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Pharmacology > Exam #4- Endocrinology > Flashcards

Exam #4- Endocrinology Flashcards

1
Q

thyroid

A

produces T4 and T3 regulated by hypothalamic-pituitary-thyroid axis

regulates normal G&D of body temp and energy levels

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2
Q

thyroid autoimmune disorders

A

thyrotoxicosis (hyper) or hypothyroidism

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3
Q

thyroid hormones

A

iodon is ESSENTIAL for thyroid hormone production (T3 and T4)

if you don’t have iodine- you can’t make thyroid hormone!!

iodine is easily absorbed, so if you have enough in your diet, you’re fine

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4
Q

hypothyroidism incidence/prevalence

A

hypothyroidism is common (WOMEN more so) and effects pretty much every body system

ranges from mild/unrecognized to severe myxedema

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5
Q

primary hypothyroidism

A

d/t thyroid gland

dx (increased TSH, low T4)

w/diseased thyroid, pituitary says to thyroid “you need to make more hormone”.

increased TSH THYROID GLAND DOES NOT RESPOND TO IT= DECREASED T4

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6
Q

secondary hypothyroidism

A

pituitary is not doing it’s job

its not making enough TSH (decreased, TSH), low T4

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7
Q

causes of hypothyroidism

A

hashimoto thyroiditis (most common cause)

drugs (lithium, amiodarone)

iodine deficiency

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8
Q

s/s of hypothyroidism

A

sloooooooooowed down

weight gain, fatigue, depression, cold intolerance, dry skin, constipation, HA, carpal tunnel syndrome, menorrhagia (heavy periods)

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9
Q

PE of hypothyroidism

A

decreased HR, diastolic HTN, thin nails/hair, peripheral edema, puffy eyes/face, delayed DTR’s, palpable thyroid=goiter

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10
Q

labs for hypothyroidism

A

decreased T3 and T4

increased TSH

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11
Q

labs for hyperthyroidism

A

increased T3 and T4

decreased TSH

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12
Q

tx for hypothyroidism

A

usually permanent

lifelong thyroid hormone replacement

synthesis levothyroxine (LT4) is the drug of choice

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13
Q

titration for levothyroxine

A

Q4-6 weeks until normal TSH

start low and go slow

1/2 life is long so it takes a while for thyroid to respond.

need higher dose with pregnancy

check labs Q4-6 weeks (TSH, T4)

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14
Q

factors affecting levothyroxine absorption

A

should take on empty stomach, fasting administration helps w/absorption

take at bedtime seems to help

when pharmacy CHANGES GENERIC BRAND of drug it can AFFECT LEVELS so check labs and adjust dose

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15
Q

dosing considerations for levothyroxine

A

increased TSH= under-replacement (assess for angina, diarrhea, malabsorption)

T4 requirements increase w/ PO estrogen therapy!!- HUGE changes w/pregnancy

don’t take it w/multivitamins or food

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16
Q

hyperthyroidism/thyrotoxicosis

A

hypermetabolic status d/t excess thyroid hormone

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17
Q

most common cause of hyperthyroidism

A

toxic diffuse goitet (GRAVES DISEASE)= autoimmune- IgG antibodies bind to TSH receptors and release of thyroid hormone

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18
Q

other causes of hyperthyroidism

A

toxic adenoma or multinodular goiter, silent and subacute thyroiditism, postpartum thyroiditis, iodine-induced

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19
Q

s/s of hyperthyroidism

A

hyperactivity, heat intolerance, weight loss w/increase appetite, goiter, hyperreflexia, A-FIB, tachycardia, diarrhea, hair loss, infertility

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20
Q

eye manifestations of hyperthyroidism

A

retraction of upper lid, lid lag, stare

proptosis, extra-ocular muscle weakness, decreased visual acuity

think of the lady with the crazy eyes

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21
Q

labs for hyperthyroidism

A

decreased TSH, increased T3 and T4

thyroid is pumping out all this thyroid hormone, so the pituitary thinks you don’t nee thyroid hormone so pituitary doesn’t release TSH

