• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/183

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

183 Cards in this Set

  • Front
  • Back
effects of thyroid hormones
-growth, development, function, and maintenance of all body tissues
-critical for nervous, skeletal, and reproductive tissues
-can lead to mental retardation and dawarfism if thyroid deprivation occurs early in life
adverse effects of overactive thyroid hormone
resemble those of increased sympthetic nervous system activity
(but catecholamine levels are normal)
manifestations of hyperthyroidism
skin (warm, moist, skin)

eyes (retraction of upper lid, wide stare)

GI (inc appetite and inc bowel movement)

CNS (nervousness)

Metabolic (inc BMR, hyperglycemia, dec cholesterol)
manifestations of hypothyroidism
skin (pale, cool, puffy)

Eyes (drooping of eyelids, periorbital edema)

GI (dec appetite, dec bowel movements)

CNS (lethargy, slowed mental process)

Metabolic (dec BMR, increased cholesterol)
2 types of anti-thyroid medication
-propylthiouracil (PTU)

-Methimazole (Tapazole)
Tests of the HPT axis
TSH
TRH
tests of thyroid gland function
radioactive iodine uptake

thyroid scan
types of hypothyroidism
Primary
-Hashimoto's thyroidititis
-iatrogenic
-iodine deficiency
-enzymatic deficit in the thyroid
-ingestion of goitrogens

Secondary
-pituitary disease
-hypothalamic disease
myxedma coma
a medical emergency that is precipitated by stress

clinical presentation
- progessive stupor, paranoid psychosis, seizures

physical findings
-puffy face/ eyelids, cardiomegaly
4 goals of thyroid therapy
1. restore thyroid hormone in tissue
2. Provide symptomatic relief
3. Prevent neurologic deficits
4. Reverse biochemical abnormalities
thyroid hormone products
1. desiccated thyroid
2. liothyronine
3. Liotrix
4. Levothyroxine
thyroid needs for preggers pts
inc need for T4
increased TBG (thyroxine-binding globulin)
45% inc in baseline T4
4 reasons for Monthly monitoring of TSH
1. therapy of myxedema - aggressive therapy even has high mortality rates 60-70% are common
2. thyroid hormone replacement
3. maintenance of vital function
4. elimination of precipitating factors
gonadal hormones usage
-replacement therapy
-contraception
-management of menopausal symptoms
-osteoporosis

Antagonists are effective in cancer chemotherapy
Estrogens
-estradiol
-estone and estriol
-ethinyl estradiol
mechanism of action of estrogens
2 estrogen subtypes α and β
thioamides
PTU and Tapazole
-prevent thyroid hormone (T3 and T4) synthesis by inhibiting THYROID PEROXIDASE
side effects of thioamides
-thioamide toxicity that causes maculopapular pruritic rash with fever in 3-12% of pts

-vasculitis (rare)
estradiol
an estrogen that is naturally produced by the ovary and is the most potent estrogen
estrone
formed in the liver and adrenal gland
1/10 the potency of estradiol
estriol
formed in the liver and adrenal gland
1/10 the potency of estradiol
ethinyl estradiol
synthetic form of estrogen that has LESS first pass metabolism and is more effective at lower doses
alpha estrogen domain
the classic domain
Beta estrogen subtype
contains the repressor domain
American college of ObGYN statement about HRT
hormone replacement therapy's risks outweigh the benefits

