (TH) T3 & T4

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21
Q

Monitoring Thyroid Function:

What are the thyroid hormones? Which is more active?

A

T3 (more active form), T4

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22
Q

Regulation of Thyroid Hormone Release (2 of 2):

Negative feedback: What is it?

A

Response to stimulus decreases synthesis and secretion of hormone

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23
Q

Regulation of Thyroid Hormone Release (2 of 2):

Negative feedback: What happens?

A

Increased T3 & T4 levels feedback on pituitary & hypothalamus to inhibit TRH & TSH

Decreased synthesis of thyroid hormones

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24
Q

Monitoring Thyroid Function:

What is 1st line for screening, diagnosis and treatment monitoring?

A

Serum TSH

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25
Q

Monitoring Thyroid Function:

What does Serum TSH distinguish between?

A

Distinguishes primary VS secondary disorders

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26
Q

Monitoring Thyroid Function:

1° disorder: Thyroid gland is at fault

What do primary disorders cause?

A

These disorders cause 2ndry feedback of pituitary TSH

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27
Q

Monitoring Thyroid Function:

What are primary disorders?

A

1° disorder: Thyroid gland is at fault

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28
Q

Monitoring Thyroid Function:

1° disorder: Thyroid gland is at fault

What happens when the TH is high?

A

When TH is high (hyperthyroid), TSH secondarily decreases because of neg feedback

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29
Q

Monitoring Thyroid Function:

What happens when TH is low?

A

When TH is low (hypothyroid), the TSH will be elevated because it’s trying to increase thyroid gland production of TH

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30
Q

Monitoring Thyroid Function:

What is a secondary disorder?

A

2° disorder: related to pituitary gland disorder

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31
Q

Monitoring Thyroid Function:

What occurs in secondary disorder?

A

Excessive TSH production –> TH is elevated secondary to the primary elevation of TSH concentration

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32
Q

Monitoring Thyroid Function:

2° disorder: related to pituitary gland disorder

What does low TSH production lead to?

A

Low TSH production –> TH decreased

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33
Q

Alterations of Thyroid Function:

Primary thyroid disorders: What is it?

A

Dysfunction or disease of thyroid

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34
Q

Alterations of Thyroid Function:

Primary thyroid disorders: What happens to TH levels?

A

Increased or decreased thyroid hormone (TH)

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35
Q

Alterations of Thyroid Function:

Primary thyroid disorders: How is it caused?

A

Idiopathic, caused by autoimmune mechanisms

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36
Q

Alterations of Thyroid Function:

Primary thyroid disorders: What do these cause?

A

These disorders will cause secondary feedback effects on pituitary TSH

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37
Q

Alterations of Thyroid Function:

Primary thyroid disorders: These disorders will cause secondary feedback effects on pituitary TSH

What is an example?

A

E.g. Decreased TH from thyroid–> Ant. Pit. TSH increases

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38
Q

Alterations of Thyroid Function:

Central (secondary) thyroid disorders: What are they?

A

Disorders of pituitary gland thyroid stimulating hormone (TSH) production

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39
Q

Alterations of Thyroid Function:

Central (secondary) thyroid disorders: What does this lead to?

A

Inadequate TSH –> TH level low

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40
Q

Hypothyroidism: How are T3 and T4 levels?

A

Decreased T3 and T4

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41
Q

Hypothyroidism: What occurs with T3 and T4?

A

Destruction of thyroid

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42
Q

Hypothyroidism: What can it cause?

A

Endemic goiter,

Hashimoto’s

thyroiditis

Cretinism

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43
Q

Hypothyroidism: Patho & Diagnosis:

What age does it occur?

A

Can occur at any age

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44
Q

Hypothyroidism: Patho & Diagnosis

Primary Thyroid disorder: How is it?

A

Deficient production of TH and increase TSH and TRH

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45
Q

Hypothyroidism: Patho & Diagnosis

Primary Thyroid disorder: What are most common causes of it?

A

Autoimmune thyroiditis (Hashimoto’s)

Surgical or radioactive treat of hyperthyroid

Head/neck radiation

Iodine deficiency congenital defects

Meds

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46
Q

Hypothyroidism: Patho & Diagnosis

Primary Thyroid disorder: What occurs with hormone levels?

A

TH is decreased, TSH elevated

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47
Q

Hypothyroidism: Patho & Diagnosis

Secondary disorder:

A

2°: pituitary failure to produce adequate amts of TSH or lack of TRH

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48
Q

Hypothyroidism: Patho & Diagnosis

Secondary disorders: How common are they?

A

Much less common

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49
Q

Hypothyroidism: Patho & Diagnosis

Secondary disorder: What are examples?

A

Eg: pit tumors compressing pituitary cells or consequences of their tx,

traumatic brain injury,

subarachnoid hemorrhage

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50
Q

Hypothyroidism: Patho & Diagnosis

Secondary disorder: How are levels of TH, TSH and TRH?

A

Low levels of TH, TSH, TRH

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51
Q

Hypothyroidism: Patho & Diagnosis

What is a third cause of hypothyroidism? Not primary or secondary disorder

A

Subclinical- mild thyroid failure

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52
Q

Pathophysiology of Primary Hypothyroidism:

How is the thyroid normally supposed to work?

