Exam #4- Endocrinology Flashcards
(106 cards)
1
Q
thyroid
A
produces T4 and T3 regulated by hypothalamic-pituitary-thyroid axis
regulates normal G&D of body temp and energy levels
2
Q
thyroid autoimmune disorders
A
thyrotoxicosis (hyper) or hypothyroidism
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
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
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
6
Q
secondary hypothyroidism
A
pituitary is not doing it’s job
its not making enough TSH (decreased, TSH), low T4
7
Q
causes of hypothyroidism
A
hashimoto thyroiditis (most common cause)
drugs (lithium, amiodarone)
iodine deficiency
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)
9
Q
PE of hypothyroidism
A
decreased HR, diastolic HTN, thin nails/hair, peripheral edema, puffy eyes/face, delayed DTR’s, palpable thyroid=goiter
10
Q
labs for hypothyroidism
A
decreased T3 and T4
increased TSH
11
Q
labs for hyperthyroidism
A
increased T3 and T4
decreased TSH
12
Q
tx for hypothyroidism
A
usually permanent
lifelong thyroid hormone replacement
synthesis levothyroxine (LT4) is the drug of choice
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)
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
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
16
Q
hyperthyroidism/thyrotoxicosis
A
hypermetabolic status d/t excess thyroid hormone
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
18
Q
other causes of hyperthyroidism
A
toxic adenoma or multinodular goiter, silent and subacute thyroiditism, postpartum thyroiditis, iodine-induced
19
Q
s/s of hyperthyroidism
A
hyperactivity, heat intolerance, weight loss w/increase appetite, goiter, hyperreflexia, A-FIB, tachycardia, diarrhea, hair loss, infertility
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
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
22
Q
classic triad of graves disease
A
hyperthyroidism, ophthalmopathy, dermopathy (skin lesions)
23
Q
exogenous thyrotoxicosis
A
happens when pt takes too much levothyroxine-suspect in thyrotoxic pt w/out palpable thyroid and suppressed radioiodine study
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
25
thioamides
methimazole and PTU
1st line treatment for hyperthyroidism
26
MOA of thioamides
inhibit thyroid peroxidase rxns, iodine organification, and conversion of T4 to T3
27
ADE of thioamides
GI s/s, rash, hypothyroidism, serious ADE= rare
28
iodides MOA
inhibits iodine organification and hormone replacement
decreased size and vascularity of thyroid
29
ADE of iodides
rare but do NOT use in pregnancy
30
I-131 radioidine
safe, effective ablative therapy for hyperthyroidism
preferred treatment for adults >21 y.o.
31
contraindication of I-131
CI in pregnancy
may cause transient worsening of hyperthyroidism
32
surgical treatment of hyperthyroidism
quick, effective (especially w/large goiters)
invasive
permanently hypothyroid
may be choice in pregnant pts if they have major SEs from anti-thyroid drugs
33
symptomatic thyroid therapy w/beta blockers
helps control adrenergic s/s (tachycardia, anxiety)
**PROPANOLOL** inhibits peripheral conversion of T4 to T3 (drug of choice)
**caution w/ CHF and asthma**
34
pregnancy considerations for hyper and hypothyroidism
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
35
amiodarone and thyroid
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
36
follow up for thyroid
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
37
estrogen
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
38
progesterone
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
39
hormonal contraceptives
effect of the estrogen component vs. progestin component
either combo of estrogen and progestin or just progestin alone
40
MOA of progestin hormonal contraceptives
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!!!**
41
MOA of estrogen hormonal contraceptives
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)
42
patient evaluation/considerations when choosing contraceptives
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**
43
categories for OC's
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
category 3 OC's
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
category 4 OC's
<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
types of OCP's
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
potential non-contraceptive benefits of OCP's
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
estrogen common and serious ADE
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
two components of combination contraceptives (CHC)
synthetic estrogen= ethinyl estradiol (EE)= most common
synthetic progestins= numerous formations
50
monophasic agents and concept of extended cycle agents
SAME amount of estrogen and progestin for 21 days followed by placebo for 7 days
51
multiphasic agents and concept of extended cycle agents
VARIABLE amounts of estrogen and progestin for 21 days followed by placebo for 7 days
52
extended-cycle formations and concept of extended cycle agents
decreased frequency of menses to Q3 months (less periods/year)
53
yasmin and yaz
monophasic or CHC (EE+drospirenone)
54
drospirenon
newer progestin derived from spironolactone
anti-androgenic and anti-mineralcorticoid activity
55
benefits of spironolactone analog formulations (drospirenone and yasmin, yaz)
decreased water retention and anti-androgen effects (good for hirsutism and acne)
56
disadvantages of spironolactone analog formulations (drospirenone and yazmin, yaz)
increased risk of thrombosis (more so than others), caution in renal/hepatic dx, caution w/ other meds that increase K+ levels
57
contraindications of spironolactone analong formulations (drospirenone and yazmin, yaz)
renal/adrenal insufficiency, hepatic dysfunction, hx DVT/PE
BBW: smoking and CV events!!!