-should only be used at the LOWEST dose for the SHORTEST amount of time

-contains substantially less estrogen than oral contraceptives
when should HRT be prescribed
vasomotor symptoms
vaginal atrophy
estrogen use in postmenopausal hormone therapy
1. hot flashes
2. Risk of osteoporosis
3. for women who have NOT had a hysterectomy - ALWAYS add a progestin to the estrogen (reduces risk of endometrial carcinoma)
4. women who HAVE had a hysterectomy estrogen without progestin is indicated
osteoporosis treatment
estrogen can effectively treat osteoporosis
-so can aldendronate
estrogen use in primary hypogonadism
estrogen therapy in combo with progestins can stimulate development of 2* sex characteristics in young women with hypogonadism
2 synthetic estrogen analogs
1. ethinyl estradiol
2. mestranol
Metabolism of estrogens
-reduced 1st pass metabolism
-may be given via transdermal patch, intravaginally, or by injection to reduce first pass metabolism
side effects of estrogens
N/V = most common
thromboembolism, MI, breast and endometrial cancer
selective estrogen receptor modulators (SERM)
reserved for compounds that display selective agonism or antagonism to a tissue type
3 drugs that are selective estrogen receptor modulators
tamoxifen
raloxifene
clomiphene
mechanism of action for tamoxifen
competes with the natural hormone for the estrogen receptor
usage of tamoxifen
-estrogen antagonist in breast cancer
-partial agonist in the uterus for endometrial hyperplasia
-used for palliative care in advanced breast cancer and can also cause regression of breast cancer tumors
side effects of tamoxifen
hot flashes
N/V
-hyperplasia and malignancies due to the estrogenic activity in the endometrium
use of raloxifene
the preventive tx of osteoporosis
how does raloxifene prevent osteoporosis
-decreases bone resoprtion and overall bone turnover leading to an inc in bone density and dec in vertebral fractures
benefits of using raloxifene
-second gen SERM
-little to no effect on the endometrium
- possible to reduce the incidence of breast cancer in postmenopausal women
side effects of raloxifene
inc risk of DVT, PE, and retinal-vein thrombosis
clomiphene
-inc the secretion of gonadotropin-releasing hormone and causes stimulation of ovulation
role of progestin
-promotes the secretory endometrium that can accommodate implantation of a newly forming embryo
-the 2nd half of the menstrual cycle inhibits further ovulation bc of high levels of progesterone
3 major clinical uses of progestins
1. rectify hormonal deficiency
2. contraception
3. control of dysfunctional uterine bleeding
4 types of synthetic progestins used in contraceptives
** they are more stable to first pass metabolism bc they are synthetic

1. medroxyprogesterone acetate
2. hydroxyprogesterone acetate
3. norethindrone
4. norgestrel
norethindrone and norgestrel
AKA norestosterone progestins bc they are similar to androgen structurally
side effects of progestins
1. edema, depression, hirstism, and weight gain
2. norethindrone and norgestrel can also increase LDL/HDL ratio
mifepristone
an antiprogestin that is a progestin antagonist
-used in early pregnancy to induce an abortion
most common intervention to prevent pregnancy
interference with ovulation
combination birth control pills
usually combine estrogen and progestin

-have a constant low dose of estrogen for 21 days COMBINED with
-a low increasing dose of progestin given over 3 seven day periods
triphasic regimen
-have a constant low dose of estrogen for 21 days COMBINED with
-a low increasing dose of progestin given over 3 seven day periods
3 types of combination BCPs
ethinyl estradiol
mestranol
norethindrone
progestin pills
aka the mini-pill and contains progestin only but it is less effective (making it have limited acceptance bc of inc risk of pregnancy)
2 types of progestin only pills
1. norethindrone
2. norgestrel
progestin implants
subdermal capsules that contain LEVONORGESTREL
-offers long term contraception-- 5 years
- 6 capsules are placed subcutaneously in the upper arm
-cheaper and very reliable bc they don't depend on pt compliance
-totally reversible
side effect of progestin implants
irregular menstrual bleeding and headaches
postcoital contraception
morning after pill- take within 72 hours
OR
2 doses of ethinyl estradiol PLUS norgestrel within 72 hours followed by another 2 doses 12 hours later
OR
Mifepristone
mechanism of action of the BCP
- inhibits ovulation bc of the combination of estrogen and progestin
- estrogen provides a negative feedback of the release of LH and FSH by the pituitary (preventing ovulation)
- Progestin stimulates normal bleeding at the end of the menstrual cycle and thickens the cervical mucus preventing access by sperm
side effects of the BCP
the estrogen causes adverse effects
thromboembolism is the most serious
HTN, MI, inc risks in women over 35 who smoke
positives effect of BCP
decreases the incidence of endometrial and ovarian cancer
serum lipid changes on BCP
-estrogen increases HDL
-progestin lowers HDL

norgestrel - causes greatest inc in the LDL/HDL ratio

estrogen-dominant preparations are best for people with high cholesterol
androgens general info
-steroids that have anabolic or masculinizing effects in both males and females