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22
Q

classic triad of graves disease

A

hyperthyroidism, ophthalmopathy, dermopathy (skin lesions)

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23
Q

exogenous thyrotoxicosis

A

happens when pt takes too much levothyroxine-suspect in thyrotoxic pt w/out palpable thyroid and suppressed radioiodine study

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24
Q

pharmacologic options for hyperthyroidism

A

thioamides (methimazole and PTU)

iodides (lugol’s solution, saturated solution of potassium iodide (SSKI), potassium iodide tabs)

1-131 radioidine

surgical tx

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25
Q

thioamides

A

methimazole and PTU

1st line treatment for hyperthyroidism

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26
Q

MOA of thioamides

A

inhibit thyroid peroxidase rxns, iodine organification, and conversion of T4 to T3

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27
Q

ADE of thioamides

A

GI s/s, rash, hypothyroidism, serious ADE= rare

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28
Q

iodides MOA

A

inhibits iodine organification and hormone replacement

decreased size and vascularity of thyroid

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29
Q

ADE of iodides

A

rare but do NOT use in pregnancy

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30
Q

I-131 radioidine

A

safe, effective ablative therapy for hyperthyroidism

preferred treatment for adults >21 y.o.

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31
Q

contraindication of I-131

A

CI in pregnancy

may cause transient worsening of hyperthyroidism

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32
Q

surgical treatment of hyperthyroidism

A

quick, effective (especially w/large goiters)

invasive

permanently hypothyroid

may be choice in pregnant pts if they have major SEs from anti-thyroid drugs

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33
Q

symptomatic thyroid therapy w/beta blockers

A

helps control adrenergic s/s (tachycardia, anxiety)

PROPANOLOL inhibits peripheral conversion of T4 to T3 (drug of choice)

caution w/ CHF and asthma

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34
Q

pregnancy considerations for hyper and hypothyroidism

A

hyper- cause is usually graves dx. preferred tx is I-131 prior to pregnancy. PTU during 1st trimester only. BBW- only used for pts that can’t tolerated I-131 or surgery. 2nd trimester=surgery or methimazole

hypo- adequate levothyroxine ESSENTIAL for early fetal brain development!!! that’s why you automatically go up 30% and go up if you need more

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35
Q

amiodarone and thyroid

A

amiodarone contains 37% iodine so it can have multiple effects on thyroid function- hyper or hypo

just know that amiodarone can cause hypo OR hyperthyroidism b/c it contains iodine

need to check TSH regularly if on amiodarone

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36
Q

follow up for thyroid

A

check WBC at intervals in pts taking thioureas or in sore throat or febrile illness

free T4 levels Q2-3 weeks during initial tx

hypothyroidism common mos-years. after I-131 or subtotal thyroidectomy

lifelong clinical f/u w/TSH and free T4 measurements

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37
Q

estrogen

A

metabolic and CV effects

increase blood blotting (why OC increases blood clot risks), decrease resorption rate of bone (why women are protected against osteoporosis until menopause), increase HDL and decreased LDL, helps w/ structure/function of skin and blood vessels in women, and stimulates parts of SNS and production of corticotropin-releasing hormone

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38
Q

progesterone

A

synthetic- used as OC, used for HRT (hormone replacement therapy) to prevent endometrial CA, and helps promote and maintain pregnancy

AEs- increase BP, decrease HDL and bone density, stimulates fat deposition

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39
Q

hormonal contraceptives

A

effect of the estrogen component vs. progestin component

either combo of estrogen and progestin or just progestin alone

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40
Q

MOA of progestin hormonal contraceptives

A

PROGESTINS provide MOST of contraceptive effect

works prior to fertilization to prevent pregnancy

progestins thicken cervical mucus to prevent sperm penetration and slows tubal motility to delay sperm transport and induce endometrial atrophy

progestins block LH to inhibit ovulation!!!