A

Pituitary gland –> TSH –> Thyroid gland –> T3 and T4

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53
Q

Pathophysiology of Primary Hypothyroidism:

How does the thyroid work in hypothyroidism? (What it the process)

A

Pituitary –> TSH–> Thyroid gland is unable to respond to TSH stimulation –> Thyroid gland does not produce T3 and T4–> Thyroid tissue is destroyed and hypothyroidism occur?

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54
Q

Hypothyroid conditions:

What is the most common cause of thyroid conditions?

A

Hashimoto DX (thyroiditis)

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55
Q

Hypothyroid conditions

Hashimoto DX (thyroiditis): What causes it?

A

Genetic risk factors & associated with other autoimmune conditions

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56
Q

Hypothyroid conditions:

What occurs in Hashimoto’s (thyroiditis)?

A

T lymphocytes, antithyroid Abs, NK cells infiltrate thyroid –> gradual inflammatory destruction of thyroid tissue

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57
Q

Hypothyroid conditions:

In Hashimoto’s, T lymphocytes, antithyroid Abs, NK cells infiltrate thyroid, What does this lead to?

A

T lymphocytes, antithyroid Abs, NK cells infiltrate thyroid –> gradual inflammatory destruction of thyroid tissue

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58
Q

Hypothyroid conditions:

What happens to the thyroid gland? What does this lead to?

A

Destruction of the gland reduces the production of T3 and T4

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59
Q

Hypothyroid conditions:

What does it result from?

A

Results from the body’s production of antibodies that attack the thyroid gland

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60
Q

Low levels of iodine lead to what?

A

Low levels of iodine → Endemic goiter

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61
Q

What kind of goiter is an endemic goiter?

A

Nontoxic goiter

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62
Q

Low levels of iodine → Endemic goiter:

Where is this seen? What conditions?

A

Usually seen in areas where there are low iodine levels in the soil and food

Use of non-ionized salt in the diet instead of iodized salt

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63
Q

Low levels of iodine → Endemic goiter:

Why is iodine important for thyroid?

A

Iodine is the fuel used by the thyroid gland to synthesize T3 and T4.

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64
Q

Low levels of iodine → Endemic goiter:

What does decreased iodine intake lead to (having to do with T3 and T4)?

A

With decreased iodine intake, the production of T3 and T4 decreases.

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65
Q

Low levels of iodine → Endemic goiter:

With decreased iodine intake, the production of T3 and T4 decreases: What does this lead to?

A

The hypothalamus then compensates by increasing its production of thyrotropin releasing hormone (TRH) to stimulate the pituitary to release thyroid stimulating hormone (TSH) to increase the production of T3 and T4.

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66
Q

Low levels of iodine → Endemic goiter:

Decreased iodine= low T3/T4 = hypothalamus makes more TRH = stimulates pituitary thyroid stimulating hormone (TSH) to increase T3 and T4: What does this lead to?

A

The increased TSH produces hyperplasia and hypertrophy in the thyroid gland which results in goiter formation.

Look at picture on slide 20

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67
Q

Goiter:

A

Enlargement of thyroid gland

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68
Q

Goiter: Enlargement of thyroid gland

What are the types of goiters?

A

Nontoxic goiter

Toxic goiter

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69
Q

Goiter: Enlargement of thyroid gland

Nontoxic goiter: What is it?

A

Enlargement of thyroid not associated with overproduction of TH

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70
Q

Goiter: Enlargement of thyroid gland

What are the types of nontoxic goiters?

A

Simple or Diffuse Nontoxic Goiter:

Multinodular Nontoxic Goiter:

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71
Q

Nontoxic Goiter:

Simple or Diffuse Nontoxic Goiter: What is it?

A

thyroid gland is uniformly enlarged.

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72
Q

Nontoxic Goiter:

Multinodular Nontoxic Goiter: What is it?

A

Multiple nodules are present but do not result in hormone overproduction

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73
Q

Goiter: Enlargement of thyroid gland

Nontoxic goiters: What can be causes?

A

Iodine deficiency, genetics, exposure to goitrogens (cabbage, broccoli)

Thyroiditis

Hormonal changes

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74
Q

Goiter: Enlargement of thyroid gland

Toxic Goiter: What is it associated with?

A

Associated with hyperthyroidism

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75
Q

Goiter: Enlargement of thyroid gland

Toxic goiter: What occurs with this?

A

Thyroid gland produces an excess amount of thyroid hormones (T4 and T3)

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76
Q

Goiter: Enlargement of thyroid gland

Toxic goiter: What are the types of goiters?

A

Toxic Multinodular Goiter (Plummer’s Disease):

Toxic Adenoma:

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77
Q

Goiter: Enlargement of thyroid gland

Toxic goiter: Toxic Multinodular Goiter (Plummer’s Disease): What is it?

A

Multiple nodules in the thyroid produce excess thyroid hormones.

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78
Q

Goiter: Enlargement of thyroid gland

Toxic goiter: Toxic Adenoma: What is it?

A

A single nodule in the thyroid becomes overactive and produces excess hormones.

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79
Q

Goiter: Enlargement of thyroid gland

Toxic goiter: Toxic Adenoma: What causes it?

