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Pharm Final

Pharmacology: Supplements and Toxicology

A manufacturer can product does something: beneficial, BUT CANNOT MAKE MEDICAL CLAIMS; there are a few exceptions like folic acid, calcium and osteoporosis, sodium and HTN, etc.
Nutrient rich products with limited health claims Nutraceuticals
Any modified food or ingredient that may provide a benefit beyond the traditional nutrients it contains Ex: bread with extra fiber in it Functional Foods
Foods that are derived from naturally occurring ingredients Ex: soy has one Foods that are derived from naturally occurring ingredients (soy has phytoestrogen)
made by steeping and soaking herb in water for a few minutes tea
the herb is soaked in alcohol, glycerin or an alcohol-water combination to extract active components Tinctures
A tincture that has been filtered or distilled Extract
herbs are dried, pulverized to a powder, and placed in capsules or shaped into pills Tablets and capsules
An herb is added to an emollient like petrolatum, lanolin, or a proprietary cream Topical
Ginseng: Uses and Adverse U: stress reliever, performance enhancer, energizer; A: HTN, or HypoTN, estrogen-like effects, HA; Antioxidant effects reduce LDL, may lower blood postprandial glucose in type 2 DM, and improve effectiveness of ABX in acute bronchitis
Ginkgo: Uses (3) and Adverse U: 1) improvement of blood flow 2) Anti-oxidant 3) Blocks effects of platelet aggregating factors A: similar to poison ivy, and can have similar effects and INCREASED bleeding risk
4 specific uses for Ginkgo 1) claudication 2) Alzheimers 3) Cerebral insufficiency 4) SSRI-induced sexual dysfn
Garlic: Use U: claims improved lipid profile, but study showed no effect
Black Cohosh: Use and Adverse U: Menopausal and PMS Sx, though not proven in NIH study for hot flashes and night sweats. A: liver damage
Echinacea: Use and Adverse U: prophylaxis/Tx of cold and flu Sx (immune system stimulation). Studies mixed on Tx, probably doesn't prevent. A: immunosuppresive w/ continuous use, Rxns in people w/ allergies to daisy family.
St. John's Wort (Hypericum): Use and Adverse U: DEPRESSION (SSRI quality), anxiety, anti-viral (not effective). A: Photosensitive skin rxns, substantial effects on cytochrome P450 system
Saw Palmetto: Use and Adverse U: 5 alpha reductase inhibitor activity (inhibits Test ->DHT), possibly BPH. A: not for use during PREGNANCY
Valerian: Use and Adverse U: Promote sleep and anti-anxiety (Increase GABA levels in CNS) A: withdrawl, potentiate benzos
Ma Huang or Ephedra: Use and Adverse U: bronchial asthma, wt loss, performance enhancer A: CNS stimulation and vasoconstriction, HTN, arrythmias, MI, stroke, seizures, death. CAN BE USED TO CREATE METH
Glucosamine: Use and Adverse U: Tx of osteoarthritis (strengthens cartilage). A: Shellfish allergies, may decrease effectiveness of insulin
S-adenosylmethionine- SAMe: Use and Adverse U: depression, arthritis, liver disease, HD (produce and break down serotonin, dopamine etc). A: dry mouth, N/G/D/HA, SEROTONIN effects
Coenzyme Q10: Use U: acts as anti-oxidant, may decrease BP, helpful post MI.
Melatonin: Use and Adverse U: dementia, jet lag, insomnia, anti-aging. A: impairs gonadal development in children
Omega 3s: Use, Deficiency, Adverse U: Essential for brain fn, reduce inflammation, Significantly lower triglyceride levels, CAD (minimal heart benefit), high BP. D: fatigue, poor memory, dry skin. A: bleeding problems
Creatine: Use and Adverse U: increase in muscle mass, heart muscle strength, body wt, endurance in HF pts. A: Dehydration and rhabdomyolysis, muscle cramps, muscle tears
T/F: Although chicken is less expensive, gram for gram, it is less effective than whey protein or amino acid supplement FALSE, cheaper and more protein; Eat a balanced diet: don't need supplements
What are 2 anabolic steroid precursors? What do they convert to? Are they effective? Adverse? DHEA and Andro; Convert to testosterone; Minimally or not effective; A: liver damage and cause opposite gender features in person and respectively increase prostate or uterine cancer.
