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120 Cards in this Set
- Front
- Back
Name that toxidrome:
symptoms: tinnitis, acidosis |
salicylate toxidrome
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Name that toxidrome:
symptoms: black body diarrhea |
Acids
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Name that toxidrome:
symptoms: vomitus thick and slimy |
Base
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Name that toxidrome:
symptoms: immediate pain in buccal cavity and esophagus |
acids
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Name that toxidrome:
symptoms: pinpoint pupil, repiratory depression/arrest |
Opiates
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Name that toxidrome:
symptoms: Dilated pupils & increase in HR |
Meperidine (Demerol)
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Name that toxidrome:
Source: automatism, what is it? |
Barbituates
automatism is forgetting that you already took your dose |
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Name that toxidrome:
symptoms: low body temp and death due to respiratory depression |
Barbituates
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What is toxicology?
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Primarily a multidisciplinary science that is based on other sciences including:
Pharmacology Pathology (disease/death) Chemistry Epidemiology |
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Children under 5 years old are usually poisoned by:
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Plants, cosmetics, salicylates, hydrocarbons, detergents and acetaminophen.
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name that toxidrome?
treatment: atropine, pralidoxime |
parathion
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name that toxidrome?
signs: deep and rapid breathing, tinnitis |
salicylates
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name that toxidrome?
treatment: cranberry juice (100X increase in excretion) |
PCP overdose
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name that toxidrome?
signs: chloracne, limited systemic effects, death? |
dioxin
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name that toxidrome?
source: herbicides, cigarette smoke, smoke from burning trash and debris |
dioxin
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main targets of toxicity are ...
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small intestines, stomach, liver, CNS, kidney
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chelating drug of choice:
mercury (hg) poisioning |
primary DOC: BAL
secondary DOC: N-acetylpenicillamine (NAP) |
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chelating drug of choice:
Methyl mercury |
Primary DOC: NAP
secondary: L-cysteine |
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chelating drug of choice:
Iron |
primary deferoxamine
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chelating drug of choice:
Lead |
Primary: BAL, EDTA
Secondary: EDTA, succimer |
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chelating drug of choice:
arsenic |
primary: BAL
secondary: Penicillamine |
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Chelating drug of choice:
Cadmium |
primary: EDTA
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Chelating drug of choice:
Copper |
Primary: NAP
secondary: Penicillamine |
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Name that toxicon:
symptoms: headache, metallic taste, NVD, cough, dyspnea, chills, fever, muscle depression, memory |
Mercury vapors
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Name that toxicon:
Symptoms: Nausea, vomiting, hematemesis, renal tubular necrosis, bloody diarrhea, intestinal mucosa necrosis, CV collapse |
inorganic mercury
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name that toxicon:
effects: neurologic effects, tunnel vision, hearing loss, memory loss, tremors, when blood levels > 20-40 ng/ml |
organic mercury
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treatment for mercury poisioning
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ABC's,
Ipecac, lavage, Charcoal BAL Antibiotics Electrolytes Sodium formaldehyde sulfoxylate |
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Name that toxicon:
SymptomsL nausea & vomiting metallic taste epigastric pain hepatic & renal failure |
Copper
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RX for copper poisioning
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ABC's, dialysis, penicillamine or NAP
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what are the two types of Urine tests used to ID drugs?
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Immunoassay (EMIT, ELISA)
Thin Layer Chromatography (TLC) |
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Urine/Blood tests
used to identify toxins |
HPLC
GCMS Coma and Stimulant panels |
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Gastric lavage is ...
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washing of the stomach
insert a tube through the nose or mouth, down into the stomach. Stomach contents can be removed using suction, immediately followed by irrigation with fluids |
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Name a cathartics.
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Mg sulfate
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Pralidoxime
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is a nucleophillic reagent that ties up the organophosphates and permits its excretion
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methemoglobin
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Chelator is made in the body
Used for CYANIDE overdose |
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Give an example of
Accelerating rate of excretion |
Compete with reabsorption (Renal Tubules).
I.e. For Sr2+ or Ra2+ radiation give Ca2+; For Br1- poisoning give Cl1- to aid in excretion. |
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Name that toxicon:
[dry mouth, mydriasis, hyperpyrexia, increase HR, decreased GI motility] |
Tricyclic Antidepressants
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insulin MOA
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Mechanism of Action: Binds to insulin receptors in cell membranes consisting of alpha subunits on the outside surface and cytoplasmic beta subunits having tyrosine kinase activity. Binding of insulin to two receptors (forming a dimer) brings the beta subunits into close proximity, resulting in phosphorylation of tyrosine residues (autophosphorylation) on the beta subunits, and chronicly elevated tyrosine kinase activity. This ultimately results in the activation of other intracellular kinases including ras and MAPK. The network of phosphorylations within the cell results in multiple effects including a translocation of glucose transporters (GLUT 1-5 subtypes) to the cell membrane, with a resultant increase in glucose uptake, glycogen synthase activity & increased glycogen formation, increased protein synthesis, lipolysis, and lipogenesis.