58
initiation of contraceptives
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
effectiveness of OCP can be decreased by drug interactions that do what?
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
ADE's of high estrogen OCP
nausea, breast pain, increased blood pressure, HA, bloating
61
ADE's of low estrogen OCP
early cycle breakthrough bleeding, hypomenorrhea
62
ADE's of high progestin OCP
fatigue, irritability, breast tenderness, HA
63
ADE's of high androgen OCP
weight gain, acne, oily skin, increased LDL, decreased libido
64
progesterone contraceptives
LT injectable contraception
"mini pill"
progestin implant (nexplanon-etonogestrel)
65
LT injectable contraception
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
"mini pill"
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
progestin implant (nexplanon)
ADE: irregular menstrual bleeding, HA, vaginitis, weight gain, acne, drug interactions/potent CYP450 inducers
68
vaginal ring (nuvaring)
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
IUD
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
MOA of IUD
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
CI of IUD
PID, active STI, un-dx abnormal vaginal bleeding, GU malignancy, uterine anomalies or fibroids, allergy to IUD components
72
ADE of IUD
insertion-related complications, menstrual irregularities, expulsion, PID
73
paragard IUD
increased menstrual blood flow and dysmenorrhea
can be in place 10 years
74
mirena IUD
decrease in dose over time
can be in place 5 years
75
skyla IUD
left in place 3 years
76
levonorgestrel IUD's produce local effects
endometrium suppression
decreased menstrual blood loss
mirena- indication for menorrhagia
increased spotting initial 6 months
77
transdermal patch- ortho evra (CHC)
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
emergency contraception (plan B)
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
monitoring needed for CHC users
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
patient education for contraceptives
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
endocrine pharmacologic application of hormone replacement vs. antagonists
REPLACEMENT therapy for hormone DEFICIENCY
ANTAGONISTS for dx caused by EXCESS production of pituitary hormones
dx tools to ID endocrine abnormalities
82
growth hormone (GH)
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
prolactin
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
hyperprolacetmia causes and treatment
causes: meds (SSRI's, haldol, reglan, dopamine antagonists) or porlactin-secreting adenomas
Tx: dopamine agonist (bronocriptine (parlodel))
85
vasopressin/ADH
effects: secreted in response to increase plasma osmolality or DECREASED BP
antidiuretic and vasopressor properties
deficiency- DI
86
oxytocin
effect: stimulates uterine and breast contractions
clinical uses: induction of labor. control of postpartum hemorrhage.
87
glucocorticoids/mineral-corticoids
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
metabolic effects of glucocorticoids
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
immunosuppressive effects of glucocorticoids
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
catabolic effects of glucocorticoids
effects muscle, lymph and connective tissue, skin, bone which decreases muscle mass, thinning skin, osteoporosis, limited growth in kids
91
other effects of glucocorticoids
CNS (behavior), gastric acid secretion, CV integrity and contractility
92
cortisol
it **follows circadian rhythm** that is REGULATED by **pulses of ACTH** (peak in early morning and after meals)
93
clinical uses of corticosteroids
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
how corticosteroids are used for diagnosis of adrenal disorders
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
adrenocortical insufficiency (addison's dx) s/s
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
tx of addison's dx
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
ADE of treatment for addison's disease (glucocorticoids)
increase BG, glycosuria, Na+ retention w/ edema/HTN, decreased K+, peptic ulcer, osteoporosis, hidden infections
98
glucocorticoids: indications that are non-adrenal related
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
causes of hypercortisolism (adrenal hyperactivity- cushing's syndrome)
cushing's syndrome (ACTH-secretin pituitary adenoma) or iatrogenic (glucorticoids administered in high doses in tx of nonendocrine disorders)
100
s/s of cushing's syndrome
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
dx of cushing's dynrome
dexamethasone suppression test: give PO dex at night then measure plasma cortisol in AM
>5mcg/dL= cushing's
102
treatment of cushing's
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
corticosteroid weaning
**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
mineralcorticoids
effect of aldosterone
aldosterone= major natural mineralcorticoid
promotes reabsoprtion of Na+ from renal tubules
105
hyperaldosteronism
excess levels of aldosterone (produced by tumors/overdosage w/synthetic mineralcorticoids), decreased K+, metaboic alkalosis, increase plasma volume, HTN
106
fludrocortisone
potent steroid w/glucocorticoid and mineralcorticoid activity
often not needed in tx of adrenal insufficiency
also used for orthostatic hypotension