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41
Q

MOA of estrogen hormonal contraceptives

A

estrogen suppresses FSH release from pituitary (helps block LH surge and prevent ovulation)

estrogen’s main role is to stabilize endometrial lining and provide cycle control (why we take OC to regulate pds)

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42
Q

patient evaluation/considerations when choosing contraceptives

A

thorough H&P (and CI), give pt info (risk vs. benefits, ADE’s, efficacy, issues of adherence, temporary/reversible)

OC’s do not prevent STI’s!!!- educate patients on this

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43
Q

categories for OC’s

A

category 1= no restriction

category 2= advantages outweigh risks

**CATEGORY 3= **risks usually outweigh advantages (relative CI’s)

**CATEGORY 4= ABSOLUTE CI’s (unacceptable health risks)- these are important

44
Q

category 3 OC’s

A

PMH breast CA, hx DVT/PE, HTN, smoking <15 cigs/day and >age 35, DM, CVD

don’t give OC’s to someone who smokes and is >35 yo

45
Q

category 4 OC’s

A

<21 days postpartum, current breast CA, hx/current DVT/PE and not on anticoags, thrombogenic mutations, major surgery w/prolonged immobilization, SBP>160/100, SMOKING!, current/hx ischemic heart dx or stroke, complicated valvular deart disease, migraines w/aura, SLE, liver CA, severe cirrhosis, complicated solid organ transplant

46
Q

types of OCP’s

A

monophasic- combination estrogen-progestin tabs taken in CONSTANT DOSE through menstrual cycle

biphasic and triphasic-combination preparations. progestin or estrogen dosage, or both, CHANGES during month (more closely mimics hormonal changes in menstrual cycle)

progestin-only preparations

47
Q

potential non-contraceptive benefits of OCP’s

A

decreased dysfunctional uterine bleeding, decreased amount of blood lost during period, decreased anemia, decreased s/s of benign cystic breast dx, decrease in functional ovarian cysts, decreased PID and ectopic pregnancy, decreased acne, prevents ovarian CA and endometrial CA

48
Q

estrogen common and serious ADE

A

common: N/V, vaginal bleeding, breast tenderness, HA/migraine, increased BP, edema, gallbladder dx, mood changes, melasma/chloasma, acne/rash
serious: DVT/PE, MI/stroke, HTN, pancreatitis, anaphylaxis, ocular lesions/retinal thrombosis

49
Q

two components of combination contraceptives (CHC)

A

synthetic estrogen= ethinyl estradiol (EE)= most common

synthetic progestins= numerous formations

50
Q

monophasic agents and concept of extended cycle agents

A

SAME amount of estrogen and progestin for 21 days followed by placebo for 7 days

51
Q

multiphasic agents and concept of extended cycle agents

A

VARIABLE amounts of estrogen and progestin for 21 days followed by placebo for 7 days

52
Q

extended-cycle formations and concept of extended cycle agents

A

decreased frequency of menses to Q3 months (less periods/year)

53
Q

yasmin and yaz

A

monophasic or CHC (EE+drospirenone)

54
Q

drospirenon

A

newer progestin derived from spironolactone

anti-androgenic and anti-mineralcorticoid activity

55
Q

benefits of spironolactone analog formulations (drospirenone and yasmin, yaz)

A

decreased water retention and anti-androgen effects (good for hirsutism and acne)

56
Q

disadvantages of spironolactone analog formulations (drospirenone and yazmin, yaz)

A

increased risk of thrombosis (more so than others), caution in renal/hepatic dx, caution w/ other meds that increase K+ levels

57
Q

contraindications of spironolactone analong formulations (drospirenone and yazmin, yaz)

A

renal/adrenal insufficiency, hepatic dysfunction, hx DVT/PE

BBW: smoking and CV events!!!

58
Q

initiation of contraceptives

A
  1. sunday start (most popular)- **start pill on 1st sunday after menses begins
  2. start on 1st day of menses
  3. start on day 5 after onset of menses (5th day after cycle begins)

use backup method for at least 7 days after initiation!

59
Q

effectiveness of OCP can be decreased by drug interactions that do what?

