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287 Cards in this Set
- Front
- Back
What are the top two leading causes of death?
How much of population in industrialized countries will be diagnosed with cancer? how many will receive chemo? |
1 = Cardiovascular disease
2 = cancer 25% 75% |
|
With chemo,
Is cure likely? Remission? prolongation of life? |
Cure NOT likely with just chemo
remission is likely Expect life prolongation |
|
What is cancer initiation/development usually correlated with?
|
GENETIC abnormalities (DNA!)
|
|
what are the two main processes that are altered during carcinogenesis?
|
Altered environmental signals
Altered Genetic info |
|
WIth increased or decreased expression of tumor suppressor genes is carcinogenesis more likely?
Oncogenes? |
Decreased Tumor Suppressor genes
Increased Oncogenes |
|
what is the difference bw cure and palliation of cancer?
|
Cure is killing ALL cancer cells and sparing normal cells, while Palliation is killing AS MANY CANCER CELLS AS POSSIBLE, and TRYING to spare normal cells.
|
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2 things Palliation of cancer does?
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Reduces symptoms
Reduces potential toxicity |
|
In general, how is a localized neoplastic cell mass first reduced?
Followed by what? |
First with Surgery and/or radiation
Second with chemo |
|
when is a cancer growth physically detectable and symptomatic usually?
|
1 gm
|
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what type of process is the killing of cancer cells by chemo?
what does this mean? |
FIRST ORDER
a constant FRACTION of cells are killed |
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For palliative treatment of cancer, is the size of tumor usually reduced?
What happens to survival? |
no, usually just stops it at the size it is.
Survival is extended |
|
In general, do cancer cells or normal cells grow faster?
|
Cancer cells grow much faster
|
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what are cell cycle specific drugs good at treating?
what are 3 examples of these drugs |
High growth fraction malignancies, where the majority of the cells are growing
Antimetabolites, Vinca Alkaloids, Etoposide |
|
What are cell cycle non-specific drugs good at treating?
3 examples? |
good against low growth, solid tumors
AND high growth fraction tumors Alkylating agents (Mechlorethamine) Antibiotics (doxorubicin) Cisplatin |
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what are 2 unwanted side effects of chemo?
|
non-selective killing of cells
low therapeutic index |
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Do cancers have intrinsic resistance?
How many develop resistance? WHat is common strategy to treat resistant cancers? |
Some do
Most do Combination therapy |
|
what is the significance of drug sanctuaries for cancer and chemo?
how do you treat sanctuaries? |
Drugs may have limited access to some tissues, as the larger the tumor the larger chance that there is necrosis and the tumor is not well perfused
Treat with INTRATHECAL admin of drug and targeted drug admin, (biological, physical/surgical) |
|
what type of cells/tissues are most susceptible to chemotherapeutic agents?
which 3 in particular and what side effects do they give? |
Those that proliferate rapidly.
1. Bone Marrow - acute myelosuppresion 2. Intestinal epithelium - Weight loss, NV, GI inflammation and destructino 3. Hair follicles - alopecia |
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why can't we use lower doses of chemo for high growth fraction tumors?
Low growth fraction tumors? |
High - bc they may not be sufficiently
killed Low - bc they are refractory to many chemo agents (colon and lung cancer) |
|
what is the combination therapy for Acute Lymphocytic Lymphoma?
|
Prednisone
Oncovine L-asparaginase Daunorubicin use bc ALL POLD (pulled) all the lymphocytes awayI |
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What is the combination therapy for Non-hodgkin's lymphoma?
|
Prednisone
Oncovin Cyclophosphamide Daunorubicin (Hydroxydaunomycin) BC people Non-Hodgkin's lymphoma usually have COPD |
|
what are the three advantages of combination therapy?
|
Maximal kill with lower toxicity
effective against heterogenous tumor population Slows/prevents development of drug resistance |
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What general process does chemotherapy attack?
|
REPLICATION OF DNA
|
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What is the primary mechanism of action for attacking DNA replication of tumor cells?
|
Alkylation
(cross link DNA, incorporate a false base, Alkylate a base and promote mutation) |
|
What are the 5 nitrogen mustards?
|
Mechloroethamine
cyclophosphamide Isosfamide melphalan Chlorambucol (I C eM! C eM?!) |
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What is the net result of nitrogen Mustards for chemotherapy?
|
Extensive CROSSLINKING of DNA
therefore, DNA cannot unwind and replicate |
|
4 ways alkylating agents cause large amounts of DNA damage?
|
Activate DNA repair pathways
Induce Cell-cycle arrest Induce Apoptosis May lead to extensive mutations I AIM to alkylate DNA! |
|
what type of drug is O6-methylguanine?
How does it work? |
It is an alkylating agent, that is GUANINE (methyl-guanine) almost identical to the normal guanine in DNA. However, it has a nitrogen with a lone pair of electrons, and therefore cannot H-bond with Cytosine at that point.
This induces tautomerization, turning Cytosine into a Tyrosine. Thus, overall, the O6-methylguanine turns a G:C base pair to an A:T base pair |
|
what are 6 mechanisms for resistance to alkylating agents?
|
1. cross-link formation can be slow and effectively repaired (ie - guanine O6 alkyl transferase reverses action of O6 methylguanine
2. p53 gene mutation 3. increased metabolism of drug (via P450s et al) 4. Increased production of "good" nucleotides that react with drug so there is no damage 5. entry of drug into cell is decreased (Transport system decreased, efflux system UP regulated) 6. gene duplication of affected host protein (DHFR) |
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what was the first antibiotic used as chemotherapy?
How does it work? |
Dactinomycin
(actinomycin D) intercalates into duplex DNA, with selectivity for G:C. Inhibits replication and duplication |
|
What are doxorubicin/daunorubicin?
How do they work? what 4 ways in particular? |
anthracycline antibiotics that mediate DNA strand breaks by:
1. intercalating into DNA 2. Inducing apoptosis 3. inhibiting topoisomerase II 4. Creating free radicals |
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2 main side effects for using antibiotics (doxorubicin/daunorubicin) for chemotherapy?
|
1. myelosuppression
2. Myopathies (Arrhythmias and CHF) RUBicins RUB the heart the wrong way |
|
What is mitoxantrone?
what are it's advantages and dis? what is it used for? |
an antibiotic used in chemo
advantages are less Myopathies compared to Doxorubicin and Daunorubicin disadvantages are less effective in creating free radicals which mediate strand breaks use LIMITED for breast, prostate cancer, leukemias, and MS. MYTOXic effects are less than doxirubicin and daunorubicin but i don't work as well! |
|
what is Bleomycin?
