Term
| What is the drug class/mechanism of action of albuterol? |
|
Definition
B-adrenergic agonist
Selective beta2 agonist |
|
|
Term
| What is the drug class/mechanism of action of cromolyn sodium? |
|
Definition
Mast cell stabilizer
Alter/inhibit delayed Cl-channels on Mast and SM cells |
|
|
Term
| What is the drug class/mechanism of action of epinephrine? |
|
Definition
B-adrenergic agonist
Nonselective alpha, beta1, beta2 agonist. |
|
|
Term
| What is the drug class/mechanism of action of fluticasone? |
|
Definition
Corticosteroid
Binds steroid R complex to change t/s |
|
|
Term
| What is the drug class/mechanism of action of formoterol? |
|
Definition
beta-adrenergic agonist
Selective B2 agonist |
|
|
Term
| What is the drug class/mechanism of action of ipratropium bromide? |
|
Definition
Antimuscarinic
Muscarinic M1,3 antagonist |
|
|
Term
| What is the drug class/mechanism of action of montelukast? |
|
Definition
Leukotriene antagonist
Leukotriene T1 R antagonist |
|
|
Term
| What is the drug class/mechanism of action of omalizumab? |
|
Definition
Anti-IgE monoclonal Ab
Binds circulating IgE |
|
|
Term
| What is the drug class/mechanism of action of prednisone? |
|
Definition
Corticosteroid
Binds steroid R complex to change t/s |
|
|
Term
| What is the drug class/mechanism of action of salmeterol? |
|
Definition
beta-adrenergic agonist
Selective B2 agonist |
|
|
Term
| What is the drug class/mechanism of action of terbutaline? |
|
Definition
B-adrenergic agonist
Selective beta2 agonist |
|
|
Term
| What is the drug class/mechanism of action of theophylline? |
|
Definition
Methylxanthine
Uncertain - likely adenosine R |
|
|
Term
| What is the drug class/mechanism of action of triamcinolone? |
|
Definition
Corticosteroid
Binds steroid R complex to change t/s |
|
|
Term
| What is the drug class/mechanism of action of zileuton? |
|
Definition
Leukotriene antagonist
Inhibits lipoxygenase |
|
|
Term
| What is the drug class/mechanism of action of diphenhydramine? |
|
Definition
First generation H1 antagonist
Prototype |
|
|
Term
| What is the drug class/mechanism of action of chlorpheniramine? |
|
Definition
| First generation H1 antagonist |
|
|
Term
| What is the drug class/mechanism of action of promethazine? |
|
Definition
| First generation H1 antagonist |
|
|
Term
| What is the drug class/mechanism of action of fexofenadine? |
|
Definition
Second generation H1 antagonist
prototype |
|
|
Term
| What is the drug class/mechanism of action of cetirazine? |
|
Definition
| Second generation H1 antagonist |
|
|
Term
| What is the drug class/mechanism of action of desloratadine? |
|
Definition
| second generation H1 antagonist |
|
|
Term
| What is the drug class/mechanism of action of famotidine? |
|
Definition
|
|
Term
| What is the drug class/mechanism of action of cimetidine? |
|
Definition
|
|
Term
| What drugs to treat asthma are bronchodilators? |
|
Definition
Beta adrenergic agonists: SABA, LABA
Methylxantines: theophylline
Muscarinic antagonists: ipratropium bromide |
|
|
Term
| What drugs are used for asthma prophylaxis (antiinflammatory) or suppressive therapy? |
|
Definition
Anti-inflam agents: inhaled/oral CS
Inhibition of mast cell degran: cromolyn sodium, omalizumab
Inhibition of cytokine action, leukotriene pathway inhibitors: zileuton, montelukast |
|
|
Term
| What is used for an asthma-related emergency? |
|
Definition
O2 to relieve hypoxemia
SABA and ipratropium bromide
Systemic CS |
|
|
Term
| What are the types of alkylating agents and examples of each? |
|
Definition
Nitrogen Mustards
Cyclophosphamide
Nitrosoureas
Carmustine
Heavy Metal compounds
Cisplatin
Carboplatin |
|
|
Term
| What are characteristics of tumors that make them sensitive to chemotherapy? |
|
Definition
| Tumors are most sensitive to chemotherapy when the tumor is small and the growth fraction is high. |
|
|
Term
| what is the log-kill hypothesis? |
|
Definition
| “cell kill” hypothesis states that a certain % of cancer cells (not a certain number of cells) will be killed with each course of chemotherapy. Thus, the tumor burden will never reach absolute zero. |
|
|
Term
| What is important to keep in mind when combining antineoplastic drugs? |
|
Definition
each drug is a good treatment as a single agent for that particular tumor
The drugs should have non-cumulative toxicities (but lots of myelosuppression)
The optimal dose and schedule of each agent should be used.
The drugs should be scheduled at consistent intervals |
|
|
Term
| What are Cell cycle specific agents? |
|
Definition
Act at specific stages of the cell cycle especially those stages representing active cell proliferation
Not very effective in G0 |
|
|
Term
| What are cell cycle non-specific agents? |
|
Definition
| Cytotoxic to both cells that are actively cycling as well as to cells in the G0 phase |
|
|
Term
| What are the general areas that are impacted by antineoplastic drugs? |
|
Definition
Hematologic cells: myelosuppression
Epithelium of the GI tract: diarrhea
Hair Follicles: alopecia
Reproductive cells: ability to have children |
|
|
Term
| What is primary resistance of antineoplastic drugs? |
|
Definition
the cancer cells are not susceptible to the cytotoxic effects of the drug
ex. 5FU does not work in leukemia |
|
|
Term
| What is acquired resistance of antineoplastic drugs? |
|
Definition
the cancer cells were originally susceptible to the agent, however, following a course of therapy the cancer cells become resistant to the same drug
ex. 5FU on colorectal cancer works at first and then stops
Specific – cell becomes resistant to only a singe agent or single class of agents
General – multi-drug resistance gene turns on(MDR)- gene directs expression of P-glycoprotein which is a cell membrane pump that pumps drugs out of the cells |
|
|
Term
| Describe the mechanism of general acquired resistance to antineoplastic drugs? |
|
Definition
| General – multi-drug resistance gene turns on(MDR)- gene directs expression of P-glycoprotein which is a cell membrane pump that pumps drugs out of the cells |
|
|
Term
| Where are alkylating agents metabolized? How does that contribute to their function? |
|
Definition
Are metabolized by the liver to form highly reactive electrophiles that react with nucleophilic groups to crosslink DNA and RNA
bifunctional alkyl groups - 2 sites on molecule that can undergo this interaction
1. mispair G-T rather than G-C during DNA synthesis
2. destabilize G ring causing DNA damage
3. bifunctional akylating agents: DNA helix is irreversibly X-linked and causes loss of DNA function |
|
|
Term
| What is the dose-limiting toxicity of cyclophosphamide? |
|
Definition
| Dose limiting toxicity = bone marrow suppression (leukopenia nadir = 8-14 days) |
|
|
Term
| What is cyclophosphamide used for? |
|
Definition
1. NH lymphoma
2. combo treatment breast cancer
3. single agent Burkitt's lymphoma
4. purge lymphoma/leukemic cells before bone marrow transplant |
|
|
Term
| What are the side effects of cyclophosphamide? |
|
Definition
Hematologic cells: BM suppression and leukopenia
Epithelium of the GI tract: severe nausea/vomiting
Hair Follicles: alopecia
Reproductive cells: amenorrhea
hemorrhagic cystisis possible but minimized by diluting urine or coadmin mesna (thiol compound) |
|
|
Term
| What alkylating agent causes hemorrhagic cystitis? How do you prevent it? |
|
Definition
| hemorrhagic cystisis possible but minimized by diluting urine or coadmin mesna (thiol compound) |
|
|
Term
| How does Carmustine work? |
|
Definition
| Non-enzymatic degradation to highly reactive intermediates that alkylate DNA bases. |
|
|
Term
| What is carmustine used for? |
|
Definition
Primary brain tumors, H lymphoma
topically for cutaneous T-cell lymphomas (mycosis fungoides) |
|
|
Term
| What is the dose-limiting toxicity associated with carmustine? |
|
Definition
| MYELOSUPPRESSION: late (3-5wk) leukopenia |
|
|
Term
| What are the SE of carmustine? |
|
Definition
Hematologic cells: myelosuppression
Have to inject with OH: DRUNK |
|
|
Term
| How do cisplatin and carboplatin work? |
|
Definition
Enter cell by passive diffusion
Intercellular removal of Cl activates the platinum
Bifunctional akylating agent to form both intrastrand and interstrand links w/ DNA through N7 G and A
Stops DNA replication but still cell cycle nonspecific!! |
|
|
Term
| How can a patient develop resistance to cisplatin? |
|
Definition
1. Decreased accumulation = stop passive diffusion
2. increased intracellular gluathione that inactivates cisplatin
3. Alterations in the rate of DNA repair |
|
|
Term
| What are cisplatin and carboplatin used for? |
|
Definition
Solid tumors
1. Combo treatment of testicular cancer = curable
2. +paclitaxel first line for stage 3/4 ovarian cancer
3. NSC lung cancer, bladder cancer, head/neck cancers |
|
|
Term
| What is the dose-limiting SE of cisplatin? |
|
Definition
Nephrotoxicity: damage to proximal and distal renal tubules
Hyperhydrating patients can help prevent this |
|
|
Term
| What are the SE of cisplatin? |
|
Definition
1. High dose/prolonged dose neurotoxic
peripheral neuropathy w/ paresthesia in fingers/toes
2. ototoxicity = tinnitus and loss of hearing in high frequency
3. nephrotoxicity!!
