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Block 10 week 1 > Thyroid and Parathyroid Pharm- Burkin > Flashcards

Thyroid and Parathyroid Pharm- Burkin Flashcards

1
Q

What is this:

A protein synthesized in the thyroid gland; its tyrosine residues are used to produce thyroid hormone

A

thyroglobulin

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2
Q

What is this:

Excess thyroid hormone

A

thyrotoxicosis
hyperthyroidism
graves disease

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3
Q

What is this:

lack of sufficient thyroid hormone

A

hypothyroidism/hashimoto thyroiditis

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4
Q

Thyroid follicular cells synthesize lare amounts of (blank)

A

thyroglobulin.

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5
Q

Thyroglobulin is a glycoprotein hormone that is stores in the colloid in the (blank)

A

follicular lumen

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6
Q

Thyroglobulin contains (blank) tyrosin residues

A

134

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7
Q

TSH (thyrotropin) is secreted from cells in the anterior pituitary called (blank). What does TSH do?

A

thyrotrophs

Binds to receptors on epithelial cells in the thyroid gland and stimulates that gland to release thyroid hormones

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8
Q

What does the thyroid hormone inhibit (i.e has negative feedback)?

A

TRH (from the hypothalamus)

TSH (from the pituitary gland)

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9
Q

Explain the synthesis of thryglobulin?

A
  1. TSH stimulates Iodine to get pumped into follicular cells,
  2. Iodide is oxidized to hypoiodoate and combined with tyrosine residues on thyroglobuin.
  3. Thyroid peroxidase results in formation of DITs and MITs (thyronine residues) onto the thyroglobulin. Iodinated thyroglobulin is taken into follicular cell via endocytosis
  4. Iodinated thyroglobulin is taken into the follicular cell by endocytosis and thyroglobulin is degraded.
  5. three to five thyroxine molecules are released per Tg molecule in a ratio of T3:T4 1:4
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10
Q

T4 is converted to T3 peripherally by an enzyme called (blank)

A

5-iodinase

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11
Q

Where is Type I iodinase present?
What does it do?
How can you block this?

A

kidney and liver
formation of T3 for rest of body
Propylthiouracil

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12
Q

Where is type II iodinase present?

What does it do?

A

Pituitary and adipose tissue

sensor for TSH

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13
Q

How do you block iodine transport and thus inhibit formation of thyroid hormones?

A
  • thiocyanate

- perchlorate

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14
Q

Thyroid hormone circulates bound to (blank) and (blank)

A

thyroid binding globulin

albumin

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15
Q

Only (blank) is active thyroid hormone and only 0.5% of this is free at any one time

A

T3

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16
Q

What is the T 1/2 for T4?

For T3?

A

7 days

2 days

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17
Q

T3 acts in responsive tissues in a manner similiar to the steroid homrones.
How so?

A

It binds unique receptors that bind to the genome and alter gene transcription

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18
Q

Mammalial thyroid hormone receptors are encoded by (blank) genes which are alternatively spliced to generate (blank) different thyroid hormone receptors which are,,,,?

A

2
4
alpha 1, alpha 2, beta 1, beta 2

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19
Q

Thyroid hormone receptors possess 3 functional domains what are they?

A
  • a transactivation domain
  • a DNA binding domain
  • ligand-binding and dimerization domain
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20
Q

What is this:

a domain at the amino terminus that interacts with other transcription factors to repress or activate transcription

A

Transactivation domain

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21
Q

What is this:

a domain that binds to sequences of promoter DNA known as hormone response elements

A

DNA binding domain

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22
Q

What is this:

domian located at the carboxy terminus

A

Ligand-binding and dimeriztion domain

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23
Q

How do thyroid hormones affect growth and development?

So what happens if you have iodine deficiency during development?

A
  • particularly important in the brain and nervous system (axonal and dendritic development)
  • results in mental retardation in children
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24
Q

How does thyroid hormone increase metabolic rate?