A

interfere w/ GI absorption, increase intestinal motility by altering bacteriologic flora, altered metabolism, excretion/ binding of OCPs

lower the dose- lower the efficacy

ex: antiepileptics, antimicrobial interactions

educate pts regarding use of backup methods- especially if breakthrough bleeding

60
Q

ADE’s of high estrogen OCP

A

nausea, breast pain, increased blood pressure, HA, bloating

61
Q

ADE’s of low estrogen OCP

A

early cycle breakthrough bleeding, hypomenorrhea

62
Q

ADE’s of high progestin OCP

A

fatigue, irritability, breast tenderness, HA

63
Q

ADE’s of high androgen OCP

A

weight gain, acne, oily skin, increased LDL, decreased libido

64
Q

progesterone contraceptives

A

LT injectable contraception

“mini pill”

progestin implant (nexplanon-etonogestrel)

65
Q

LT injectable contraception

A

depo-provera- given Q12 weeks

BBW: risk of loss of BMD (bone mineral density) in use >2 years

ADE: irregular bleeding, breast tenderness, weight gain

may take up to 12 months for fertility to return

66
Q

“mini pill”

A

progestin only

not as effective as other pills we talked about

take a real pill (no placebo) every day

benefits: can be used if estrogen intolerance or CI. can be used during breastfeeding.
risks: MUCH LESS EFFECTIVE!!

**must be taken at EXACT SAME TIME EVERYDAY( even 3 hours- need backup BC method)

67
Q

progestin implant (nexplanon)

A

ADE: irregular menstrual bleeding, HA, vaginitis, weight gain, acne, drug interactions/potent CYP450 inducers

68
Q

vaginal ring (nuvaring)

A

releases over period of 3 weeks

new ring inserted on same day of the week as the last cycle

use: pt inserts/removes ring

when backup contraceptives need: if expelled>3 hours

ADE: similar ADE and CI like other CHC; other=vaginitis, vaginal discomfort, foreign body sensation, ring expulsion

69
Q

IUD

A

3 devices available: levonorgestrel (mirena, skyla) and copper (paragard)

benefits: efficacy>99%, no adherence issues, LT contraception, return to fertility w/in 30 days

70
Q

MOA of IUD

A

inhibit sperm migration, damage to non-fertilized and fertilized ovum, and disrupt ovum transport

progestin containing (mirena and skyla) have added effects of thickened cervical mucus and endometrial suppression

71
Q

CI of IUD

A

PID, active STI, un-dx abnormal vaginal bleeding, GU malignancy, uterine anomalies or fibroids, allergy to IUD components

72
Q

ADE of IUD

A

insertion-related complications, menstrual irregularities, expulsion, PID

73
Q

paragard IUD

A

increased menstrual blood flow and dysmenorrhea

can be in place 10 years

74
Q

mirena IUD

A

decrease in dose over time

can be in place 5 years

75
Q

skyla IUD

A

left in place 3 years

76
Q

levonorgestrel IUD’s produce local effects

A

endometrium suppression

decreased menstrual blood loss

mirena- indication for menorrhagia

increased spotting initial 6 months

77
Q

transdermal patch- ortho evra (CHC)

A

advantages: convenient, increased adherence. patch applied weekly x3 weeks. 4th week- no patch.

apply to abdomen, butt, upper torso, upper arm on 1st day of menses

if patch is detached>24 hours, start new 4 week cycle and use backup method for 7 days

ADE: like other CHC and increased risk of DVT/PE d/t increased estrogen exposure. skin irritation and decreased efficacy if BMI>35

78
Q

emergency contraception (plan B)

A

how it works: need to take w/in 72 hours

ADE: N/V, HA, dizziness, breast tenderness, abd and leg cramps

give w/ antiemetic b/c it won’t work if they throw the pill up

79
Q

monitoring needed for CHC users

A

BP annually in all CHC users

glucose levels in pts w/ hx glucose intolerance/DM

cytologic screening annually.

assess regularly for ADE

evaluate DMPA users Q3 months for: weight gain, menstrual cycle disturbances, STI risks

monitor nexplanon users annually for: menstrual cycle disturbances, weight gain, local inflammation/infection at implant site, acne, breast tenderness, HA, hair loss