4. Severe nausea/vomiting needs pretreatment w/ anti-emetics |
|
|
Term
| What is carboplatin most frequently used for? |
|
Definition
| Lung/ovarian cancer but similar clinical application as cisplatin |
|
|
Term
| What is SE profile of carboplatin? How is it different from cisplatin? |
|
Definition
NO ototoxicity, peripheral neuropathy
Has nausea and vomiting (less severe)
Less common kidney disease
CAUSES MYELOSUPPRESSION (neutropenia/thrombocytopenia = DL toxicity |
|
|
Term
| What are the antimetabolite antineoplastic drugs? |
|
Definition
Folic acid antagonists
Methotrexate
Pyrimidine Antagonists
5FU
Cytarabine (AraC) |
|
|
Term
| How does methotrexate work? |
|
Definition
Competitive inhibitor of DHFR that converts FH4 to methylene FH4
Thus metFH4 can't be used to add a methyl group to dUMP->dTMP
THUS DEPLETION OF TH4 CAUSES INHIBITION OF dTMP SYNTH
Additionally: interfere w/ purine biosynthesis and RNA synthesis
CELL CYCLE SPECIFIC IN S PHASE |
|
|
Term
| Is methotrexate cell cycle specific? What phase? |
|
Definition
|
|
Term
| What is leucovorin used for? |
|
Definition
Given a day after methotrexate for planned rescue of noncancer cells
Provides TH4 for cells w/o going through enzyme steps. |
|
|
Term
| What cancers get high-dose methotrexate + leucovorin? |
|
Definition
osteosarcoma
less often: advanced NH lymphoma |
|
|
Term
| How does cancer develop resistance to methotrexate? |
|
Definition
1. Decreased transport
2. Alteration in DHFR
- induce expression to increase enzyme activity
- make altered DHFR |
|
|
Term
| What is methotrexate used for? |
|
Definition
Acute lymphoblastic leukemia
NH lymphoma
choriocarcinoma
Osteosarcoma
Breast cancer/bladder cancer
Given intrathecally for CNS leukemia, lymphoma, brain metastasis |
|
|
Term
| What are the dose limiting toxicities of methotrexate? |
|
Definition
myelosuppression and mucositis
(max at 10 days) |
|
|
Term
| What are the SE of methotrexate? |
|
Definition
1. myelosupp and mucositis
2. High dose = severe nephrotoxicity b/c of precipitates and metabolites in acidic urine
= alkalinization and hydration of pt
MUST MONITOR IF ON HIGH DOSE REGIMEN (>100MG/M2) |
|
|
Term
|
Definition
Gets converted to F-dUMP which is an inhibitor of thymidylate synthase so dTMP cannot be made for DNA synthesis
Can also be converted to F-UTP which is incorporated into RNA
CELL CYCLE SPECIFIC IN S AND G1 phases of cell cycle |
|
|
Term
|
Definition
| treatment of solid tumors in colon, head/neck, breast |
|
|
Term
| Why would you give leucovorin with 5FU? |
|
Definition
Causes high levels of reduced folates in cell - helps FdUMP bind tighter to thymidylate synthase causing it to be more toxic to tumor/host
=> used for colorectal cancer |
|
|
Term
|
Definition
If given as bolus: Myelosuppression
If prolonged infusion: diarrhea, mucosidis
combo w/ leuco = mucositis |
|
|
Term
| How does cytarabine work? |
|
Definition
Prodrug metabolized by deoxycytidine kinase to AraCMP gets incorporated into DNA stoping template function and DNA elongation
Cell cycle specific during S phase |
|
|
Term
| How do tumor cells develop resistance to AraC? |
|
Definition
1. deficiency in activity of deoxycytidine kinase for activation
2. increased activity of enzymes that convert AraCMP to inactive metabolites |
|
|
Term
| What is Cytarabine used for? |
|
Definition
Very important for acute myelogenous leukemia
Other leukemias and NH lymphomas
LD intrathecally into CSF or liposomally for brain tumors
High doses used to overcome R, overwhelm system or consolidating treatment |
|
|
Term
| What are SE of Cytarabine? |
|
Definition
SEVERE MYELOSUPPRESSIVE EFFECTS = leukopenia, thrombocytopenia, anemia
GI: nausea, vomiting, diarrhea subside after stopping treatment
HD:
ocular toxicity = keratoconjunctivitis - secreted in tears that should be prevented with prophylactic steroid drops
Cerebellar toxicity
Skin rash
Palmar-plantar erythrodysesthesia (hand-foot syndrome) |
|
|
Term
| What class of drug does irinotecan belong to? |
|
Definition
| topoisomerase I antagonist |
|
|
Term
| How does irinotecan work? |
|
Definition
topo I is an enzyme that produces a single-standed nick in DNA to relax localized supercoiling of DNA during unwinding of DNA helix and results in formation of cleavable complexes in DNA strand that are needed for DNA rep and RNA t/s to proceed
noncovalently acts on topo I to prevent religation ofDNA strands -> causes ds brankes |
|
|
Term
|
Definition
|
|
Term
| How do cells develop resistance to irinotecan? |
|
Definition
| Mutations in topoI or make decreased amounts of topo I |
|
|
Term
| What is the dose-limiting toxicity associated with irinotecan? |
|
Definition
Neutropenia
Other SE:
1. Acute Diarrhea that is Ach related
Prevent by giving IV atropine
2. Delayed GI slowing 7 days later treated w/ lopiramide OTC above the amount given for recommended dose
3. thrombocytopenia
4. Alopecia
5. Headache/fever |
|
|
Term
| What class does vimcristine belong to? |
|
Definition
| Antimitotic agent - Vinca alkaloid |
|
|
Term
| What is MOA of Vimcristine? |
|
Definition
| binds to tubulin protein to preent polimerization of MTs to disrupt mitotic spindle, prvent completion of mitosis and arrest cell division in metaphase |
|
|
Term
|
Definition
|
|
Term
| How do you develop resistance to Vincristine? |
|
Definition
| Increased expression of MDR-1 with enhanced activity of P glycoprotein so decreased accumulation |
|
|
Term
| What are SE of vincristine? |
|
Definition
Neurological toxicity: disruption of axonal mts: manifests as numbness and tingling of extremities, loss of deep tendon reflexes, weakness of limbs
- reversible on discontinuation or reduction of dose; warranted on development of motor dysfunction
advanced motor dysfunction is irreversible
Myelosuppression is less frequent |
|
|
Term
| What is MOA of paclitaxel? |
|
Definition
| binds to beta tubulin of mts and prevents disassembly or depolymerization of this complex and causes inhibition of their ability to reorganize; mts are nonfunctional and cells arrest in mitosis |
|
|
Term
| What is MOA of docetaxel? |
|
Definition
| binds to beta tubulin of mts and prevents disassembly or depolymerization of this complex and causes inhibition of their ability to reorganize; mts are nonfunctional and cells arrest in mitosis |
|
|
Term
| What causes resistance to taxanes? |
|
Definition
Alterations in MT structure or assembly causing diminished effectiveness of drug
Or increased expression of P-glycoproteins |
|
|
Term
| what are the dose-limiting toxicities of the taxanes? |
|
Definition
| Myelosuppression = neutropenia and leukopenia; associated w/ development of peripheral neuropathy and present as 'stocking and glove' numbness and paresthesia |
|
|
Term
| What is the SE of paclitaxel not seen with docetaxel? |
|
Definition
