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DPT 530 > Endocrine Meds > Flashcards

Endocrine Meds Flashcards

1
Q

what categories of drugs are included in endocrine pharmacology?

A

thyroid meds

drugs that affect bone mineral homeostasis

diabetic meds

adrenocorticosteroids

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2
Q

what are the fxns of the thyroid?

A

growth and development

metabolism

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3
Q

does hypo or hyperthyroidism result in being hot all the time, weight loss, and tachycardia?

A

hyperthyroidism

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4
Q

does hypo or hyperthyoidism result in being cold all the time, weight gain, and bradycardia?

A

hypothyroidism

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5
Q

what is thyrotoxicosis?

A

hyperthyroidism

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6
Q

what are some cuases of hyperthyroidism?

A

Goiter

Grave’s disease

Thyroiditis

thyroid tumors

hypothalamus/pituitary gland pathology

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7
Q

how does Goiter cause hyperthyroidism?

A

enlargement and hyperfunctioning of the thyroid

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8
Q

how does Grave’s disease cause hyperthyroidism?

A

it is an autoimmune disorder that causes antibodies to be released, stimulating the thyroid to overproduce thyroid hormone

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9
Q

how does thyroiditis cause hyperthyroidism?

A

inflammation of the thyroid gland causes leakage of thyroid hormone, increasing level in the bloodstream

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10
Q

t/f: thyroiditis sometimes occur post partem

A

true

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11
Q

how does hypothalamus and/or pituitary gland pathology cause hyperthyroidism?

A

it can lead to excessive TRH and TSH

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12
Q

what are the s/s of hyperthyroidism?

A

increased in SNS symptoms

tachycardia, dysrhythmias, HF

increased RR

restlessness/anxiety

fatigue

hair loss

muscles wasting

changes in menstruation

unexplained weight loss

calcium metabolism (dec bone density)

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13
Q

what s/s are older ppl more at risk for with hyperthyroidism?

A

CV s/s

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14
Q

what are the rx options for hyperthyroidism?

A

anti-thyroid agents

thyroidectomy

iodide or radioactive iodine

beta blockers

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15
Q

do beta blockers treat hyperthyroidism at the thyroid level?

A

nope, just the cardiac symptoms (tachycardia)

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16
Q

what is thionamide?

A

an anti-thyroid agent used to treat hyperthyroidism

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17
Q

what is PTU?

A

a type of thionamide that inhibits thyroid hormone synthesis

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18
Q

what is Methimazole (Tapazole)?

A

a type of thionamide that is 10x more potent than PTU

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19
Q

describe the pharmacokinetics of antithyroid agents

A

slow onset (about 2-3 weeks)

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20
Q

what is a contraindication for antithyroid agents?

A

being pregnant or nursing

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21
Q

why is it contraindicated to use antithyroid agents when pregnant or nursing?

A

bc it can cause hypothyroidism in the fetus that can affect growth and development

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22
Q

what are the side effects of antithyroid agents?

A

nausea, GI distress

black, tarry stool

painful/difficult urination

maculopapular rash (not very serious)

severe liver disease

cholestatic jaundice (obstruction of bile flow in the liver)

agronulocytosis (dangerous but rare)

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23
Q

what is cholestatic jaudice?

A

obstruction of bile flow in the liver

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24
Q

what is agranulocytosis?

A

granulosis or granulopenia

leukocytopenia so monitor WBC count and bone marrow count

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25
Q

what does iodide do?

A

inhibits all steps involved in thyroid hormone synthesis and release

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26
Q

does iodide work fast or slow?

A

fast

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27
Q

is iodide a large or small dose?

A

large

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28
Q

t/f: iodide can be used to protect the thyroid from radiation

A

true

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29
Q

effects of iodide begin to diminish after how long?

A

about 2 weeks

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30
Q

t/f: susceptible individuals can have a severe hypersensitive rxns to iodide

A

true

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31
Q

what can be a temporary treatment for hyperthyroidism b4 permanent rx like ablation or removal?

A

iodide

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32
Q

what is radioactive iodine?

A

radioactive dye that is only absorbed by the thyroid tissues causing radioactive destruction of the thyroid gland

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33
Q

what are common side effects of radioactive iodine?

