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Pharmacology > Exam 3 Endocrine Drugs > Flashcards

Exam 3 Endocrine Drugs Flashcards

1
Q

methods for treating hypotitutiarism

A
  • replace missing hormones
  • ACTH, TSH, FSH/LH
  • growth hormone (somatropin)
  • vasopressin (AVP akak ADH)
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2
Q

growth hormone indication

A

hypopituitarism

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3
Q

growth hormone MOA

A

synthetic growth hormone, acts on bone, skeletal muscle, fat.
increase RBC mass, transport of water, electrolyte and other fluid functions

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4
Q

growth hormone AE

A

fluid retention

muscle and joint pain

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5
Q

growth hormone drug

A

Somatotropin

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6
Q

vasopressin (AVP) indication

A

hypopituitarism

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7
Q

vasopressin (AVP) MOA

A

increases aquaporins on cell membrane, water is reabsorbed

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8
Q

vasopressin (AVP) drugs

A

DDAVP

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9
Q

What is DDAVP also used for

A

nocturia

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10
Q

vasopressin (AVP) AEs

A

dry mouth

hyponatremia

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11
Q

vasopressin (AVP) main role

A

decrease water excretion by causing increased urine concentration

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12
Q

vasopressin (AVP) is aka….

A

ADH

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13
Q

1st line treatment for excessive glucorticoids

A

surgery

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14
Q

2nd line treatment for excessive glucocorticoids

A

medication (usually pre or post op or if surgery is contraindicated or fails)

  • steriodgenesius inhibitors (block cortisol synthesis)
  • glucocorticoid antagonist (blocks cortisol binding to receptor)
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15
Q

treatment used for glucocorticoid deficiency

A

replace glucocorticoids with steroids

hydrocortisone

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16
Q

treatment for mineralocorticoid excess

A

use aldosterone receptor antagonist

  • spironolactone
  • eplerenone
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17
Q

treatment for mineralocorticoid deficiency

A

use fludrocortisone

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18
Q

testosterone replacement indication

A

androgen deficiency

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19
Q

testosterone replacement route

A

IM, subcut injection or pellet, patch, gel, solution, nasal spray, buccal

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20
Q

testosterone replacement IM concerns

A

variable sx relief, mood changes

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21
Q

testosterone replacement AE

A
  • possible increased risk of MI, stroke, CV death
  • prolonged use can cause hepatoxicity
    (IM associated with hepatic adenomas)
  • infertility with large doses
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22
Q

anabolic-androgenic steroids (AAS)

A

DHEA - banned by FDA but markets as a nutritional supplement

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23
Q

anabolic-androgenic steroids (AAS) AE

A 
acne
MI, CV death from arrhythmia, VTE
Cancer
Infection
Musculoskeletal - tendon/ligament rupture
insomnia, mood disorders
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24
Q

Forms of contraception

A
  • combo oral
  • IUD
  • injection
  • progestin only pill
  • progestin only implant
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25
Q

combined oral contraceptive AEs

A 
increased BP
n/v
weight gain
acne
depression
topical rxn
RARE: DVT/PE, stroke, MI
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26
Q

IUD AE

A

rare pelvic inflammatory disease

- copper associated with increased bleeding (anemia)

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27
Q

estrogen and progesterone indication

A

post-menopausal hormone replacement therapy

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28
Q

estrogen alone indication

A

if no uterus

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29
Q

estrogen route

A

PO, transdermal patch/spray, topical gel/solution, vaginal ring/cream

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30
Q

estrogen AE

A 
nausea
HA
breast tenderness
vaginal bleeding
endometrial cancer
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31
Q

progesterone route

A

PO, patch

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32
Q

progesterone AE

A

bloating, headache, weight gain, irritability

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33
Q

estrogen and progesterone known risks

A

DVT, PE, breast cancer

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34
Q

alpha-adrenergic antagonists indication

A

benign prostatic hypertrophy (enlarged prostate gland)

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35
Q

alpha-adrenergic antagonists MOA

A

relax smooth muscle in prostate and bladder neck (urination is easier)