HS rxn of dyspnea, bronchospasm, hypotension, urticaria b/c of cremophor EL vehicle
Give antihistamines and CS like dexamethasone proph |
|
|
Term
| What is the SE of docetaxel not seen w/ paclitaxel? |
|
Definition
fluid retention; increase in cap permeability seen as peripheral edema and weight gain
Severely causes pleural effusion, dsypnea at rest and cardiac tamponade
Premed w/ steroids to reduce severeity and delay onset of severe fluid retension
half of people get vesicular pruritic rash w/ localized eruptions on hands/ feet/ forearms but can get to face/thorax; resolves w/in weeks of discontinuation
alopecia in everyone |
|
|
Term
| What class of drugs does doxorubicin belong to? |
|
Definition
|
|
Term
| What is MOA of doxorubicin? |
|
Definition
| Intercalation of DNA; DNA breakage and interference w/ DNA replication -> results in intracellular generation of free radicals causing mito destruction |
|
|
Term
|
Definition
| Nooo =. Cell cycle nonspecific but majority of cytotoxic effects on S phase of cell cycle |
|
|
Term
| How do you develop resistance to doxorubicin? |
|
Definition
| INcreased expression of P-glycoproteins |
|
|
Term
| What is the SE profile of doxorubicin? |
|
Definition
Bone marrow suppression that is short term
Total hair loss
Cardiomyopathy!! (don't give to people w/ hten or cardiac disease and give continuous IV to prevent cardiotox)
Acute: electrophysiology changes; devlt of arrhythmias and sinus tachy
Chronic: cumulative, dose-related; CHF not responsive to dig therapy - fatal so stop when see cardiac toxicity
RAdiation recall
Mucositis, diarrhea |
|
|
Term
| What class of drugs does bleomycin belong to? |
|
Definition
|
|
Term
| What is MOA of bleomycin? |
|
Definition
| Binds to DNA w/ O2 and Fe to make O2 free radicals to cause DNA scission |
|
|
Term
|
Definition
| Yes and max cytotoxic effects in S and G2 phase of cell cycle |
|
|
Term
| What causes resistance to bleomycin? |
|
Definition
| Increased drug inactivation |
|
|
Term
| What are SE of bleomycin? |
|
Definition
Little/no myelosuppression so given when other drugs have caused myelosupp
Pulmonary toxicity!! pneumonitis w/ pulm fibrosis: dry cough, rales, dyspnea - may be irreversible and can cause death
Cutaneous effects: erythema, hyperkeratosis, hyperpigmentation, ulceration in pressure areas like hands, fingers, joints |
|
|
Term
| What class of drug does tamoxifen belong to? |
|
Definition
| hormonal agent: selective ER modulator |
|
|
Term
| What is the MOA of tamoxifen? |
|
Definition
| antagonist on ER - so only works on ER+ breast carinomas |
|
|
Term
| What cancers would you use tamoxifen for? |
|
Definition
meatastatic breast cancer in post-men women and in women at high risk of recurrence: cytotoxic
used after surgery/radiation
Used in pre-me women but other therapy also needed
Chemopreventive in women that are at high risk for breast cancer |
|
|
Term
| What are SE of tamoxifen? |
|
Definition
Only seen in half of people:
mimic menopause: hot flashes, nausea, fluid retension
LT: endometrial proliferation and develop endometrial cancer
thrmoboembolism maybe b/c of partial agonist effects on ERs
Good for bones/lipoproteins |
|
|
Term
| What class does anastrozole belong to? |
|
Definition
| Hormone agent: Aromatase inhibitor |
|
|
Term
| What is MOA of anastrozole? |
|
Definition
Competative Nonsteroidal aromatase inhibitor
aromatase: cytochrome P450 containing enzyme that acts in final step to convert androstenedione, testosterone to estradiol and estrone in muscle, fat, liver, epi, stromal cells |
|
|
Term
| What is anastrozole good for? |
|
Definition
in post-menopausal women, see decrease in levels of E but do not see decrease in mineralocorticoids or glucocorticoid synthesis
First line in breast cancer in post-men women w/ hormone R+ or hormone R status unkown diesease that is locally advanced or metostatic
Advanced breast cancer in post-men women w/ disease progression following tamoxifen treatment |
|
|
Term
| What are SE of anastrozole? |
|
Definition
Well tolerated, ST similar to tamoxifen
nausea, hot flashes, back pain, arthralgias, myalgia and osteoporosis
vaginal bleeding, remits after few weeks |
|
|
Term
| What drug class does leupromide belong to? |
|
Definition
| hormonal agent: gonadotropin (LH) releasing hormone agonist |
|
|
Term
| What is MOA of leupromide? |
|
Definition
analog of GnRH and acts as agonist at GnRH R in anterior pituitary
initially stimulation of R and incrase in FSH/LH
eventually downregulation of GnRH R w/ loss of FSH/LH production
decreased T synthesis by leydig cells of testis and E synth by ovaries
occurs 1-2 wks after admin |
|
|
Term
| What does leupromide treat? |
|
Definition
Advanced prostate cancer; medical castration and alternative to surgery
Premeno somen w/ ER+ breast cancer |
|
|
Term
| What are SE of leupromide? |
|
Definition
hot flashes, diaphoresis, testicular atrophy, impotence
1. initally cuases flaring of bone pain w/ prostate cancer b/c of increase in FSH/LH
minimized if you give antiandrogen flutamide |
|
|
Term
| What class does flutamide belong to? |
|
Definition
| Hormonal agent: antiandrogen |
|
|
Term
| What is MOA of flutamide? |
|
Definition
| Nonsteroidal compound that inhibits T binding to androgen R |
|
|
Term
| What does flutamide treat? |
|
Definition
| metastatic prostate cancer and used w/ leuporomide |
|
|
Term
| What are SE of flutamide? |
|
Definition
decreased libido, impotence, hot flashes, gynecomastia
Hepatotoxicity: reversible or hepatic necoris leading to liver failure |
|
|
Term
| What class does prednisone belong to? |
|
Definition
|
|
Term
| How does prendisone have an antineoplastic effect? |
|
Definition
marked lympholytic effects;
binds to cytoplasmic glucocort R and hormone-R complex acts on GRE on genes to activate/inhibit gene t/s
In leukemic/lymphoid cells causes cell death via apoptosis through induction/repression of pro-apoptotic and anti-apoptotic genes |
|
|
Term
| How do cancers develop resistance to prednisone? |
|
Definition
| increased expression of p-glycoprotein |
|
|
Term
| Are ty kin inhibitors CCS? |
|
Definition
|
|
Term
| Are ty kin inhibitors CCS? |
|
Definition
|
|
Term
| What class odes imatinib belong to? |
|
Definition
|
|
Term
| What is the imatinib MOA? |
|
Definition
CML due to philadelphia chromosome where abl from chrom 9 is translocated to chrom 22 in front of bcl gen:
bcl-abl ty kin is constituitvely active and causes CML to increase cell prolif, enhanced cell survivial due to inhibition of apoptosis and alteration in cell adhesion to BM stroma or ECM, also accumulates more malignant transfmrations
Competitive inhibitor at the ATP binding site of bcl-abl and so prevents ability to phos proteins |
|
|
Term
| What does imatinib treat? |
|
Definition
CML in chronic phase after failure/intolerance of IFN-alpha therapy, in accelerated phase or in blast crisis