A

hypothyroidism

diarrhea

nausea

burning and metallic taste in the mouth

swollen salivary glands

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34
Q

what is a contraindication for radioactive iodine?

A

pregnancy or planning of getting pregnant in the next 6 months

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35
Q

why do you need to be in an isolated environment for a few days after receiving radioactive iodine?

A

bc you emit radioactivity

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36
Q

how do beta blockers treat hyperthyroidism?

A

they symptomatically treat CV symptoms of hyperthyroidism

antihypertensive and antiaginal

they suppress cardiac symptoms related to hyperthyroidism (tachycardia, palpitations, restlessness)

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37
Q

what do beta blockers end in?

A

-olol

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38
Q

what is the most common endocrine disorder, esp in women over 50?

A

hypothyroidism

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39
Q

what is a common cause of hypothyroidism?

A

Hashimoto disease

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40
Q

what is Hashitmoto disease?

A

the most common cause of hypothyroidism in the US

autoimmune disorder primarily affecting middle aged populations

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41
Q

what does iodine deficiency cause?

A

hypothyroidism

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42
Q

where do we get iodine from?

A

our diet in foods like soy milk and shellfish

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43
Q

what are the s/s of hypothyroidism?

A

decreased metabolism

bradycardia

jt and muscle pain

lethargy

depression

changes in menstruation

mental impairment

weight gain

dry skin and hair

cold intolerance

myxedema

increased LDL and CV disease

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44
Q

what is myxedema?

A

thickening of the skin

non pitting peripheral edema

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45
Q

what is the rx for hypothyroidism?

A

Levothyroxine (Synthroid)

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46
Q

what is Levothyroxine (Synthroid)?

A

synthetic thyroid hormone (t4)

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47
Q

does Levothyroxine (Synthroid) work fast or slow?

A

slow

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48
Q

people on Levothyroxine (Synthroid) need dose adjustments every ___ weeks

A

4-8

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49
Q

what is the 1/2 life of Levothyroxine (Synthroid)?

A

about 6 days

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50
Q

what is the pro of the long half life of Levothyroxine (Synthroid)?

A

it reduces misdosing

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51
Q

what are the s/s of overdose of Levothyroxine (Synthroid)?

A

s/s of hyperthyroidism (CV risks and fx risk)

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52
Q

what are the adverse effects of Levothyroxine (Synthroid)?

A

vomiting, diarrhea

tachycardia

dysrhythmias

hair loss

insomnia

changes in menstrual cycle

weight/appetite changes

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53
Q

what are the drug/food interactions with Levothyroxine (Synthroid)?

A

calcium carbonate

iron supplements

antacids with albumin or magnesium

walnuts

grapefruit juice

high fiber foods

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54
Q

what elements are involved in management of bone mineral density?

A

calcium and phosphate

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55
Q

what are the primary regulators of calcium and phosphate homeostasis?

A

parathyroid hormone (PTH)

fibroblast growth factor 23

vitamin D

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56
Q

how does PTH regulate calcium and phosphate?

A

by increasing blood calcium by breaking down bone

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57
Q

how does fibroblastgrowth factor 23 regulate calcium and phosphate?

A

by decreasing phosphate levels in the blood

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58
Q

how does vitamin D regulate calcium and phosphate?

A

by increasing the absorption of calcium and phosphate from the intestines and kidneys

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59
Q

what are the secondary regulators of calcium and phosphate?

A

calcitonin

glucocorticoids

estrogen

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60
Q

what are some disorders affecting bone mineral homeostasis?

A

hypoparathyroidism

hyperparathyroidism

osteoporosis

Paget’s disease

chronic kidney disease

vitamin D deficiency

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61
Q

what are some drugs to maintain bone mineral homeostasis?

A

calcium supplement

vitamin D analog

bisphosphonate

calcitonin

estrogen

rPTH, RANKL inhibitor, calcimimetics, thiazide diuretics

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62
Q

what are the indications for a calcium supplement?

A

deficiency

hypocalcemia

osteoporosis

hypoparathyroidism

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63
Q

a calcium supplement is often combined with ___ and ___

A

vit D, bisphosphonate

64
Q

what are the side effects of calcium supplements?