How does it work? |
An antibiotic used for Chemo
Forms complexes with Copper and Iron, leading to strand breakage of DNA |
|
what suffix is common to ALL Platinum coordination complexes?
What do they do? |
Platin (Cisplatin, Carboplatin, Oxaliplatin) (like PLATINum!)
Crosslinks Guanine to induce DNA damage (intra and interstrand crosslinks) |
|
what are epipodophyllotoxins?
what do they do? What are they used for? |
CHemo agents from mandrake plant
(etoposide, teniposide) Inhibits topoisomerase II (like Fluoroquinolones), so that the first cut is STILL MADE, but it prevents "re-sealing", so DNA breakage used for Testicular tumors, non-hodgkins and Acute NON-lymphocytic lymphoma |
|
what is the name of the chemo agent that inhibits topoisomerase I?
Where does it come from? Is it widely used today? why? |
Camptothecin
comes from camptotheca acuminata (happy tree in china and tibet) When you go CAMPing, you get HAPPY, and inhibit topoisomerase I not widely used today bc: unpredictable toxicity, myelosuppression, hemorrhagic cystitis |
|
How do anti-mitotic drugs used for Chemo prevent mitosis exactly?
what are the 2 anti-mitotic drugs used? |
Prevents Chromosomes from segregating!
Vinca alkaloids Taxols |
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what cell part is essential for equally distributing DNA into daughter cell during cell division?
|
Microtubules
|
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What are vinca alkaloids?
How do they work? |
Anti-mitotic drug used for Chemo
work by inhibiting tubulin polymerization, ande therefore mitosis is blocked in METAPHASE, and chromosomes don't segregate Vinca, the mean russian lady, blocked the METs from winning the worlds series |
|
What are taxols?
How do they work? |
Anti-mitotic drug for Chemo
work by Promoting tubulin polymerization (whereas vinca alkaloids inhibit it) This STABILIZES tubulin and stops cell from completing metaphase |
|
What are 2 short term adverse effects of anti-mitotic drugs (taxols and vinca alkaloids)?
5 long terms? |
1. Neuritic pain
2. constipation 1. leukopenia 2. muscle wasting 3. sensory loss 4. Parasthesias (ESP. lips and mouth) 5. alopecia (Anti mitotics over long term can lead to a trip to the PALMS for therapy) |
|
what does tetrahydrofolate do specifically?
3 reactions in specific? How do humans synthesize it? |
carries ONE-CARBON units and is necessary cofactor in methyltransfer reactions (methyl=1 carbon!)
conversion of dUMP to DUTP de novo purine synthesis Serine and glycine synthesis WE DON'T, we get it from diet or intestinal flora |
|
what does dihydrofolate reductase do?
what is major chemo agent that inhibits this? |
changes dihydrofolate to tetrahydrofolate (folic acid) in last step
METHOTREXATE |
|
is methotrexate or sulfonamide-trimethoprim better at inhibiting dihydrofolate reductase?
by how much? |
Methotrexate
10^-10 M v. 10^-5 M |
|
what 3 things does Methotrexate decrease the levels of by inhibiting dihydrofolate reductase?
what is net result? |
dATP, dGTP, and dTTP
Net result is less DNA and RNA synthesized and more DNA damage! |
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What type of cell does Methotrexate ONLY work on?
|
actively growing cells (bc it inhibits dihydrofolate reductase which makes folate, which is only necessary when cell is growing and DNA is being produced
|
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What 3 conditions is methotrexate used for (DHFR inhibitor)
|
ALL
Choriocarcinoma Psoriasis Rheumatoid Arthritis (CRAP, I have to take Methotrexate!) |
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3 ways cells become resistant to Methotrexate (DHFR inhibitor)?
|
1. Reduced influx or increased efflux
2. Polyglutamylation ? 3. increased expression of DHFR |
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What do you do to combat Methotrexate resistance?
why does it work? |
1. give huge dose of Methotrexate
2. Give Leucovorin (folinic acid) later - this is similar to folic acid and bypasses DHFR so folate is RESUPPLIED and RESCUED |
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what is used to rescue folate levels after a large dose of methotrexate is given (for MTX resistant cells)?
|
Leucovorin (Folinic Acid)
|
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what is the name of the chemo drug that inhibits Thymidylate sythase, so that DNA and RNA aren't made?
what type of tumor is this effective in? |
5 - Fluoro-uridine monophosphate (5-FU)
Effective in SLOW growing SOLID tumors (FU im slow because i'm solid!) |
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what are 3 adverse effects of 5-FU (5-Fluoro-uradine monophosphate) toxicity?
|
1. SEVERE ulceration of oral and GI mucosa
2. Anorexia 3. Hand-foot syndrome |
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What are 2 modulators of 5-FU and what does each do?
|
1. Methotrexate - increases 5-FU anabolism, and increases incorporation of RNA
2. Leucovorin - increases inhibition of thymidylate synthase and supplies folate needed for other purposes |
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What is cytosine arabinoside?
how does it work? what is it used for? |
an analog of RIBOSE (sounds like arabinose)
Cytarabine and AraC incorporated into DNA (instead of ribose) causing DNA damage,and INHIBITING conversion of rCDP to dCDP and inhibiting DNA replication used for Acute Myelocitic Leukemia |
|
How do purine analogues work as chemo agent?
what are they also used as? 3 examples? |
block SALVAGE pathways (re-use) of nucleotide biosynthesis so DNA is not made bc no nucleotides!
also used as antiviral agents Thioguanine Mercaptopurine Azathioprine |
|
how does Hydroxuyurea work as a Chemotherapeutic agent?
|
Inhibits RIBONUCLEOTIDE REDUCTASE (RNR)
Thereby blocking ribose conversion to deoxyribose for DNA |
|
how do bisphosphonates work?
What do they work like, how are they different? 3. uses? |
Inhibit osteoclasts
Work like statins, but bisphosphonates have a much higher affinity for bone Osteoporosis Bone Metastasis Multiple Myeloma |
|
what are four adverse effects of bisphosphonates?
|
1. Osteonecrosis of the Jaw (MANDIBLE more often than max)
2. Esophageal erosion + other GI probs 3. Severe pain in bone, joints, and muscles 4. Decrease dose in CKD Decrease DOSE in bisphosphonates! |
|
what three cancers depend on hormones for growth?
|
Breast
Ovarian Prostate |
|
what are the two different Hormone therapeutic strategies for cancer?
