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108 Cards in this Set

  • Front
  • Back
Drugs that stimulate Activity (Oxytocics)
1. Oxytocin
2. Dinoprostone
3. 15-methyl PGF2a - Carboprost Tromethamine
4. Ergonovine Maleate
5. Methylergonovine Maleate
6. Mifepristone - RU486
Drugs that inhibit uterine Activity (tocolytic)
1. Terbutaline sulfate
2. Magnesium Sulfate
3. Prostaglandin-synthetase Inhibitors - Indomethacin
Therapeutic Indications for drugs that stimulate uterine motility
1. induce labor
2. control postpartum uterine hemorrhage
3. cause uterine contraction
4. Induce abortion
Therapeutic indications for drugs that inhibit uterine motility
1. delay or prevent premature labor (<37 weeks)
2. slow delivery so other therapeutic measures can be performed
Production of oxytocin
sensory stimuli (stretching) from cervix, vagina, and breast causes the release from nerve terminals into the circulation
MOA of Oxytocin
binds to specific receptors, activates receptors on myometrial smooth muscle cells increases intracellular calcium and leads to contractions of smooth muscle
Indications for use of Oxytocin for labor induction
1. risk to mother, fetus, or both
2. erythroblastosis fetalis
3. placental insufficiency
4. prolonged pregnancy (>42 weeks)
Other uses of Oxytocin
1. stimulate milk ejection
2. reduce postpartum hemorrhage (USE BIG DOSE)
Adverse Effects of Oxytocin
1. decrease in blood pressure, increased heart rate, arrhythmias
2. Sustained uterine contractions **
Prostaglandins for uterine motility
1. Dinoprostone
2. 15-methyl PGF2a - Carboprost Tromethamine
3. PGE1 analog - Misoprostol
Uses of dinoprostone
1. cervical ripening **
2. induce contractions
Cervical Ripening
prostaglandins stimulate uterine contractions and cause softening and dilation of the cervix
Application of Dinoprostone
1. Cervical gel - Prepidil
2. Vaginal inserts - Cervidil
ADRs and Contraindications of Dinoprostone
1. GI disturbances
2. Uterine hyperstimulation


1. Abnormal fetal position, fetal distress
15-methyl PGF2a - Carboprost Tromethamine
control postpartum bleeding - given IM
OR
induce abortion in the 2nd trimester
PGE1 analog Misoprostol
used with the antiprogestin Mifepristone RU486 for early termination of pregnancy
Ergot Alkaloids to stimulate uterine motility
1. Ergonovine Maleate
2. Methylergonovine Maleate
Ergonovine Maleate & Methylergonovine Maleate
USE: postpartum/postabortion hemorrhage

MOA: activate alpha 1 receptors - induce intense contractions of uterus

ADRs: HTN, nausea, vomiting, diarrhea
Mifepristone - RU486
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
Terbutaline
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
Magnesium Sulfate
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
1. Mechlorethamine
2. Cyclophosphamide
Alkylating Agent - Nitrogen Mustards
1. Carmustine
Alkylating Agent - Nitrosoureas
1. Cisplatin
Alkylating Agent - Platinum Complexes
1. Methotrexate
Antimetabolite - Folic Acid Analog
1. Mercaptopurine
Antimetabolite - Purine Analog
1. Fluorouracil
2. Cytarabine
Antimetabolite - Pyrimidine
1. Daunorubicin HCl
2. Doxorubicin HCl
Antibiotics - Atracycline
1. Vinblastine Sulfate
2. Vincristine Sulfate
3. Etoposide
4. Paclitaxel
Vinca Alkaloids, Epipodophylotoxins and Taxanes
1. Prednisone
2. Dexamethasone
Adrenocorticosteroids
1. Tamoxifen
Estrogen and Antiestrogens
1. Imatinib Mesylate
Tyrosine Kinase Inhibitors
1. Trastuzumab
Monoclonal Antibodies
Mechanism of Action of Alkylating Agents
*Cell Cycle Non-Specific

1. Miscode DNA strands
2. Incomplete repair of alkylated segment
3. Excessive crosslinking of DNA and inability for strand separation
Which Alkylating Agent is most lipid soluble
Carmustine
ADRs of Cisplatin
Nephrotoxicity and otoxicity
Toxicity of Alkylating Agents, Antimetabolites
1. Nausea and Vomiting
2. Bone Marrow Depression
Methotrexate
*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
Uses of Methotrexate
leukemia, lymphoma; breast, head, neck carcinoma; osteosarcoma; bladder, gastric AND immunosuppressant
Part of the cell cycle affected by Mercaptopurine, Fluorouracil, and Cytarabine
S-Phase - Antimetabolites
MOA of Daunorubicin HCl and Doxorubicin HCl
*Cell Cycle Non-Specific - max effect in S-phase*