A

thrist

frequent urination

bone and muscle pain

fatigue

confusion (more severe if hypercalcemia is not resolved soon)

nausea/vomiting

cardiac arrythmias, HTN

65
Q

what are the indications for a vitamin D analog?

A

hypocalcemia, vit D deficiency secondary to malabsorption of hepatic diseases

66
Q

what is the prescription vitamin D analog?

A

Calcitrol (Calcijex, Vectocal, ROcaltrol)

67
Q

what is vit D toxicity?

A

hypercalcemia

calcium stones, renal failure, mood changes, seizures

68
Q

increasing ____ and _____ enhances bone formation

A

calcium and phosphate

69
Q

is a vit D analog used alone going to be effective for osteoporosis?

A

nope

70
Q

t/f: biphosphanates are antiresorptive

A

true

71
Q

what does it mean if a drug is anti-reabsorptive?

A

it inhibits the osteoplastic activity in the reabsorption bone phase

72
Q

what are the indications for biphosphanates?

A

osteoporosis

Paget’s disease

73
Q

do biphosphanates have a high or low bioavailability?

A

very low

74
Q

are biphosphanates taken daily?

A

no!

75
Q

how often is the bisphosphonate Alendronate (Fosamax) taken?

A

weekly

76
Q

how often is the bisphosphonate Risedronate (Actonel) taken?

A

weekly or monthly

77
Q

how often is the bisphosphonate Ibandronate (Boniva) taken?

A

every 3 months

78
Q

how often is the bisphosphonate Zoledronate (Reclast) taken?

A

yearly injection (usually have bone pain few days after)

79
Q

what are the side effects of biphosphanates?

A

bone pain (with injection)

GI disturbances (should be taken with plenty of water and maintain upright position for 30 min after)

80
Q

t/f: calcitonin is an anti-reabsorptive drug

A

true

81
Q

what are the indications for calcitonin?

A

osteoporosis

hypercalcemia

Paget’s disease

82
Q

what are the 2 types of calcitonin?

A

human calcitonin (Fortical)

salmon calcitonin (Miacalcin)

83
Q

how is calcitonin administered?

A

SQ, IM, or intranasal

84
Q

t/f: calcitonin use can lead to flushing of the hands and face

A

true

85
Q

what are the side effects of calcitonin?

A

nausea, vomiting

paresthesia (tingling hands and feet) - very mild symptom

86
Q

what are the indications for estrogen replacement therapy?

A

osteoporosis in females post-menopause

87
Q

why does estrogen replacement therapy work in post menopausal women with osteoporosis?

A

bc menopause decreased estrogen and estrogen helps with bone formation, so increasing estrogen can increase bone density

88
Q

what are the side effects of estrogen replacement therapy?

A

increased risk of endometrial and breast cancer

increased risk of CV disease (already at risk post-menopause)

89
Q

what is the common estrogen replacement therapy drug?

A

selective estrogen receptor modulators (SERMs)

90
Q

what do SERMs do?

A

they act as estrogen agonist in bones and estrogen antagonist in breast and uterine tissues

91
Q

what are the names of a couple of SERMs?

A

Raloxifene (Evista)

Tamoxifen (Soltamox)

92
Q

what are the side effects for estrogen replacement therapy?

A

flu-like symptoms

hot flushes

leg cramps

peripheral edema

93
Q

what meds increase risk for osteoporosis?

A

anticoagulants that affect hepatic vit D metabolism (phenytoin, carbamazepine)

anticoagulants (heparin, warfarin)

immunosuppressants (cyclosporine A, methotrexate, tacrolimus)

PPIs (Omeprazole, esomeprazole, pantoprazole,)

thiazolidinedrones (Proglitazone)

SSRIs (sertraline, paroxetine, fluoxentine)

94
Q

what are the PT implications for durgse to maintain bone mineral homeostasis?

A

be aware of s/s of hypercalcemia

don’t take oral bisphosphonate w/food and take w/lots of water

schedule pt about an hour after taking meds (don’t lay down within half hour of taking meds)

potential side effects of the drugs

pt education (exercise to Rx and prevent osteoporosis, adherence to med regimine)

exercises for osteoporosis (weight bearing, plyometrics, jumping)

95
Q

what is type 1 DM?

A

born with it

insulin supply problem

96
Q

what is type 2 DM?