-synthetic modifications cause solubility and susceptibility change during enzymatic breakdown
therapeutic use for androgens
hypogonadism
senile osteoporosis
skeletal growth in prepubertal boys with dwarfism
endometriosis
hypogonadism
caused by Leydig cell dysfunction or failure of the hypothalamic pituitary unit

-treatment androgen therapy
anabolic steroids treatment
treats senile osteoporosis and severe burns
danazol
a mild androgen that treats endometriosis
side effects of androgens
Females-masculinization: acne, facial hair, voice change, and contraindicated during pregnancy

Males- stimulates growth of the prostate

-increase LDL and lower HDL
when is testosterone contraindicated?
during pregnancy bc it virilizes the female fetus
types of anabolic steroids
DHEA
Nandrolone
Stanozolol
side effects of anabolic steroids
-premature closure of the epiphysis of the long bones

-reduction of testicular size
-increased aggression "roid rage"
antiandrogens
interferes with the synthesis of androgens by blocking their receptors
4 types of antiandrogens
1. finasteride
2. cyproterone
3. flutamide
4. bicalutamide
finasteride
treats BPH
cyproterone and flutamide
act as competitive inhibitors of androgens at the target cell
cyperterone
treats hirsutism in females
bicalutamide
treats metastatic prostate cancer
function of the cortex
synthesizes and secretes adrenocorticoids (glucocorticoids and mineralocorticoids) AND adrenal androgens
function of the medulla
secretes epi
function of the outer zona glomerulosa
produces mineralocortioids (aldosterone)
aldosterone
regulated by the renin-angiotensin system
function of the middle zona fasciculata
synthesizes glucocorticoids (cortisol)
function of the inner zona reticularis
secretes adrenal androgens (dehydroepiandosterone)
function of glucocorticoids
feedback inhibitors of corticotrophin and CRH (corticotrophin releasing hormone) secretion
where are glucocorticoid receptors located
distributed to excretory organs
-kidneys, salivary and sweat glands
glucocorticoids
ie cortisol
cortisol
principal human gluccocorticoid
-produced diurnally (peak in early morning and a smaller peak in late afternoon)
6 major functions of glucocorticoids
-promotes normal intermediary metabolism (favors gluconeogensis by increasing AA uptake by the liver and kidney)

increases resistance to stress- providing the body with energy

cause an inc in BP bc of vasoconstriction of small vessels (caused by adrenergic stimuli)

Alters blood cell levels in plasma

anti-inflammatory action- by inhibiting phospholipase A

interferes with mast cell degranulation decreasing histamine reslease and capillary permeability
what do glucocorticoid stimulate
protein catabolism (break down)
what results from glucocorticoid insufficiency
hypOglycemia
phospholipase A
blocks the release of arachidonic acid
arachidonic acid
the precursor of the prostaglandins and leukotrienes
what results from the altered blood cell levels in plasma from glucocorticoids
dec in eosinos, basos, monos, lymphos, by redistributing them to the lymphoid tissue thus compromising the ability to fight infection

inc in hemoglobin, RBCs, platelets, and PMNs
what results form the anti-inflammatory action of glucocorticoids
anti-inflammatory response is the most therapeutic property by reduces immunity bc lymphos and monos were redistributed to the lymphoid tissue