Intercalates and binds DNA - uncoils DNA helix - destroys DNA template
Toxicity of Daunorubicin HCl and Doxorubicin HCl
Cardiotoxicity
MOA of Vinblastine Sulfate and Vincristine Sulfate
*Cell Cycle Specific - M phase*

binds tubulin - disrupts mitotic spindle apparatus - prevents metaphase
Toxicity of Vinblastine Sulfate and Vincristine Sulfate
Neurological toxicity
MOA of Etoposide
*G2-Phase*

forms complex with topoisomerase II and DNA - DNA breaks - cell death
MOA of Paclitaxel
*G2 and M Phase*

Antimicrotubule agent - inhibits microtubule assembly
MOA of Tamoxifen
*G1 Phase*

competes with estradiol for binding to cytoplasmatic estrogen receptors - DNA, RNA, and protein synthesis reduced
ADRs of Tamoxifen
SHORT: hot flashes, nausea, vomiting

LONG: visual disturbances, hypercalcemia, vaginal bleeding
Uses of Tamoxifen
Breast Carcinoma
MOA of Imatinib Mesylate
*G1 Phase*

Bcr-Abl protein tyrosine kinase inhibition - cell proliferation inhibition and induction of apoptosis
ADRs of Imatinib Mesylate
SHORT: ab pain, nausea, vomiting, diarrhea

LONG: fatigue, join pain, fluid retention, cramps, edema, rash
USES of Imatinib Mesylate
1. Philadelphia Chromosome positive chrominic myeloid leukemia

2. c-Kit (CD117) receptor positive-gastrointestinal stromal tumor
MOA of Trastuzumab
*G1-Phase*

binding to extracellular domain of human epidermal growth factor receptor HER-2 - downregulation of EGF receptor tyrosine kinase signaling activity
ADRs of Trastuzumab
SHORT: nausea, vomiting, diarrhea

LONG: anemia, neutropenia, infections, fatigue, infusion reactions, rash
USES of Trastuzumab
1. adjuvant breast cancer (in EGF 2 receptor positive tumor)

2. metastatic breast cancer
Cause of Cushing's Syndrome
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
Symptoms of Cushing's Syndrome
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
LD50 - Lethal Dose 50
dosage of a chemical that is needed to produce death in 50% of treat animals
LC50 - Lethal Concentration 50
same as LD50 but applies to exposure to gasses
NOAEL - No Observed Adverse Effect Level
highest dose that does not produce a statistically significant toxic effect
RfD - Reference Dose
estimate of the daily exposure to an agent that is assumed to have no adverse health impact on the human population

NOAEL / 100
Anticholinergic Syndrome
*Think Atropine*

SIGNS: tachycardia, dry flushed hot skin, urinary retention

COMMON CAUSES: atropine, scopolamine, antihistamines

TREATMENT: Physostigmine
Sympathomimetic Syndrome
*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)
Opiate Syndrome
*Think Heroin*

SIGNS: hypotension, bradycardia, coma, resp depression, miosis

COMMON CAUSES: narcotics

TREATMENT: symptomatic and maybe naloxone
Non-Opiate Syndrome
*Think Alcohol*

SIGNS: hypotension, bradycardia, coma, resp depress, miosis

COMMON CAUSES: barbiturates, benzos, alcohol

TREATMENT: symptomatic, maybe flumazenil, IV saline
Cholinergic Syndrome
*Think insecticides, nerve agent*

SIGNS: confusion, CNS depression, muscle twitching, weakness/paralysis

COMMON CAUSES: organophosphates, carbamate insecticides

TREATMENT: atropine, 2-PAM(organophosphates)
Non-Specific Antidotes to Ingested Toxins
1. Activated Charcoal
2. Polyethylene Glycol PEG 3350)
non-specific chelator, limits drug absorption, not as efficacious if drug is rapidly absorbed
Activated Charcoal
Whole-Bowel Irrigation - polyethylene glycol
useful when the ingestion of a drug occurs that is poorly absorbed by activated charcoal
Organophosphates
*Acetylcholine esterase inhibitors*