How are they different? |
Hormone Responsive
v. Hormone Dependent Hormone responsive strategy involves ADDING the hormone to regress tumor (USUALLY ONLY PALLIATIVE) Hormone Dependent involves REMOVING hormone to regress tumor (via surgery or receptor antagonists) |
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What is the exception to the rule that says the Hormone Responsive route to treating cancer in ONLY PALLIATIVE?
|
Glucocorticoids kill lymphocytes
|
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what are some positive effects of hormone replacement therapy with estrogen?
|
reverses postmenopausal atrophy
affects HT control of NE secretion Protective effect of CV disease Lowers LDL and increases HDL Decreases bone resorption |
|
does estrogen have an effect on bone resorption?
Bone formation? |
Decreases resorption
NO EFFECT on bone formation |
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what are some potential negative effects of hormone replacement therapy with estrogen?
|
possible CANCER increase
increased mutagenesis and proliferation (estrogen and quinone derivatives may induce DNA damage) Thromboembolic disease changes in carb and lipid metabolism migraines mood swings |
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what does it mean that Selective Estrogen Receptor Modulators are tissue sensitive?
|
Designed to be AGONISTS in:
Bone Brain Liver ANTAGONISTS in: Breast and ovarian tissues |
|
what are 4 uses of Selective Estrogen Receptor Modulators?
|
after mastectomy
advanced and metastatic breast cancer high risk individuals long term treatment after radiation and chemo of breast cancer |
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5 side effects of Selective Estrogen Receptor Modulators (SERM)?
|
1. anti-resorptive effect on bone
2. decreases total cholesterol, but doesn't increase HDL 3. affects vasomotor function (Hot flashes) 4. Causes thickening/prolif of endometrium (ovarian cancer?) 5. Decrease CV risk?? |
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what causes resistance to SERMs
(Tamofixen and Raloxifene)? |
low levels of estrogen receptor expression (ER negative cancers)
Mutations of estrogen receptors |
|
How do estrogen-synthesis inhibitors work (Aminoglutathimide, Exemestane and Anastrazole)?
|
Inhibit Aromatase
which converts testosterone to 17beta-estradiol. |
|
what are megasterol acetate and Flutamide?
how are they the same? different? |
both deal with testosterone to treat cancer.
However, Megasterol is a steroid itself(STEROL), and is a partial/weak agonist at the androgen receptors, therefore COMPETITIVELY inhibiting testosterone Flutamide is NON_STEROIDAL, that prevents androgen receptor translocation to nucleus. it acutally INCREASES testosterone levels, but the testosterone cannot get to nucleus and work! |
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what are three adverse effects of Flutamide (synthetic non-steroidal anti-androgen)
|
1. GI
2. Gynecomastia 3. HOT FLASHES |
|
how do Tamoxifen and Raloxifene work?
|
They are SERMs
Bind to estrogen receptor, but fail to stimulate transcription |
|
what is a side effect to both tamoxifen AND flutamide?
why does this make sense? |
HOT FLASHES
bc both work on hormones (tamoxifen=estrogen, flutamide = androgens), and the levels increase with both of them, but effectiveness decreases |
|
What is a NON-selective hormone treatment for cancer?
WHat type exactly? What else is it used for? |
Prednisone! (binds to glucocorticoid receptors)
used for lymphomas also used for immunosuppression |
|
Do normal cells have high or low levels of Asparagine Synthetase?
Cancer cells? WHat does asparagine synthetase do in the cell? what Drug acts on it? |
Normal cells have high levels, cancer cells have low.
It converts aspartate to asparagine for protein synthesis L-asparaginase blocks asparagine synthetase, so asparagine is not formed |
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How does L-asparaginase work on cancer cells without affecting all cells significantly?
|
Normal cells have high levels of asparagine synthetase and can overcome the effects of the enzyme.
However, cancer cells have low levels of asparagine synthetase, and are therefore MORE SENSITIVE to L-asparaginase's effect |
|
2 disadvantages of L-asparaginase?
|
must be given by IV
does not enter cells |
|
what are 2 examples of monoclonal antibodies given for cancer?
which one's in particular? |
Rituximab = Non-hodgkin's lymphoma
Trastuzumab = Breast cancer |
|
How does Rituximab work?
what cancer is it used for? |
A monoclonal antibody that binds to
CD20 antigen of B lymphocytes used for non-hodgkin's lymphoma there are 20 CLONES wearing tuxes that all look like they have non-hodgkins lymphoma |
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How does trastuzumab work?
what cancer does it treat? |
Binds to HUMAN EPIDERMAL GROWTH FACTOR RECEPTOR 2 (HER2), which is overexpressed in 25% of breast cancers
breast cancer |
|
what is the main disadvantage to using monoclonal antibodies (Rituximab and Trastuzumab)?
|
TOXICITY leads to Antigenic response
|
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In what 4 conditions is there excessive angiogenesis?
|
Diabetic retinopathy
Age-related macular degeneration Rheumatoid arthritis Cancer (it's darc with all these new blood vessels blocking everything!) |
|
3 drugs that are anti-angiogenic?
|
Angiostatin
Batimastat, Marimastat, carboxyamino-triazole Genistein |
|
are levels of PGE2 high or low in cancer cells?
what drug works on this specifically? what is its drawback? |
HIGH
Celecoxib (Celebrex) = COX 2 inhibitor Need HIGH PLASMA CONCENTRATIONS to be effective |
|
3 cancer treatments currently being developed?
|
1. Telomerase inhibitors - shorten ends of chromosome and force apoptosis
2. Anti-sense approaches - complementary to and binds specific RNA, blocking translation of key proteins 3. Engineered or novel transcription factors - target specific promoters and repress transcription |
|
what 2 things is mucositis/stomatitis common after?
what is it due to? |
1. Induced Leukopenia
2. Methotrexate due to mucosal overgrowth and erosion lots of cytokine signaling bacterial and fungal overgrowth |
|
How do you manage drug related Mucositis/Stomatitis?
|
short course glucocorticoids
optimum oral hygeine Mouthwash with L-GLUTAMINE (NO EVIDENCE ANY OTHER MW WORKS!) |
|
What 2 things does xerostomia cause?
How do you treat xerostomia? what does xerostomia do to taste? |
causes caries and candidiasis
treat with ice chips, sugarless candy and gum, SYSTEMIC MUSCARINIC CHOLINERGIC AGONISTS (severe cases) Alters taste |
|
what 4 types of infections are common with bone marrow suppression due to antineoplastic drugs?
|
1. overgrowth of bacteria and fungi
2. Reactivation of HSV (treat with acyclovir) 3. Candidiasis 4. Bacterial infections |
|
How many people on bisphosphonates get osteonecrosis of the jaw?
which jaw is more common? after what specifically is it more common? |
15%
Mandible more common Most common after invasive procedure (ie extraction) |
|
What is the curative treatment for Osteonecrosis of the jaw?
|
THERE IS NONE!