-phospholipase A is inhibited
what type of action does cortisol have
cortisol is a glucocortioid and it has an anti-inflammatory action bc it suppresses immunity
mineralocorticoids function
a common mineralocorticoid is ALDOESTERONE
- it causes reabsorption of sodium, bicarb, water
-inc elimination of K and H in the urine
side effects of elevated aldosterone (mineralocorticoid)
inc blood volume
inc BP
alkalosis
HYPOkalemia
tx of HYPERaldosteronism
spironolactone
therapeutic uses for adrenocorticosteroids
1. anti-inflammatory agents
2. treatment of Primary adrenocortical insufficiency aka Addison's disease
3. treatment in 2* or 3* adrenocortical insufficiency
4. diagnosis of Cushings
5. glucocorticoids reduce redness, swelling, heat and tenderness
6. tx of bronchial asthma, allergic rhinitis, and drug, serum, and transfusion allergic rxns
hydrocortisone
-identical to natural cortisol

treats Addison's, adrenocortical insufficiency, and 2* or 3* adrenocortical insufficiency
fludrocortisone
a synthetic mineralocorticoid with some glucocorticoid activity which raises mineralocorticoid activity
-may be used with hydrocortisone to treat addison's
diagnosis of Cushings
Dexamethasone test

-dexamethasone suppresses cortisol release if it is pituitary-dependent Cushings

-it will NOT suppress glucocorticoid release from adrenal tumors (so it can differential what's actually causing the problem)
what is a frequent cause of Cushings
high dose of glucocorticoids for a long period of time
how do glucocorticoids reduce inflammation
causes eosinos, basos, monos, and lymphos to be redistributed to the lympoid tissue decreasing the number of circulating lymphos and macros

-leads to decreased histamine permeability and interference of mast cell degranulation

-dec production of prostaglandin and leukotrienes bc glucocorticoids inhibit phospholipase A so no arachidonic acid can be produced
beclomethasone administration
inhalation so there is a dec in side effects

-reduces need for oral steroids
beclomethasone usage
bronchial asthma
allergic rhinitis
drug, serum or transfusion allergic rxn
triamcinolone
inhalable corticoid steroid that is used for
bronchial asthma
allergic rhinitis
drug, serum or transfusion allergic rxn
tx for respiratory distress syndrome
beclomethasone administered IM 48 and 24 hrs before birth

-fetal CORTISOL regulates lung maturation
side effects of adrenocorticoids
osteoporosis that is NOT prevented by alternative dosing
pts should be prescribed with a bisphosphonate if they are on long-term oral glucocorticoid therapy

-cataracts
-hyperglycemia
-hypokalemia

acute adrenal insuffiency syndrome if the drug is not tapered
method to reduce the change of HPA axis suppression
alternate-day administration of glucocortiods if pt is taking large extended doses
withdrawal of corticosteroids
drug must be TAPERED
-could cause acute adrenal insufficiency syndrome that can be lethal
inhibitors of adrenocorticoid biosynthesis
1. metyrapone
2. dexamethasoze
3. tamoxifen
4. aminoglutethimide
5. ketoconazole
6. spironolactone
7. eplerenone
metyrapone
replaced by dexamethasone to test for Cushings

-inhibitor of adrenocorticoid biosynthesis
Tamoxifen (as a inhibitor of adrenocorticoid biosynthesis)
replaced aminoglutethimide for breast cancer tx
ketoconazole
an inhibitor of adrenocorticoid biosynthesis

an antifungal that inhibits gonadal and adrenal steroid hormone synthesis

-treatment for Cushings
treatmetn for Cushings
ketoconazole
eplernone
an inhibitor of adrenocorticoid biosynthesis

binds to mineralocorticoid receptors

-avoids side effects of spironolactone

- can be used as an anti-hypertensive
spironolactone
inhibits sodium absorption by competing with mineralocorticoid receptor

