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
what does iodide do?
inhibits all steps involved in thyroid hormone synthesis and release
26
does iodide work fast or slow?
fast
27
is iodide a large or small dose?
large
28
t/f: iodide can be used to protect the thyroid from radiation
true
29
effects of iodide begin to diminish after how long?
about 2 weeks
30
t/f: susceptible individuals can have a severe hypersensitive rxns to iodide
true
31
what can be a temporary treatment for hyperthyroidism b4 permanent rx like ablation or removal?
iodide
32
what is radioactive iodine?
radioactive dye that is only absorbed by the thyroid tissues causing radioactive destruction of the thyroid gland
33
what are common side effects of radioactive iodine?
hypothyroidism diarrhea nausea burning and metallic taste in the mouth swollen salivary glands
34
what is a contraindication for radioactive iodine?
pregnancy or planning of getting pregnant in the next 6 months
35
why do you need to be in an isolated environment for a few days after receiving radioactive iodine?
bc you emit radioactivity
36
how do beta blockers treat hyperthyroidism?
they symptomatically treat CV symptoms of hyperthyroidism antihypertensive and antiaginal they suppress cardiac symptoms related to hyperthyroidism (tachycardia, palpitations, restlessness)
37
what do beta blockers end in?
-olol
38
what is the most common endocrine disorder, esp in women over 50?
hypothyroidism
39
what is a common cause of hypothyroidism?
Hashimoto disease
40
what is Hashitmoto disease?
the most common cause of hypothyroidism in the US autoimmune disorder primarily affecting middle aged populations
41
what does iodine deficiency cause?
hypothyroidism
42
where do we get iodine from?
our diet in foods like soy milk and shellfish
43
what are the s/s of hypothyroidism?
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
44
what is myxedema?
thickening of the skin non pitting peripheral edema
45
what is the rx for hypothyroidism?
Levothyroxine (Synthroid)
46
what is Levothyroxine (Synthroid)?
synthetic thyroid hormone (t4)
47
does Levothyroxine (Synthroid) work fast or slow?
slow
48
people on Levothyroxine (Synthroid) need dose adjustments every ___ weeks
4-8
49
what is the 1/2 life of Levothyroxine (Synthroid)?
about 6 days
50
what is the pro of the long half life of Levothyroxine (Synthroid)?
it reduces misdosing
51
what are the s/s of overdose of Levothyroxine (Synthroid)?
s/s of hyperthyroidism (CV risks and fx risk)
52
what are the adverse effects of Levothyroxine (Synthroid)?
vomiting, diarrhea tachycardia dysrhythmias hair loss insomnia changes in menstrual cycle weight/appetite changes
53
what are the drug/food interactions with Levothyroxine (Synthroid)?
calcium carbonate iron supplements antacids with albumin or magnesium walnuts grapefruit juice high fiber foods
54
what elements are involved in management of bone mineral density?
calcium and phosphate
55
what are the primary regulators of calcium and phosphate homeostasis?
parathyroid hormone (PTH) fibroblast growth factor 23 vitamin D
56
how does PTH regulate calcium and phosphate?
by increasing blood calcium by breaking down bone
57
how does fibroblastgrowth factor 23 regulate calcium and phosphate?
by decreasing phosphate levels in the blood
58
how does vitamin D regulate calcium and phosphate?
by increasing the absorption of calcium and phosphate from the intestines and kidneys
59
what are the secondary regulators of calcium and phosphate?
calcitonin glucocorticoids estrogen
60
what are some disorders affecting bone mineral homeostasis?
hypoparathyroidism hyperparathyroidism osteoporosis Paget's disease chronic kidney disease vitamin D deficiency
61
what are some drugs to maintain bone mineral homeostasis?
calcium supplement vitamin D analog bisphosphonate calcitonin estrogen rPTH, RANKL inhibitor, calcimimetics, thiazide diuretics
62
what are the indications for a calcium supplement?
deficiency hypocalcemia osteoporosis hypoparathyroidism
63
a calcium supplement is often combined with ___ and ___
vit D, bisphosphonate
64
what are the side effects of calcium supplements?
thrist frequent urination bone and muscle pain fatigue confusion (more severe if hypercalcemia is not resolved soon) nausea/vomiting cardiac arrythmias, HTN
65
what are the indications for a vitamin D analog?
hypocalcemia, vit D deficiency secondary to malabsorption of hepatic diseases
66
what is the prescription vitamin D analog?