Phentermine appetite suppressant; amphetamine like substance w/o habituating properties as it didn’t have as strong of a mental stimulation
Locaserin: Use, MOA and Adverse for chronic weight management in BMI>30 or >27 w/DM2/HTN/Dyslipidemia. 5HT-2c agonist (most control over satisfaction/satiation). A: HA, cognitive impairment, fatigue, hypoglycemia.
Qysmia: Use, MOA, Wt loss? Adverse chronic weight management in BMI>30 or >27 w/DM2/HTN/Dyslipidemia. combines phentermine and ER topiramate (anti-seizure). 20 lbs wt loss/year. A: monitor for suicidal thoughts/behavior, cognition, fatigue, dysgeusia (exacerbates weird metallic taste)
Orlistat: Use and Adverse Alli; U: inhibits pancreatic lipases w/ break down fat molecules. A: Oily, leaky, fatty discharge and lowers absorption of fat soluble vitamins
Sibutramine: Use and Adverse U: inhibits NT reuptake in brain (esp norepinephrine), enhances feeling of satiety. PULLED from US markets but still slipped into conterfeit products. A: Part of fen-phen combination and an amphetamine.
Metformin: Use U: overweight and DM2 (lowers glucose, increase insulin sensitivity, appetite suppressant).
Adverse for Stimulant Rx drugs: Increased BP, HR, nervousness, irritability
T/F: Prescription diet drugs work well independantly FALSE, very minimal results w/o diet and exercise
Difference between ephedra and ephedra replacements Ephedra replacements have no active ingredient and there is no published evidence to support them for appetite suppressing
T/F: Xenadrine contains ephedrine and synephrine False, it USED TO contain those, now it contains heavy caffeine and and other stimulants.
First steps on approaching a poisoned patient Airway, Breathing, Circulation (ABCs)
6 questions you want to ask with a toxicology patient 1) What? 2) When? 3) How much? 4) How? 5) Why? 6) Anything else?
LC50 The concentration of a toxin or toxicant needed to produce death (lethality) in 50% of the exposed population
EC50 The dose producing an effect (good or bad) in 50%
IC50 The dose inhibiting a physiologic end-point in 50%; great if toxin has several levels of physiologic impact.
What is the measure to define carcinogenic effects? NO MEASURE
Delaney Clause zero tolerance for any agent that caused cancer in humans or animals – mandated removal from the market any food or drug ingredient that had been linked to cancer, even in miniscule amounts.
5 key toxidromes 1. sympathomimetic 2. serotoninergic 3. opiate 4. anticholinergic 5. cholinergic
Serotoniergic Toxidrome: Why, Dx, Tx, Ex Adverse rxn to serotonergic agents. Dx: 1) high temp, 2) mental status changes, 3) autonomic instability 4) Neuromuscular abnormalities. Tx: Antipyretics and Benzos (for seizures and muscle relaxant); Ex: SSRI OD
Anticholinergic Toxidrome: Dx, Tx, Ex Dx: Dry mucus membranes, mental status changes, flushed skin, mydriasis (very dilated pupils), fever, tachy, hyperprexia, HTN. Tx: Supportive care or cholinergics if they are super tachycardic. Ex: Atropine
Cholinergic Toxidrome: Dx, Tx, CNS interaction, Ex Dx: DUMBELLS (diarrhea, urinatio, miosis, bradycardia, bronchospasm, emesis, lacrimation, limp, salivation/sweating) LOTS OF SECRETING; Tx w/ anti-cholinergics. Entry of cholinergics into the CNS will cause SEIZURES; Ex: pesticides (organophosphates)
Opioid toxidrome: Dx, Tx Dx: respiratory depression, miosis (pinpoint pupils), hypoactive bowel sounds. Tx: naloxilone
Sympathomimetics: Dx, Ex HTN, Tachycardia, hyperpyrexia WITH SWEATING, mydriasis (dilated pupils), anxiety Ex: Cocaine (LIKE anti-cholinergics except SWEATING)
What toxins cause bradycardia? PACED Propanolol, anticholinesterases, CCBs, Ethanol, Digoxin
What toxins cause tachycardia? CAAASST Cocaine, Anticholinergics, Antihistimines, Amphetamines, Sympathoimetics, Solvents, Theophylline