NOT EVEN DISCONTINUING DRUG |
|
what 3 things cause increased bleeding in chemo?
|
1. Leukopenia due to bone marrow suppression
2. Decrease in platelets 3. Anemia |
|
what are 4 dental anomalies from chemo especially seen in children?
what is preferred treatment of these kids? |
1. Delayed eruption
2. Non-eruption 3. crown/root malformation 4. discolorations (esp. crown) Do not treat unless necessary! |
|
What are the four classes of endocrine hormones?
|
Steroids
Proteins Polypeptides DNA derivatives (thyroxine) |
|
what are the three uses of endocrine drugs?
|
1. replace missing or deficient hormone
2. testing responsiveness of organ 3. treating a disease with supraphysiological levels |
|
What is the process called that controls regulation of endocrine hormones and what does it include?
|
OVERLAPPING
Positive and negative feedback! |
|
what are the 2 metabolic functions of glucocorticoids?
2 anitinflammatory? |
1. increase glucogenesis/glycogenolysis
2. increase protein catabolism and decrease anabolism 1. decrease prostaglandins 2. decrease proliferation of lymphocytes and macrophages |
|
how are gluco and mineralocorticoids eliminated and excreted?
|
Eliminated by LIVER metabolism
Excreted as17-hydroxysteroids by KIDNEYS |
|
what are three therapeutic uses of glucocorticoids?
|
1. Immunosuppression/anti-inflammatory
2. Adrenal insufficiency 3. Myeloproliferative diseases (Leukemia) |
|
what 3 glucocorticoid drugs are used for chronic anti-inflammatory treatment?
what is half life? Mineralocorticoid activity? |
1. Prednisone
2. Prednisolone 3. Methylprednisolone intermediate half life low mineralocorticoid activity |
|
what are 2 glucocorticoid drugs that are used for acute anti-inflammatory treatment?
what is half life? mineralocorticoid activity? |
1. Dexamethasone
2. Betamethasone prolonged half life minimal mineralocorticoid activity |
|
7 adverse effects and toxicity with glucocorticoids?
|
Iatrogenic Cushing's syndrome
Immune Suppression Osteoporosis suppression of feedback axis Hyperglycemia, diabetes mellitus growth retardation in children muscle wasting |
|
what does coadministration of glucocorticoids with inducers of hepatic metabolism result in in terms of effect and induction?
|
Less effect
Possibly greater induction |
|
how does administration of glucocorticoids affect the following:
Diabetes mellitus Hypothyroidism NSAIDS Infection Herpes Labialis |
makes diabetes worse
suppresses pituitary more so makes hypothyroidism worse additive with NSAIDS makes infection more common Causes reactivation of oral herpes lesions due to immunosuppression |
|
What are three therapeutic uses of mineralocorticoids like aldosterone?
|
1. primary adrenal insufficiency
2. Hypoaldosteronism 3. Idiopathic orthostatic hypotenstion |
|
how do you treat glucocorticoid excess like that seen in Cushing's syndrome?
Mineralocorticoid excess drug? |
with the Adrenal steroid receptor blocker:
RU 486 Spironolactone (Diuretic that blocks channels in kidney) |
|
what two dental conditions are glucocorticoids used to treat?
what one dental condition do they cause frequently? what 2 things do dentists have to think about with patients on glucocorticoids? |
1. oral ulceration
2. TMJ arthritis 1. Thrush 1. may need higher doses under stress (like dental procedures) 2. prophylactic Abs might be warranted due to immunosuppression by glucocorticoids |
|
what are the 6 fxns of estrogen?
|
1. secondary sex characteristics
2. closure of epiphyseal discs 3. maintains bone mass 4. stimulates prolactin 5. endometrial proliferation 6. Inhibits FSH/LH |
|
What are the 4 fxns of progestin?
|
1. mammary gland development
2. uterine changes for embryo implantation (opposite of estrogen induced proliferation) 3. Maintenance of pregnancy 4. Inhibits FSH/LH |
|
5 therapeutic uses of estrogens or estrogen receptor partial agonists?
|
1. Menopausal symptoms
2. Osteoporosis 3. CV disease prevention 4. Ovarian failure 5. Prostate cancer |
|
4 therapeutic uses of progestins?
|
1. Oral contraception
2. Dysfxnl uterine bleeding 3. Endometrial cancer 4. endometriosis |
|
2 therapeutic uses of combined estrogen/progestin?
|
1. Oral contraceptives
2. Chronic Menopausal symptoms |
|
5 routes of estrogen/progestin administration?
|
1. Oral
2. Transdermal patch 3. IM injection 4. Silastic implant 5. Intravaginally |
|
Out of Natural estrogens, esterified estrogens, and synthetic estrogens, which one has:
Highest potency? lowest oral bioavailability? protection against hepatic inactivation? activation necessary to bind ER? |
Synthetic estrogens
Natural estrogens Synthetic estrogens Esterified estrogens (must break ester bond!) |
|
5 major side effects of high-dose estrogen therapy?
|
Thromboembolic disorders
High BP Migraines Increased risk of endometrial cancer worsening of endometriosis |
|
4 contraindications for estrogen therapy?
|
1. pregnancy
2. estrogen dependent breast cancer 3. abnormal vaginal bleeding 4. thromboembolic disorders (since this is a major side effect of high dose estrogen therapy) |
|
what is common about the bioavailabilty of natural estrogens and progestin/progesterone? Why?
|
extremely low bioavailabilty because there is extensive first pass metabolism by liver
|
|
2 side effects of high dose Progesterone therapy?
|
1. Menstrual abnormalities
2. Abnormal glucose tolerance |
|
what does estrogen/progesterone therapy do for:
Salivary content Dry socket incidence Gums |
1. alters salivary content promoting plaque formation
2. increases dry sockets 3. Gingival hyperplasia and bleeding |
|
3 therapeutic uses of ovarian steroid receptor blockers?
examples of each? |
1. breast and prostate cancer (Tamoxifen and Raloxifene)
2. Contragestation (RU 486 (antiprogesterone)) 3. Ovulation induction (Clomiphene (anti-estrogen)) |
|
what 4 things can elevated androgen production in females cause?
|
1. adrenal/ovarian tumors
2. Polycystic ovarian syndrome 3. Congenital steroidogenesis enzyme defects 4. imbalance in gonadotropin secretion |
|
5 therapeutic uses for androgens?
