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List the prototypes and describe the MOA and toxicities of the major classes of oral antidiabetic agents: Alpha-glucosidase inhibitors: Protypes: Acarbose & Miglitol

MOA: block alpha-glucosidase, an enzyme needed for carbohydrate metabolism

Toxicity: gas, abdominal discomfort
List the prototypes and describe the MOA and toxicities of the major classes of oral antidiabetic agents: Sulfonylureas: prototypes: tolbutamide & chlorpropamide (1st generation)

glipizide, glimepiride, glyburide (second generation)

MOA: stimulates the release of insulin from the pancreatic Beta-cells

Toxicities: hypoglycemia
List the prototypes and describe the MOA and toxicities of the major classes of oral antidiabetic agents: Biguanide: Prototype: Metformin

MOA: decreases the liver's production of glucose, inhibits the breakdown of fatty acids used to produce glucose, and increases the removal of glucose from muscle, the liver, and other body tissues where it is stored.

Toxicities: lactic acidosis, diarrhea, nausea, vomiting, bloating, gas, diminished appetite
List the prototypes and describe the MOA and toxicities of the major classes of oral antidiabetic agents: Thiazolidinediones (glitazones): P: Rosiglitazone, Pioglitazone

MOA: Binds to the PPAR receptors and increases insulin sensitivity

Toxicity: Anemia, redistribution of body fat,
List the prototypes and describe the MOA and toxicities of the major classes of oral antidiabetic agents: Meglitinides: P: Rapaglinide

MOA: insulin secreatagoge, regulates potassium efflux from the pancreatic Beta-cells

Toxicity: hypoglycemia
List the prototypes and describe the MOA and toxicities of the major classes of oral antidiabetic agents: Phenylalanine Derivatives: P: Nateglinide

MOA: regulates potassium efflux from pancreatic beta-cells

Toxicity: has lower incidence of hypoglycemia compared to other secreatagogues
Describe the indications/contraindications and advantages/disadvantages of each class of oral hypoglycemic drugs: alpha glucosidase inhibitors: Indications: Type II diabetes
Contraindications: digestive problems, history of diabetic ketoacidosis, IBD, intestinal disorders, liver or kidney disease

Advantages: non-systemic, few contraindications, no weight gain, no hypoglycemia, prevents diabetes
Disadvantages: moderate reduction in A1c levels, pre-meal dosing, GI symptoms, drug interactions with MAOIs
Describe the indications/contraindications and advantages/disadvantages of each class of oral hypoglycemic drugs: sulfonylureas: Indications: Type II diabetes
Contraindications: hypersensitivity to the drgus, diabetic ketoacidosis, renal and hepatic insufficiency

Advantages: very effetive (2-3% reduction in A1c), once daily dosing, immediate benefits, well-tolerated, well-characterized, inexpensive
Disadvantages: weight gain, hypoglycemia, caution in patients with hepatic and renal dysfunction
Describe the indications/contraindications and advantages/disadvantages of each class of oral hypoglycemic drugs: Biguanides: Indications: Type II diabetes
Contraindications: Servere infection, CHF, metabolic acidosis, history of alcohol abuse, kidney & liver disease

Advantages:no weight gain, advantages lipid effects, no hypoglycemia, long record of safety, decreased macrovascular complications, prevents diabetes
Disadvantages: multiple contraindications, creatine> 1.5 mg/dl, CHF, GI side effects
Describe the indications/contraindications and advantages/disadvantages of each class of oral hypoglycemic drugs: Thiazolidinediones: Indications: Type II diabetes
Contraindications: Type I diabetes, liver and heart failure

Advantages: No hypoglycemia, can be used in pts with renal insufficiency, improve triglycerides and HDL-C, prevents diabetes

Disadvantages: weight gain, edema, increases LDL, multiple contraindications, delayed onset of action, long term outcomes unknown
Decribe the indications/contraindications and the advantages/disadvantages: Meglitinides: Indications: Type II diabetes
Contraindications: type I diabetes, renal and hepatic insufficiency