A

Graves’ & nodules (Autonomous functioning secrete TH despite normal regulatory mechanisms

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80
Q

Cretinism: Who does it occur in?

A

Infants

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81
Q

Cretinism: What is the issue with the thyroid?

A

Thyroid tissue absent or hereditary defects

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82
Q

Cretinism:

What is TH essential for (in general not having to do with disease)?

A

TH essential for fetal growth, brain development

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83
Q

Cretinism: What can this lead to if left untreated?

A

Can lead to developmental & cognitive disabilities if untx’d

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84
Q

Cretinism:

What are symptoms of cretinism?

A

Protruding tongue,

potbelly,

dwarfish stature,

hypothermia,

constipation,

lethargy,

cold mottled skin,

bradycardia

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85
Q

Cretinism: What happens to skeletal growth in this disease? WHy?

A

Skeletal growth stunted due to impaired protein synthesis, poor nutrient absorption, lack of bone mineralization

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86
Q

Cretinism: What happens to development of nervous system?

A

Impaired development of nervous system, bones, teeth, brain tissue, difficulty feeding, lethargy

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87
Q

Cretinism: What develops on the abdomen?

A

Umbilical hernia due to hypotonic abdominal muscles

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88
Q

Cretinism: When will it be evident?

A

May not be evident until 4 months of age

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89
Q

Cretinism: What is needed for cretinism?

A

Immediate TX necessary

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90
Q

Cretinism: How long is treatment?

A

Continued treatment until 3yo then stopped for 4 weeks to r/o permanent or transient deficiency

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91
Q

Cretinism: What is something that can be lifelong with cretinism?

A

↑ TSH & ↓ T4 ~ continued lifelong

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92
Q

Clinical Manifestations of Hypothyroidism:

What does hormone levels do to metabolic rate?

A

↓ T3, T4resulting in a decreased metabolic rate

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93
Q

Clinical Manifestations of Hypothyroidism:

Why does ↓ T3, T4 resulting in a decreased metabolic rate occur?

A

Hyposecretion of thyroid hormones

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94
Q

Clinical Manifestations of Hypothyroidism: What may or may not be present with hypothyroidism?

A

Goiter (enlarged gland) may or may not be present; may have hoarseness if present

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95
Q

Clinical Manifestations of Hypothyroidism: Why is Goiter (enlarged gland) may or may not be present; may have hoarseness if present?

A

Overstimulation of thyroid gland from TSH released from pit. in response to low TH levels; pressure on vocal cord leads to changing voice

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96
Q

Clinical Manifestations of Hypothyroidism:

How is the skin? How is the hair?

How do they tolerate the cold?

A

Pale, cool skin

Loss of hair, coarse, brittle hair

Cold intolerance

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97
Q

Clinical Manifestations of Hypothyroidism: Why does pale, cool skin, occur in Hypothyroidism?

A

Decreased metabolic rate, bradycardia, and decreased blood flow to skin

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98
Q

Clinical Manifestations of Hypothyroidism: Why does loss of hair, coarse, brittle hair, cold intolerance and weight gain with decreased appetite occur in Hypothyroidism?

A

Decreased metabolic rate

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99
Q

Clinical Manifestations of Hypothyroidism: How is weight and appetite?

A

Weight gain with decreased appetite

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100
Q

Clinical Manifestations of Hypothyroidism:

How does the face appear?

A

Myxedema (nonpitting edema seen as facial puffiness, periorbital edema, and thick tongue)

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101
Q

Clinical Manifestations of Hypothyroidism: Why does Myxedema (nonpitting edema seen as facial puffiness, periorbital edema, and thick tongue) occur?

A

Increased mucopolysaccharides in the dermis and other tissues from lack of thyroid hormones and improper metabolism

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102
Q

Clinical Manifestations of Hypothyroidism: How is the heart?

A

Bradycardia (less than 60 beats per minute),

enlarged heart,

heart failure

103
Q

Clinical Manifestations of Hypothyroidism: Why does bradycardia occur?

A

Decreased cardiac contractility

104
Q

Clinical Manifestations of Hypothyroidism:

Effects on GI, Muscles, reflexes?

A

Constipation, muscle weakness, hyporeflexia

105
Q

Clinical Manifestations of Hypothyroidism:

Why does constipation, muscle weakness, hyporeflexia occur?

A

Hypotonic muscles

106
Q

Clinical Manifestations of Hypothyroidism:

How are they intellectually?

A

Lethargic, slow intellectual functions

107
Q

Clinical Manifestations of Hypothyroidism:

Why does lethargy, slow intellectual functions occur in hypothyroidism?

A

Decreased mental alertness from decreased metabolic rate and decreased blood flow from bradycardia

108
Q

Myxedema coma- What is it?

A

Myxedema coma = severe hypothyroidism with severely decreased metabolic rate which slows everything down into a coma

109
Q

Myxedema coma: How is it viewed?

A

Myxedema coma – med emergency

110
Q

Myxedema coma: What is it a clinical manifestation of?

A

Severe deficiency, profound presentation of hypothyroidism

111
Q

Myxedema coma (in severe hypothyroidism): What causes it?