|
1. testicular insufficiency
2. Hypogonadotropic hypogonadism 3. Congenital Microphallus 4. anorexia from chronic diseases 5. decreased libido |
|
5 therapeutic uses of anti androgens?
|
1. prostate hyperplasia/cancer
2. Acne 3. Hirsutism 4. Precocious puberty 5. Alopecia |
|
what are the two androgen receptor blockers?
|
Cyproterone Acetate
Flutamide |
|
what are the three androgen synthesis inhibitors?
|
Finasteride (blocks conversion of T to DHT)
Spironolactone Ketoconazole |
|
what is the major drug given for prostatic hyperplasia? how does it work?
|
Finasteride
An androgen synthesis inhibitor that blocks conversion of T to DHT |
|
is first pass effect high or low for naturally occurring testosterones?
|
High (same as estrogens and progesterones)
|
|
4 routes of androgen administration?
|
Oral
Scrotal transdermal patch Transdermal patch IM injection |
|
what is the major cause of growth hormone excess?
what are 2 symptoms what are 2 treatments? |
1. excessive bone growth
2. acromegaly 1.dopamine agonists 2. somatostatin (GHIH) |
|
3 side effects of growth hormone therapy?
|
1. diabetes mellitus
2. excessive growth 3. acromegaly |
|
4 causes of prolactin excess?
|
1. prolactin secreting tumors
2. Dopaminergic antagonists 3. Primary hypothyroidism (high TRH) 4. Injury |
|
what are three symptoms of prolactin excess in females?
Males? how do you treat it? |
1. Amenorrhea, Galactorrhea, Infertility
1. Infertility, Galactorrhea, Impotence Treated with BROMOCRIPTINE (dopamine agonist bc dopamine is PIH) |
|
4 major side effects of bromocriptine (dopamine agonist)?
|
Low BP
Severe headaches Seizures Stroke |
|
What is the most common thyroid disorder?
Is it more common in men or women? How many women over 40 have it? |
HYPOthyroidism
WOMEN 10% |
|
3 main causes of hypothyroidism?
3 main symptoms? |
Iodine deficiency
Pituitary/HT failure Autoimmune thyroiditis Cold/Dry skin/edema Poor appetite Lethargy |
|
what is most common form of thyrotoxicosis?
|
Graves diesease
|
|
how does iodide work as an antihyperthyroid med?
|
It inhibits synthesis and release of Thyroid hormones due to negative feedback
|
|
what drug inhibits iodination of thyroglobulin to treat hyperthyroidism?
|
Methimazole
Thyroglobulin can't make it out of the meth maze to find it's iodine! |
|
what is the name of the antihyperthyroid drug that inhibits conversion of T4 to T3?
|
Propylthiouracil
|
|
what are the names of the 2 ionic inhibitors that inhibit active transport of iodide into the thyroid to treat hyperthyroidism?
|
Perchlorate
Thiocyanate If you don't bring TP you can't get into the party iodine |
|
what is used to non-surgically destroy the thyroid in a hyperthyoidic patient?
what is necessary afterwards? |
Radioactive iodide
Need to treat for hypothyroidism, bc the thyroid no longer works |
|
what are 3 adjuvant drugs for hyperthyroidism and how does each work?
|
1. Corticosteroids - inhibit T4 to T3 conversion (like propylthiouracil)
2. Beta-adrenergic receptor antagonists (propanolol - treats catecholaminergic effects of hyperT 3. Ca channel blockers - For tachycardia and arrhythmias |
|
for dentistry, what do we have to worry about for unmanaged hypothyroid patients?
what is contraindicated? Why? |
LOW BP
Opioids, barbiturates, and other depressants due to CNS and CV depression |
|
4 side effects of iodide therapy?
|
Brassy taste
Burning in mouth and gums Soreness of teeth and gums More salivation |
|
3 drugs to treat central diabetes insipidus?
|
Vasopressin
Lysopressin Desmopressin |
|
2 adverse effects of vasopressin analogs? (Lysopressin, Desmopressin)
|
Water intoxication
NSAIDS and carbamazapines can increase ADH effects |
|
what major HT hormone inhibits insulin release?
|
Somatostatin (makes sense bc if that's there, it's telling the body not to grow, and insulin is a storage hormone
|
|
what are the effective drugs to treat Diabetes Mellitus type I?
|
INSULIN (with diet and exercise)
ONLY effective drug |
|
what are the different half lives for insulin when:
Alone? With Zinc suspension? WIth protamine? |
short - 5-7hrs
Long - 30-40 hrs Intermediate - 6-14 hrs |
|
what type of drug is sulfonylurea?
what is it used to treat? how does it work? |
it's a hyperglycemic agent
used to treat TYPE II DIABETES works by sensitizing pancreatic beta cell to glucose and increases insulins effect on glucose uptake and storage by liver |
|
What are biguanides (metformin)?
what are they used to treat? how do they work? what DON"T they do? |
anti-hyperglycemic agent
used to treat TYPE II DIABETES works by increasing TISSUE sensitivity to insulin DOES NOT cause insulin release or hypoglycemia |
|
what becomes elevated in hypoglycemia? what does this cause?
|
Epinephrine (to try and compensate for no sugar)
Rapid heart rate, weakness, trembling, cold sweats Neural fxn is also impaired with blurred vision, incoherant speech, confusion |
|
What are the dental considerations of someone with poorly controlled Diabetes Mellitus?
|
Oral infection
Attachment loss Gingivitis Decreased saliva Increased caries |
|
What part(s) of BV have anticoagulant properties?
Which have Coagulant? |
Inner Endothelial layer has Anti
ALL other layers have anticoagulant (so that if it ruptures a clot is formed |
|
what is the difference bw primary and secondary hemostasis?
|
Primary = PLATELET PLUG from platelets and BV wall interactino
Secondary = FIBRIN CLOT replaces platelet plug |
|
what activates platelets during primary hemostasis when vessel wall is damaged?
|
von Willenbrand factor
|
|
what protein mediates platelet aggregation to form a plug?
|
Fibrinogen
|
|
What are the 2 major pathways in secondary hemostasis?
|
Intrinsic and Extrinsic (Primary) coagulation pathways
|
|
What is the pathway of primary (extrinsic) pathway of secondary hemostasis?
|
VII and TF
X Prothrombin to Thrombin Fibrin and XIII crosslinked fibrin polymer |
|
what is released from endothelium to inhibit platelet aggregation and vasodilates?
|
Prostacyclin
|
|
What inactivates thrombin and other factors?
|
Antithrombin III
|
|
What do protein C and protein S do?