Advantages: well-tolerated, les hypoglycemia than SFU
Disadvantages:Expensive, three times a day, weight gain
List the types of estrogens that are used therapeutically?: estradiol, diethylstilbestrol, estrone, estriol, ethinyl estradiol, mestranol, conjugated estrogens, estradiol benzoate
Explain their therapeutic actions (of estrogens DES, mestranol, premarin, and ethinyl estradiol): Estradiol: contraception
conjugated estrogens: HRT for post menopausal women
DES: morning after pill and prostate cancer drug
mestranol: in some birth control
Describe the adverse effects of estrogens: (1) increased incidence of breast cancer
(2) endometrial carcinoma
(3) tender breasts and breast enlargment
(4) thromboembolic events
(5) nausea and vomiting
(6) migraines, dizziness, headache
(7) Vaginal bleeding
(8) edema
(9) hyperpigmentation
(10) hypertension
List the contraindications for estrogen therapy: (1) pregnancy
(2) suspected or known breast cancer
(3) estrogen-receptor positive neoplasia
(4) History of thromboembolic events
(5) Heavy smoking
(6) unexplained vaginal bleeding
Recognize the therapeutic uses for antiestrogens: (1) infertility treatment especially due to anovulation (Clomiphene)
(2) estrogen-receptor positive breast cancer (Tamoxifen & raloxifene)
Know what a SERM is: Selective estrogen receptor modulators (SERMs) is a class of medication that acts on the estrogen receptor. A characteristic that distinguishes these substances from receptor agonists and antagonists is that their action is different for various tissues, thereby granting the possibility to selectively inhibit or stimulate estrogen-like action in various tissues.

Members are:

* clomifene
* raloxifene
* tamoxifen
List the reasons for the use of progesterone in oral contraceptives: More effective anti-contraception
Have different mechanisms
List other uses for progestin and their adverse effects: (1) dysmenorrhea, endometriosis
(2) control of irregular bleeding

Adverse effects
(1) Weight gain
(2) irregular bleeding, spotting,
(3) edema
(4) Depression
(5) Thrombophlebitis
(6) Pulmonary embolism
Describe the most common progestins used in contraception: pill: norethindrone, norgestrel,
IUD: Levonorgestrel
shot: medroxyprogesterone
List the clinical and non-clinical uses for androgen?: Testosterone cypionate - hypogonadism (clinical), muscle building/body building (non-clinical)

Danazol - fibric breast disease and endometriosis in women

Stanazol - Hereditary angioedema

Fluoxymesterone -androgen responsive mammary cancer in women, Replacement therapy
Recognize the side effects of androgen?: increased LDL, lowered HDL, increased aggression, Closure of epiphyses (ends of long bones), edema, cholestatic (stopping flow of bile) jaundice, priapism, decreased sperm count, masculanizaiton with acne
Recognize the clinical uses for antiandrogens?: Finasteride: for BPH (prostatic carcinoma) & for male patterned baldness

Mifepristone: Abortifacient and for tamoxifen-resistant breast cancer
Explain how oral contraceptives work: Estrogen -
(1) feedback inhibition preventing the release of LH and FSH from the pituitary
(2) makes the endometrium inhospitable to implantation
(3) causes a thicking of the cervical mucuous leading to decreased sperm penetration
(4) changes in the motility and secretion in the uterine tubes

Progesterone
(1) low dose - changes to cervical mucus, endometrial & uterine changes similar to estrogen,
(2) high dose - inhibitory feedback on GnRH release from the hypothalamus
List the adverse effects of oral contraceptives: Adverse effects:
estrogen-associated: breast tenderness and enlargement, thromboembolitic events,
increased incidence of breast cancer, endometrial carcinoma, nausea and vommiting, hypertension, vaginal bleeding, headache and dizziness.

progesterone-associated: weight gain, edema, depression, thrombophlebitis, pulmonary embolism
Recite the contraindications for oral contraception: (1) pregnancy
(2) thromembolitic events
(3) estrogen receptor positive neoplasia
(4) known or suspected breast cancer
(5) heavy smoking
(6) undiagnosed abnormal genital bleeding
Explain the statement "dose differentiates a poision from a remedy": Paracelsus - basically at low doses a drug can be therapeutic or have no toxic side effects, often you need a very high dose to see toxic side effects.
Distinguish between a pharmacological effect and a toxic effect: pharmacological effects are intended
the toxic effects are side effects that occur from the drug acting at non-target receptors
Describe special terms or acronyms which are used to define toxicity or safety: TLV - threshold limit value
LD50 - half subjects die
TI - TD50/ED50, large # safter
Acute toxicity - single dose in 24 hrs
Chronic toxicity - daily exposures up to a lifetife
NOEL - no observal effect level
ADI - allowable daily intake = NOEL/x
STEL - Short term exposure levels
ALD - Average lethal dose
Toxicon - toxic principle or a given chemical entity
Describe the basis of selective toxicity: one man's poision is another man's pill