A

Hypotension, hypoglycemia, respiratory depression, hypothermia, lethargy –> coma

112
Q

Myxedema coma:
Hypotension, hypoglycemia, respiratory depression, hypothermia, lethargy –> coma:

Why does hypotension occur?

A

Hypotension due to hypotonic (flabby) heart muscle from decreased metabolism

113
Q

Myxedema coma:
Hypotension, hypoglycemia, respiratory depression, hypothermia, lethargy –> coma:

Why does hypoglycemia occur?

A

Hypoglycemia due to decreased production of glucose from low levels of thyroid hormones

114
Q

Myxedema coma:

Hypotension, hypoglycemia, respiratory depression, hypothermia, lethargy –> coma:

Why does hypothermia occur?

A

Hypothermia without shivering due to decreased metabolic rate

115
Q

Myxedema coma:

Hypotension, hypoglycemia, respiratory depression, hypothermia, lethargy –> coma:

Why does hypoventilation occur?

A

Hypoventilation due to decreased metabolic rate and hypotonic respiratory muscles

116
Q

Myxedema coma: When can it occur?

A

May occur after acute illness

117
Q

Myxedema coma:

Why does loss of consciousness occur?

A

Loss of consciousness due to decreased perfusion to brain from hypotension

118
Q

Myxedema coma:

Who is at risk for developing this?

A

At risk: older adults with comorbidities & mod or untreated hypothyroidism

119
Q

Myxedema coma:

Why else would it occur (having to do with drugs)?

A

May occur after overuse of narcotics or sedatives

120
Q

Myxedema coma:

What is treatment for this?

A

Adjunct TX w/ GCs

121
Q

Myxedema coma:

What is the adjunct treatment for this?

A

Treatment – IV Levothyroxine (SyntheticT4)

122
Q

Hypothyroidism: Life Span Issues

During Pregnancy: How can it effect first trimester?

A

In first trimester can result in permanent neuropsychologic deficits in the child

123
Q

Hypothyroidism: Life Span Issues

During Pregnancy: What are the signs and symptoms?

A

Minimal s/s or asymptomatic

124
Q

Hypothyroidism: Life Span Issues

During pregnancy: What is the treatment?

A

Early-DX & TX necessary

125
Q

Hypothyroidism: Life Span Issues

During pregnancy: If diagnosis is before pregnancy, how should dosing be?

A

For prior DX ~ ↑ supplement dose by 50%

126
Q

Hypothyroidism: Life Span Issues

During pregnancy: When is increased dosage of thyroid supplements needed?

A

Increased dosage of thyroid supplements needed between 4-8 wks gestation, levels off by week 16

127
Q

Hypothyroidism: Life Span Issues

In infants: How are effects of hypothyroidism?

A

May be permanent or transient

128
Q

Hypothyroidism: Life Span Issues:

In infants: What are the effects of hypothyroidism?

A

Can cause intellectual disability and derangement of growth

129
Q

Hypothyroidism: Life Span Issues

Older adults: What is important to remember about symptoms?

A

Hypothyroid symptoms should never be attributed to normal age-related changes

130
Q

TX for Hypothyroidism: Thyroid Supplementation

What are the meds?

A

Levothyroxine (Synthroid)

131
Q

TX for Hypothyroidism: Thyroid Supplementation

What is the drug of choice for all forms of hypothyroidism regardless of cause?

A

Levothyroxine (Synthroid)-
DOC for all forms, regardless of cause

132
Q

TX for Hypothyroidism: Thyroid Supplementation

What is Levothyroxine (Synthroid)- its ingredient?

A

Synthetic preparation of thyroxine (T4)

133
Q

TX for Hypothyroidism: Thyroid Supplementation

PKs: How is it absorbed?

A

Absorption reduced by food

134
Q

TX for Hypothyroidism: Thyroid Supplementation

PKs: How should they be taken?

A

Take on empty stomach in AM, 30-60 min before breakfast

135
Q

TX for Hypothyroidism: Thyroid Supplementation

PKs: What does it do?

A

Med is converted to T3 –> normal levels of T3 & T4

136
Q

TX for Hypothyroidism: Thyroid Supplementation

PKs: How is it bound to protein? How does this effect half life?

A

Highly protein bound –> prolonged half-life of 7d

137
Q

TX for Hypothyroidism: Thyroid Supplementation

PKs: How are hormone levels with dosing?

A

Hormone levels remain steady with daily dosing but takes 1 month to reach a plateau so delayed onset of full effects

138
Q

TX for Hypothyroidism: Thyroid Supplementation:

? interchangeability: What does this mean?

A

Inconclusive results between FDA & endocrinology society regarding equivalence of brand-name & generic products

139
Q

TX for Hypothyroidism: Thyroid Supplementation

Dosing & administration: How is it normally taken? How is it take for myxedema coma?

A

PO for most

IV - myxedema coma 200-500mcg
pts who can’t take PO

140
Q

TX for Hypothyroidism: Thyroid Supplementation:

Dosing & administration: How are therapeutic effects evaluated?

A

Resolution of s/sx

TSH

141
Q

TX for Hypothyroidism: Thyroid Supplementation:

Dosing & administration: How are TSH levels with treatment of hypothyroidism?