A

acquired

peripheral resistance to insulin

97
Q

does insulin inc or dec blood glucose levels after eating?

A

dec

98
Q

____ is converted to ____ to be stored in the liver

A

glucose, glycogen

99
Q

how is insulin administered?

A

SQ with a small syringe or needle tipped pen

insulin pump

IV in emergencies

100
Q

what are the types of insulin?

A

insulin aspart

insulin glulisine

insulin lispro

regular (R)

NPH (N)

insulin detemir

insulin glargine

101
Q

what lifestyle factors affect insulin dosing?

A

eating habits and exercise habits

102
Q

what are the non-insulin pharmacotherapy options?

A

sulfonureas

biguanides (Metformin)O

thiazolidinediones (Proglitazone)

Semaglutide injection (Ozempic)

103
Q

what is the only non-insulin med that can be used for both type 1 and 2 DM?

A

sulfonylureas

104
Q

what is the target of sulfonylureas?

A

pancreatic beta cells

105
Q

what is the MOA of sulfonylureas?

A

inc insulin release

106
Q

what are the adverse effects of sulfonylureas?

A

hypoglycemia

107
Q

what is the target of Biguanides (Metformin)?

A

liver, peripheral tissues

108
Q

what is the MOA of Biguanides (Metformin)?

A

dec glucose production by liver

dec peripheral insulin resistance

109
Q

what are the adverse effects of Biguanides (Metformin)?

A

GI disturbance

110
Q

what is the target of Thiazolidinediones (Pioglitazone)?

A

liver, peripheral tissues

111
Q

what is the MOA of Thiazolidinediones (Pioglitazone)?

A

dec glucose production by liver

dec peripheral insulin resistance

inc peripheral insulin sensitivity

112
Q

what are the side effects of Thiazolidinediones (Pioglitazone)?

A

headache, dizziness, fatigue/weakness, back pain; worsen HF

113
Q

what is the target of Semaglutide injection (Ozempic)?

A

pancreatic beta cells

brain

liver

114
Q

what is the MOA of Semaglutide injection (Ozempic)?

A

inc insulin release

dec glucose production by liver

dec glucagon release

115
Q

what are the side effects of Semaglutide injection (Ozempic)?

A

increased risk of thyroid cancer; affects muscle-can lead to muscle wasting (encouraged to have higher protein diet)

116
Q

what are common adverse reactions to anti-diabetic meds?

A

hyperglycemia and hypoglycemia

117
Q

what are the s/s of hyperglycemia?

A

extreme thirst

frequent urination

extreme hunger

weakness

blurred vision

upset stomach/vomiting

SOB

fruity breath

Dec/loss of consciousness

confusion

seizure

118
Q

which is the greater risk, hyperglycemia or hypoglycemia?

A

hyperglycemia

119
Q

what are the s/s of hypoglycemia?

A

shakiness/tremor

pale skin

hunger

weakness

dizziness/lightheadedness

sweating

sudden changes in behavior/mood

nervousness/irritability

headache

numbness/tingling around the mouth

clumsy/jerky movements

120
Q

are interactions bw anti-DM drugs and beta blockers usually bw selective or non selective beta blockers?

A

non-selective beta blockers

121
Q

what is the problem with interactions bw DM meds and beta blockers?

A

beta blockers may lead to a delayed response to hypoglycemia bc they keep tremors and tachycardic symptoms are bay

122
Q

t/f: pts with DM should be advised or use selective beta blockers is they must be on beta blockers

A

true

123
Q

when is cortisone, released?

A

in the morning

124
Q

what is the role of adrenocorticosteroids?

A

to controll glucose metabolism and coping with stress

125
Q

if there is too much cortisol or steroids, what may happen?

A

DM-like insulin resistance

126
Q

t/f: steroids are immunosupressants and anti-inflammatory

A

true

127
Q

what is the role of glucocorticoids?

A

increased blood glucose, anti-inflammatory, and immunosuppressant effects

128
Q

how do muscles cells increase glucose when cortisol acts on it?

A

by breaking down protein

129
Q

how do fat cells increase glucose when cortisol acts on it?

A

by breaking down fat

130
Q

how do liver cells increase glucose when cortisol acts on it?