selectivity is a specific drug acting only on one receptor ...
Define the mechanisms by which specific antidotes produce their salutary effects: 1. increase conversion of toxic drug to nontoxic metabolite
2. Prevent break down of nontoxic compound into toxic metabolites
3. Complexation
4. Accelerating rate of excretion
5. competition for essential receptors
6. Repair or bypass effects fo poision
7. blockade of receptors responsible for toxic effects
Descibe the three aims of treatment of a poisioned patient: 1. ABCs,make sure the pt is alive
2. ID drug (urine & blood samples)
3. get rid of drug
Describe the general ways to prevent absorpition of ingested drugs or chemicals: 1. activated characol - give drug that binds to toxin, preventing absorption
2. ion trapping - change pH so that it is ionized and cannot cross lipid membranes
3. dilution with water
4. demulcents - cover interior of stomach with mucus so that it cannot be absorbed
5. gastric lavage
6. emesis
Indicate the appropriate laboratory tests to determine whether a patient has been poisioned: 1. blood tests
2. urine tests (immunoassays, TLX, HPLC)
3. gastric contents
List the agent or procedures used to detoxify or elminate poisions from the body after they have absorbed: 1. Alteration of the pH of the urine
2. diuresis
3. hemodialysis
Describe the toxic effects of common household products: 1. Cleaners, soldering flux, and bleaches = Acids
Toxic effects: burns, black, bloody diaarrhea, epigastric pain, esophageal strictures, 50% mortality; immediate pain in buccal cavity and esophagus

2. Lye, liquid plumber, oven cleaner = bases
toxicity: swallowing is painful and difficult, vomitus thick and slimy and may contain blood, shock, esophageal strictures, causes progressive damage ... 25% mortality, Chemical burns, rapidly penetrating liqueactive necrosis, esophageal perforation.
Describe the general treatment of poisoning for specific agents: 1. Acids : ABCâ€™s, Demulcents, lots of water (no neutralizer unless on skin), steroids for esophageal strictures, analgesics and antibiotics.

2. Bases: ABCâ€™s, demulcents, lots of water, analgesics, steroids, antibiotics, no lavage or emetics

3. Opiates: ABCâ€™s, Naloxone, gastric lavage and supportive care.

4.Meperidine: ABCâ€™s, Gastric lavage (if oral), diazepam for seizures and naloxone for depressive effects (not for tremors)

5. Atropine: ABCâ€™s, Lavage with 4% tannic acid, pilocarpine or physostigmine, aspirin (antipyretic) and alcohol sponges.

6. Barbiturates: ABCâ€™s, Lavage with KmNO4, charcoal, alkaline diuresis (NaHCO3), hemodialysis (long acting barbs)

7. Benzodiazepines: ABCâ€™s, emesis, gastric lavage, antidote: flumazenil short T1/2 may require multiple doses.

8. Ethanol: ABCâ€™s, gastric lavage with bicarb, caffeine, hemodialysis (if >500mg%)

10. Neuroleptics: ABCâ€™s, lavage (even hours hours later due to lower gastric motility), Treat arrhythmias as needed and diphenhydramine for EPS.

11. Kerosene: ABCâ€™s, large amounts of water, olive oil and saline cathartic, antibiotics, corticosteroids to reduce kerosene pneumonitis, no emetics or lavage.

12. Parathion: ABCâ€™s, atropine, pralidoxine, lavage with 5% NaHCO3, wash affected areas, avoid morphine, barbituates and phenothiazines.

13. Salicylates: ABCâ€™s, emetics, gastric lavage 5% NaHCO3, monitor pH, barbituates or benzoâ€™s for seizures, hemodialysis if needed.

14. Acetaminophen: ABCs, emetics, lavage, charcoal, N-acetylcysteine to restore glutathione earlier the better (grapefruit juice), monitor liver enzymes.