80
Q

patient education for contraceptives

A

take pill w/a daily ritual to increase compliance.

advise patients that neither OC tabs nor DMPA protect against STDs

if pt misses 1 or 2 ombo OC tabs, take 1 tab as soon as possible followed by 1 tablet twice daily until missed tablets have been taken.

pts that miss >2 need a backup contraceptive

progestin-only have to take at same time every day (need back up if late >3 hours)

inform HCP if they get pregnant/plan to become pregnant

81
Q

endocrine pharmacologic application of hormone replacement vs. antagonists

A

REPLACEMENT therapy for hormone DEFICIENCY

ANTAGONISTS for dx caused by EXCESS production of pituitary hormones

dx tools to ID endocrine abnormalities

82
Q

growth hormone (GH)

A

importance: needed for normal G&D through adolescence and regulator of lipid and carb metabolism throughout adulthood

GH def. tx; somatotropin (recombinant form of GH) used for GH def. in kids and adults. tx children w/ genetic dx r/t short status (turner syndrome and prader-willi syndrome)

GH excess tx: somatostatin analogs like octreotide and lanreotide

83
Q

prolactin

A

principal hormone for lactation

hyperprolactemia- increase prolactin which inhibits GnRH secretion- s/s of amennorhea and galactorhhea in women, infertility, decreased libido in men

84
Q

hyperprolacetmia causes and treatment

A

causes: meds (SSRI’s, haldol, reglan, dopamine antagonists) or porlactin-secreting adenomas

Tx: dopamine agonist (bronocriptine (parlodel))

85
Q

vasopressin/ADH

A

effects: secreted in response to increase plasma osmolality or DECREASED BP

antidiuretic and vasopressor properties

deficiency- DI

86
Q

oxytocin

A

effect: stimulates uterine and breast contractions

clinical uses: induction of labor. control of postpartum hemorrhage.

87
Q

glucocorticoids/mineral-corticoids

A

glucocorticoid secretion from adrenal cortex is stimulated by adrenocortioctropic hormone (ACTH) or corticotropin that is released from the anterior pituitary in response to the hypothalamic mediated release of corticotropin-releasing hormone (CRH)

corticosteroids are steroid hormones made by the adrenal cortex

glucocorticoids-important effects on metabolism, catabolism, immune responses, and inflammation

mineral corticoids- regulate Na+ and K+ reabsorption in kidney’s collecting tubules

88
Q

metabolic effects of glucocorticoids

A

stimulate gluconeogenesis and glycogen synthesis which increase BG.

regulates carb, protein, and fat metabolism.

releases AA’s by muscle catabolism.

inhibits peripheral glucose uptake (insulin resistance)

89
Q

immunosuppressive effects of glucocorticoids

A

inhibit cell-mediated immunologic function.

profound suppression of inflammatory process (increased neutrophils, decreased lymphocytes, eosinophils, basophils, and monocytes)

migration of leukocytes inhibited.

does not interfere w/development of normal acquired immunity.

90
Q

catabolic effects of glucocorticoids

A

effects muscle, lymph and connective tissue, skin, bone which decreases muscle mass, thinning skin, osteoporosis, limited growth in kids

91
Q

other effects of glucocorticoids

A

CNS (behavior), gastric acid secretion, CV integrity and contractility

92
Q

cortisol

A

it follows circadian rhythm that is REGULATED by pulses of ACTH (peak in early morning and after meals)

93
Q

clinical uses of corticosteroids

A

adrenal disorders: dx and tx adrenal dysfunction (dexamethasone suppression test) and replacement in adrenal insufficiency (acute and or chronic)

non adrenal disorders: uses r/t ability to suppress inflammatory and immune responses. stimulates lung maturation in fetus.

