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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
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1. desiccated thyroid
2. liothyronine 3. Liotrix 4. Levothyroxine |
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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
|
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estrone
|
formed in the liver and adrenal gland
1/10 the potency of estradiol |
|
estriol
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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
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the classic domain
|
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Beta estrogen subtype
|
contains the repressor domain
|
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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
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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
|
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function of the medulla
|
secretes epi
|
|
function of the outer zona glomerulosa
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produces mineralocortioids (aldosterone)
|
|
aldosterone
|
regulated by the renin-angiotensin system
|
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function of the middle zona fasciculata
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synthesizes glucocorticoids (cortisol)
|
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function of the inner zona reticularis
|
secretes adrenal androgens (dehydroepiandosterone)
|
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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 |