When should you evaluate effects of meds on TSH levels?

A

Levels fall (but effect is slow)

Don’t evaluate until 6-8 wks after starting tx, lags behind TH

142
Q

TX for Hypothyroidism: Thyroid Supplementation

Dosing & administration-Evaluating Therapeutic effect: How are T3 and T4?

A

T3 & T4 (normal to high range)

143
Q

TX for Hypothyroidism: Thyroid Supplementation

Dosing & administration: For most people, how long is treatment?

What kind of treatment is it?

A

For most people tx is lifelong

Symptomatic relief only (not cure)

144
Q

TX for Hypothyroidism: Thyroid Supplementation

Dosing & administration: Even if symptoms improve, what should you NOT do?

A

Although sx improve, do not stop tx

145
Q

Thyroid Supplementation cont. Levothyroxine:

What are adverse effects of this medication?

A

Hyperthyroidism

146
Q

Thyroid Supplementation cont. Levothyroxine:

What rare hyperthyroidism symptoms that can occur with levothyroxine use?

A

Tachycardia, angina, tremor,

Nervousness, insomnia,

Hyperthermia

Heat intolerance, sweating

147
Q

Thyroid Supplementation cont. Levothyroxine:

Geriatric ADEs, precautions

A

Accelerated bone loss –> fracture risk

A. fib

148
Q

Thyroid Supplementation cont. Levothyroxine

What can occur? What is this called? (A negative effect)

A

Acute overdose

thyrotoxicosis

149
Q

Thyroid Supplementation cont. Levothyroxine:

Interactions: What type of drugs does it cause interactions with? So how should these drugs be taken?

A

Drugs that reduce it’s absorption ~ separate 4h, most PO

Drugs that accelerate it’s metabolism

Warfarin

Stimulant, sympathomimetics, EPI

150
Q

Thyroid Supplementation cont. Levothyroxine:

Drugs that reduce it’s absorption ~ separate 4h, most PO: What are the drugs?

A

H2RA
PPIs
Sucralfate
AL-containing antacids
Ca & Fe supplements
Mg salts

151
Q

Thyroid Supplementation cont. Levothyroxine

Drugs that accelerate it’s metabolism include:

A

Seizure drugs:

Rifampin, sertraline (Zoloft)

152
Q

Thyroid Supplementation cont. Levothyroxine

Drugs that accelerate it’s metabolism include: Seizure drugs

What are examples of seizure drugs?

A

phenytoin,

carbamazepine,

phenobarbital,

153
Q

Thyroid Supplementation cont. Levothyroxine:

Interactions:
Drugs that accelerate it’s metabolism- What should you do with levothyroxine?

A

↑ dose of levothyroxine dose when taking these drugs (while taking drugs that accelerate its metabolism)

154
Q

Thyroid Supplementation cont. Levothyroxine:

Warfarin- effect on levothyroxine?

A

Levothyroxine accelerates the breakdown of Vit K clotting factors –> enhanced warfarin effects

155
Q

Thyroid Supplementation cont. Levothyroxine:

Warfarin: What may you have to do with warfarin dose?

A

Warfarin dose may need to be reduced

156
Q

Thyroid Supplementation cont. Levothyroxine:

Stimulant, sympathomimetics, EPI: What does it cause with levothyroxine use?

A

Increase cardiac responsiveness to catecholamines

157
Q

Thyroid Supplementation cont. Levothyroxine:

Stimulant, sympathomimetics, EPI: What medical condition should you be cautious of when taking this with levothyroxine?

A

Caution dysrhythmias

158
Q

Hyperthyroidism/Thyrotoxicosis: Patho & Diagnosis: What occurs?

A

Excess amts of TH (T3 & T4) secreted from thyroid gland

159
Q

Hyperthyroidism/Thyrotoxicosis: Patho & Diagnosis:

Primary causes:

A

1°: most caused by Graves disease (autoimmune TSIs mimic TSH),

toxic multinodular goiter (Plummer DX),

& solitary toxic adenoma

160
Q

Hyperthyroidism/Thyrotoxicosis: Patho & Diagnosis:

1°: most caused by Graves disease (autoimmune TSIs mimic TSH), toxic multinodular goiter (Plummer DX), & solitary toxic adenoma

What are diagnostic labs of this?

A

Elevated T3, T4 & suppressed TSH are diagnostic

161
Q

Hyperthyroidism/Thyrotoxicosis: Patho & Diagnosis:

Secondary cause:

A

2°: less common, caused by TSH-secreting pituitary adenoma

162
Q

Hyperthyroidism/Thyrotoxicosis: Patho & Diagnosis:

Secondary cause: What are labs?

A

Normal to increased TSH despite elevated TH concentrations

163
Q

Hyperthyroidism/Thyrotoxicosis: Patho & Diagnosis:

What is treatment in general do?

A

Tx: control excessive TH production, secretion, or action

164
Q

Hyperthyroidism/Thyrotoxicosis: Patho & Diagnosis:

Treatment: control excessive TH production, secretion, or action

How is this done?

A

Antithyroid drug tx,

radioactive iodine tx,

surgical removal of nodules or part of thyroid gland

165
Q

Hyperthyroidism/Thyrotoxicosis: Patho & Diagnosis:

What is a major complication of treatment?