A
  • increased O2 utilization in muscle and other metabolically active tissues
  • maintains body temp
  • T3 is inotropic and increases CO
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25
Q

How does T3 increase inotropy and CO?

A

-alters myosin isozymes (V1/V3) resulting in increased Ca2+ ATPase activity and increased contraction force

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26
Q

Thyroid disease affects (blank)% of the general population.

A

5-15%

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27
Q

Females (blank) more likely than males to develop thyroid disease

A

3-4X

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28
Q

Typical thyroid disease includes ….?

A

hypothyroidsm, hyperthyroidism, nodular disease and thyroid cancer

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29
Q

(blank) is an autoimmune disorder and most comon cause of primary hypothyroidism.

A

Hashimoto’s thyroiditis

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30
Q

What are other causes (besides hashimotos thyroiditis) causes primary hypothyroidism?

A
  • iatrogenic destruction of gland after radioiodie therapy or surgery
  • drug induced hypothyroidism can occur in susceptible patients (tx with iodide, lithium, interferon-alph)
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31
Q

What is the most common form of hyperthyroidism?

What are the other causes of hyperthyroidism?

A

Grave’s disease

Toxic autonomous nodular goiter

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32
Q

What is the most common cause disorder of thyroid function?

What do you call this when it is severe?

A

hypothyroidism

myxedema

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33
Q

Hypothyroid caused by (blank) causing a goiter, remains a common worldwide problem

A

iodine deficiency

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34
Q

Primary hypothyroidism is characterized by high leves of circulating antibodies to (blank), (blank) or (blank)

A

thyroid peroxidase, thyroglobulin or TSH receptor

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35
Q

What causes primary hypothyroidism?
Secondary?
Tertiary?

A

Broken thyroid gland
Broken pituitary gland
Broken hypothalamus

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36
Q

What are the symptoms of hypothyroidism?

A

Fatigue, Lethargy, Cold intolerance, Mental slowness, Depression, Dry skin, Mild weight gain, Fluid retention, Muscle aches and stiffness, irregular menses, infertility, anemia

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37
Q

What are the common signs of primary hypothyroidism?

A

Goiter, bradycardia, delayed relaxation phase of the deep tendon reflexes, cool and dry skin, hypertension, nonpitting edema, and facial puffiness

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38
Q

What are the common signs of neonatal hypothyroidism?

A

feeding problems, failure to thrive, constipation, sleepiness, mental retardation, impaired linear bone growth and bone maturation

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39
Q

When can neonatal hypothyroidism cause permanent retardation of mental function?

A

if not treated so start treatment soon!

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40
Q

How do you diagnose thyroid hypofunction?

A
  • elevated serum TSH

- decrease T4 in central hypothyroidism

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41
Q

What are the drugs used to treat hypothyroidism?

A
  • thyroid USP
  • thyroglobulin (proloid)
  • levothyroxine Na (synthroid)
  • thyrotropin
  • protirelin or thyrogen
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42
Q

What is this:

acetone powder of pig thyroid gland

A

thyroid USP

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43
Q

What is this

purified pig thyroid

A

thyroglobulin (proloid)

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44
Q

What is this:

Na salt of T3 and available in 25-300 micrograms tablets

A

Levothyroxine Na (synthroid)

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45
Q

What is this:

TSH from bovine pituitary (diagnostic)

A

Thyrotropin

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46
Q

What is this:

synthetic or human recombinant TSH (stimulate thyroid gland)

A

Protirelin or thyrogen

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47
Q

(blank) is a condition caused by elevated levels o free thyroid hormones

A

Thyrotoxicosis

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48
Q

What is the most common way to get increased thyroid hormone?

A
  • TSH receptor stimulation

- increase iodine uptake by the thyroid gland

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49
Q

(blank) is an autoimmune disorder characterized by increased thyroid hormone production, diffuse goiter and IgG antibodies that bind to and activate the TSH receptor.