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Insulin tissue effects: liver
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* Liver: increased storage of glucose as glycogen. This involves insertion of GLUT 2 into liver cell membranes & increased synthesis of enzymes involved in glucose metabolism. Insulin also decreases the breakdown of proteins.
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Insulin tissue effects: muscle
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* Muscle: stimulates glycogen & protein synthesis. Increased GLUT 4 insertion into cell membranes.
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insulin tissue effects: adipose tissue
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* Adipose tissue: facilitates triglyceride storage by activating plasma lipoprotein lipase. Increased glucose transport into cells via GLUT 4, reduced breakdown of lipid (reduced intracellular lipolysis).
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Name ultra & short acting insulin
What is it used for? |
insulin lispro & insulin aspart
prandial insulin replacement |
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insulin used iv for emergencies
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crystalline zinc insulin
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intermediate acting insulins
What type of insulins are they? |
-isopane insulin suspension (NPH insulin)
-lente insulin (Basal insulins) |
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If you want to mix intermediate acting insulin with regular insulin, use ...
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NPH and lente b/c lente can retard the onset of action of regular insulin
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Difference between lente and NPH?
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lente: can retard the onset of action of regular insulin
lente also has a longer duration of action |
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long acting insulin
When do you administer it? |
ultralente insulin
- administer it in the morning only basal insulin formation |
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Ultra long acting insulin
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insuilin glargine
-peakless delivery of 20-24 hours basal insulin |
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When does glargine achieve steady state?
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- 2 hours after administration
-peakless delivery |
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insulin delivery systems
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-inhaled
-subcutaneous injection -pump ( continuous infusion pump) -portable pen-sized injection |
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hazards of insulin use
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-hypoglycemia
-antigenic toxic effects (due to the development of antibodies) |
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which insulins are basal insulins?
Which are prandial insulins? |
Basal: NPH, Lente, Ultralente, glargine
Prandial: regular, lispro, aspart. |
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acarbose MOA
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alpha glucose inhibitors
MOA: inhibits the activity of enzymes required to break carbohydrates down into simple sugars within the intestines |
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Drugs that increase insulin duration or sensitivity
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-Biguanides (metformin)
-Thiazolidinedioness (glitazones) Rosiglitazone, Pioglitazone |
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sulfonylurea MOA
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stimulates the release of insulin from B cells
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causes a permanent reduction in thyroid activity
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radioactive iodine (131 I)
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the antithyroid drug with the most rapid onset of antithyroid action is
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ipodate
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a symptom that would be expected to occure in the event of chronic overdose with exogenous T4 is
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weight loss
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When initiating T4 therapy for an elderly patient with long standing hypothyroidism, it is important to begin with small doses to avoid
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overstimulation of the heart
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radiocontrast medium that is also useful in thyrotoxicosis
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ipodate is a radioactive contrast agent
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before surgical removal, a large, highly vascular thyroid gland should be prepared by administration of a short couse of
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iodide ion
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treatment for anabolic protein synthesis
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stanozolol
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men who use large doses of anabolic steroids are at increased risk of
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cholestatic jaundice and elevation of aspartate transaminase levels in the blood.
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which of the second generation sulfonylureas are most potent?
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glipizide & glyburide
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sulfonylureas that are largely protein bound
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tolbutamine and chlorpropamide are extensively bound to serum proteins and drug that compete for protein binding may enhance their hypoglycemic effects
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an important effect of insulin is
(a) increased conversion of amino acids into glucose (b) increased gluconeogensis (c) incresed glucose transport into cells (d) inhibition of lipoprotein lipase (e) stimulaiton of glycoenolysis |
C - increased glucose transport into cells
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why is glucagon given to a 62 year old man with severe bradycardia and hypotension resulting from ingestion of an overdose of atenolol
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glucagon acts through cardiac glucagon receptors to stimulate the rate and force of contaction of the heart. Makes glucagon useful in the treatment of B-blocker induced cardiac depression.
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succimer uses
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lead poisioning (2nd choice)
arsenic mercury |
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a 2 year old child was brought to the emergency room 1 hour after ingestion of tablets he had managed to obtain from a bottle on top of the refrigerator. His symptoms included marked gastrointestinal distress, vomiting (with hematemesis), and epigastric pain. metabolic acidosis and leukocytosis were also present. This patient is most likely to have ingested tablets of
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iron !