-remission of 95% of chronic phase
- not as good in other stages
also for inoperatible GI stromal tumors b/c inhibits Kit ty kin (TM R ty kin that is consit active in malignant cells) |
|
|
Term
|
Definition
GI irritation, muscle cramps, fluid retension
- mild/moderate peripheral edema; 1-2% get fluid retension; neutropenia, thrombocytopenia, severe hepatotoxic rxns |
|
|
Term
| What causes resistance to imatinib? |
|
Definition
| No blc-abl signaling or amplification of bcl-abl |
|
|
Term
| What class does trastuzumab belong to? |
|
Definition
|
|
Term
| What is the MOA of trastuzumab? |
|
Definition
Ab against EC domain of HER2 protein
Her2 gene makes TM ty kin R that makes more DNA and faster growth rates; increased metasisis and hormone-indep breast cancer
action:
1. NK cells/monocytes destroy ab-coated cells
2. R internalization or downregulation
3. disrupt shedding of her2 protein - short forms have enhanced signaling properties |
|
|
Term
| What is trastuzumab used to treat? |
|
Definition
first line treatment in metastatic breast when used w/ paclitaxcel
2nd/3rd line agent when used alone
better if pts have marked exp of Her2
approved for women w/ Her2+ breast cancer after surgery |
|
|
Term
| What are SE of trastuzumab? |
|
Definition
cardiomyopathy causing CHF (III-IV) when alone
increased when use doxorubicin and cyclophos
symp: dyspnea, cough, edema, S3 gallop, reduced EF, death, mural wall thrombosis and stroke
Must monitor cardiac function
Severe HS rxn is rare w/ ARDS and fatal anaphylactic shock |
|
|
Term
| What class does cetuximab belong to? |
|
Definition
| humanized monoclonal Ab that is anti-angiogenic |
|
|
Term
| What is MOA of cetuximab? |
|
Definition
| humanized monoclonal Ab for EGFR; blocks tumor growth/invasion and metastasis dep on EGFR activity |
|
|
Term
| What are SE of cetuximab? |
|
Definition
interstitial lung disease, severe achneform rash which can develop superinfictions (these rashes indicate that the drug is killing the tumor though),
hypotension,
infusion rxn: rarely fatal, includid rapid onset of airway obstruction, urticaria, hypotension |
|
|
Term
| What class of drugs does bevacizumab belong to? |
|
Definition
| humanized monoclonal AB for VEGF |
|
|
Term
| What is MOA of bevacizumab? |
|
Definition
blocks binding of VEGF to R to prevent growth/maintenance of bv that sustain tumors
- used w/ 5FU and leucovorin |
|
|
Term
| What are SE of bevacizumab? |
|
Definition
heachache, nausea, vomiting, anorexia, constipation, URI, epitaxis, dyspnea, proteinuria
less prevalent: hyperten crisis, nephrotic syndrome, hemorrhage, CHF, GI perofiration, wound healing complications! |
|
|
Term
| What does high intake of iodine cause? What happens after 2 weeks? |
|
Definition
Inhibits the hormone biosynthesis for 10-14 days in normal thyroid glands (the reason for using iodine for treatment of thyrotoxicosis): inhibits organification, trapping and proteolysis
May cause hypothyroidism in susceptible thyroid glands that are not able to escape from the inhibitory effects of iodine (e.g. autoimmune thyroiditis).
Can induce hyperthyroidism in patients with MNG or Grave’s disease (lack of autoregulation). |
|
|
Term
| How does I- get into follicular cells? Why is it concentrated there? |
|
Definition
| NA-I symporter is only expressed on follicular cells; Peroxidase converts I- to I to trap it there |
|
|
Term
| What compounds inhibit TSH release? |
|
Definition
somatotropin, dopamine, dopamine agonists (bromocriptine), and glucocorticoids
Acute/chronic disease |
|
|
Term
|
Definition
ganglioside: activates adenylate cyclase, more cAMP, PK activated, PO4 I transporter to increaseuptake
gycoprotein site: PI activates next steps (peroxidase) of TH synthesis |
|
|
Term
|
Definition
on TR that can be homodimer or heterodimer w/ retinoid X receptor (RXR)
T3+TR causes conformation hange and HAT recruitment which acetylates histones causing open histone to make more mRNA
T3 has 10 times higher affinitiny than T4 for TR
cyotosolic/intranuclear T3 concentration higher than T4 (cytosolic 5'-deiodinase converts T4 to T3)
40% of TR is occupied normally so baseline TH is always needed |
|
|
Term
| Symptoms of hypothyroidism? |
|
Definition
Weight gain, lethargy, cold feeling, croaky voice, constipated
Signs: Puffy face, slow reflexes, low pulse, dry skin,� |
|
|
Term
| signs of hyperthyroidism? |
|
Definition
Symptoms: Weight loss, diarrhea, anxiety, palpitations
Signs: Soft skin, high pulse rate, high BP� |
|
|
Term
| Most common cause of hypothyroidism? |
|
Definition
|
|
Term
| Most common cause of hyperthyroidism? |
|
Definition
|
|
Term
| Function of TH in the body? |
|
Definition
1. Normal growth and function of thyroid hormone-responsive organs (all except spleen & testes
2. Normal metabolism of carbohydrate, lipid, protein, and vitamin, and thus maintain normal basal metabolic rate (BMR)
3. Normal calorigenesis and thermogenesis
4. Normal synthesis, secretion, and degradation of other hormones and neurotransmitters e.g. catecholamines = THIS IS WHY YOU USE BETA BLOCKERS IN THYROID STORM |
|
|
Term
| What is the MOA of levothyroxine Sodium? |
|
Definition
|
|
Term
| What is the MOA of liothyronine sodium? |
|
Definition
|
|
Term
| Advantages/disadvantages of levothyroxine sodium? |
|
Definition
|
|
Term
| Advantages/DA of liothyronine Sodium? |
|
Definition
Fast onset of action (~1 hr), but has short half-life (1 day), and expensive
will cause low T4, norm/high T3 and normal TSH
don't use in elderly b/c of bone/heart problems |
|
|
Term
| What can cause lack of response to exogenous T4 administration? |
|
Definition
Insufficient dose of T4
Lack of compliance
Lack of GI absorption
-Malabsorption syndrome
-Drugs affecting T4 absorption: calcium
iron
cholestyramine |
|
|
Term
| How do you manage a pt w/ hypotyroidism during pregnancy? |
|
Definition
T4 therapy should be adjusted closely during pregnancy (increased during pregnancy and decreased to the baseline after delivery).
Fetus is dependent on maternal thyroid hormone before the 11th week of gestation, therefore untreated pregnancy can cause hypothyroidism in newborn (mental retardation and neurological defects). |
|
|
Term
|
Definition
| Autoimmune production of TSH receptor antibody (TRAB) that can stimulate I- transporter & thyroid hormone synthesis |
|
|
Term
| What is toxic multinodular or toxic adenoma? |
|
Definition
| Focal and/or diffuse hyperplasia of thyroid follicular cells with autonomic function |
|
|
Term
| What drug can elevate I and cause thyrotoxicosis? |
|
Definition
● Amiodarone 1) is an antiarrhythmic drug
2) contains ~37 % iodine by weight
3) is stored in fat, myocardium, liver, and lung and has a half-life of about 50 days.
● 2% of patients treated with amiodarone develop thyrotoxicosis.