Calcitrol (Calcijex, Vectocal, ROcaltrol)
67
what is vit D toxicity?
hypercalcemia calcium stones, renal failure, mood changes, seizures
68
increasing ____ and _____ enhances bone formation
calcium and phosphate
69
is a vit D analog used alone going to be effective for osteoporosis?
nope
70
t/f: biphosphanates are antiresorptive
true
71
what does it mean if a drug is anti-reabsorptive?
it inhibits the osteoplastic activity in the reabsorption bone phase
72
what are the indications for biphosphanates?
osteoporosis Paget's disease
73
do biphosphanates have a high or low bioavailability?
very low
74
are biphosphanates taken daily?
no!
75
how often is the bisphosphonate Alendronate (Fosamax) taken?
weekly
76
how often is the bisphosphonate Risedronate (Actonel) taken?
weekly or monthly
77
how often is the bisphosphonate Ibandronate (Boniva) taken?
every 3 months
78
how often is the bisphosphonate Zoledronate (Reclast) taken?
yearly injection (usually have bone pain few days after)
79
what are the side effects of biphosphanates?
bone pain (with injection) GI disturbances (should be taken with plenty of water and maintain upright position for 30 min after)
80
t/f: calcitonin is an anti-reabsorptive drug
true
81
what are the indications for calcitonin?
osteoporosis hypercalcemia Paget's disease
82
what are the 2 types of calcitonin?
human calcitonin (Fortical) salmon calcitonin (Miacalcin)
83
how is calcitonin administered?
SQ, IM, or intranasal
84
t/f: calcitonin use can lead to flushing of the hands and face
true
85
what are the side effects of calcitonin?
nausea, vomiting paresthesia (tingling hands and feet) - very mild symptom
86
what are the indications for estrogen replacement therapy?
osteoporosis in females post-menopause
87
why does estrogen replacement therapy work in post menopausal women with osteoporosis?
bc menopause decreased estrogen and estrogen helps with bone formation, so increasing estrogen can increase bone density
88
what are the side effects of estrogen replacement therapy?
increased risk of endometrial and breast cancer increased risk of CV disease (already at risk post-menopause)
89
what is the common estrogen replacement therapy drug?
selective estrogen receptor modulators (SERMs)
90
what do SERMs do?
they act as estrogen agonist in bones and estrogen antagonist in breast and uterine tissues
91
what are the names of a couple of SERMs?
Raloxifene (Evista) Tamoxifen (Soltamox)
92
what are the side effects for estrogen replacement therapy?
flu-like symptoms hot flushes leg cramps peripheral edema
93
what meds increase risk for osteoporosis?
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
what are the PT implications for durgse to maintain bone mineral homeostasis?
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
what is type 1 DM?
born with it insulin supply problem
96
what is type 2 DM?
acquired peripheral resistance to insulin
97
does insulin inc or dec blood glucose levels after eating?
dec
98
____ is converted to ____ to be stored in the liver
glucose, glycogen
99
how is insulin administered?
SQ with a small syringe or needle tipped pen insulin pump IV in emergencies
100
what are the types of insulin?
insulin aspart insulin glulisine insulin lispro regular (R) NPH (N) insulin detemir insulin glargine
101
what lifestyle factors affect insulin dosing?
eating habits and exercise habits
102
what are the non-insulin pharmacotherapy options?
sulfonureas biguanides (Metformin)O thiazolidinediones (Proglitazone) Semaglutide injection (Ozempic)
103
what is the only non-insulin med that can be used for both type 1 and 2 DM?
sulfonylureas
104
what is the target of sulfonylureas?
pancreatic beta cells
105
what is the MOA of sulfonylureas?
inc insulin release
106
what are the adverse effects of sulfonylureas?
hypoglycemia
107
what is the target of Biguanides (Metformin)?
liver, peripheral tissues
108
what is the MOA of Biguanides (Metformin)?
dec glucose production by liver dec peripheral insulin resistance
109
what are the adverse effects of Biguanides (Metformin)?