15. Cocaine: ABCâ€™s, charcoal, diazepam (seizures), lidocaine (arrhythmias), no dialysis or lavage.

16. PCP: Lock in padded room, diazepam, antipsychotic agent (Haloperidol), cranberry juice (100x increase in excretion)

17. Tricyclic antidepressants: ABCâ€™s, emesis, lavage, physostigmine (till ACS stops), treat arrhythmias (phenytoin, bicarb)

18. Methaqualone
: ABCâ€™s, emesis, lavage, hemodialysis

19. Digoxin: ABCâ€™s Dose adjustment, drug withdrawal, lavage, charcoal, emesis, Digibind, K+ supplement, treat arrhythmias (lidocaine, phenytoin, propranolol)

20. Phenytoin: ABCâ€™s, emesis (if conscious), lavage, charcoal, cathartics, discontinue phenytoin

21. Theophylline: ABCâ€™s, discontinue drug, charcoal, emesis, fluids and anticonvulsants (diazepam) as needed

22. Dioxin: ABCâ€™s, alkaline diuresis, If recent ingestion: [emesis, lavage, charcoal, cathartic], mainly supportive care
Describe the toxicology of prototypical drugs as a guide for explaining the toxicology of other agents in the same categories: 1. Sympathomimetic Toxidrome: Agitation, hallucinations, paranoia, mydriasis, Seizure, hypertension, tremor, hyperreflexia, hyperthermia

2. Sedative/Hypnotic Toxidrome: Hypothermia, decrease reflexes, hypotension, coma, decreased respiration, mydriasis

3. Opioid/Opiate: Hypothermia, hypotension, triad, histamine release, PPP, decreased respiration, coma.

4. Anticholinergic Toxidrome: Fever, dry skin, flushing, urinary retention (ACS) [Hot, dry, mad, red, blind], Agitation, and mydriasis.

5. Cholinergic Toxidrome: Fasciculation, incontinence, salivation, wheezing, lacrimation, bradycardia (SLUDE), coma, PPP.

6. Tricyclic Antidepressant Toxidrome: Arrythmias, convulsions, hypotension, mycoclonus, hyperthermias, mydriasis, coma, agitation

7. Salicylate Toxidrome: Diaphoresis, tinnitis, agitation, alkalosis (early), acidosis (late), fever
increased respiration.
Explain the basis for distinguishing acute vs. chronic toxicity: unknown
List at least one good chelating agent for each of the major heavy metals: lead - EDTA
mercury - BAL
Arsenic - Dimercaprol (BAL in oil)
List antidotes for specific agents when they exist and their mechanisms: (1) Acetaminophen - N-acetylcyssteine (increase glutathione stores, combines directly with acetaminophen, enhances sulfate conjugation)

(2) Anticholinergics - physiostigmine salicylate (a reversible acetylcholinesterase inhibitor capable of directly antagoizing the CNS manifestations of anticholinergic activity).

(3) Arsenic - Dimercaprol (BAL in oil) (heavy metal chelator)

(4) Benzodiazepines - Flumazenil (Benzodiazepine antagonist)

(5) Digioxin - Digibind (binds digioxin, which keeps it from acting toxically.

(6) Lead - EDTA (heavy metal chelator)

(7) Mercury - BAL (heavy metal chelator)

(8) Methanol - Ethanol (competition for enzyme that converts methanol to formaldehyde) or Leucovorin (helps get rid of formic acid)

(9) morphine - naloxone - mu opioid receptor antagonists

(10) Organophosphates - Pralidoxime for organophosphates
Explain the basic methods used to determine a causative relationship between an environmental exposure and health outcomes: 1. Determine that the compound has inherent toxicity

2. Need to determine if the there is a completed pathway (i.e. ate lead, you can't lead poisioning by touching a painted wall)

3. Compare incident to known health standards/info
Describe workplace health standards, and general health standards that are used to protect against harmful effects: In the workplace, agencies like the EPA, OSHA, NIOSH, and ACGIH evaluate and set safety exposure levels. Such standards address conditions under which individuals maybe exposed to a chemical without experiencing an adverse effect. There are standards for both acute and chronic exposure. (IDLH, TLV, PEL, REL, STEL, ERPG)
Discuss the mechanisms by which drugs and other chemcials produce their harmful effects: various mechanisms, for instance

CO - binds with greater affinity to Hb, thereby brain and heart do not receive adequate O2

Can inactivate enzymes, for instance, Mercury blocks.. â€“SH containing enzymes, lead inactivates proteins by binding to their sulfhydryl groups.