● Thyrotoxicosis is caused due to excessive iodine or amiodarone-induced thyroiditis (inflammation and release of stored hormone into the bloodstream). |
|
|
Term
| What are symptoms of a thyroid storm? |
|
Definition
fever, nausea, vomiting, diarrhea, agitation, restlessness, delirium, tachycardia w/ A fib
Medical emergency |
|
|
Term
| What is the MOA of potassium perchlorate? |
|
Definition
Inhibits I- binding to NIS & inhibits I– release to lumen; stimulate discharge of I from thyroid gland
� |
|
|
Term
| What are the SE of potassium perchlorate? |
|
Definition
GI irritation; Nausea, vomiting, fever, rashes; Aplastic anemia
� |
|
|
Term
| What is the MOA of propylthiouracil? |
|
Definition
Inhibits thyroid peroxidase reaction (no iodination/coupling rxn) & peripheral 5’-deiodinase
(5’-DID) |
|
|
Term
| What is SE of propylthiouracil? |
|
Definition
Bitter taste; Rashes; agranulocytosis; GI discomfort; hepatitis
|
|
|
Term
| What is the MOA of methimazole? |
|
Definition
DOC
Inhibits peroxidase reaction
NO activity on DID |
|
|
Term
| What are the SE of methimazole? |
|
Definition
Obstructive jaundice, agranulocytosis
NOT USED IN 1ST TRIMESTER OF PREGNANCY |
|
|
Term
| What function does propranolol play in hyperthyroidism? What is the class? |
|
Definition
Beta blocker
reduces peripheral actions of TH
rapid temp symptomatic releif in thyroid storm
May inhibit DID
BAD for asthmetics, late stage CHF |
|
|
Term
| How do you manage hyperthyroidism in pregnant/nursing women? |
|
Definition
Most common etiology is Graves disease
The goal is to keep the mother’s free T4 in the high-normal range (non-pregnant level) using the lowest drug since thionamides cross placenta and can cause hypothyroidism in fetus.
PTU for first trimester and MMI from second trimester are used for treatment of hyperthyroidism (teratogenicity of MMI-aplasia cutis, tracheoesophageal fistulas, choanal atresia).
Both MMI and PTU safe for nursing mothers |
|
|
Term
| How are TH and antiTH drugs metabolized? |
|
Definition
99% T4 and T3 TBG bound; in plasma mostly deiodinated- excreted in feces
75% PTU is protein bound; excreted in urine
liver disease decrease met of MMI |
|
|
Term
| Describe the mechanism for insulin secretion in beta cells. |
|
Definition
increased glu levels -> GLUT2 transports inside
metabolism of glu through glycolysis and oxphos making ATP
ATP causes closure of specific ATP-sensitive K+ channels (Katp) in cell membrane
Depol opens Ca channels and increase in Ca causes insulin exocytosis |
|
|
Term
| Describe insulin action on R of target tissues. |
|
Definition
binding of insulin to alpha subunit
Beta subunis autophosphorylate at tyrosine sites
phosphorylate specific proteins called IRS-1 and 2
activates several proein kinases
Activation of PI3-kinase causes mobilization of GLUT4 to cell membrane and glucose uptake |
|
|
Term
| What are the ultra short-acting insulin preparations? How long is their duration of action? |
|
Definition
|
|
Term
| What are the short acting insulins? |
|
Definition
Regular insulin
works for 3-6 hours |
|
|
Term
| What are the intermediate acting insulins? |
|
Definition
| NPH works for 10-16 hours |
|
|
Term
| What are the long acting insulins? |
|
Definition
Detemir for 14-20 hours
Glargine for 20-26 hours |
|
|
Term
| What is pramlintide? What is it's MOA? SE? |
|
Definition
Analog of amylin for T1 and 2 diabetics
Amylin is cosecreted w/ insulin - give before a meal
1. slows gastric emptying into intestine
2. suppresses glucagon and endogenous glucose production by liver during/after meals
3. satiating effect
SE: nausea, vomiting, headache, anorexia |
|
|
Term
| What are the SE of insulin therapy? |
|
Definition
1. hyoglycemia!! (excessive hunger, sweating, paresthesias, palpitations, tremor, anxiety, not concentrating, confusion, weakness, feelign of warmth, dizziness, blurred vision) -> give sugar, IV dextrose, glucagon injection
2. insulin allergy/resistance- b/c of protamine in the formulation; antihist or glucocortocoids for insulin resistance
3. lipoatrophy and lipohypertrophy: atrophy or enlargment of subQ fat deposits at site of repeated injections; rotate sites
3. insulin edema: edema, ab bloating, blurred vision b/c of severe hyperglycemia and ketoaidosis treated w/ high doses of insulin |
|
|
Term
| How is insulin metabolized? |
|
Definition
50% in the liver; 35% kidney; rest in peripheral tissue
decrease doses in reenal insufficiency b/c of greater liklihood of hypoglycemia |
|
|
Term
| glipizide belongs to what class of drug? What is MOA? |
|
Definition
2nd gen sulfonylureas.
Block Katp channel to cause more insulin secretion |
|
|
Term
| acarbose belongs to what class of drug? What is the MOA? |
|
Definition
alpha-glucosidease inhibitor
stop alpha glucosidase hydrolase and alpha amylase in gut lumen to delay absorption and metabolism of carbs |
|
|
Term
| Metformin belongs to what class of drug? What is the MOA? |
|
Definition
Biguanides
Decrase insulin R by unknown mechanism
Decrease hepatic glu production by stopping gluconeogenesis and increase glu uptake and metabolism in adipose/muscle cells |
|
|
Term
| Pioglitazone belongs to what class of drug? What is the MOA? |
|
Definition
Thiazolidinedione
Activates TF peroxisome proliferation-R activator gamma that increase t/s of genes in lipid/glu metabolism (like GLUT4) |
|
|
Term
| Repaglinide belongs to what class of drug? What is the MOA? |
|
Definition
Meglitinide
Incrase isnulin secretion via unique R and have no intracellular action |
|
|
Term
| Sitagliptin belongs to what class of drug? What is the MOA? |
|
Definition
DPP4 inhibitor
stop degredation of incretins (GLP1 and GIP) that potentiate insulin synthesis and release by pancreating beta cells and decrease glucagon production by alpha cells in glu-dep manner to lower serum glu concentration |
|
|
Term
| Exenatide belongs to what class of drug? What is the MOA? |
|
Definition
incretin mimetics
enhances glu-stimulated insulin secretion from pancreas and exhibits antihyperglycemic actions like incretins (GLP2)
Not used in type 1 patients other than treating hyperglycemia/ketoacidosis |
|
|
Term
| What are the SE of glipizide? |
|
Definition
disulfiram rxn: inhibits aldehyde dehydrogenase that breaks down aldehyde generated by OH - aldehyde toxicity upon drinking
Don't use if renal/liver problems
hypoglycemia, weight gain, GI discomfort, blood dyscrasias, cholastatic jaundice,
increased liver function tests |
|
|
Term
| What are the SE of acarbose? |
|
Definition
LIVER PROBLEMS: test liver often, use other drugs
Gas and GI discomfort = slow titration
increased LFT values |
|
|
Term
| What are the SE of metformin? |
|
Definition
lactic acidosis IF RENAL INSUFFICIENCY OR REASONS B/C OF TISSUE HYPOXIA AND EXCESSIVE LACTIC ACID PRODUCTION (MI)
GI discomfort so slow administration
alteration of taste,
megaloblastic anemia
DOES NOT CAUSE HYPOGLYCEMIA
excreted in urine so not to be given if renal insufficiency |
|
|
Term
| What are the SE of pioglitazone? |
|
Definition
FDA warning b/c CV system accumulation if used alone
Mild/moderate edema
anemia
increased blood chol
fluid accumulation in HF pts (retain H20 and Na)
LFT needed |
|
|
Term
| What are the SE of repaglinide? |
|
Definition
hypoglycemia
weight gain
no disulfiram rxn b/c no sulfur |
|
|
Term
| What are the SE of sitagleptin? |
|
Definition
Well tolerated
no weight gain/hypoglycemia |
|
|
Term
| What are the SE of exenatide? |
|
Definition
hypoglycemia, don't used w/ pregnant women
BUT WEIGHT LOSS SO GOOD |
|
|
Term
What is hydrocortisone?
