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108 Cards in this Set
- Front
- Back
Drugs that stimulate Activity (Oxytocics)
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1. Oxytocin
2. Dinoprostone 3. 15-methyl PGF2a - Carboprost Tromethamine 4. Ergonovine Maleate 5. Methylergonovine Maleate 6. Mifepristone - RU486 |
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Drugs that inhibit uterine Activity (tocolytic)
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1. Terbutaline sulfate
2. Magnesium Sulfate 3. Prostaglandin-synthetase Inhibitors - Indomethacin |
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Therapeutic Indications for drugs that stimulate uterine motility
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1. induce labor
2. control postpartum uterine hemorrhage 3. cause uterine contraction 4. Induce abortion |
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Therapeutic indications for drugs that inhibit uterine motility
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1. delay or prevent premature labor (<37 weeks)
2. slow delivery so other therapeutic measures can be performed |
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Production of oxytocin
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sensory stimuli (stretching) from cervix, vagina, and breast causes the release from nerve terminals into the circulation
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MOA of Oxytocin
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binds to specific receptors, activates receptors on myometrial smooth muscle cells increases intracellular calcium and leads to contractions of smooth muscle
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Indications for use of Oxytocin for labor induction
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1. risk to mother, fetus, or both
2. erythroblastosis fetalis 3. placental insufficiency 4. prolonged pregnancy (>42 weeks) |
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Other uses of Oxytocin
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1. stimulate milk ejection
2. reduce postpartum hemorrhage (USE BIG DOSE) |
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Adverse Effects of Oxytocin
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1. decrease in blood pressure, increased heart rate, arrhythmias
2. Sustained uterine contractions ** |
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Prostaglandins for uterine motility
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1. Dinoprostone
2. 15-methyl PGF2a - Carboprost Tromethamine 3. PGE1 analog - Misoprostol |
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Uses of dinoprostone
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1. cervical ripening **
2. induce contractions |
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Cervical Ripening
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prostaglandins stimulate uterine contractions and cause softening and dilation of the cervix
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Application of Dinoprostone
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1. Cervical gel - Prepidil
2. Vaginal inserts - Cervidil |
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ADRs and Contraindications of Dinoprostone
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1. GI disturbances
2. Uterine hyperstimulation 1. Abnormal fetal position, fetal distress |
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15-methyl PGF2a - Carboprost Tromethamine
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control postpartum bleeding - given IM
OR induce abortion in the 2nd trimester |
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PGE1 analog Misoprostol
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used with the antiprogestin Mifepristone RU486 for early termination of pregnancy
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Ergot Alkaloids to stimulate uterine motility
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1. Ergonovine Maleate
2. Methylergonovine Maleate |
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Ergonovine Maleate & Methylergonovine Maleate
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USE: postpartum/postabortion hemorrhage
MOA: activate alpha 1 receptors - induce intense contractions of uterus ADRs: HTN, nausea, vomiting, diarrhea |
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Mifepristone - RU486
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MOA: antiprogestin or progesterone receptor antagonist = causes detachment of the products of conception
USES: 1st trimester termination of pregnancy - restricted distribution program ADRs: bleeding and cramping |
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Terbutaline
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MOA: beta 2 receptor agonist - increase in cAMP may decrease contraction of smooth muscle
ADRs: maternal pulmonary edema and hyperglycemia BLACK BOX WARNING: fetal and maternal tachycardia |
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Magnesium Sulfate
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MOA: relaxes uterine smooth muscle - decreases levels of myometrial intracellular free calcium
ADRs: flushing, sweating, hypotension *drug of choice for patients with contraindications for beta 2 agonists |
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1. Mechlorethamine
2. Cyclophosphamide |
Alkylating Agent - Nitrogen Mustards
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1. Carmustine
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Alkylating Agent - Nitrosoureas
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1. Cisplatin
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Alkylating Agent - Platinum Complexes
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1. Methotrexate
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Antimetabolite - Folic Acid Analog
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1. Mercaptopurine
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Antimetabolite - Purine Analog