Can damage organs, for instance acetaminophen can bind hepatocytes leading to hepatotoxicity.
Explain the basic principle of toxicology described by Paracelsus: Dose, dose, dose (accumulation and time also matter)
Discuss the basis of reversible versus irreversible effects of environmental agents: Reversibility and irreversibility has to do with dose and exposure levels. If the pt is exposed to a low concentration, the effects will be reversible, but if they are exposed to a high enough concentration, the effects can be irreversible.
Describe the effects of insulin on the liver, muscle, and adipose tissue: Liver: Insulin increases the storage of glucose as glycogen in the liver. This involves the insertion of additional GLUT 2 glucose transport molecules in cell membranes, increased synthesis of the enzyme, pyruvate kinase, phosphofructokinasem and glucokinase, and the suppression of several other enzymes. Insulin also decreases protein catabolism
Identify the types of insulin preparations available and their pharmacology: 1) Rapid/short acting: insulin lispro and insulin aspart

2) short acting insulin: Crystalline zinc (regular) insulin - given IV

NPH insulin and lente suspensions

3) Long acting insulin & insulin glargine

Everything else is intramuscular injection
Describe the hazards of insulin use: hypoglycemia
immunotoxic effects from the development of antibodies
Describe the effects of insulin on the muscles: Muscle: Insulin stimulates glycogen sythesis and protein synthesis. Glucose transport into muscle cells is facillitated by insertion of additional GLUT 4 transport molecules into cell membranes
Describe the effects of insulin on the adipose tissue: Adipose tissue: Insulin facilitates triglyceride storage by activating plasma lipoprotein lipase, by increasing glucose transport into cells via GLUT 4 transporters and by reducing intracellular lipolysis.
Describe the synthesis of the thyroid hormone: Start out with I-, this gets transported across the thyroid membrane, then it is oxidized by a peroxidase, which is then converted to MIT-DIT-T3-T4, which is called thyrogloubulin. Thyroglobulin is broken down (proteolyzed) to T4 and T3 in the blood, which is then distributed to the rest of the body
point out the sites of action for inhibitors of thyroid hormone synthesis: In the thyroid hormone pathway, there are multiple points of inhibition

1) anions can compete with I- ions to prevent them from being pumped into the thyroid gland

2) iodides and thioamides block the conversion of I to the thyroglobulin

3) iodides can also block proteolysis of Thyroglobulin to T4 and T3 in the blood

4) Last ipodate, b-blockers, and corticosteroids can block the conversion of T4 --> T3
Explain the therapeutic effets of thyroid hormones in the treatment of hypothyroidism: Thyroid hormones are used to treat hypothyroidism. Use

1) Triodothyronine (T3) - replacement therapy

2) levothyroxine or thyroxine (T4 is converted to T3, also results in altered gene expression)
Explain the therapeutic effects of anti-thyroid drugs in the treatment of hyperthyroidism: Anti-thyroid drugs are used to treat hyperthyroidism

1) Propylthiouracil: prevents thyroid hormone synthesis by inhibiting the thyroid peroxidase catalyzed reactions and also blocks coupling of iodotyrosines, inhibits the peripheral deiodination D1 of T4 and T3
2) methimazole (block thyroid peroxidase like PTU but doesn't inibit D1)

3) Potassium iodide - inhibiton of thyroidal peroxidase

4) Radioactive iodine - is incorporated into storage follicles.

5) Iopanoic acid & ipodate sodium - inhibits the conversion of T4 --> T3 in the liver, kidney, pituitary, and brain.
What are the two main things we were told to remember about herbal medications?: 1. In many cases, the medical value of these substances has not been demonstrated in controlled clincial trials

2. These substances are marked without governmental review of efficacy and safety.
Describe the proposed medical uses and adverse effects of dehydroepiandrosterone: MOA: DHEA is an androgen precursor, converted to estradiol in the peripheral tissues

Uses: Possibly value in AIDS patients (women only) and women with systemic lupus erythematosus?

Adverse effects: androgenic side effects; androgenization in postmenopausal women, feminization in young men
Describe the proposed medical uses and adverse effects of melatonin: MOA: a serotonin derivative thought to regulate sleep=wake cycles.

Uses: Decreases jet lag symptoms and useful as a sleeping aide.