A

by increasing transformation of glycogen to glucose

131
Q

t/f: steroids affect bone marrow homeostasis and can lead to osteoporosis

A

true

132
Q

t/f: steroids also have CNS and CV effects

A

true

133
Q

what are endocrine disorder associated with glucocorticoid use?

A

adrenocortical insufficiency

congenital adrenal hyperplasia

adrenocortical hypersecretion

after adrenalectomy or destruction of pituitary gland

134
Q

what is primary adrenocortical insufficiency?

A

deficient glucocorticoid from deficient adrenal cortex

Addison’s disease

135
Q

what is secondary adrenocortical insufficiency?

A

lack of ACTH (adrenocorticotropic hormone) release from the anterior pituitary gland which normally signals the release of glucocorticoids

136
Q

what is congenital adrenal hyperplasia?

A

enlarged adrenal cortex leads to adrenal cortex not releasing cortisol

low cortisol, high ACTH

137
Q

what is adrenocortical hypersecretion?

A

Cushing’s syndrome from too much glucocorticoids

inc glucose in blood can lead to DM

138
Q

what are the non-endocrine disorders associated with glucocorticoid use?

A

inflammatory conditions of bones and joints (ie. RA, OA, gout)

allergic reactions

skin diseases

organ transplant (meds suppress immune system)

autoimmune disorders (ie. RA, MS

chronic infections (ie. tuberculosis)

resp disorders

GI tract diseases

hyperthyroidism

139
Q

what are examples of glucocorticoids?

A

short to medium-acting

intermediate-acting

long-acting

140
Q

what are the short to medium- acting glucocorticoids?

A

hydrocortisone-short

prednisolone- medium

methylprednisolone-medium - intraarticular injections

141
Q

what is the half life of short to medium-acting glucocorticoids?

A

3-12 hours

142
Q

what are the intermediate-acting glucocorticoids?

A

triamcinolone

paramethasone

143
Q

what is the half life of intermediate-acting glucocorticoids?

A

12-36 hours

144
Q

what are the long-acting glucocorticoids?

A

dexamethasone (one of the most commonly seen meds in PT) where the drug molecules are pushed across the skin using US or electricity

betamethasone

145
Q

what is the half life of long-acting glucocorticoids?

A

36-72 hours

146
Q

what is the physiologic dose?

A

the dose used for replacement therapy bc the body doesn’t make enough of the steroid

147
Q

what is the pharmacological (supraphysiololgic) dose?

A

the dose given for inflammation for RA, MS, allergies, etc

adrenal steroids given at higher dose to produce a specific benefit

148
Q

what are the different routes of administration of steroids?

A

systemic (oral or IV)

topical

intra-articular

inhalation (for asthma)

ophthalmic

nasal

otic

149
Q

t/f: glucocorticoids are metabolized mostly in the liver

A

true

150
Q

do glucocorticoids have a high or low first pass effect?

A

high

151
Q

does half life inc or dec with liver damage?

A

inc

152
Q

how are glucocorticoids excreted?

A

urination

153
Q

what are the adverse reactions to glucocorticoids?

A

immunosuppression

Iatrogenic Cushing syndrome-drug induced Cushing syndrome from taking too much oral steroid/hormone

breakdown of connective tissues-skin, muscles, and bones (osteoporotic changes in bone, muscles wasting, thin skin, etc) bc cortisol wants to inc blood glucose by converting fatty tissue into glucose and amino acids from muscle cells into glucose, etc

hyperglycemia

HTN

slow growth in children (from stunted bone and musc growth)

ocular side effects

psychosis

peptic ulcer

154
Q

what are the general principles of glucocortioid use?

A

local administration is preferred

LT use is potentially hazardous

no abrupt withdrawal after >2-3 weeks of administration
–> may precipitate adrenal insufficiency
–> body learns to produce less steroid bc of exogenous source

155
Q

what are the PT implications for glucocorticoids?

A

proceed with caution when selecting treatments and modalities

infection control (immunosuppressant effect)

monitor signs of developing osteoporosis or DM (hyperglycemia s/s)

monitor vitals (HTN secondary to corticosteroid use)

FALL RISK (visual disturbances)

skin integrity

muscles wasting (MMT)

DPT 530 (14 decks)

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