antagonizes aldosterone and testosterone synthesis

treats hyperaldosteronism and hisutism
side effects of spironolactone
hyperkalemia and gynecomastia
which corticosteroid is an antiemetic
dexamethasone
3 causes of peptic ulcer disease
1. H pylori
2. inc hydrochloric acid secretion
3. poor mucosal defense
2 places where peptic ulcers might occur
gastic ulcers
duodenal ulcers
three tests for H pylori infection
1. endoscopy
2. serological testing
3. breath tests for urea
2 methods to eradicate H pylori
triple therapy
quadruple therapy
triple therapy
1. PPI PLUS
2. metronidazole OR amox PLUS
3. clarithromycin
quadruple therapy
1. PPI OR H2-antagonist PLUS
2. tetracycle PLUS
3. metronidazole PLUS
4. bismuth subsalicylate
bismuth salts
cause an increase secretion of mucus leading to inc in protection
gastic acid
secreted by parietal cells
stimulated by Ach, gastrin, and histamine
prostaglandin E2
diminishes gastric acid secretion along with somatosatin
somatostatin
cuases gastric acid secretetion to diminish along with prostaglandin E2
4 types of H2 receptor antagonists
1. cimetidine
2. ranitidine
3. famotidine
4. nazatidine

-less commonly used now bc of PPIs
function of h2 receptor antagonists
inhibits basal, food-stimulated, and nocturnal secretion of gastric acid
what are the actions of h2 receptors antagonists
no effect on h1 receptors
partially inhibit gastic acid secretion by acetylcholine
COMPLETELY inhibit gastic acid secretion by histamine and gastrin
uses for H2 receptor blockers
1. peptic ulcer healing of both duodenal and gastric ulcers
2. 50% of GERD pts feel relief
how do h2 receptor antagonists work
by stopping acid secretion

-symptoms may not be relieved for 45 minutes
cimetidine
h2 receptor antagonist

-inactivated by the livers microsomal MIXED FUNCTION OXYGENASE SYSTEM
-interferes with metabolism of other drugs
-acts as a nonsteroidal antiandrogen
side effects of cimetidine
gynecomastia
galactorrhea
reduced sperm count
-inhibits cytochrome P450
-slows the metabolism of warfarin
ranitidine
h2 receptor antagonist
-long acting and no interference with the livers mixed-function oxygenase system
-does not affect conc of other drugs
nizatidine
h2 receptor antagonist
-eliminated by the kidney
side effects of cimetidine, ranitidine, and nizatiodine
does not include famotidine

-inhibits gastric first pass metabolism of ETHANOL
-ketonazole and other drugs that depend on stromach acid for absorption will not be efficiently absorbed
4 proton pump inhibitors
--prazoles

omeprazole
lansoprazole
rabeprazole
pantoprazole
esomeprazole
use of PPIs
preffered drugs for erosive esophagitis, duodenal ulcer and Zollinger-Ellison syndrome, GERD, ulcer prevention from NSAIDs
action of PPIs
inhibits both basal and gastric acid secretion more than 90%
-acid suppression begins in 1-2 hours
omeprazole
binds to the proton pump of the parietal cell
suppresses the secretion of hydrogen ions into the gastric lumen
***interferes with the oxidation of warfarin
side effects of PPIs
low Vit B12
rare drug interactions
prostaglandins E2
inhibits the secretion of HCl and stimulates secretion of mucus and bicarb

- cytoprotective effect
gastric mucosa
produces prostaglandin E2

-thought that deficiency in prostagladins are involved with development of peptic ulcers
misoprostol
analog of prostaglandin E
-inhibits secretion of HCL and stims secretion of mucus and bicarb (cytoprotective)

-used ONLY for pts at high risk of developing NSAID-induced ulcers aka the elderly
when is misoprostol contraindicated
during pregnancy
3 types of antacids
1. aluminum hydroxide (causes constipation)
2. magnesium hydroxide (causes diarrhea)
3. calcium carbonate (can cause metabolic alkalosis)
calcium carbonate side effect
can cause metabolic alkalosis when it systemically absorbs sodium bicarb