AE: sedation, drowsiness, and headache, also contraindicated in pregnant women
Describe uses, adverse effects and potential for drug interactions: Ma-huang (ephedra): MOA; contains ephedrine and pseudophedrine, which release NE from sympathetic nerve endings

Uses: weight loss and athletic performance, pressor agent

AE: diziness, insomnia, anorexia, flushing, tachycardia, urinary retention

high doses of ephedra can cause hypertension, cardiac arrhythmias, and psychosis

Contraindications: pregnancy, heart failure, bulimia, cardiac arrhythmias, diabetes, hypertesnsion, glaucoma, hyperthyroidism.
Describe uses, adverse effects and potential for drug interactions: St. John's wort: MOA: hypericin and hyperforin decrease serotonergic reuptake systems

Uses: moderate to severe depression

AE: GI discomfort, drug interactions with drugs metabolized by cyt-p450 or transported by p-glycoproteins (oral contraceptives, cyclosporine, digoxin, etc.)
Describe uses, adverse effects and potential for drug interactions: Ginko: MOA: contains glycosides and terpenoids, which have antioxidant, radical-scavaging effects, and increase NO formation.

Uses: intermittent claudication (limping) and Alzheimer's disease

AE: GI effects, anxiety, insomnia, headache, may be epileptogenic (avoid in patients with seizure disorders).
Describe uses, adverse effects and potential for drug interactions: Ginseg: MOA: contains ginsenosides (saponin glycosides)

Uses: unknown, improve mental & physical performance

AE: Estrogenic effects (vaginal bleeding), insomnia, nervousness, and hypertension
Describe uses, adverse effects and potential for drug interactions: Saw Palmetto: MOA: contains lavonoids, polyprenes, aliphatic alcohols, and phytosterols, which inhibit 5-alpha reductase and androgen receptors

Uses: BPH (Benign prostatic hypertrophy)

AE: abdominal pain, decreased libido, headache, hypertension.
Describe the role of cytochrome P450 in pharmacokinetic drug/drug, drug/herb, and drug/food interactions: Hepatic CYTP450 enzymes metabolize many drugs via redox reactions. There are many substates, inducers, and inhibitors of the CYTP450 pathway that can lead to major drug interactions.
Explain the role of the p-glycoprotein drug transport in drug/drug, drug/herb, and drug/food interactions: P-glycoprotein is a drug transporter that can transport a lots of different substrates out of a cell; this reduces drug effectiveness because they do not reach their target site.

In kidney: responsible for renal excretion

Part of BBB: prevents drugs from crossing the BBB

in biliary excretion: causes drugs to be excreted in feces

There are lots of different substrates, inducers, and inhibitors of p-glycoprotein, which leads to drug interactions
Apply knowledge of cytochrome p450 substrate specificities to predict drug/drug, drug/food, and drug/herb interactions in clinical cases: CYT P450 system:

substrates effected: oral contraceptives, warfarin, atorvastatin (all statins), indinavir, cyclosporins, tamoxifen, tacrolimus,

drugs that increase substrate concentration by INHIBITING cyt-p450: grapefruit juice, cimetidine, indinavir (other -avirs too), diltiazem, amiodarone, fluconazole (other azoles), erythromycin, etc.

Drugs that decrease substrate concentration by INDUCING CYTp450: rifampin, carbamazepine, barbituates, phenytoin, phenobarbital, efavirenz, St. John's wort
Apply knowledge of p-glycoprotein substrate specificities to predict drug/drug, drug/food, and drug/herb interactions in clinical cases: p-glycoprotein substrates: digoxin, simvastatin, verapamil

p-glycoprotein inducers increase drug transport out of the cell: St. John's wort, Rifampin

p-glycoprotein inhibitor inhibits transport of substrate out of the cell: amiodarone.
------ and ----- have low oral bioavailability due to a large first pass metabolism. Therefore, even a mild inhibition of cyp3a4 activity will produce a 10-20 fold increase in systemic levels.: Simvastatin & Lovastatin
statins that are low affinity substrates of cyp3a4 with high bioavailability: Atorvastatin and cerivatstatin - systemic levels are not effected as much by cytp450 inhibition
------- are high affinity substrates for cyp3a4 and therefore compete for metabolism (they function as competitive inhibitors): Simvastatin, lovastatin, cyclosporine, and verapamil.
What do cyp2d6 metabolizers block?: beta blockers and antiarrhythmics. The cyp 2d6 poor metabolizers will be at high risk for serious adverse reactions with antiarrhythmics
Explain drug interactions amiodaraone and digoxin: Amiodarone inhibits the renal excretion of digoxin via PGP
explain the drug interaction: amiodarone & warfarin: Amiodarone inhibits cyp 2c9 mediated metabolism of warfarin, which increases its plasma levels.

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