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gingivitis, discolored gums, and loose teeth are common symptoms of chronic exposure to this agent
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mercury vapor
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this agent has been reported to cause lupus erythematosus and hemolytic anemia
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penicillamine
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high doses of this agent may cause histamine release and extreme vasodilation
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iron
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the most likely drug to be needed in an overdose due to this substance is an anticonvulsant, but B-blockers are appropriate when cardiac arrhythmias are present.
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theophylline
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Symptoms: drowsiness, agitation, convulsions, muscle spasms, tremor & rigidity, inability to sit still, miosis,
orthostatic hypotension and hypothermia (poikliothermia), ventricular tachyarrhythmias, coma |
Toxicon: Phenothiazines
Treatment: gastric lavage, activated characol |
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Symptoms: nystagmus (horizontal, vertical), ataxia, slurred speech, lethargy & confusion, coma & seizures,
hypotension. Chronic side effects: gingival hyperplasia, hirsutism (excessive hairiness), rashes, acne. |
toxicon: Phenytoin (sodium channel blocker)
treatment: Activated charcol, hemodialysis & hemoperfusion |
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Symptoms: Acid-base disturbances vary with the severity of toxicity. Initially, hyperventilation a respiratory
alkalosis develops secondary to direct stimulation of the respiratory centers. This may be the only consequence of mild salicylism. A severe metabolic (ketolactic) acidosis with compensatory respiratory alkalosis may develop with severe salicylate intoxication. Potassium moves from the intracellular space to the extracellular space. Excretion of hydrogen ions produces acidic urine. A paradoxical aciduria (hydrogen ion excretion) occurs with the depletion of sodium bicarbonate and potassium. Ototoxicity, tinnitus, tachycardia, CNS depression, seizures, nausea & vomiting, GI hemorrhage, prolonged bleeding time, dehydration. |
toxicon: salicylates
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salicylate treatment
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Treatment: ABCs.
Gastric lavage activated charcoal Hemodialysis Sodium bicarbonate Monitor glucose |
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Symptoms: nausea, sinus tachycardia, tremors, seizures, hypotension, and significant
dysrhythmias. |
Toxicon:Theophylline
Treatment: activated charcoal & bowel irrigation. Propranolol, Phenobarbital, Hemodialysis |
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Symptoms: tachycardia, hypotension, confusion or hallucinations, mydriasis, dry mucous membranes
and skin, decreased bowel sounds, urinary retention, seizures, QRS prolongation & arrhythmias. |
Toxicon: Tricyclic antidepressants
treatment: activated characoal, sodium bicarbonate, benzodiazepines |
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Indications: chelator for lead (Pb) & cadmium (Cd)
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Drug: EDTA (ethylene diamine tetra acetic acid)
Mechanism of Action: used as a disodium calcium salt. Forms a soluble heavy metal chelate in the blood which is excreted through the urine |
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primary drug of choice for methyl mercury & copper poisoning.
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N-acetylpenicillamine (NAP)
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secondary
agent for treatment of copper & arsenic poisoning |
Penicillamine
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Mechanism of Action: Forms a chelate by binding sulfhydryl groups with arsenic, mercury, lead, and gold,
thus increasing both urinary and fecal excretion of the metals. |
BAL
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Indications: Treatment of prostatic carcinoma & as a postcoital contraceptive.
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DES
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Pharmacokinetics: As a "morning after pill" - take within 72 hrs of unprotected coitus to prevent blatocyst
implantation w/ a dose regimen of 2.5 mg twice daily for 5 day |
Drug: Ethinyl Estradiol (Estinyl ®)
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if used for a long period of time, will decrease HDL levels and lead to
atherosclerosis. |
progestins
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Tamoxifen MOA
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Mechanism of Action: two mechanisms - 1) decreases estrogen-induced mitogen production by antagonizing
estrogen receptors; 2) it can directly induces growth factor inhibitors. |
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Mechanism of Action: has effects on bone, but does not stimulate the endometrium or breast.