What is it used for? |
|
Definition
Cortisol - major carb-regulating steroid in humans
PREFERRED DRUG FOR REPLACEMENT THERAPY
Not good for anti-inflammatory/salt-retaining actions
Short half life (1-2hrs)
Used for tapering of glucocorticoid therapy |
|
|
Term
|
Definition
increased anti-inflammatory potency and decreased mineralocorticoid activity.
Anti-inflammations are 10X greater than salt-retaining actions
Good choice for chronic anti-inflamm therapy b/c of intermediate half-life. |
|
|
Term
|
Definition
C(16)methyl fluro-derivatives of prednisolone.
High anti-inflammatory potency w/ essentially no mineralocorticoid activity and long half life (36hrs)
GOOD FOR ACUTE ANTI-INFLAMMATORY THERAPY WHERE YOU WANT MAX STRENGTH (septic shock, cerebral edema)
Not good choice for chronic use b/c growth suppressive and bone demineralization actions |
|
|
Term
|
Definition
Established to protect the right of consumer access and availability to safe dietary supplements
1) Provide a venue to augment daily diets, promote wellness and provide health benefits
2) Potential connection between dietary
supplement use, reduced healthcare
expenses, and disease prevention
Dietary supplements are in a special •
category under the general umbrella of "foods" so must have ingredient label, ID as dietary supplement and manufacturer is responsible for making sure it's safe/don't lie about what the drug does |
|
|
Term
| What is FDA's role in regulating dietary supplements versus the manufacturer's responsibility for marketing them? |
|
Definition
Manufacturers do not need to register supplement products with FDA before producing or selling them
FDA has the responsibility for showing that supplement is "unsafe”, before it
can take action to restrict the product's use or removal from the marketplace
FDA does not regulate minimal standard of practice: can have contaminants/other ingredients
Manufacturer (not FDA) is responsible for ensuring the accuracy and truthfulness of claims:
Health Claims
Structure/Function Claims
Nutrient Content Claims |
|
|
Term
| What are the niacin-drug interactions? |
|
Definition
Lipid-lowering drugs (i.e., “statins”) –
increase side effects of statins
Anti-convulsants (i.e., carbamazepine)
– levels of anti-convulsants increased
Anti-diabetic agents (i.e., metformin,
glipizide) – actions antagonized
Anti-hypertensive drugs (i.e., nitrates,
Ca2+ channel blockers or alpha1 receptor antagonists) – potentiate hypotension |
|
|
Term
| What forms is vitamin B3 available in? Water/fat soluble? what is the prescription form used to treat? |
|
Definition
Water-soluble vitamin
•Vital in cell metabolism
•Available as a supplement in three forms: nicotinic acid (nicotinate),
niacinamide, and inositol hexaniacinat
Script used to lower cholesterol |
|
|
Term
| What are the potential uses of niacin supplements? |
|
Definition
Reduces Cholesterol
Useful for Circulatory Problems (i.e., relaxes blood vessels)
Has Anti-inflammatory Effect(i.e., benefit in rheumatoid arthritis)
Repairs cartilage (i.e., benefit in osteoarthritis |
|
|
Term
| What are the adverse effects of niacin? |
|
Definition
Skin Flushing
GI distress
Severe liver damage
Myopathy and Maculopathy
Metabolic Acidosis
Blood Disorder |
|
|
Term
| What are the contraindications of niacin? |
|
Definition
Individuals with liver disease, gout or ulcers
Individuals with diabetes
High alcohol consumption |
|
|
Term
| Is Vitamin C fat/water soluble? What forms is it available in? |
|
Definition
Essential water-soluble vitamin
Supplements: ascorbic acid, calcium ascorbate, sodium ascorbate, or a combination of these forms |
|
|
Term
| What is Vitamin C used for? |
|
Definition
Vitamin C deficiency
(Helps the body produce collagen
Acts as an antioxidant
Involved in the metabolism of phenylalanine and tyrosine
Enhances iron absorption from supplements and plant foods)
CV disease
Cancer
But megadoses do not help w/ colds or heart disease or cancer progression |
|
|
Term
| What are adverse effects of Vitamin C toxicity? |
|
Definition
GI distress: diarrhea, gas, bloating
Interfere with copper and selenium absorption
Cause iron overload |
|
|
Term
| What are the Vitamin C-drug interactions? |
|
Definition
Preparations containing grapefruit flavonoids inhibit cytochrome P450
Drugs affected:
felodipine (Ca 2+ channel blocker)
cyclosporine
lovastatin and simvastatin
carbamazepine (anti-convulsant agent |
|
|
Term
| Is vitamin D fat/water soluble? What forms does it come in? |
|
Definition
Fat-soluble vitamin
Two major forms of vitamin D:
Vitamin D3(formed in skin by exposure to sunlight)
Vitamin D2(added to milk and other foods, and used as a supplement) |
|
|
Term
| What is Vitamin D used for? |
|
Definition
Prevention and treatment of osteoporosis
Individuals who have reduced ability to
absorb dietary fat (i.e., Crohn’s disease)
Breast-fed infant |
|
|
Term
| What are the adverse effects of vitamin D toxicity? |
|
Definition
GI distress: nausea, vomiting, constipation
Poor appetite and weight loss
Raise blood levels of calcium – resulting in confusion and cardiac arrhythmias
Calcinosis (the deposition of calcium and phosphate in soft tissues like the kidney) |
|
|
Term
| What are the contraindications to Vitamin D? |
|
Definition
| Individuals with sarcoidosis or hyperparathyroidism |
|
|
Term
| What are the vitamin D-drug interactions? |
|
Definition
Verapamil (Ca •2+channel blocker)
Thiazide diuretics – result in elevated Ca2+levels
Steroids – may impair vitamin D metabolism |
|
|
Term
| What is coenzyme Q10? is it fat/water soluble? Where is it found in the body? |
|
Definition
Vitamin-like substance
Lipophilic, water-insoluble substance Belongs to family of ubiquinones
Essential component of the electron transport chain in mitochondria
Antioxidant activity in mitochondria and cellular membranes
- protects against peroxidation of LDL-cholesterol |
|
|
Term
|
Definition
Cardiovascular Disease: CHF, HBP
Parkinson’s Disease
Periodontal Disease
Doxorubicin: prevent cardiomyopathy
Fatigue
Aging
A bajillion other things: AIDS, HD, lyme disease, immune booster, MD, exercise tolerance
Overall Therapeutic Efficacy = neither
convincing evidence supporting nor refuting evidence of benefit or harm |
|
|
Term
| What are adverse effects of CoQ10 toxicity? |
|
Definition
GI distress: nausea, vomiting, constipation
Skin rash
Interferes with blood pressure control
during and after surger |
|
|
Term
| What are CoQ10-drug interactions? |
|
Definition
Statins decrease CoQ10 levels
Ameliorate the cardiotoxicity of doxorubicin
Propanolol (beta blocker) inhibits some CoQ10-dependent enzymes
Antidiabetic medications may need dose adjusting (CoQ10 may improve glycemic control in type II diabetes)
Red yeast (herbal supplement used for lipid-lowering) might reduce coenzyme Q10 levels |
|
|
Term
| What is glucosamine? Where is it found in the body? |
|
Definition
Murine product
Found in cartilage and synovial fluid
Supplement derived from shellfish
Usually taken in combination with chondroitin |
|
|
Term
| What is glucosamine used for? |
|
Definition
Severe osteoarthritis
Overall Therapeutic Efficacy = similar or slightly better than Celebrex® (selective COX-2 inhibitor)
No efficacy in mild to moderate osteoarthritis
MOA:
Enhance cartilage proteoglycan synthesis
help maintain equilibrium between
cartilage catabolic and anabolic
processe |
|
|
Term
| What are the adverse effects of glucosamine and it's contraindications? |
|
Definition
Adverse Effects
GI Disturbances
Contraindications
Allergy to shellfish and shellfish products
Patients with asthma (exacerbated when taking glucosamine/chondroitin combination)
Diabetes (glucosamine impairs insulin secretion |
|
|
Term
| What are the glucosamine-drug interactions? |
|
Definition
Anti-diabetic agents – reduced effectiveness
Aspirin, anticoagulants, heparin, or NSAIDS – increased risk of bleeding |
|
|
Term
| What is omega3 FA? What are sources? How does it compare to omega6? |
|
Definition
Alpha-linolenic acid (ALA)
sources: leafy green vegetables, nuts, and vegetable oils
converted to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in body
sources: fish meat
natural ratio of EPA to DHA is ~ 3:2
benefit ratio, higher omega-3:omega-6 |
|
|
Term
| What are omega3 FA used for? |
|
Definition
Cardiovascular Disease
Reduces all-cause mortality and various CVD outcomes (i.e., sudden death, cardiac death, and myocardial infarction)
Lowers blood triglyceride levels in a dose-dependent manner via inhibition of
lipogenesis and stimulation of fatty acid oxidation in live
Joint Inflammation
Reduces joint tenderness and need for corticosteroid drug in RA due to inhibition of the synthesis of pro-inflammatory lipid products (i.e., prostaglandin and leukotriene) and
cytokine |
|
|
Term
| What are the adverse effects and contraindications of taking omega3 FA? |
|
Definition
Adverse Effects
GI Disturbances
High doses may increase risk of bleeding
Contraindications
Hemophiliacs
Patients taking warfarin or aspirin, NSAIDS, heparin
Fish oil supplements should be stopped before any surgical procedure |
|
|
Term
| What are the omega3-drug interactions? |
|
Definition
| Aspirin, anticoagulants, heparin, or NSAIDS – increased risk of bleeding |
|
|
Term
|
Definition
Herbal Remedy!