What toxins cause hypoventilation? SLOW Sedatives, Liquor, Opiates, Weed
What toxins cause hyperventilation? PANT PCP, Aspirin, Noncardiogenic pulmonary edema, Toxic metabolic acidosis
Bitter almonds Cyanide
Mothballs Camphor
Garlic Organophosphates, Arsenic
Peanuts Rodenticides
Carrots Water hemlock
Rotten eggs Sulfur dioxide, hydrogen sulfide
Wintergreen Methyl salicylates
Gasoline Hydrocarbons
Fruity DKA, Isopropanol consumption
Pears Chloral hydrate
What can cause EKG problems? (5) Sympathomimetics, BBs, digoxin, CCBs, CO
2 with increased anion gap and increase osmolar gap 1) Methanol 2) Ethylene glycol
What 4 things cause increased anion gap other than methanol and ethylene glycol? 1) Lactic acidosis 2) Ketoacidosis 3) Salicylate poisoning 4) Chronic renal failure
Normal anion gap? 8-12
Coma Cocktail (3) Dextrose, Naloxone (Txs opiates), Thiamine (malnourishment)
T/F: Lavage is TOC with ingestion of corrosives due to risk of perforation False, CONTRA, replaced with charcoal
T/F: Treat the poison first False, TREAT THE PATIENT NOT THE POISON
T/F: Pepto-bismol can cause a salicylate overdose True, bismuth subsalicylate!
Metabolism of Salicylates Metabolism is first order until serum level reaches 30mg/dL, then it becomes zero order (constant rate)
Salicylate overdose Sx (5) N/V (dehydration), diaphoresis, tinnitius, hyperventilation, hypokalemia
Worse the toxicity, worse the hypokalemia
Tx of salicylate overdose (3) 1) Tx of metabolic acidosis and hypokalemia 2) Activated charcoal (multi-use, best for extended release) 3) Urine alkalization
Indications for dialysis in salicylate overdose (7) 1) Serum levels >100 in acute 2) Levels >60 in chronic 3) Pulmonary edema 4) Renal failure 5) CHF 6) Poor response to Tx 7) Altered mental status/academia
Acetaminophen or APAP is the most common annual cause of 1) Pharmaceutical poisoning 2) Pharmaceutical poisoning death 3) Acute liver failure in US (even more than alcohol!)
Max dose of acetaminophen in Peds 60mg/kg/day
Max dose of acetaminophen in adults 4 grams/day
What part of acetaminophen is the most toxic? What does it do? What detoxifies it? NAPQI (4% of breakdown), binds cellular proteins, altering cell function resulting in cell death. Detoxified by glutathione (which is only produced in a finite amount)
What else lowers glutathione? (2) Ethanol and phenobarbital
Acetaminophen overdose phase 1 “silent overdose”, N/V/Abd pain
Acetaminophen overdose phase 2 hepatic damage (LFT elevated), RESOLUTION OF PHYSICAL Sxs
Acetaminophen overdose phase 3 N/V/abd pain reoccur, LFT maximally elevated, coagulopathy, hepatic necrosis (orange pt), coma -> death
Acetaminophen overdose phase 4 if pts survives 4 days -> recovery phase. LFTs decrease over several weeks.
Normogram guideline for determining who should be treated for a single acute ingestion
Tx for acetaminophen? What does it do? N-acetylcysteine (NAC), donates for glutathione regeneration
Greatest benefit for administration w/in how long for acetaminophen 8 hours, though after 8 hours can work (even up to a few days)
Worst part about NAC Very foul “rotten egg” odor when in liquid form
Adverse of IV N-acetylcysteine anaphylactoid rxn: rash, HypoTN, bronchospasm, death
T/F: Tx if any sign of liver injury even w/o Hx of APAP ingestion unless AST/ALT normal True!
T/F: Late presenting sick pts may not have detectable acetaminophen levels True!
What does the rule of 150's describe? Acute toxic dose:>150mg/kg (also pediatric) or >7.5g. Chronic toxic dose: >150mg/kg/day or 7.5g/day.. Tx indicated if: Level above 150mcg/dL at 4 hours or Ingestion of 150 mg/kg in children
Created by: crward88



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