A

Major complication of treatment is hypothyroidism

166
Q

Hyperthyroid conditions include:

A
  1. Graves disease (most common)
  2. Toxic multinodular goiter (Plummer disease)
  3. Toxic adenoma
  4. Thyroid medication
167
Q

Hyperthyroid conditions: What is the most common hyperthyroid condition?

A
  1. Graves disease (most common)
168
Q

Hyperthyroid conditions:

Graves disease (most common): What kind of response is this?

A

Autoimmune response

169
Q

Hyperthyroid conditions:

Graves disease (most common):
What occurs?

A

Thyroid stimulating Abs (TSIs) attach to TSH receptors

170
Q

Hyperthyroid conditions:

In Graves disease when Thyroid stimulating Abs (TSIs) attach to TSH receptors, what does this act like?

A

Thyroid stimulating Abs (TSIs) attach to TSH receptors

Acts like pit hormone TSH, stimulates thyroid to release TH

171
Q

Hyperthyroid conditions:

In Graves disease, what does TSIs stimulate thyroid to do? What does this cause?

A

TSIs stimulate thyroid to make T3 and T4, overriding negative feedback cycle –> overproductions

172
Q

Hyperthyroid conditions:

In Graves disease, TSIs stimulate thyroid to make T3 and T4, overriding negative feedback cycle –> overproductions;

What does this result in?

A

Results in hyperplasia & goiter from growth of the thyroid and increased secretion of T3 and T4.

173
Q

Hyperthyroid conditions:

In Graves Disease, what happens to metabolic rate? Why?

A

Metabolic rate is increased from the excessive release of TH

174
Q

Hyperthyroid conditions:

Graves disease is what type of hypersensitivity reaction?

A

Type II hypersensitivity reaction

175
Q

Hyperthyroid conditions:

Toxic multinodular goiter (Plummer disease): What happens?

A

Several hyperfunctioning nodules

176
Q

Normally, in what circumstances would a thyroid gland enlarge?

A

Normally, thyroid gland enlarges in response to increased demand (eg pregnancy, puberty, iodine-deficient states) for TH

177
Q

Normally, thyroid gland enlarges in response to increased demand for TH: What are examples of increased demand?

A

(eg pregnancy, puberty, iodine-deficient states)

178
Q

Normally, when would normal thyroid gland size return after it was enlarged?

A

When condition resolves, TSH secretion subsides, and normal thyroid size returns

179
Q

Hyperthyroid conditions:

What occurs in Toxic multinodular goiter (Plummer disease)? Be specific

A

Irreversible changes occur in follicular cells, TSH receptor mutated, nodules form, function autonomously & produce excessive TH

180
Q

Hyperthyroid conditions:

Toxic multinodular goiter (Plummer disease)- What would several hyperfunctioning nodules lead to?

A

Several hyperfunctioning nodules –> toxic multinodular goiter

181
Q

Hyperthyroid conditions:

How is Toxic multinodular goiter (Plummer disease) similar to Graves Disease?

A

Same clinical sx as Graves’ except exophthalmos

182
Q

Hyperthyroid conditions:

  1. Toxic adenoma- what occurs with nodule (s)?
A

1 hyperfunctioning nodule

183
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

How are T3 and T4 levels? What does this lead to?

A

↑ T3, T4 leading to an increased metabolic rate

184
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why are there ↑ T3, T4 leading to an increased metabolic rate?

A

Overstimulation to TSH receptors –> increased production of thyroid hormone

185
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

What are major distinguishing features of this disease?

A

Exophthalmos (major distinguishing feature)

Pretibial edema (major distinguishing feature)

186
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why are there Exophthalmos and decreased blink and eye movements?

A

Increased tissue mass (fat and fluid) in the orbit pushing the eyeball forward

Increased sympathetic stimulation affecting the eyelids

187
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

What occurs with the eyes?

A

Decreased blink and eye movements

188
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why does pretibial edema occur?

A

Lumpy, swollen appearance on the anterior and lateral aspects of the legs resulting from accumulation of connective tissue, pinkish purple discoloration

189
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

What develops?

A

Toxic goiter

190
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why does toxic goiters occur?

A

Hyperplasia and hypertrophy of thyroid from overactive thyroid

191
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

How is the skin? How is heat/cold tolerance?

How is hair?

A

Skin flushed and warm, sweaty palms, heat intolerance

Thin hair

192
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why is skin flushed and warm, sweaty palms, heat intolerance?

A

Increased metabolic rate & vasodilation for heat loss

193
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why does thin hair occur?

A

Increased metabolic rate with excessive metabolism of macronutrients –> thinning hair

194
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

How is heart? Bp?

A

Tachycardia, increased blood pressure, eventually heart failure

195
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why does tachycardia, increased bp, and eventual heart failure occur?

A

Increased tissue sensitivity to the sympathetic nervous system from increased thyroid hormones and increased metabolism

Over time, the heart cannot meet body’s metabolic demands –> heart failure

196
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

What happens with weight and appetite?

A

Weight loss, with increased appetite

197
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why does weight loss and increased appetite occur?