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1. Fluorouracil
2. Cytarabine |
Antimetabolite - Pyrimidine
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1. Daunorubicin HCl
2. Doxorubicin HCl |
Antibiotics - Atracycline
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1. Vinblastine Sulfate
2. Vincristine Sulfate 3. Etoposide 4. Paclitaxel |
Vinca Alkaloids, Epipodophylotoxins and Taxanes
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1. Prednisone
2. Dexamethasone |
Adrenocorticosteroids
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1. Tamoxifen
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Estrogen and Antiestrogens
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1. Imatinib Mesylate
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Tyrosine Kinase Inhibitors
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1. Trastuzumab
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Monoclonal Antibodies
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Mechanism of Action of Alkylating Agents
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*Cell Cycle Non-Specific
1. Miscode DNA strands 2. Incomplete repair of alkylated segment 3. Excessive crosslinking of DNA and inability for strand separation |
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Which Alkylating Agent is most lipid soluble
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Carmustine
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ADRs of Cisplatin
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Nephrotoxicity and otoxicity
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Toxicity of Alkylating Agents, Antimetabolites
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1. Nausea and Vomiting
2. Bone Marrow Depression |
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Methotrexate
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*FOLIC ACID ANALOG*
MOA: blocks the conversion of folic acid to tetrahydrofolate leads to a block in DNA, RNA, protein synthesis ; S-phase specific ADRs: mild nausea/vomiting, bone marrow depression |
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Uses of Methotrexate
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leukemia, lymphoma; breast, head, neck carcinoma; osteosarcoma; bladder, gastric AND immunosuppressant
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Part of the cell cycle affected by Mercaptopurine, Fluorouracil, and Cytarabine
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S-Phase - Antimetabolites
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MOA of Daunorubicin HCl and Doxorubicin HCl
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*Cell Cycle Non-Specific - max effect in S-phase*
Intercalates and binds DNA - uncoils DNA helix - destroys DNA template |
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Toxicity of Daunorubicin HCl and Doxorubicin HCl
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Cardiotoxicity
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MOA of Vinblastine Sulfate and Vincristine Sulfate
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*Cell Cycle Specific - M phase*
binds tubulin - disrupts mitotic spindle apparatus - prevents metaphase |
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Toxicity of Vinblastine Sulfate and Vincristine Sulfate
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Neurological toxicity
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MOA of Etoposide
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*G2-Phase*
forms complex with topoisomerase II and DNA - DNA breaks - cell death |
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MOA of Paclitaxel
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*G2 and M Phase*
Antimicrotubule agent - inhibits microtubule assembly |
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MOA of Tamoxifen
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*G1 Phase*
competes with estradiol for binding to cytoplasmatic estrogen receptors - DNA, RNA, and protein synthesis reduced |
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ADRs of Tamoxifen
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SHORT: hot flashes, nausea, vomiting
LONG: visual disturbances, hypercalcemia, vaginal bleeding |
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Uses of Tamoxifen
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Breast Carcinoma
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MOA of Imatinib Mesylate
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*G1 Phase*
Bcr-Abl protein tyrosine kinase inhibition - cell proliferation inhibition and induction of apoptosis |
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ADRs of Imatinib Mesylate
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SHORT: ab pain, nausea, vomiting, diarrhea
LONG: fatigue, join pain, fluid retention, cramps, edema, rash |
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USES of Imatinib Mesylate
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1. Philadelphia Chromosome positive chrominic myeloid leukemia
2. c-Kit (CD117) receptor positive-gastrointestinal stromal tumor |
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MOA of Trastuzumab
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*G1-Phase*
binding to extracellular domain of human epidermal growth factor receptor HER-2 - downregulation of EGF receptor tyrosine kinase signaling activity |
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ADRs of Trastuzumab
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SHORT: nausea, vomiting, diarrhea
LONG: anemia, neutropenia, infections, fatigue, infusion reactions, rash |
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USES of Trastuzumab
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1. adjuvant breast cancer (in EGF 2 receptor positive tumor)
2. metastatic breast cancer |
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Cause of Cushing's Syndrome
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1. caused by a tumor or excess growth (hyperplasia) of the pituitary gland. This gland is located at the base of the brain.