A

Graves disease

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50
Q

At what age do you commonly get graves disease? and in what gender?

A

females

20 and 50 but may occur at any age

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51
Q

What are these symptoms of:
Excessive heat production, increased motor activity, and increased production of catecholamines, warm, moist and flush skin, muscles are weak and tremulous, heart rate is rapid, heartbeat is forceful, atrial pulses are prominent and bounding. Increased appetite, weight loss, insomnia, intolerance to heat, increased bowel movements, angina, arrhythmias, Heart failure in older patients, muscle wasting.

A

thyroxicosis

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52
Q

How do you diagnosis thyrotoxicosis (thyroid hyperfunction)?

A
  • TSH

- T4

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53
Q

(blank) (thyrotropin alfa) is available to test the ability of thyroid tissue to take up radioactive iodine and release thyroglobulin.

A

Recombinant human TSH

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54
Q

What are the kinds of thiourylene anti thyroid drugs?

A
  • methimazole
  • propylthiouracil
  • thiourea
  • carbimazole
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55
Q

What do thiourylenes do?

How long does it take to start working?

A
  • bind and inactivate peroxidase enzymes

- takes several weeks to see effects due to resevoir of hormone in the gland

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56
Q

Why is propylthiouracil different than all the other thiourylenes?

A

-it blocks peripheral conversion of T4 to T3

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57
Q

What are the ionic inhibitor anti-thyroid drugs?

A

-thiocyanate and perchlorate which intefere with uptake of iodide by the thyroid gland

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58
Q

Why do you give iodide in hyperthyroidism?

A

it has a paradoxical effect (KI solution) so it will dessicate (dry up) that gland prior to surgery

59
Q

What is radioiodine [131 I] and what is it used for?

A
  • T 1/2= 8 days
  • emits x-rays, radio-ablation of the gland, emits x rays and b particles. selectively irradiates the parenchymal cells of the gland
60
Q

(blank) directly interferes with the first step in thyroid hormone biosynthesis in the thyroid gland

A

Methimazole

61
Q

How does methimazole work?

A

binds to thyroid peroxidase and inhibits the incorporation of iodide into the thyroglobulin. Thyroid hormone depleted
AND
inhibits iodotyrosyl residue coupling thus inhibition of thyroglobulin synthesis. THyroglobulin depleted

62
Q

How is methimazole degraded?

A

it is iodinated and degraded within the thyroid gland

63
Q

(blank) directly interferes with the first step in thyroid hormone biosynthesis in the thyroid gland.

A

Methimazole

64
Q

Methimazole acts as a substrate for the (blank), methimazole inhibits the incorporation of iodide into the thyroid hormone precursor, thyroglobulin.

A

catalyst thyroid peroxidase

65
Q

What causes this:

Oxidized iodine is diverted away from thyroglobulin, which effectively diminishes the biosynthesis of thyroid hormone.

A

methimazole

66
Q

Methimazole can inhibit the coupling of (blank) to form thyroglobulin. Methimazole may interfere with the oxidation of the iodide ion and iodotyrosyl groups. Eventually, thyroglobulin is depleted and circulating thyroid hormone levels diminish.

A

iodotyrosyl residues

67
Q

What does methimazole do to thyroxine (T4) and triiodothyronine (T3) in the circulation or stored in the thyroid gland?

A

It does not alter their action

additionaly, does not effect exogenously administered thyroid hormones

68
Q 
What does this:
blocks peripheral conversion of T4 to T3
Bind and inactivate peroxidase
enzyme which is responsible for
oxidation of iodine and iodotyrosyl
groups.
A

Propylthiouracil

69
Q

Can you use propylthiouracil in pregnant women?

A

should be used with caution in pregnant or breast feeding women (less neg effects that methimazole)

70
Q

What are the toxic effects of propylthiouracil?

A

skin rash (common) and severe immune reactions (rare)

71
Q

What do you use for well differentiated thyroid cancer (papillary and follicular)?