A

Increased catabolism from increased metabolic rate leads to weight loss even though appetite is often increased

198
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

What are other symptoms of hyperthyroidism?

A

Restless, nervous tremors

Hyperreflexia

Diarrhea

199
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why does diarrhea occur?

A

Hypermotility of gastrointestinal tract

200
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why does hyperreflexia occur?

A

Hyperexcitability of reflexes

201
Q

Clinical Manifestations of Hyperthyroidism (Graves’ Disease):

Why does restlessness and nervous tremors occur?

A

Increased tissue sensitivity to the sympathetic nervous system from increased TH

202
Q

What is Exophthalmos?

A

Exophthalmos (large and protruding eyeballs)

203
Q

Hyperthyroid conditions cont’d:

What is another name for Thyrotoxic storm?

A

Thyrotoxic crisis (AKA thyroid storm)

204
Q

Hyperthyroid conditions cont’d:

Thyrotoxic crisis (AKA thyroid storm): How common is it?

A

Rare but dangerous, TH levels rise dramatically

205
Q

Hyperthyroid conditions cont’d:

Thyrotoxic crisis (AKA thyroid storm): How long can it take death to occur?

A

Death can occur within 48hrs w/o tx

206
Q

Hyperthyroid conditions cont’d:

Thyrotoxic crisis (AKA thyroid storm): When does it happen?

A

Happens in undx’d/partially tx’d Graves & subject to physiologic stressors/triggers

207
Q

Hyperthyroid conditions cont’d:

Thyrotoxic crisis (AKA thyroid storm): Happens in undx’d/partially tx’d Graves & subject to physiologic stressors/triggers.

What is an example?

A

E.g. infection

208
Q

Hyperthyroid conditions cont’d:

Thyrotoxic crisis (AKA thyroid storm)
What are symptoms?

A

Sx:

hyperthermia,

tachycardia,

heart failure,

atrial tachydysrhythmias,

agitation/delirium,

n/v/d

209
Q

Hyperthyroid conditions cont’d:

Thyrotoxic crisis (AKA thyroid storm): What are treatments?

A

Tx: drugs that block TH synthesis (PTU & methimazole),

beta-blockers (for cardiac sx),

glucocorticoids,

radioactive iodine (shrinks the gland),

supportive care (F&E, cooling measures, nutritional support)

210
Q

Hyperthyroid conditions cont’d:

Thyrotoxic crisis (AKA thyroid storm): If there is no response to treatment drugs, what must be done?

A

If no response –> surgical tx –> thyroidectomy

211
Q

Complications of HyperthyroidismThyrotoxic crisis or thyroid storm

Manifestation:
How is temperature?

A

Severe hyperthermia, over 104◦F

212
Q

Complications of HyperthyroidismThyrotoxic crisis or thyroid storm:

Why does Severe hyperthermia, over 104◦F occur?

A

Excessive release of thyroid hormones, increasing metabolic rate

213
Q

Complications of HyperthyroidismThyrotoxic crisis or thyroid storm:

Manifestation: What happens with the heart?

A

Severe tachycardia, over 140 beats per minute

Heart failure (shortness of breath, edema, fatigue)

214
Q

Complications of HyperthyroidismThyrotoxic crisis or thyroid storm:

Why does Severe tachy, over 140 bpm occur?

A

Excessive release of thyroid hormones, increasing sensitivity of tissues to sympathetic nervous system stimulation and excessive catecholamine release

215
Q

Complications of HyperthyroidismThyrotoxic crisis or thyroid storm:

Why does Heart failure (shortness of breath, edema, fatigue) occur?

A

Heart cannot continue to meet the high oxygen demand needed for an increased metabolic rate

216
Q

Complications of HyperthyroidismThyrotoxic crisis or thyroid storm:

Manifestation: What happens with the consciousness/alertness?

A

Delirium

217
Q

Complications of HyperthyroidismThyrotoxic crisis or thyroid storm:

Why does delirium occur?

A

Decreased neurological functioning

218
Q

Drugs for HyperthyroidismAntithyroid drugs include:

A

Methimazole

Propylthiouracil

219
Q

Hyperthyroidism: What is the first line drug for this condition?

A

Methimazole

220
Q

Hyperthyroidism: Methimazole

Mode of action: What does it inhibit?

A

Inhibits synthesis of thyroid hormones

221
Q

Hyperthyroidism: Methimazole

Mode of action: What does destroy/not destroy?

A

Does not destroy existing stores of thyroid hormone, suppresses thyroid synthesis

222
Q

Hyperthyroidism: Methimazole

Mode of action: How long does it take for effects to occur?

A

May take 3 to 12 weeks for euthyroid state

223
Q

Hyperthyroidism: Methimazole

What is it used for?

A

Uses: Graves, adjunct to radiation, suppress TH in prep for thyroid surgery, thyrotoxic crisis

224
Q

Hyperthyroidism: Methimazole

Kinetics: How is it absorbed?

A

Well absorbed,

crosses placenta,

Half life 6 -13 hours, so dosing is once a day

225
Q

Hyperthyroidism: Methimazole

Kinetics: How often is maintenance dose?