GI disturbance
110
what is the target of Thiazolidinediones (Pioglitazone)?
liver, peripheral tissues
111
what is the MOA of Thiazolidinediones (Pioglitazone)?
dec glucose production by liver dec peripheral insulin resistance inc peripheral insulin sensitivity
112
what are the side effects of Thiazolidinediones (Pioglitazone)?
headache, dizziness, fatigue/weakness, back pain; worsen HF
113
what is the target of Semaglutide injection (Ozempic)?
pancreatic beta cells brain liver
114
what is the MOA of Semaglutide injection (Ozempic)?
inc insulin release dec glucose production by liver dec glucagon release
115
what are the side effects of Semaglutide injection (Ozempic)?
increased risk of thyroid cancer; affects muscle-can lead to muscle wasting (encouraged to have higher protein diet)
116
what are common adverse reactions to anti-diabetic meds?
hyperglycemia and hypoglycemia
117
what are the s/s of hyperglycemia?
extreme thirst frequent urination extreme hunger weakness blurred vision upset stomach/vomiting SOB fruity breath Dec/loss of consciousness confusion seizure
118
which is the greater risk, hyperglycemia or hypoglycemia?
hyperglycemia
119
what are the s/s of hypoglycemia?
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
are interactions bw anti-DM drugs and beta blockers usually bw selective or non selective beta blockers?
non-selective beta blockers
121
what is the problem with interactions bw DM meds and beta blockers?
beta blockers may lead to a delayed response to hypoglycemia bc they keep tremors and tachycardic symptoms are bay
122
t/f: pts with DM should be advised or use selective beta blockers is they must be on beta blockers
true
123
when is cortisone, released?
in the morning
124
what is the role of adrenocorticosteroids?
to controll glucose metabolism and coping with stress
125
if there is too much cortisol or steroids, what may happen?
DM-like insulin resistance
126
t/f: steroids are immunosupressants and anti-inflammatory
true
127
what is the role of glucocorticoids?
increased blood glucose, anti-inflammatory, and immunosuppressant effects
128
how do muscles cells increase glucose when cortisol acts on it?
by breaking down protein
129
how do fat cells increase glucose when cortisol acts on it?
by breaking down fat
130
how do liver cells increase glucose when cortisol acts on it?
by increasing transformation of glycogen to glucose
131
t/f: steroids affect bone marrow homeostasis and can lead to osteoporosis
true
132
t/f: steroids also have CNS and CV effects
true
133
what are endocrine disorder associated with glucocorticoid use?
adrenocortical insufficiency congenital adrenal hyperplasia adrenocortical hypersecretion after adrenalectomy or destruction of pituitary gland
134
what is primary adrenocortical insufficiency?
deficient glucocorticoid from deficient adrenal cortex Addison's disease
135
what is secondary adrenocortical insufficiency?
lack of ACTH (adrenocorticotropic hormone) release from the anterior pituitary gland which normally signals the release of glucocorticoids
136
what is congenital adrenal hyperplasia?
enlarged adrenal cortex leads to adrenal cortex not releasing cortisol low cortisol, high ACTH
137
what is adrenocortical hypersecretion?
Cushing's syndrome from too much glucocorticoids inc glucose in blood can lead to DM
138
what are the non-endocrine disorders associated with glucocorticoid use?
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
what are examples of glucocorticoids?
short to medium-acting intermediate-acting long-acting
140
what are the short to medium- acting glucocorticoids?
hydrocortisone-short prednisolone- medium methylprednisolone-medium - intraarticular injections
141
what is the half life of short to medium-acting glucocorticoids?
3-12 hours
142
what are the intermediate-acting glucocorticoids?
triamcinolone paramethasone
143
what is the half life of intermediate-acting glucocorticoids?
12-36 hours
144
what are the long-acting glucocorticoids?
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
what is the half life of long-acting glucocorticoids?
36-72 hours
146
what is the physiologic dose?
the dose used for replacement therapy bc the body doesn't make enough of the steroid
147
what is the pharmacological (supraphysiololgic) dose?
the dose given for inflammation for RA, MS, allergies, etc adrenal steroids given at higher dose to produce a specific benefit
148
what are the different routes of administration of steroids?
systemic (oral or IV) topical intra-articular inhalation (for asthma) ophthalmic nasal otic
149
t/f: glucocorticoids are metabolized mostly in the liver
true
150
do glucocorticoids have a high or low first pass effect?
high
151
does half life inc or dec with liver damage?
inc
152
how are glucocorticoids excreted?
urination
153
what are the adverse reactions to glucocorticoids?
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
what are the general principles of glucocortioid use?
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
what are the PT implications for glucocorticoids?
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)