A member of the buttercup family
Root of the plant has medicinal properties
Historically used for malaise, gynecological disorders, kidney
disorders, malaria, rheumatism, and
sore throat |
|
|
Term
| What is black cohosh used for? |
|
Definition
Dysmenorrhea
Premenstrual Syndrome Symptoms
Menopausal Symptoms (i.e., hot flashes)
Alternative to Hormone Replacement Therapy
Overall Therapeutic Efficacy = no efficacy with hot flashes |
|
|
Term
| What are the adverse effects of black cohosh? |
|
Definition
Nausea
Dizziness
Decreased heart rate
Increased perspiration
Weight gain
Cramping |
|
|
Term
| What are the contraindications of black cohosh? |
|
Definition
Women taking hormone replacement therapy
Women who are pregnant – can increase the risk of miscarriage
Women who have breast cancer
Some reports of heptatoxicity – monitor liver function |
|
|
Term
| What are the black cohosh-drug interactions? |
|
Definition
Transitioning from higher doses of estrogen will result in breakthrough hotflashes and other symptoms
Oral contraceptives – may interfere with
hormone levels
Antihypertensive agents – black cohosh slightly lowers blood pressure
Heptatoxic agents (kava, acetaminophen) –
increases the risk of heptatoxicity |
|
|
Term
|
Definition
Herbal supplement
Common name - Purple coneflower
Stimulates the overall activity of the
cells responsible for fighting all kinds of infection
Immune-stimulating components are the large polysaccharide |
|
|
Term
| What are some of the uses of echinacea? |
|
Definition
Upper Respiratory Infections
Colds and Flu
Skin Conditions: acne, eczema, insect bites
Wounds and Burns
GI: Crohn’s Disease, ulcers
Mouth Infections: canker sores, gingivitis
General Immune-boosting
MOA:
Stimulates phagocytosis
Increases the number and activity of immune system cells, including anti-tumor cells
Promotes T-cell activation
Inhibits the bacterial enzyme hyaluronidas
With long-term use, echinacea appears to lose effectiveness
Overall Therapeutic Efficacy = Unclear benefit in decreasing the incidence and duration of the common cold |
|
|
Term
| What are some of the toxic effects of echinacea? |
|
Definition
Rashes, itching, occasional swelling of the face
Difficulty breathing
Dizziness
Hypotensio |
|
|
Term
| What are some of the contraindications of echinacea? |
|
Definition
Individuals with progressive systemic or
autoimmune disorders such as tuberculosis, AIDS,
multiple sclerosis, collagen disease, leukosis
that's why herbal meds are stupid |
|
|
Term
| What are the Echinacea-drug interactions? |
|
Definition
Immunosuppressants (cyclosporine)
CS
Antifungals |
|
|
Term
| What is feverfew? What are the active components? |
|
Definition
Herbal supplement
Belongs to the flower family that includes daisies and sunflowers
Leaves of the plant are used medicinally
Parthenolide and chrysanthenyl acetate, the active compounds of feverfew, block substances involved in vascular tone
regulation and inflammation
Prevents a migraine, but cannot relieve a migraine |
|
|
Term
| What are the potential uses of feverfew? |
|
Definition
Prevention of chronic, recurrent migraine headaches
Reduces the frequency and symptoms of pain, nausea, vomiting, and sensitivity to light and noise
Overall Therapeutic Efficacy = Minimal
efficacy in migraine prevention (similar to beta-blockers and valproic acid) |
|
|
Term
| What are the adverse effects of feverfew? |
|
Definition
Orally, well tolerated
Slight GI distress
Sores and inflammation of the mucous membranes of the mouth if chewing leaves
Skin contact can cause a rash |
|
|
Term
| What are the contraindications of fever-few? |
|
Definition
Pregnant women as it can cause unwanted uterine contractions
Individuals on anticoagulant and anti-inflammatory medications
Individuals taking prescription headache drug |
|
|
Term
| What are the feverfew-drug interactions? |
|
Definition
Anticoagulants such as warfarin or heparin – feverfew inhibits platelet activity (i.e., blood clotting)
Anti-inflammatory agents such as aspirin
or other NSAIDs – increase the risk of
stomach problem |
|
|
Term
| What is ginko biloba? What are the active ingredients? What are beliefs about it? |
|
Definition
Herbal supplement prepared from the leaf of the ginkgo tree
Has two groups of active substances, terpene lactones (ginkgolides) and flavonoids
Enhance circulation in the brain: benefits – improve short and
long-term memory, increase reaction time and improve mental clarity
May help to counteract the effects of aging, including mental fatigue and lack of energy |
|
|
Term
| What are the potential uses of ginko biloba? |
|
Definition
Cerebral insufficiency (i.e., memory loss)
Intermittent claudication and other •
circulatory diseases (i.e., diabetic
peripheral vascular disease, Raynaud's
syndrome, hemorrhoids and varicose veins)
->Ginkgolides inhibit platelet activating factor
Reduces bronchoconstriction and airway
hyperactivity
Decreases T-lymphocyte proliferation and
cytokine production
Reduces inflammation
Minimizes changes in vascular permeability
Tinnitus and vertigo
Respiratory conditions (i.e., asthma, altitude sickness)
Overall Therapeutic Efficacy = None
Flavonoids act as anti-oxidants, inhibit nitric oxide production and increase serotonin release and uptake |
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Term
| What are adverse effects of ginkgo biloba? |
|
Definition
Cardiovascular: heart palpitations
CNS: dizziness
GI distress |
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Term
| What are contraindications of gingko biolba? |
|
Definition
History of allergy to the herb
Individuals with bleeding disorders or before elective surgery due to increased bleeding potential associated with chronic use |
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Term
| What are gingko bioba-drug interactions? |
|
Definition
MAO inhibitors – potentiates its actions
Thiazide diuretics – results in increased capillary permeability
Antithrombolytic agents – spontaneous
bleeding due to PAF inhibition by ginkgo
Antidepressants (i.e., SSRIs, MAOIs, tricyclics) – offset sexual dysfunction
symptoms
Cyclosporine (immunosuppressant) |
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Term
|
Definition
Herbal supplement
Adaptogen (increases body’s ability to
adapt to emotional and physical stress)
Medicinal part is the root |
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Term
| What are the potential uses of ginseng? |
|
Definition
Adaptogenic agent
Boost energy and stamina (Asian ginseng)
“Calming” effect (American ginseng)
Immune stimulation
Diabetes
Overall Therapeutic Efficacy = None
Ginsenosides affect the hypothalmus- pituitary-adrenal axis; stimulate insulin release and increase insulin receptors Panaxans lower blood sugar
Polysaccharides, complex sugars, enhance
immune system |
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Term
| What are the adverse effects of ginseng? |
|
Definition
Basically at high doses the opposite of what you take this crap for.