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Drug: Raloxifene (Evista ®)
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Indications: prevention of post-menotpausal osteoporosis
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Drug: Raloxifene (Evista ®)
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Drug Class: Estrogen partial agonist / antagonist
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Drug: Raloxifene (Evista ®)
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Drug: Stanozolol (Winstrol ®)
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Drug Class: Anabolic Steroid, Synthetic Testosterone Analog
Mechanism of Action: Similar to testosterone Indications: Hereditary Angioedema. (Abused by atheletes). |
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Drug: Fluoxymesterone (Halotestin ®)
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palliation of androgen responsive recurrent mammary cancer in postmenopausal women
• replacement therapy in conditions associated with symptoms of deficiency or absence of endogenous testosterone in men (e.g. hypogonadism or delayed puberty). |
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Intended Use: Prevent jet lag & to induce sleep (reduce insomnia)
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Melatonin
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Melatonin contraindication
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pregnancy or desire to conceive
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Melatonin MOA
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Mechanism of Action: A serotonin derivative that is released by the pineal gland & is believed to be inolved in
regulating sleep-wake cycles. Melatonin release coincides with darkness & is suppressed by daylig |
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Intended Use: Diet suppressant, bronchodialator, stimulant
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Herb: Ma-huang (ephedra)
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Herb: Ma-huang (ephedra)
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Ephedrine has both direct (alpha and
beta) agonist effects and indirect (amphetamine or tyramine - like) sympathomimetic effects. |
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Herb: Ma-huang (ephedra) toxicity
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an increased risk of stroke, myocardial infarction and sudden death in those using ephedra
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Side Effects: higher than normal incidence of myocardial infarction, stroke and sudden death. Hypertension,
insomnia. Pharmacokinetics: tachyphylaxis develops with repeated dosing. |
Herb: Ma-huang (ephedra)
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herbal med: similar efficacy as some prescribed
antidepressants for mild to moderate depression. However, clinical trials indicate that it is not effective against major or severe depressio |
St. John's wort
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Intended Use: Treatment of cerebrial insufficiency & Alzheimer dementia
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Herb: Ginkgo (Ginkgo Biloba)
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Herb: Ginkgo (Ginkgo Biloba
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Mechanism of Action: has antioxidant and free-radical scavenging properties that may reduce ischemic injury
and oxidative stress. Ginkgo has been shown to increase blood flow and reduce blood viscosity (antiplatelet effect). Enhancment of nitric oxide may be involved. |
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Ginkgo
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Ginkgo has antiplatelet properties & for cerebrial insufficiency & Alzheimer dementia
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Intended Use: To improve physical and mental performance, enhancement of immune function
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Herb: Ginseng
Mechanism of Action: active principles appear to be a dozen or more triterpenoid saponin glycosides called ginsenosides or panaxosides. |
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use cautiously when taking any other psychiatric, estrogenic or hypoglycemic
medication. Should not be used in combination with warfarin |
ginseg has antiplatelet properties
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Intended Use: Treatment of benign prostatic hyperplasia
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Herb: Saw Palmetto
more effective than placebo in reducing nocturnal urinary frequency, daytime urinary frequency and increasing peak urinary flow |
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Intended Use: Relief of age-related disorders, weight loss, reduced risk of heart disease, prevention of cancer,
boosting the immune system |
Herb: Dehydroepiandrosterone (DHEA)
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DHEA MOA & SE
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Mechanism of Action: a precursor hormone (to as many as 50 different hormones) that is secreted by the
adrenal cortex & CNS. It is converted to androstenedione, testosterone & androsterone. In peripheral tissues aromatase converts DHEA to estradiol. In the plasma, DHEA is converted to DHEA sulfate (DHEAS) Side Effects: Adrongenic side effects are common |
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ipodate, B-blockers, and corticosteroids effect on T3 levels
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Drugs such as ipodate, B-blockers, and corticosteroids, and severe illness or starvation inhibit the 5’-deiodinase necessary for the conversion of T4 to T3, resulting in low T3 and high rT3 levels in the serum.
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iodide organification
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Iodide is then oxidized by thyroidal peroxidase to iodine, in which form it rapidly iodinates tyrosine residues within the thyroglobulin molecule to form monoiodotyrosine (MIT) and diiodotyrosine (DIT)-IODIDE ORGANIFICATION
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Characterized by decreased BMR, CO, fatigue, myxedema, lethargy, etc.
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hypothyroidism
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antithyroid drugs adverse effects
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agranulocytosis (reversible)
rash (most common) edema. |
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inhibits thyroid hormone release.
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potassium iodide
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treat thyroid storm
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Propranolol blunts sympathetic stimulation that occurs in hyperthyroidism.
2. Potassium iodide inhibits thyroid hormone release. 3. Large doses of propylthiouracil |
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BTEX (Benzene, toluene, ethylbenzene and xylene)
gasoline causes |
CNS depressants, nausea, vomiting, mucous membrane irritation, pulmonary irritation, skin irritation and convulsions (high dose).
Treatment: Discontinue exposure, ABC’s, no emesis, anticonvulsants as needed |
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leading causes of death in the workplace.
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Hydrogen sulfide
MOA: Most likely an inhibitor of cytochrome oxidase. Resulting in increase anaerobic activity, causing a metabolic acidosis. |
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CNS Depression
Coma Respiratory paralysis and collapse. |
H2S
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dypsnea, pneumonitis, Pneumothorax
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inorganic mercury
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Acute renal tubular necrosis
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inorganic mercury
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cadmium antidote
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No specific antidote for cadmium poisoning
BAL is contraindicated due to evidence that large concentration of cadmium in the kidney will lead to greater damage. |