A

surgical thyroidectomy, radioiodine and levothyroxine to suppress TSH

72
Q

What do you use for low risk patients with stage 1 or 2 thyroid cancer?

A

maintain TSH just below reference range

73
Q

Most well differentiated thyroid carcinomas accumulate very little (blank). Stimulation of iodine uptake with (blank) is required to treat metastases effectively.
How do you do this?

A

iodine

TSH

74
Q

How do you treat thyroid carcinoma after a patient has a thyroidectomy with or without radioactive ablation of residual thyroid tissue?

A

You stop thyroid hormone therapy and give thyrogen (recombinant human TSH) to test the capacity of thyroid tissue (normal or malignant)
i.e tells you if the thyroid is taken up iodine and secreting thyroglobulin

75
Q

Why is thyroglobulin a good drug to use when treating thyroid carcinoma?

A

because you can use it to assess thyroid function without having to stop suppressing thyroglobulin and thus prevents patients from becoming hypothyroid.

76
Q

TSH suppressive therapy with (blank) is indicated in all patients after treatment with thyroid cancer.

A

levothyroxine.

77
Q

What are the 2 most important minerals for cellular function?

A

calcium and phosphate

78
Q

Where do you find 98% of the calcium and 85% of phosphorous>

A

in the bone

79
Q

There are complex mechanisms that regulate calcium and phosphate homeostasis with a dynamic exchange b/w what 2 things

A

bone and the mineral in extracellular fluid

80
Q

Abnormalities in bone metabolism can lead to a wide variety of cellular dysfunction resulting in (blank X 3), defects in structural support resulting in (blank), and loss of hematopoietic activity (blank)

A

muscle weakness, coma and tetany
osteoporosis
infantile osteopetrosis

81
Q

What will decreased calcium cause?

What will this hormone do?

A

an increase in parathyroid hormone

  • conversion of calcifediol to calcitriol
  • decreased exretion of calcium by kidney, increased calcium absorption in the intestin and mobilization of calcium from bone which causes a rise in plasma calcium concentration
82
Q

PTH is an (Blank) amino acid peptide. Amino acids (blank) of PTH confer activity.

A

1-34

83
Q

How do you regulate PTH?

A
  • a calcium-sensitive protease cleaves intact hormone into fragments which limits production of PTH
  • a calcium-sensing receptor in the parathyroid gland is stimulated by calcium to reduce PTH production and secretion
  • PTH gland contains Vit D receptor and CYP27B1 to produce active metabolite of vit D to suppress PTH production
84
Q

The parathyroid gland contains the (blank) receptor and (blank) to produce the active metabolite of vitamin D to suppress PTH production.

A

vitamin D

CYP27B1

85
Q

What are the synthetic human parathyroid drugs?

A

parathar or teriparatide

86
Q

What does PTH do?

A
  • mobilizes bone calcium
  • decreases renal excretion of calcium
  • stimulates Vit D3 synthesis
  • promotes phosphate excretion
87
Q

Do you use PTH often clinically?

A

no, D3 and calcium are preferred

88
Q

What is the biosynthesis of vit D?

A

7-dehydrocholesterol + heat-> D3 (cholecalciferol)-> 24,25 (OH)2D3 (secalciferol)-> 1,25(OH)2D3 (calcitriol)

89
Q

Calcitriol is derived from the diet and generated in the skin as (blank). Calcitriol is formed by hydroxylation steps that take place in the (blank and blank)

A

pro-vitamin D3

liver and kidney

90
Q

Formation rom calcifediol is increased by (blank)

A

PTH

91
Q

Vit D and its metabolites circulate in the blood bound to (blank) and is rapidly cleared by (blank) from the blood

A

vit D binding protein

liver

92
Q

Calcitriol (vit D) stimulates the absorption of calcium and (Blank) in the (blank) and the mobilization of calcium from (blank)

A

phosphate
intestine
bone

93
Q

What do you use calcitriol (vit D) to treat?

