tox final Flashcards
CO2 produced by
Incomplete oxidation of fossil fuels (gas, wood, coal)
CO2 forms ____ when bound to hemoglobin
Carboxy-hb
CO2 leads to what type of cyanosis
Cherry red cyanosis
CO2 primary target organs
Brain (Parkinson), Myocardium (MI/ angina)
Initial SS of CO2 poisoning
Headache, confusion
CO2 poisoning managed by
100% O2, Hyperbaric O2
Hb oxidizing agents
Nitrogen oxides- nitrates, nitrites, chlorates, meds
Heme Fe2 oxidized to
Heme Fe3 (methemoglobin)
Methemoglobin normally <5% due to
Methemoglobin reductase
Methemoglobin reductase deficiency
Methemoglobinemia (blue baby syndrome) FERTILIZER IN WELL WATER
Methemoglobin causes _____ cyanosis
Chocolate cyanosis
Strong inorganic acids cause
Precipitative necrosis at site of contact w/ Eschar
Strong acid burn management
Wash w/ cold running water 15 minutes
Strong inorganic bases cause
Dissolution necrosis at site of contact. No scar, progressive penetrative damage to underlying tissue possible
Salicylates
Acetylsalicylic acid (aspirin), sodium salicylate
Salicylate uses
Analgesic, antipyretic, anti-inflammatory, OSTEOARTHRITIS
Salicylate toxicity mechanisms
Acid base imbalance (stimulate medullary respiratory nuclei) ->
Hyperventilation/ respiratory acidosis –>
Oxidation uncoupled from phosphorylation ->
Heat released from ETC -> hyperthermia
Salicylate toxicity symptoms
Reye’s syndrome in children (when aspirin given for viral fever)
Tinnitus
Aggravate gouty arthritis
NSAIDs
Aspirin, ibuprofen, naproxen
Steroidal anti-inflammatory drugs all related to
Hydrocortisone- cortisol, prednisone, betamethasone, dexamethasone
Steroids used
Advanced OA, asthma
Steroid mechanism
Inhibit phospholipase A2, prevent arachidonic acid formation -> decreased prostaglandin
Steroid toxicity
Hyperglycemia, Cushing’s (fat trunk, shoulders, face) (moon face, buffalo hump)
Protein catabolic effect - > muscle wasting, difficulty healing
Immunosuppression
Pituitary suppression (decreased ACTH)
Narcotic analgesics
morphine, codeine, hydrocodone, oxycontin
Narcotic analgesics suppress __ and ___
CNS (central reflexes depressed), Medulla (CV and respiratory collapse- CHEYNE STOKES RESPIRATORY PATTERN)
Narcotic analgesics stimulate
vagus (sinus bradycardia and projectile vomiting)
EW nuclei- miosis/ pinpoint pupils
Most important non-narcotic analgesic
Acetaminophen in tylenol
Acetaminophen mechanism
Inhibits prostaglandin synthesis IN BRAIN ONLY. NOT ANTI-INFLAMMATORY
Acute acetaminophen overdose effect
Centrilobular hepatic nedcrosis
Chronic acetaminophen overdose effect
Kidney failure
MAO inhibitor
Tranylcypromine
MAO inhibitor usage
Anti-depressant
Tranylcypromine mechanism
Increase activity at aminergic synapses (NE, serotonin)
MAO inhibitor toxicity
Hypertensive crisis when combined with fermented food -> stroke
Tricyclic antidepressant
imipramine
Imipramine effect on ECG
Prolongs QT interval
Imipramine mechanism
Anticholinergic (block muscarinic Ach muscle receptors, exocrine glands, SA node)
Imipramine toxic effects
Flaccid intestinal stasis, pupil dilation, decreased sensation, dry mucous membranes
SSRIs
Prozac, zoloft
SSRI toxicity
Serotonin syndrome
Antifreeze
Ethylene glycol
Ethylene glycol mechanisms
CNS depression like ethyl alcohol
Forms oxalic acid in liver-> hypocalcemia -> decreased heart contraction and peristalsis
Calcium oxylate formation in ST
Oxalic acid metabolized by ___ and ___
Alcohol dehydrogenase and aldehyde dehydrogenase
Methyl alcohol AKAs
Methanol, Woos Spirit
Methanol use
Solvent, de-icer
Methanol toxicity mechanism
Forms formaldehyde, formate -> destroys retinal ganglion cells
Methanol toxic effect
Blindness
Methanol overdose treatment
Titrated doses of ethyl alcohol (preferred substrate for enzymes)