|
Vitamin K dependent that inactivate factors 5 and 8 in secondary hemostasis
|
|
What converts plasminogen to plasmin and cleaves crosslinked fibrin?
|
tPA
tissue plasminogen activator |
|
name the four antiplatelet agents
|
COX inhibitors - aspirin
Phosphodiesterase inhibitors ADP receptor antagonists GPIIb-IIIa antagonists Anti Platelets Get Clots! |
|
name the 3 anticoagulants
|
Heparin
Warfarin/coumadins Hirudin |
|
name 2 thrombolytic agents that dissolve clots
|
Streptokinase
tPA |
|
what is the ONLY irreversible NSAID? How?
|
Aspirin
acetylates COX |
|
For low dose aspirin prophylaxis, does a higher than 81 mg dose work better? what else
|
No, it doesn't work and it's harmful
|
|
how do phosphodiesterase inhibitors work to decrease platelet aggregation?
|
It prevents breakdown of cAMP, therefore cAMP increases, and platelets don't aggregate when cAMP is high
|
|
what is the prototypical phosphodiesterase inhibitor and what is it used with?
|
Dipyridamole
used with warfarin or aspirin |
|
what happens when ADP binds to platelet receptors?
what drugs work on this? are they reversible? |
it promotes aggregation
ADP receptor antagonists Clopidogrel (plavix) and Ticlopidine (Ticlid) IRREVERSIBLE |
|
when is clopidogrel used?
What about Ticlopidine? (ADP receptor antagonists |
after MI with aspirin
ONLY in cerebral ischemia |
|
what is primary adverse effect of clopidogrel and ticlopidine? (ADH receptor antagonists)
others? |
Bleeding!
tiredness headache dizziness stomach diarrhea or constipation nosebleed ADH antagonists can stop you from peeing, but they can't stop you from bleeding! |
|
do clopidogrel and aspirin work after uncompicated MI? proof?
|
YES
98% v. 88% survival if you take them |
|
what are GPIIa-IIIb used to treat?
how do they work? what are they used during? |
used to make clot less stable and easier to disintegrate
Antiplatelet drugs Bind fibrinogen molecules cementing platelet aggregation used during angioplasty and can lead to excessive bleeding |
|
what does heparin do?
what does unfractionated do? what about the low molecular weight version? |
prevents clot formation
Antiplatelet unfractionated = inactivates thrombin and factor X low m weight = inactivates factor X, safer than unfractionated |
|
how do you treat a heparin od when there is excess bleeding? how does it work
|
Protamine
binds heparin |
|
how does warfarin work?
are they orally active? how soon is the onset of action? what about when you stop taking it? |
blocks regeneration of Vit k
yes orally active delayed bc doesn't work until previously synthesized factors turn over WARfarin is at WAR with vitamin K also means the actions last longer past when you stop taking it |
|
what anticoagulant has tons of drug interactions?
for what 2 reasons? |
WARFARIN
highly protein bound metabolized by P450s |
|
what main drugs increase the effect of warfarin?
|
Tylenol
NSAIDS Antibiotics statins steroids |
|
what 3 drugs decrease warfarin effect?
|
Barbiturates
Vitamin K Cholestyramine |
|
what is hirudin?
what patients is it used it? |
anticoagulant selective for thrombin
used in those that cannot tolerate heparin |
|
what 2 thrombolytic agents are active against preexistant clots?
|
Streptokinase (made by b-hemolytic strep)
tPA (produced by endothelial cells, opening clogged coronary and pulmonary arteries) |
|
when does tPA significantly improve MI survival?
when does it not? |
if given within one hour of symptom onset
DOESN'T work after 2 hours! the patient's death is TBA if the TPA is not given within 2 hrs |
|
What department publishes requirements related to prescribing, dispensing, and storing drugs?
office purchase, storage and administration? |
State departments of public health, boards of pharmacy and dentistry
|
|
what is the database called that contains preferred drugs depending on medicaid and insurance?
can they mandate generic? |
Drug formularies
CAN mandate generic |
|
is the prescription a legal document?
|
YES, subject to state, local, and federal laws
|
|
Look at prescription components, what needs to be on it, do's and don'ts, etc.
|
NOW
|
|
true or false, if you are in a general practice you need to print YOUR name on the form along with the practice name.
|
TRUE
|
|
What is the use of Latin on a prescription?
|
MALPRACTICE,
NEVER use LATIN ON PRESCRIPTIONS |
|
do you put zeroes BEFORE a decimal?
what about after one? |
ALWAYS
ie 0.25 v. .25 (bc without the 0, the patient can add something NEVER use trailing zeroes ie dont put 5.0, put just 5 |
|
how many patients are less than 90% compliant?
Why? |
50%!!
shit load of reasons, no question on this |
|
how often should you review med history including drug allergies and interactions?
|
EVERY VISIT
|
|
how do you increase compliance?
|
Good Partnership with patient
Both oral and written info rationalize drug therapy plan around patients life patient friendly packaging follow ups |
|
what are 7 signs of drug seeking behavior
|
evasive about previous doctor or med history
unable to react dentist/doctor asks for specific drug claims allergy or inefficacy with specific drugs lost prescription requests higher doeses or quantities calls late in day or weekend |
|
what do you do if you suspect drug seeking behavior?
|
contact pharmacies and get drug history
ask pharmacy to check ID of patient |
|
can you get in trouble for prescribing to a patient with known dependency or addiction history?
|
YES
|
|
summary for prescription writing?
|
BE CLEAR
BE COMPLETE |
|
what 3 things does kidney dysfunction have a large impact on for drugs?
|
Clearance
T 1/2 Adverse effects |
|
what is definition of CKD?
|
evidence of kidney damage for at least 3 months
GFR < 60 ml/min for at least 3 mo |
|
what is worst stage of CKD?
what is another name? |
Stage 5
End Stage Renal Disease |
|
what %age of population has SOME form of CKD?
|
11%!
about 1 in 10 people! |
|
5 risk factors for CKD??
|
Diabetes mellitus (45% of ESRD)
HT (23% of ESRD) CVD (2-5x risk) Family history of ESRD also >65 yo |
|
what is very well correlated with kidney disease?
|
Proteinuria (as you get older, eat less steak!)
also african americans and females have 2x greater risk |
|
what is the strongest independent predictor of progression of CKD?
|
PROTEINURIA
Albumine to Creatinine ratio |
|
what does proteinuria lead to in CKD?
|
a cycle which will make CKD worse bc body is trying to compensate
|
|
3 major complications of CKD?
|
CV problems
Anemia Osteodystrophy (defective mineralization) |
|
independent of any other factor, what is the most important factor determining survival after an MI?
|
RENAL FUNCTINO
|
|
How much higher is CVD risk in dialysis patients?
what is the major cause of mortality in CKD/ESRD? |
65X !!!