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36
Q

alpha-adrenergic antagonists AE

A

hypotension

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37
Q

5a-reductase inhibitor MOA

A

interfere with stimulatory effects of testosterone

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38
Q

5a-reductase inhibitor AE

A

hypotension

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39
Q

anticholinergic agents drugs

A

oxybutynin

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40
Q

anticholinergic agents MOA

A

antispasmodic effect on smooth muscle

- blocks acetylcholine on smooth muscle

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41
Q

anticholinergic agents AE

A

cant see, spit, pee, shit

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42
Q

B3-agrengic agonist MOA

A

relaxes detrusor muscle to decrease voiding sx

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43
Q

B3-agrengic agonist AE

A

increased BP

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44
Q

B3-agrengic agonist indication

A

benign prostatic hypertrophy

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45
Q

medication classes for benign prostatic hypertrophy

A
  • alpha-adrenergic antagonists
  • 5a reductase inhibitors
  • anticholinergic agents
  • b3-adrenergic agonist
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46
Q

calcimemtics indication

A

hyperparathyroidism

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47
Q

calcimemtics moa

A

interacts with CaSR to increase calcium affinity and decreases PTH

48
Q

calcimemtics AE

A

monitor for hypocalcemia

49
Q

bisphonates MOA

A

prevents calcium loss from bone

50
Q

what do you take for hypoparathyroidism

A

calcium and vitamin d

51
Q

levothyroxine indication

A

hypothyroidism

52
Q

levothyroxine MOA

A

synthetic version of T4 that is converted T3

53
Q

levothyroxine AE

A

NTI drug
- requires monitoring and dose adjustments

  • generally well tolerated unless you over treat (pushes you into hyperthyroidism sx)
54
Q

levothyroxine dosing

A

take on an empty stomach.

30-60 minutes before a mean or 3-4 hours after a meal

  • do not take within 4 hours of certain supplements
55
Q

levothyroxine over treatment

A

can increase risk of CVD issues

- long term over treatment can lead to decreased bone density and increased risk of fractures

56
Q

drug classes to treat hyperthyroidism

A
  1. antithyroid meds
  2. radioactive iodine
  3. thyroidectomy
57
Q

antithyroid indication

A

hyperthyroidism

58
Q

antithyroid drug

A

methimazole

59
Q

antithyroid MOA

A

blocks formation of T4 and T3 – by inhibiting oxidation of iodine

60
Q

antithyroid AE

A

common: rash GI upset, arthralgia (joint pain)
rare: agranulyctyes, heptatoxicity
- can cause hypothyroidism but less less likely than other treatments

61
Q

what antithyroid medication is preferred in pregnancy

A

PTU over methimazole

62
Q

types of osteoporosis treatment

A
  • anitresorptive therapy

- anabolic therapy

63
Q

antiresoprtive therapy MOA

A

blocks the breakdown of bone

64
Q

anabolic therapy MOA

A

increases bone formation

65
Q

calcium and vitamin D indication

A

osteoporosis

66
Q

bisphosphonates indication

A

osteoporosis

67
Q

bisphosphonates MOA

A

inhibits the natural bone turnover pathway, increases osteoclasts, to decrease bone turnover

68
Q

what is 1st line treatment for osteoporosis

A

bisphosphonates

69
Q

bisphosphonates AE

A

mild upper GI sx (GERD)

70
Q

bisphosphonates dosing

A

take w plain water 30-60 minutes before any food or meds

  • stay upright
  • absorption can be decreased by up to 90% if taken w food or water
71
Q

bisphosphonates contraindications

A
  • hypoglycemia
  • inability to remain upright
  • esophageal abnormalities with PO
72
Q

bisphosphonates rare but serious risks

A
  • atypical femur fracture
  • osetonecrosis of jaw

monitor: hypocalcemia, reports of sever joint, muscle, and bone pain

73
Q

anti-RANKL dosing

A

every 6 month in the providers office

74
Q

anti-RANKL indication

A

osteoporosis

75
Q

bisphosphonates ending

A

-dronate

76
Q

anti-RANKL MOA

A

ultimately inhibits bone resorption

77
Q

anti-RANKL AE

A

arthralgia, limb pain, derm reactions

Rare: atypical femur fraction, increased risk of infections

78
Q

Sclerosin inhibitors indication

A

osteoporosis

79
Q

Sclerosin inhibitors MOA

A

inhibits sclerotin to increase bone formation

80
Q

Sclerosin inhibitors AE

A

arthralgia

rare: hypocalcemia, atypical fractures, ONJ, incase CVD issues

81
Q

Common Oral Diabetic medication classes

A
  1. Binguanide (metformin)
  2. sulfonylureas (SU)
  3. Thiazolidinediones (TZD)
  4. Dipeptidyl-peptidase 4 inhibitors (DPP-4i)
  5. Sodium glucose co-transporter 2 inhibitors (SGLT2i)
  6. Glucagon-like peptide 1 agonist (GLP1a)
82
Q

common injectable diabetic medication classes

A
  1. glucagon-like peptide 1 agonists (GLP1a)