A

Maintenance tx daily

226
Q

Hyperthyroidism: Methimazole

Administration:

How is treatment done? When is it dc’d

A

Tx for 1-2 yrs –> d/c–> 30-40% of pts will go into remission, others relapse in 1-4 wks

227
Q

Hyperthyroidism: Methimazole

ADR and when should this drug be avoided?

A

Pregnancy – avoid during 1st trimester

Agranulocytosis!!!!

Hypothyroid state in high doses

228
Q

Hyperthyroidism: Methimazole

ADR: Why should this drug be avoided in the first trimester of pregnancy?

A

Can cause neonatal hypothyroidism, goiter, congenital hypothyroidism

229
Q

Hyperthyroidism: Methimazole

Agranulocytosis!!!! what symptoms associated with this should be reported?

A

Report sore throat & fever immediately, med must be d/c’d

Develops rapidly

230
Q

What is the second line drug for Graves’ disease?

A

Propylthiouracil (PTU)

231
Q

Propylthiouracil (PTU):

What does it do?

A

Inhibits thyroid hormone synthesis

232
Q

Propylthiouracil (PTU):

How long is the half life? How many doses does it require?

A

Short half-life (about 90 minutes)

Requires 2 or 3 daily doses

233
Q

Propylthiouracil (PTU):
How long does it take for full benefits of drugs to occur?

A

Full benefits may take 6 to 12 months

234
Q

Propylthiouracil (PTU):

How does it cross placenta? What does this mean?

A

Crosses placenta less readily
Used in 1st trimester

235
Q

Propylthiouracil (PTU):

What are therapeutic uses?

A

Graves’ disease

Adjunct to radiation therapy

Preparation for thyroid gland surgery

Thyrotoxic crisis/thyroid storm (preferred initially)

236
Q

Propylthiouracil (PTU):

Therapeutic uses: Thyrotoxic crisis/thyroid storm (preferred initially)- What does it do?

A

Blocks conversion T4 –> T3

237
Q

Propylthiouracil (PTU):

What are adverse effects:

A

Agranulocytosis (most serious)

Hypothyroidism

Can cause severe liver damage

238
Q

Propylthiouracil (PTU):

Can cause severe liver damage: How is progression? What should you teach the patient?

A

Onset sudden & progression rapid so routine LFTs check won’t help

Teach pt to report sx

239
Q

TX for Hyperthyroidism: What is another treatment?

A

TX for Hyperthyroidism: Radioactive Iodine-131

TX for Hyperthyroidism: Beta Blockers

240
Q

TX for Hyperthyroidism: Radioactive Iodine-131

What is the mode of action:

A

Destructive gamma rays & beta particles on thyroid cells

241
Q

TX for Hyperthyroidism: Radioactive Iodine-131:

Where is I-131 concentrated?

A

I-131 is concentrated in thyroid gland

242
Q

TX for Hyperthyroidism: Radioactive Iodine-131

What does it help to do?

A

Helps to reduce thyroid hormone production by selectively destroying overactive thyroid cells

243
Q

TX for Hyperthyroidism: Radioactive Iodine-131

What are uses for it?

A

Graves’ DX in adults (some require 2 treatments)

ALT for non-response to antithyroid drugs or subtotal thyroidectomy

Toxic multinodular goiter or solitary toxic adenoma (thyroid gland produces excess thyroid hormones)

Diagnostic use (tracer)

Some forms of thyroid cancer

244
Q

TX for Hyperthyroidism: Radioactive Iodine-131:

What are misconceptions?

A

⍉ tissue damage outside thyroid

245
Q

TX for Hyperthyroidism: Radioactive Iodine-131:

How does this treatment effect surrounding tissue?

A

Minimal damage to surrounding tissue

Beta particles limited to travel to other tissues outside thyroid

246
Q

TX for Hyperthyroidism: Radioactive Iodine-131:

Adverse Drug Reactions:

A

Dry mouth,

sore throat,

altered taste,

neck tenderness

247
Q

TX for Hyperthyroidism: Radioactive Iodine-131

Radiation precautions:

A

https://www.thyroid.org/radioactive-iodine/

248
Q

TX for Hyperthyroidism: Radioactive Iodine-131:

How fast are effects?

A

Delayed full effects ~ 1-3m

Initial effects apparent in days/weeks

249
Q

TX for Hyperthyroidism: Radioactive Iodine-131:

What is a complication?

A

Delayed hypothyroid is complication

250
Q

TX for Hyperthyroidism: Radioactive Iodine-131

Avoid in who?

A

Pediatrics, risks of delayed
hypothyroidism & slight risk of cancer

Pregnancy, R/O prior

Lactation

251
Q

TX for Hyperthyroidism: Beta Blockers

Uses:

A

Management of s/s in Graves’ DX
Adjunct TX for thyrotoxicosis
Administration may be oral or IV

252
Q

TX for Hyperthyroidism: Beta Blockers

MOA:

A

Suppress tachycardia

Some effect on T3 (small & slow)

253
Q

TX for Hyperthyroidism: Beta Blockers:

What is the first line beta blocker?

A

Propranolol

254
Q

TX for Hyperthyroidism: Beta Blockers

Propranolol: how is it?

A

Non-selective BB

PATHO/PHARM II (27 decks)

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