A

osteomalacia and hypocalcemia associated with hypoparathyroidism

94
Q

Calcitonin is a (blank) hormone made up of (blank) amino acids produced by the thyroid gland

A

protein

32

95
Q

What is calcitonin regulated by?

What does it do?

A

plasma calcium

inhibits osteoclasts and decreases reabsorption of both calcium and phosphate

96
Q

What is the overall effect of calcitonin?

A

lower plasma calcium

97
Q

Is there a synthetic form of calcitonin?

A

yes!

98
Q

When do you use calcitonin?

A

in the tx of hypercalcemia associated with some neoplasms

99
Q

(blank) is characterized by a reduced quantity of bone

A

osteoporosis

100
Q

(blank) is characterized by a lack of mineralization

A

osteomalacia

101
Q

(blank) is characterized by the production of abnormal bone

A

Pagets disease

102
Q

Pagets disease affects app. (blank) percent of the population over age 60

A

3

103
Q

Pagets disease of the bone presents with what symptoms?

A

bone pain
skeletal deformity
neurological complications or fractures

104
Q

Where is Pagets disease common?

Where is it rare?

A
  • Central Europe, UK, australia, new zealand, and USA

- Rare in Africa, Middle east, scandinava

105
Q

What is the pathology of Pagets disease?

A

excessive bone resorption and formation in 3 phases
Phase 1: osteolytic
Phase 2: osteoblastic
Phase 3: quiescent
(may be present in the same patient at the same time)

106
Q

(blank) is caused by decreased mineralization of new bone matrix

A

Osteomalacia

107
Q

How will osteomalacia affect children?

A

lack of calcification results in growth failure and deformity of Rickets

108
Q

How will osteomalacia affect adults?

A

adults will present with bone pain, proximal myopathy or fractures with minor trauma

109
Q

Osteomalacia is commonly caused by (blank) defiency. Biomarkers include (Blank X 3)

A

Vit D

hypocalcemia, secondary elevation in PTH, low plasma 25-hydroxyvitamin D.

110
Q

What are the causes of osteomalacia?

A
  • insufficient exposure to sunlight
  • malnutrition
  • renal tubular acidosis
  • malnutrition during pregnancy
  • malabsorption syndrome
  • hypophosphatemia
  • chronic renal failure
  • tumor induced osteomalacia
  • long term anti-convulsive therapy
  • coelaic disease
  • cadmium poisoning
111
Q

What is this:

a common disorder in post-menopausal women that may result in hip, forearm, and spinal fractures

A

Osteoporosis

112
Q

What is osteoporosis caused by?

What is it accelerated by?

A

thinning of the bone with aging

  • premature or surgical loss of ovarian function
  • drugs (e.g corticosteroids)
  • Lifestyle (alcohol or smoking)
113
Q

How do you treat osteoporosis?

A

estrogen replacement therapy (ERT) at the time of menopause inhibits the effect of osteoclasts on bone resportion and increases bone density

114
Q

What are the drugs used in hormone replacement therapy?

A
  • oral estrogens (equine estrogen, estrone sufate and miconized estradiol-20b)
  • widely prescribed to treat postemenopausal osteoporosis
115
Q

HRT results increased (blank) events especially women with a history of (blank and blank)

A

CV

heart disease and breast cancer

116
Q

(blank) can be considered for hormone resplacement therapy in patients that have not had a hysterectomy

A

Progesterone

117
Q

What was first approved as a treatment for osteoporosis?

A

Selective estrogen receptor modulator

Raloxifen

118
Q 
Raloxifene has (blank) activity but not on all sensitive tissues. What does it increase?
What does it decrease?
A

estrogenic
increases bone density and appears to decrease number of fractures
decreasese cholesterol

119
Q

Long term clinical trials with (blank) mg/day of raloxifene shows improvements in (blank) of the hip and lumbar spine

A

60

bone density

120
Q

Patients takes raloxifene for the TX of osteoporosisi were followed for cancer and found to have a (blank) in overall cancer incidence

A

50% decrease

121
Q

What are the adverse effects of raloxifene?