*should NOT be used for long term tx
*can be used as a calcium supplement for osteoporosis
what should you watch for if pt is taking antacids
watch if pt has HTN or CHF bc antacids contain sodium
Mucosal protective agents
-cytoprotective compounds that stimulate the secretion of mucus and bicarb
2 types of mucosal protective agents
1. sucralfate
2. colloidal bismuth
sucralfate
-mucosal protective agent

forms complex gels with epithelial cells and impairs diffusion of HCL and prevents degredation of mucus by pepsin and acid
2 functions of sucralfate
1. stimulates prostagladin, musuc, and bicarb release
2. heals duodenal ulcers
triggers of vomiting
2 brainstem sites
1. chemoreceptor trigger zone
2. vomiting center
chemoreceptor trigger zone
located in the area psotremea that is outside of the blood brain barrier
vomiting center
located in the lateral reticular formation of the medulla
-coordinates motor mechanisms of vomiting
-responds to the afferent input from the vestibular system (functions in motion sickness)
vomiting activating neuroreceptors
1. dopamine receptor type 2
2. serotonin type 3 (5-HT3)
13 antiemetic drugs
1. scopolamine
2. dimenhydrinate
3. meclizine
4. prochloperazine
5. ondansetron
6. granisetron
7. metoclopramide
8. droperidol
9. domperidone
10. dexamethasone
11. methylprednisolone
12. dronabinol
13. diphenhydramine
anticholinergic antiemetics
scopolamine
h1 receptor antagonist antiemetic
1. dimenhydrinate
2. meclizine
phenothiazine antiemetic
proclorperazine
5-HT3 antiemetic drugs
-setron's

1. ondansetron
2. gransetron
metoclopramide
anti-emetic that cause antidopaminergic side effects
droperidol and domperidone
block dopamine receptors

-anti-emetic
lorazepam
sedative anxiolytic and amnestic properties

-treats anticipatory vomiting
dexamethasone and methylprednisolone
effective against mild to moderate emetogenic chemo

-can be used in combo with other drugs
dronabinol
marijuana derivative that is NOT a first line antiemetic
combination therapy for anti-emetics
1. dexamethasone increases anti-emetic activity with metoclopramide
2. diphenhydramine given with metoclopramide reduces extrapyramidal rxns
draw back of h1 receptor antagonists as anti-emetics

(dimenhydrinate and meclizine)
1. ineffective against substances that act directly on the chemorecptor trigger zone
phenothiazines function as anti-emetic

(prochlorperazine)
-blocks dopamine receptors
-effective against low or moderately emetogenic chemo drugs
- extrapyramidal symptoms may occur
5-HT3 as an anti-emetic

(ondansetron)
(granisetron)
-treates emesis linked to chemo
-long duration of action
-blocks 5HT3 receptors (visceral vagal afferent fibers) and the chemorecptor trigger zone
-very expensive
major factors of diarrhea
1. increased motility of the gut
2. decreased absorption
2 types of antimotility drugs to prevent diarrhea
1. dephenoxylate
2. loperamide

- act on the gut and inhibit ACh release and decrease peristalsis
- aka opioid-like effect
side effect of dephenoxylate and loperamide
toxic megacolon
absorbents that prevent diarrhea
1. kaolin
2. pectin
3. methylcellulose

-abosrb intestinal toxins or MOs by coating the intestinal mucosa
-less effective than antimotility drugs
agents that modify fluid to prevent diarrhea
1. NSAIDs (asprin and indomethacin)
2. bismuth subsalicylate (used for travelers diarrhea)
3 categories of laxatives
1. irritants or stimulants
2. bulking agents
3. stool softeners
irritants of stimulants type laxatives
1. castor oil - increses peristalsis
2. cascara and senna - stimulates colon
3. bisacodyl - stimulates colon
bulking agents as laxatives
action: hydrophilic colloids form gels that cause water retention and intestinal distention leading to increased peristaltic activity

- Lactulose - an osmotic laxative
saline cathartics
non absorbable salts that hold water in the intestine by osmosis
stool softeners laxatives
emsification process with the stool to produce soften feces

1. docusate sodium
2. mineral oil
3. glycerin suppositories