94
Q

how corticosteroids are used for diagnosis of adrenal disorders

A

short cosyntropin-stimulation test: dx addison’s dx give a dose of cosyntropin (syntheic ACTH) IV or IM then measure plasma cortisol at 0, 30, and 60 min. ** look for increase in cortisol level to r/o dx**

dexamethasone suppression test: dx cushing’s dx given PO dex at night then measure plasma cortisol in AM >5 mcg/dL= cushing’s

95
Q

adrenocortical insufficiency (addison’s dx) s/s

A

fatigue, weakness, irritability, depression, anorexia, weight loss, dizziness, orthostatic hypotension, N/V/D, abdominal cramps, creased Na+ and BG, increased K+, anemia, hyperpigmentation of skin, mucosa, craves Na+, pallor, amenorrhea, decreased libido, impotence, HA, vision s/s, scant axillary/pubic hair, small testes, prepubertal growth deficiency, delayed puberty

(think of cartoon of old lady slunched over)

96
Q

tx of addison’s dx

A

don’t have enough cortisol so replace cortisol

drug of choice=hydrocortisone (bc it has glucocorticoid AND mineralcorticoid activity)

don’t forget stress dosing!!

pts need to carry a card/wear ID bracelet (b/c if they end up in the ED b/c they’re very sick, they need stress dosing of steroids)

if they don’t get their stress dose then they will have an adrenal crisis

adrenal crisis: parenteral glucocorticoids

97
Q

ADE of treatment for addison’s disease (glucocorticoids)

A

increase BG, glycosuria, Na+ retention w/ edema/HTN, decreased K+, peptic ulcer, osteoporosis, hidden infections

98
Q

glucocorticoids: indications that are non-adrenal related

A

allergic rxns

asthma exacerbation

collagen-vascular disorders (ex. SLE)

eye dx

systemic inflammation

hematologic disorders

joint injections w/ steroids for inflammation

antiemetic effects while on chemo/anesthesia

organ transplant

renal disorders like nephrotic syndrome

99
Q

causes of hypercortisolism (adrenal hyperactivity- cushing’s syndrome)

A

cushing’s syndrome (ACTH-secretin pituitary adenoma) or iatrogenic (glucorticoids administered in high doses in tx of nonendocrine disorders)

100
Q

s/s of cushing’s syndrome

A

enlarged supraclavicular fat pads

osteoporosis

HYPERTENSION

muscle in the extremities

poor wound healing

moon face

dark facial hair (women)

cardiac hypertrophy

obesity

abdominal striae

amenorrhea (women)

(think of the fat guy)

101
Q

dx of cushing’s dynrome

A

dexamethasone suppression test: give PO dex at night then measure plasma cortisol in AM

> 5mcg/dL= cushing’s

102
Q

treatment of cushing’s

A

surgically removed ACTH producing tumor/irradiate pituitary tumor

drugs are usually used pre-op or as adjunct therapy post op

4 classes of agents: steroidogenesis inhibitors, adrenolytic agents, neuromodulators of ACTH release, glucocorticoid receptor blocking agents

synthesis inhibitors (ketoconazole) and antagonists (mifepristone) given

FYI: side effects of giving exogenous corticosteroids look like typical findings in cushing syndrome

103
Q

corticosteroid weaning

A

abrupt cessation of glucocorticoids leads to s/s of adrenal insufficiency

wean anyone on dose comparable w/ 20 mg prednisone a day for >3 weeks, anyone on an evening/bedtime dose of >5 mg of prednisone for > a few weeks, anyone w/ a cushing like appearance

consider age, comorbids, likelihood of flare of underlying illness, psych factors, and duration of previous use of glucocrticoids

goal of tapering: generally, dose decrease of 10-20%

104
Q

mineralcorticoids

A

effect of aldosterone

aldosterone= major natural mineralcorticoid

promotes reabsoprtion of Na+ from renal tubules

105
Q

hyperaldosteronism

A

excess levels of aldosterone (produced by tumors/overdosage w/synthetic mineralcorticoids), decreased K+, metaboic alkalosis, increase plasma volume, HTN

106
Q

fludrocortisone

A

potent steroid w/glucocorticoid and mineralcorticoid activity

often not needed in tx of adrenal insufficiency

also used for orthostatic hypotension

Pharmacology (3 decks)

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