CVD! |
|
what is the main treatment for CKD?
|
Inhibit renin-angiotensin pathway
|
|
3 major drugs active on renin-angiotensin system?
|
ACE inhibitors
Angiotensin receptor antagonists Renin inhibitors (in clinical development) |
|
what is common suffix on ACE inhibitors?
|
PRIL
(captopril, enalopril, etc.) |
|
what is the major disadvantage of treatment of CKD with ACE inhibitors?
|
they are cleared by the KIDNEYS, so less clearance and less dose needed
|
|
do ace inhibitors work?
|
yes, they double the time to kidney failure
|
|
5 adverse effects of ACE inhibitors?
|
1. Teratogenic
2. Hypotension 3. Cough 4. Hyperkalemia (and arrhythmias) 5. Abnormal taste |
|
what 3 drugs have interactions with ACE inhibitors?
|
Lithium
NSAIDS (don't use) K+ supplements (bc hyperkalemia is adverse effect of ace inhibitors) |
|
what is common suffix for Angiotensin receptor antagonists?
|
SARTAN
(losartan, irbesartan, etc.) |
|
how are Angiotensin receptor antagonists cleared?
|
by LIVER, so renal fxn does not effect clearance or dose
(NOT the case for ACE inhibitors!) |
|
5 adverse effects of Angiotensin Receptor Antagonists?
|
Teratogenic (like ACE inhibitors)
Hypotension, dizziness, blurry vision muscle pain impotence hyperkalemia |
|
what teratogenic drug can leach out in breast milk and should be avoided in those breast feeding?
|
Angiotensin Receptor Antagonists
|
|
5 drug interactions with Angiotensin Receptor Antagonists?
|
Lithium
NSAIDS Fluconazole K+ sparing diuretics K+ supplements Rifampin and erythromycin |
|
decrease in renal fxn does what to Angiotensin dependent processes?
|
INCREASES THEM, which is why you use ACE inhibitors and Angiotensin receptor antagonists for it
|
|
at recommended dose, is a combo of ACE inhibitors and Angiotensin Receptor antagonists better than either alone?
|
YES COMBO BETTER
|
|
can you use General anesthetics in CKD?
Midazolam? NSAIDS? |
NO!
|
|
what do you use for perioperative analgesia with CKD?
|
Morphine or fentanyl
|
|
what do you use for postoperative analgesia with CKD?
|
tramadol or codeine
|
|
what 3 things increase acid production in stomach?
what decreases it? |
Gastrin
Ach histamine Prostaglandin decreases |
|
what is sucralfate?
what is composition? what is mechanism? |
Used for injured GI
sucrose octasulfate and aluminum hydroxide gel Coats stomach and ulcer craters, prevents acid excess. NO acid, but mucin still gets through |
|
does sucralfalate get absorbed?
how is it activated, so what shouldn't you use with it? |
NO! too much metal and R groups
activated by ACID, so don't use with antacids! |
|
what is bad with sucralfalate?
is it a first line drug for GI injury? |
more relapse
no pain relief no protection bw meals or during sleep NO due to above reasons, even though it heals and maintains ulcers as well as h2 antagonists |
|
what is action of antacids? what is it NOT?
what are the two best antacids? why? |
CHEMICAL NOT biological
Mg OH2 and AlOH3 because the mixture allows rapid (Mg) and long acting action (Al) |
|
what is worst antacid?
|
Calcium bc of rebound and long term effects
|
|
Are Ca and NA antacids recommended for gastric injury treatment?
|
NO!
|
|
Are antacids a first choice drug?
|
NO, but useful as adjunct
|
|
what does decreased acid due to antacids cause in relation to absorption rate and bioavailabilty?
|
ALTERS it, usually decreasing it
|
|
are liquid or tablets better antacids?
|
LIQUIDS
usually have to take more than recommended tablets to get effect |
|
what can chronic use of Al antacids cuase? why?
|
phosphate deficiency
bc it precipitates phosphate and fluoride and prevents absorption aluminum phosphate is a common salt! |
|
what does combo of Mg and Al antacids do to bowel movements?
|
Mg promotes diarrhea
Al promotes constipation so they cancel out!! this is also why we give them in combo |
|
what is another name for H-K-ATPase Inhibitors?
what is the common suffix for them? |
Proton pump inhibitors (H+Atpase!)
Prazole (Omeprazole (prilosec), esomeprazole (Nexium)) |
|
how are omeprazole and esomeprazole different? how are they the same?
which is generic? |
esomeprazole (nexium) is the S-isomer of omeprazole (prilosec)
and esomeprazole works at half dose, but is way more expensive! omeprazole (Prilosec) is generic |
|
how do Proton pump inhibitors block all acid productino in stomach?
|
blocks H-K-ATPase which is the ONLY way acid gets in stomach (last step)
|
|
does inhibition of H-K ATPase affect:
Gastrin IF gastric secretinos, gastric motility? |
NO!!!
|
|
how is omeprazole (Prilosec) self limiting?
|
it is a PRODRUG that must be activated by acid below pH 5, so if too much acid blocking goes on, the drug is not activated
|
|
are K-H ATPase inhibitors reversible?
What does this mean? |
NO, pseudoirreversible
means effects last for 4-5 days after done taking |
|
what is the drug of choice for ulceration and GERD?
|
H-K-ATPase inhibitors (Proton pump inhibitors)
|
|
what are adverse effects of H-K ATPase inhibitors (PPIs)?
|
not many,
rarely leukopenia and rash also, omeprazole and esomeprazole affect P450s so interactions |
|
how do PGEs work against stomach injury?
|
Inhibits gastric acid secretion (bw histamine and H-K-ATPase) from ALL stimuli
and increases mucin and bicarb |
|
what do NSAIDs do to mucin and bicarb levels in stomach? what does this do for feedback for acid secretion?
|
DECREASE IT
inhibits feedback |
|
why is misoprostol (synthetic PGE1) used instead of regular PGE2 for stomach probs?
|
bc PGE2 is an autocoid so it has terrible half life, and PGE 1 lasts longer and has longer effect
|
|
2 adverse effects of PGE2 agonists for gastric injury?
what is the approved use? |
causes abortion
uterine motility TERATOGENIC contraindicated in women during child bearing age approved for those who take large doses of NSAIDS (bc PPIs have adverse effect) |
|
how do muscarinic cholinergic antagonists work for gastric injury?
are they as good as others? adverse effects? |
decreases basal acid secretion by 50% (whereas PGEs and PPIs block ALL acid)
so not as good as others due to this dry mouth, blurred vision, urinary retentino, just like atropine od can cause hallucinations and coma |
|
what type of GI drug do belladonna and hendane, and devil's root have?
|
Muscarinic cholinergic antagonists
|
|
what used to be drug of choice for GERD and ulcers before PPIs were introduced?
|
Histamine H2 receptor antagonists
|
|
where are H2 histamine receptors abundant?
|
in the stomach which is why histamine H2 receptor antagonists are good bc they are selective (second choice)
|
|
do H2 histamine receptor antagonists block acid during day? what about at night?
is half life long or short? adverse effects? |
YES, ALL THE TIME!
short half life (3 hrs) few adverse effects |
|
What type of drug is cimetidine (Tagemet)?