2. occurs when your body is exposed to high levels of the hormone cortisol for a long time 3. occur when your body makes too much cortisol |
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Symptoms of Cushing's Syndrome
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1. Upper body obesity (above the waist) and thin arms and legs
2. Round, red, full face (moon face) 3. Purple marks, called striae, on the skin of the abdomen, thighs, and breasts 4. Thin skin with easy bruising 5. Backache, which occurs with routine activities 6. Bone pain or tenderness WOMEN - excess hair growth on face, neck, chest MEN - impotence, no desire for sex |
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LD50 - Lethal Dose 50
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dosage of a chemical that is needed to produce death in 50% of treat animals
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LC50 - Lethal Concentration 50
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same as LD50 but applies to exposure to gasses
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NOAEL - No Observed Adverse Effect Level
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highest dose that does not produce a statistically significant toxic effect
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RfD - Reference Dose
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estimate of the daily exposure to an agent that is assumed to have no adverse health impact on the human population
NOAEL / 100 |
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Anticholinergic Syndrome
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*Think Atropine*
SIGNS: tachycardia, dry flushed hot skin, urinary retention COMMON CAUSES: atropine, scopolamine, antihistamines TREATMENT: Physostigmine |
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Sympathomimetic Syndrome
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*Think Cocaine*
SIGNS: tachycardia, HTN, elevated temp, diaphoresis, mydriasis, seizures COMMON CAUSES: cocaine, amphetamine, ephedrine, caffeine TREATMENT: IV benzos (seizures), lidocaine(heart), beta blockers (HTN) |
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Opiate Syndrome
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*Think Heroin*
SIGNS: hypotension, bradycardia, coma, resp depression, miosis COMMON CAUSES: narcotics TREATMENT: symptomatic and maybe naloxone |
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Non-Opiate Syndrome
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*Think Alcohol*
SIGNS: hypotension, bradycardia, coma, resp depress, miosis COMMON CAUSES: barbiturates, benzos, alcohol TREATMENT: symptomatic, maybe flumazenil, IV saline |
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Cholinergic Syndrome
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*Think insecticides, nerve agent*
SIGNS: confusion, CNS depression, muscle twitching, weakness/paralysis COMMON CAUSES: organophosphates, carbamate insecticides TREATMENT: atropine, 2-PAM(organophosphates) |
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Non-Specific Antidotes to Ingested Toxins
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1. Activated Charcoal
2. Polyethylene Glycol PEG 3350) |
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non-specific chelator, limits drug absorption, not as efficacious if drug is rapidly absorbed
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Activated Charcoal
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Whole-Bowel Irrigation - polyethylene glycol
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useful when the ingestion of a drug occurs that is poorly absorbed by activated charcoal
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Organophosphates
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*Acetylcholine esterase inhibitors*
Irreversible - organophosphate Reversible - carbamates |
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Signs and Symptoms of Organophosphate Poisoning
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HEADACHE, miosis, nausea
1. S-Salivation 2. L-Lacrimation 3. U-Urination 4. D-Defication |
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Mechanism of Action of Organophophates
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extremely toxic----respiratory failure due to diaphragm muscle paralysis and central depression of respiratory centers
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Treatment of Organophosphate poisoning
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Atropine for both and 2-PAM
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Alcohols
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1. Methanol
2. Ethylene Glycol 3. Diethylene Glycol |
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Methanol
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SOURCE: windshield washer solvent
S/S: CNS depression like ethanol MOA: metabolized to formaldehyde - blindness TREAT: metabolic acidosis - Na bicarb IV & Fomepizole(ADH inhibitor) |
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Ethylene Glycol
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SOURCE: auto antifreeze
S/S: CNS depression, hypocalcemic tetany, oxalicaciduria(crystals present in the urine) TREAT: hypocalcemia - Ca IV & Fomepizole(ADH inhibitor) |
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Diethylene Glycol
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SOURCE: wrongly used as low-cost sub for glycerin and propylene glycol (toothpaste)
S/S: nausea, anuric renal failure, hepatitis, pancreatitis TREAT: early diagnosis w/ supportive and symptomatic |
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1. Arsenic
2. Lead 3. Methylmercury |
Metals
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Lead
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short T1/2 life in soft tissue, T1/2 life in bone is from years to decades
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Sources of Lead
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1. Consuming contaminated foods
2. ingestion of paint chips or dust 3. drinking contaminated water 4. toys made in other countries 5. gasoline 6. Occupation |
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Signs and Symptoms of Lead Poisoning
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1. hypochromic microcytic anemia
2. weak wrist or ankle extensor muscles 3. encephalopathy with delirium, hallucinations, convulsions 4. colic 5. gout 6. stillbirths |