2. insulin

83
Q

what is the only medication will discuss for T1DM

A

insulin

84
Q

Biguanide (metformin) indication

A

T2DM

85
Q

Biguanide (metformin) MOA

A

not fully known -

  1. inhibits the production of glucose
  2. inhibits intestinal absorption of glucose
  3. increases insulin sensitivity in muscle and fat
86
Q

Biguanide (metformin) AEs

A

low risk of hypoglycemia!!

common AEs: GI (n/d/cramping/bloating)
Vitamin B12 deficiency - but don’t assume! Can be misdiagnosed as peripheral neuropathy

87
Q

Biguanide (metformin) route

A

oral, oldest oral drug for T2DM

88
Q

sulfonylereas (SU) indication

A

T2DM

89
Q

sulfonylereas (SU) MOA

A

binda sulfonylurea receptor in the pancreas

- depolarization causes insulin release

90
Q

sulfonylereas (SU) AE

A

SUPER high risk hypoglycemia (esp in elderly and renal dysfunction)
weight gain

BEERS LIST

91
Q

sulfonylereas (SU) route

A

-typically taken before breakfast (must be 30 mins before a meal)

If not taken correctly can increase hypoglycemia risk

92
Q

Thiazolidinedione (TZD) indication

A

T2DM

93
Q

Thiazolidinedione (TZD) MOA

A

increases insulin sensitivity in muscle and fat, increases gene responses that influence glucose metabolism

“insulin sensitizer”
- no diuretic effect

94
Q

sulfonylereas (SU) drug

A

glipizide

95
Q

Thiazolidinedione (TZD) AEs

A

low hypoglycemia risk!!

edema
long term increase bone fracture risk (esp females)

boxed warning! (HF, monitor and avoid in pre-existing HF)

96
Q

DPP-4 Inhibitors indication

A

T2DM

97
Q

DPP-4 Inhibitors MOA

A

inhibits DPP-4 (an enzyme we all have that typically breaks down incretin hormones)
- increases insulin synthesis and release and decreases glucagon secretion

98
Q

DPP-4 Inhibitors AE

A

low risk for hypoglycemia
- very well tolerated

case reports of arthralgia (also genetic component)

99
Q

SGLT2 inhibitor indication

A

T2DM

100
Q

SGLT2 inhibitor MOA

A

blocks glucose reabsorption in the kidney at SGLT2

- increases urinary glucose excretion

101
Q

SGLT2 inhibitor AE

A

volume depletion related AEs

rare risk: DKA (more so if dehydrated or used off-label in T1DM)

102
Q

SGLT2 inhibitor “pros”

A

some can reduce risk of renal complications, CV events and HF hospitalizations

103
Q

GLP1 Receptor Agonist route

A

injectable or PO

  • sometimes used in combo with basal insulin
  • can be daily or weekly
104
Q

GLP1 Receptor Agonist MOA

A

increases insulin secretion
decreases glucagon secretion
slows gastric emptying (to increase satiety)

105
Q

GLP1 Receptor Agonist AEs

A

nausea, bloating, diarrhea

some reduce risk of CV event

106
Q

insulin indication

A

T1DM

more advanced T2DM

107
Q

insulin MOA

A

bind tyrosine kinase receptors
triggers intracellular effects
increase expression of GLUT4 receptor
increase glucose uptake

can also…
inhibit production of glucose

108
Q

insulin AEs

A

hypoglycemia! and weight gain

109
Q

basal insulin

A

always working in background

- usually once daily (sometimes twice)

110
Q

rapid bolus insulin

A

onset : 10-30 mins

duration 3-5+ hours

111
Q

regular bolus insulin

A

onset: 30 mins
direction: 4-12 hours

112
Q

bolus insulin

A

typically given before a meal (sometimes immediately after)

can be given to correct hyperglycemia
“correction insulin”
“sliding scale insulin”

113
Q

intermediate insulin (NPH)

A

direction: 12-24 hours

inject once or twice daily

114
Q

mixed insulin

A 
combo of intermediate w rapid or regular acting 
- inject before meal
70/30
70% intermediate 30% regular acting
longer acting/shorter acting
115
Q

first line T2DM treatment

A

metformin

116
Q

2nd line T2DM treatment

A

pt specific

117
Q

which medication classes have the highest risk of hypoglycemia

A

sulfonyrias and insulin

Pharmacology (11 decks)

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