What do you have to be careful of when using?why? why is this unusual? |
It is a histamine H2 receptor antagonist.
MANY drug interactions bc it prolongs half lives of drugs metabolized by P450 1A, 2C, and 3A Unusual bc cimetidine is the ONLY Histamine H2 antagonist that inhibits P450s, so other ones don't have interactions |
|
is one Histamine H2 blocker better than another?
|
NO
just be careful with cimetidine (tagemet), bc it's the only one that inhibits P450s and has interactinos |
|
other than GI problems, what other condition uses Histamine H2 blockers sometimes?
|
SEVERE URTICARIA
when H1 antagonists are not enough |
|
what are adverse effects of H2 receptor antagonists long term therapy? WHy?
|
males = loss of libido and gynecomastia
females = loss of libido and galactorrhea H2 receptors mediate some prolactin secretion Cimetidine is weak antagonist at androgen receptors Cimetidine inhibits estradiol metabolism (bc P450s) |
|
Is H. pylori more associated with duodenal or Stomach ulcers?
|
Duodenal
|
|
If H. pylori is present in a patient with ulcers, does getting rid of H. pylori cure the ulcer?
what about treating with other drugs? |
YES
other drugs may cure it, but it may relapse since h. pylori is not gone |
|
what is main disadvantage of Sucralfate?
|
No nighttime protection against acid
|
|
what two age groups are most prone to overdose on OTC drugs?
|
young adults through middle age (20-49)
Infants |
|
what are the two requirements for Prescription drugs?
what about OTC drugs? |
Safe and effective
SAFE, no rule on efficacy |
|
can advertising/labeling of OTC drug claim that it treats a specific disease?
|
NO
not unless a drug trial has been performed (excedrin for arthritis, previous rx drugs that are now OTC) |
|
Are nutritional supplements considered drugs? what does this mean?
|
NO, by law considered FOODS
meaning that they come under FOOD SAFETY regs, not DRUG SAFETY regs |
|
is ephedra legal now?
why? what NT are ephedras actions similar to? |
NO, not since 2004
bc it increases heart workload, risk of arrhythmias, and vasoconstricts similar to Epi and NE |
|
what is in xenadrine and metabolife now that ephedra is banned? is it as effective?
|
synephrine (in bitter orange)
less effective (which is why it can be used bc less side effects) |
|
how are OTC combination medicines?
why? |
rarely useful
almost always bad medicine bc doses not optimalized, not always rationalized, formulations vary without reason, high price |
|
in cough medications, what is the :
cough suppressant? Antihistamine? Decongestant? |
Dextromethorphan
Doxylamine pseudoepedrine |
|
in terms of OTC drug combinatinos, are pharmodynamic or pharmokinetic interferences most common?
|
Pharmokinetic (kinetic are kommon)
more about how the drug gets in and out (kinetic), not how it acts(dynamic) |
|
3 common misconceptions consumers have about OTC meds?
|
too weak to cause problems
no side effects due to interactions no side effects at all |
|
what in cough medicine can have interaction with heart meds? why?
|
Pseudoephedrine (decongestant)
constricts BVs, can cuase arrhythmias and increase BP |
|
for colds, are pills or nasal sprays more effective?
which has more side effects and why? |
pills more effective bc less chance of rebound
Pills have more side effects bc they are available to entire body whereas sprays stay local |
|
since tylenol is not antiinflammatory, what three types of pain does it not help with?
|
Muscle aches
achy joints arthritis |
|
are store brand OTCs different than brand names?
|
NO
usually from same manufacturer even and just put into a different box |
|
for rashes, itches and minor skin conditions, what OTC should you use?
what shouldn't you use and why? |
Use topical corticosteroids
DONT use topical "anti-itch" products with "caine" in name bc it could cause allergic rxns rapidly (like benzocaine!) |
|
for allergies and bites, which OTC shoudl you use?
what shouldn't you use and why? |
use non-drowsy antihistamines
don't use anti-allergy tablets (bc they induce sleep) don't take anything with D after the name (for decongestant) take Pseudoephedrine separately |
|
what OTC should you take for a cough?
what should you generally avoid and why? |
Dextromethorphan
avoid combinations bc nothign but the dextromethorphan does anything for a cough |
|
for runny nose and allergies, what OTC should you take during day?
at night? why are they a problem? what has been done? |
day = oral pseudoephedrine
night = 12 hr nasal spray of pseudoephedrine Now behind the counter due to crystal meth problem reformulated to contain phenylephrine instead. |
|
what are 2 problems with phenylephrine as a decongestant?
|
it doesn't last as long as a nasal spray (as pseudoephedrine)
CANNOT be taken orally, bc extensively metabolized by gut with ZERO decongestant activity |
|
For naproxen, is the OTC recommended dose the same as the Rx dose?
what about for ibuprophen? |
same for Naproxen (aleve)
OTC recommended dose for Ibuprofen is 1/2 that of prescription dose |
|
For OTC antacids, what should you use?
what should you avoid? |
Maalox or Mylanta
ANYTHING WITH MAGNESIUM AND ALUMINUM should be used Avoid those with calcium (tums) and don't treat with milk, bc calcium actually increases acid production later |
|
what should you use OTC as a laxative for constipation?
what about for diarrhea? |
Metamucil/ other bulk former (most others don't work and can be toxic)
Immodium A-D |
|
for vitamins/minerals what should you get?
what should you avoid and why? |
cheapest complete formulation with lots of minerals
avoid taking large doses of single vitamin bc it can cause malabsorption of others |
|
what OTC should you take for dandruff?
Hemorrhoids? |
anyhing with SELENIUM SULFIDE
(nothing else works) Anusol (for the anus! teehee) combined with equal part cortisol |