Nervousness
Insomnia
Euphoria
May cause menstrual abnormalities and breast
tenderness with long-term use |
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|
Term
| What are the contraindications of ginseng? |
|
Definition
Individuals with hypoglycemia
Individuals taking cardiac or hypertensive medication
Individuals suffering from anxiety or severe nervousness
Children – associated with lethal intoxication
Women who are pregnant – ginseng may be teratogenic
People who want to get drunk b/c it stimulates aldehyde dehydrogenase and increases OH clearance in kidney |
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Term
| What are the ginseng-drug interactions? |
|
Definition
Warfarin (anticoagulant) – ginseng inhibits platelet aggregation
Caffeine and other stimulants – additive
stimulant effect of ginseng
MAO Inhibitors – results in mania
Antidiabetic agents - concomitant use might enhance blood glucose lowering effects
Alcohol – lowers blood alcohol concentrations
Ginseng can interfere with drug metabolism via P450 enzymes |
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Term
| What are the phytoestrogens? What is their active ingredient? What is its main effect? |
|
Definition
Estrogen-like plant compounds Isoflavones
-Act similarly to the hormone estrogen
-Isoflavones have an anti-estrogen effect when the body's estrogen levels are high
Isoflavones and estrogen compete for estrogen receptors
-Semi-synthetic form of isoflavone, called ipriflavone
Not intended for the treatment of menopausal symptoms
Believed not to adversely affect estrogen receptor-positive breast cancer |
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Term
| What are the potential uses of phytoestrogens? |
|
Definition
Soy:
Maintain and even increase bone density
Reduce menopausal symptoms
Reduce total cholesterol and LDL while
increasing HDL
Inhibit the growth and proliferation of tumor cells (prevent breast and prostate
cancer)
Antioxidant
Overall Therapeutic Efficacy = Similar to estrogen, but little to no benefit for above use |
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|
Term
| What are the adverse effects of phytoestrogens? |
|
Definition
| GI upset: stomach pain, loose stool and diarrhea |
|
|
Term
| What are the contraindications of phytoestrogens? |
|
Definition
Soy isoflavones may not be safe for women with estrogen receptor-positive breast cancer
History of allergic reactions to soy products
Pregnant or breast-feeding women should not take soy isoflavone supplements
Individuals with thyroid disease |
|
|
Term
| What are the phytoestrogen-drug interactions? |
|
Definition
Thyroid medication – absorption reduced •
Reduces the absorption of the nutrients:
zinc, iron, and calcium |
|
|
Term
|
Definition
Perennial plant native to North •
America and Europe
Rootstock of valerian contains •
active compounds, valerenic
acid, responsible for sedative
effects
Promoted as a mild sedative and •
sleep aid for nervous tension and
insomnia |
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|
Term
| What are the uses of valerian? |
|
Definition
Insomnia •
less effective than Ambien© •
Anxiety •
Nervous stomach •
Overall Therapeutic Efficacy = Similar
to benzodiazepines
Activates GABA a R
Increases the amount of gamma aminobutyric •
acid (GABA, an inhibitory neurotransmitter)
available in the synaptic cleft
May cause GABA release from and block GABA reuptake •
into brain nerve ending |
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|
Term
| What are the adverse effects of valerian? |
|
Definition
Orally, well tolerated •
Impairment of attention for a few hours after •
taking valerian
Large doses or long-term use leads to dizziness, •
restlessness, blurred vision, nausea, stimulant,
hepatotoxicity and cardiac problems |
|
|
Term
| What are the contraindications of valerian? |
|
Definition
Avoid alcohol •
Avoid driving or performing hazardous tasks •
Individuals taking prescription sedatives or anti- •
anxiety medication |
|
|
Term
| What are the valerian-drug interactions? |
|
Definition
Benzodiazepines – additive sedative effects
Alcohol – additive sedative effects •
Barbituates – additive sedative effect |
|
|
Term
|
Definition
Native plant of North America •
with a life span of 700 years
Small palm tree found in Texas to •
South Carolina
Medicinal properties are derived •
from the blue-black berries
Fatty acids and sterols are the •
active ingredients in the berries
Native Americans used these •
berries for the treatment of
various urinary problems in men
and breast disorders in women |
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|
Term
| What are the potential uses of saw palmetto? |
|
Definition
Benign Prostatic Hyperplasia (BHP) •
Stages I and II •
Relieves difficulties and symptoms •
associated with BHP
Self-medication with saw palmetto to treat •
both chronic prostatitis and prostate
cancer is common – however, clinical data
indicates no benefit or effectiveness
Overall Therapeutic Efficacy = No benefit or effectiveness in moderate to severe BPH
Inhibition of 5-alpha-reductase (5AR) •
Enzyme that catalyzes the conversion of
testosterone to dihydrotestosterone (DHT), and DHT is associated with prostate growth
Blockade of alpha1-adrenergic R
Anti-estrogenic action
Inhibition of growth factors and prolactin-induced cell proliferation
Anti-inflammatory effect |
|
|
Term
| What are the adverse effects and contraindications of saw palmetto? |
|
Definition
Adverse Effects
Mild GI distress
Contraindications
Individuals with hormone-specific cancers – anti-androgenic, anti-estrogenic effects of saw palmetto |
|
|
Term
| What are the saw palmetto-drug interactions? |
|
Definition
Currently, there are no known drug
interactions, nor does it interact with the
enzymes) 450
drug metabolizing enzymes (P
However, caution should be used with:
Hormones or hormone-like drugs – saw •
palmetto exerts anti-androgenic and antiestrogenic actions
alpha1 adrenergic agents: saw palmetto can block alpha1 R |
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|
Term
|
Definition
Used for centuries to treat mental •
disorders, nerve pain, malaria,
wounds, burns, insect bites,
menstrual cramping, menopause,
and arthritis
Active ingredients, hypericin and •
hyperforin, may play a significant
role in the herb’s antidepressant
effect
Tannins, another active ingredient, are responsible for
the astringent effect for wound
healing |
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Term
| What are the potential uses of St. John's Wort? |
|
Definition
Mild to moderate or major depression
Sleeping disorders
Anxiety
Wounds and burns
Overall Therapeutic Efficacy = equally
effective as tricyclic antidepressants in the treatment of mild to moderate depression
Hypericin minimizes the breakdown of various neurotransmitters, including serotonin via inhibition of serotonin re-uptake
Hypericin increases theta waves in the brain, which are associated with deep meditation, serene pleasure and heightened creative activity |
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|
Term
|
Definition
|
|
Term
| What are the adverse effects of st. johns wort? |
|
Definition
Increased sensitivity to sunlight (caused by hypericum extract)
CNS: dizziness, fatigue
GI distress (due to tannins)
Increased prothrombin time and breakthrough bleeding
Dry mouth
Allergic skin reactions
Inhibit the absorption of iron (due to tannins) |
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|
Term
| What are the drug interactions w/ St. John's Wort? |
|
Definition
Decreases the levels of cyclosporine, •
indinavir, theophylline, and digoxin
Hyperforin has been suggested to be an inducer of CYP 3A4 enzyme the P450
Antidepressants (i.e., SSRIs, MAOIs, •
tricyclics) – potential serotonin syndrome
Sympathomimetics and MAO inhibitors – •
leads to hypertensive crisis
Combination oral contraceptives – leads to breakthrough bleeding and decreases OC level LIKE ON ER! |
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