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MOA of Lead
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1. believed to mimic and replace endogenous ions
2. inhibits hemoglobin synthesis resulting in anemia |
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Treatment of Lead Poisoning
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1. eliminate source
2. metal chelators (succimer being 1st line) |
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Why is lead poisoning worse in children than in adults
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absorb 40% that is ingested, blood brain barrier deteriorates which can lead to lower IQ, increased ADHD, aggressive behavior, and deliquency
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Sources of Arsenic
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1. contaminant of coal, metal ores
2. rural/municipal water supplies in the US 3. Occupational |
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Signs and Symptoms of Arsenic Poisoning
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ACUTE:
1. hemorrhagic gastroenteritis (rice water diarrhea) 2. garlic odor on breath 3. dehydration CHRONIC: 1. hyperkeratosis 2. exfoliative dermatitis 3. bone marrow depression 4. increased risk of cancer |
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MOA of Arsenic poisoning
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likely causes severe oxidative stress and disrupt protein function by binding to -SH containing amino acids
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Treatment of Arsenic Poisoning
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Metal Chelator - Dimercaprol given IM
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Arsine Gas
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1. occurs in miners
2. formed when acid touches arsenic metal 3. S/S: rapid hemolysis, renal failure 4. TREAT: none- supportive |
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Sources of Methylmercury
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1. Hg metal in dental labs, old thermometers, gold mining
2. inorganic salts used as medical specimen preservatives, insecticides 3. felt hats 4. consumption of contaminated fish and grain fungicide |
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Signs and Symptoms of Methylmercury poisoning
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1. cerebellar ataxia
2. movement disorders 3. loss of balance 4. sensory deficits 5. loss of visual field 6. deafness 7. dysarthria **ALL ARE IRREVERSIBLE** |
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MOA of Methylmercury poisoning
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unknown, shown to increase intracellular calcium and bind to metallothionein
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Women who are nursing or pregnant
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avoid consuming all predatory fish species due to teratogenic effects of MeHg
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Metal Chelators
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1. Succimer
2. Calcium EDTA |
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Calcium EDTA
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1. Given IM or IV for severe Lead Poisoning
2. Toxic to kidney at high doses 3. S/E: chills, fever, nausea, vomiting |
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Succimer
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1. first orally effective metal chelator
2. more rapidly effective 3. can be used for lead, mercury, and arsenic poisoning 4. S/E: GI distress, rash, diarrhea |
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Gases
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1. Carbon Monoxide
2. Cyanide |
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Sources of Carbon Monoxide
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*colorless, odorless, tasteless, nonirritating, ubiquitous*
1. any burning or combustion process |
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Signs and Symptoms of Carbon Monoxide Poisoning
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1. headache
2. dizziness 3. increased heart rate |
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Mechanism of Carbon Monoxide
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binds to hemoglobin in place of oxygen, reduces ability of oxygen to dissociate from hemoglobin and be delivered to deep tissues needing oxygen
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Treatment of Carbon Monoxide Poisoning
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1. remove agent
2. hyperbaric oxygen |
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Cyanide
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SOURCE: smoke(plastics, wool). industrial exposure, chemical warfare
S/S: bitter almond breath, headache, nausea, apnea, loss of consciousness, seizures, coma MOA: binds to cytochrome oxidase- inhibits electron transport chain - decreased ATP synthesis TREAT: Cyanokit (Cyanide + Hydroxocabalamin) |
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Dust and Others
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1. Asbestos
2. PCBs and Dioxin 3. Bisphenol A |
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Asbestos
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*filamentous silica*
SOURCE: older building materials S/S: none right away, mesothelioma lung cancer (15-20 years later) TREAT: no antidote, limit exposure |
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PCBs and Dioxin
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SOURCE: flame retardants, plasticizers, insulating materials in electric transformers
S/S: dermal acne-like eruptions called chloracne, nausea, headache, vomiting |
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Dioxin
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colorless odorless, highly lipid soluble, environmentally stable, contaminant of Agent Orange
TREAT: none |
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Bisphenol A (BPA)
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SOURCE: leaching from water bottles (stamped with 7 on bottom) into water, plastic lined canned food,
S/S: unkonwn MOA: unknown TREAT: none |
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Some concern with BPA
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exposure in utero results in neural and behavioral effects
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