A

increased risk of thromboembolic events similiar to estrogen. Some women report hot flashes and leg cramps

122
Q

What are bisphosphates?

What is there structure?

A

enzyme-resistant analogs of pyrophosphate (designed to mimic pyrophosphate)

POP structure replaces by PCP

123
Q

What is the results of bisphosphonates? How long do they take to work?

A

reduces turnovver of bone by preventing the number and activity osteoclasts.
-Takes 48 hours to block bone resorption

124
Q

How do bisphosphonates work?

A

blocks transformation of calcium phosphate into hydroxyapatite thus inhibiting the formation, aggregation, and dissolution of hydroxyapatite crystals in bone

125
Q

What are bisphosphonates used for?

A

osteoporosis and pagets disease

126
Q

Studies have shown what three bisphosphonates increase bone density by 4-9% over the first 3 years of tx and reduces vertebral fractures by (blank)?

A

etidronate, alendronate and risedronate

50%

127
Q

(blank) should not be given continuously as it can cause osteomalacia. Dosing is normally intermittent over 2 weeks with periods off the drugs.

A

Etidronate

128
Q

(blank) 10mg/day or (blank) 5mg/day reduce the incidence of single vertebral fractures by 50% and by 90% for multiple vertebral fractures

A

Alendronate

Risedronate

129
Q

Bisphosphates should not taken with (blank X 3) as this inhibits drug absorption

A

milk products, food or Ca2+ supplements

130
Q

What are the adverse effects of bisphosphonates?

A

GI (heartburn, nausea, and abdominal pain), incidence of gastric ulcers and erosive oseophagitis.

131
Q

How should you take bisphosphonates?

A

with water and avoid lyng in supine position for at least 30 minutes

132
Q

What is this:
a human monoclonal antibody against RANKL
What does it do?

A

Denosumab
Treats osteoporosis, bone loss and bone metastasis, rheumatoid arthritis, multiple myeloma and giant cell tumor of the bone

133
Q

Precursors of (blank) express RANK (receptor activator of nuclear kappa B), a member of the TNFR family. RANK is activated by RANKL present on the surface of (blank) which converts pre-osteoclasts to osteoclasts to resorb bone.

A

osteoclasts

oesteoblasts

134
Q

Denosumab inhibits the maturation of (blank) into osteoclasts and therefore prevents bone resorption.

A

pre-osteoclasts

135
Q

What is osteoprogenin?

A

An endogenous RANKL inhibitor

136
Q

Denosumab mimics that actions of (blank), an endogenous RANKL inhibitor that is decreased in patients with osteoporosis.

A

osteoprogenin

137
Q

Clinical trials showed Denosumab reduced (blank) in women aged 60 to 90 yeas by 35%

A

fractures

138
Q

What are the adverse effects of denosumab?

A

increased urinary and respiratory tract infections, rashes, joint pain, eczema

139
Q

What are the contraindications of denosumab?

A

hypocalcemia

140
Q

Calcium supplements have a small beneficial effect in preventing (blank)

A

bone loss

141
Q

(blank) analogs facilitate calcium absorption from the (blank) and may have an effect on bone formation and reabsorption.

A

Vit D

GI tract

142
Q

(blank) is a synthetic C-19 steroid with weak hormonal properties. What does it do?

A

Tibolone

increase bone mass in the spine and prevention of bone loss from the forearm in postmenopausal women

143
Q

What is Teriparatide? How do you use it and what is it for?

A

PTH analog
used in cyclic doses
effective in tx of osteoporosis

144
Q

How do you treat Hashimotos?

A

levothyroxine

Block 10 week 1 (4 decks)

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