Irreversible - organophosphate
Reversible - carbamates
Signs and Symptoms of Organophosphate Poisoning
HEADACHE, miosis, nausea
1. S-Salivation
2. L-Lacrimation
3. U-Urination
4. D-Defication
Mechanism of Action of Organophophates
extremely toxic----respiratory failure due to diaphragm muscle paralysis and central depression of respiratory centers
Treatment of Organophosphate poisoning
Atropine for both and 2-PAM
Alcohols
1. Methanol
2. Ethylene Glycol
3. Diethylene Glycol
Methanol
SOURCE: windshield washer solvent

S/S: CNS depression like ethanol

MOA: metabolized to formaldehyde - blindness

TREAT: metabolic acidosis - Na bicarb IV & Fomepizole(ADH inhibitor)
Ethylene Glycol
SOURCE: auto antifreeze

S/S: CNS depression, hypocalcemic tetany, oxalicaciduria(crystals present in the urine)

TREAT: hypocalcemia - Ca IV & Fomepizole(ADH inhibitor)
Diethylene Glycol
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
1. Arsenic
2. Lead
3. Methylmercury
Metals
Lead
short T1/2 life in soft tissue, T1/2 life in bone is from years to decades
Sources of Lead
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
Signs and Symptoms of Lead Poisoning
1. hypochromic microcytic anemia
2. weak wrist or ankle extensor muscles
3. encephalopathy with delirium, hallucinations, convulsions
4. colic
5. gout
6. stillbirths
MOA of Lead
1. believed to mimic and replace endogenous ions

2. inhibits hemoglobin synthesis resulting in anemia
Treatment of Lead Poisoning
1. eliminate source
2. metal chelators (succimer being 1st line)
Why is lead poisoning worse in children than in adults
absorb 40% that is ingested, blood brain barrier deteriorates which can lead to lower IQ, increased ADHD, aggressive behavior, and deliquency
Sources of Arsenic
1. contaminant of coal, metal ores
2. rural/municipal water supplies in the US
3. Occupational
Signs and Symptoms of Arsenic Poisoning
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
MOA of Arsenic poisoning
likely causes severe oxidative stress and disrupt protein function by binding to -SH containing amino acids
Treatment of Arsenic Poisoning
Metal Chelator - Dimercaprol given IM
Arsine Gas
1. occurs in miners
2. formed when acid touches arsenic metal
3. S/S: rapid hemolysis, renal failure
4. TREAT: none- supportive
Sources of Methylmercury
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
Signs and Symptoms of Methylmercury poisoning
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**
MOA of Methylmercury poisoning
unknown, shown to increase intracellular calcium and bind to metallothionein
Women who are nursing or pregnant
avoid consuming all predatory fish species due to teratogenic effects of MeHg
Metal Chelators
1. Succimer
2. Calcium EDTA
Calcium EDTA
1. Given IM or IV for severe Lead Poisoning
2. Toxic to kidney at high doses
3. S/E: chills, fever, nausea, vomiting
Succimer
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
Gases
1. Carbon Monoxide
2. Cyanide
Sources of Carbon Monoxide
*colorless, odorless, tasteless, nonirritating, ubiquitous*

1. any burning or combustion process
Signs and Symptoms of Carbon Monoxide Poisoning
1. headache
2. dizziness
3. increased heart rate
Mechanism of Carbon Monoxide
binds to hemoglobin in place of oxygen, reduces ability of oxygen to dissociate from hemoglobin and be delivered to deep tissues needing oxygen
Treatment of Carbon Monoxide Poisoning
1. remove agent
2. hyperbaric oxygen
Cyanide
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)
Dust and Others
1. Asbestos
2. PCBs and Dioxin
3. Bisphenol A
Asbestos
*filamentous silica*

SOURCE: older building materials

S/S: none right away, mesothelioma lung cancer (15-20 years later)

TREAT: no antidote, limit exposure
PCBs and Dioxin
SOURCE: flame retardants, plasticizers, insulating materials in electric transformers

S/S: dermal acne-like eruptions called chloracne, nausea, headache, vomiting
Dioxin
colorless odorless, highly lipid soluble, environmentally stable, contaminant of Agent Orange

TREAT: none
Bisphenol A (BPA)
SOURCE: leaching from water bottles (stamped with 7 on bottom) into water, plastic lined canned food,

S/S: unkonwn

MOA: unknown

TREAT: none
Some concern with BPA
exposure in utero results in neural and behavioral effects