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Pharm Exam 4 > Toxicology Buzzwords > Flashcards

Toxicology Buzzwords Flashcards

1
Q

True or False… Dioxin causes cancer via DNA mutation

A

FALSE: causes cancer by epigenetic changes

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1
Q

List the 3 types of mercury and their respective symptoms

A

1) HG0 (elemental) - *gingivitis* + CNS tremor and excitability 2) HG2+ (inorganic) - renal failure (necrosis of prox tubule) 3) Methyl-HG: accumulates in brain! resuls in neurotoxicity (numbness/ataxia/vision probs…)

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2
Q

5 most common physical exam findings for acute poisoning

A

1) coma 2) cardiac arrythmias 3) metabolic acidosis 4) seizures 5) GI probs

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2
Q

What deficiencies can lead to and increased sensitivity to toxicants?

A

Vit. E or C (anti-oxidants) deficiency Selenium def. (req. to make glutathione peroxidase) GSH depletion (via malnutrition/fasting) Superoxide Dismutase genetic deficiency

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3
Q

Cyanide MOA, symptoms and source

A

MOA = cytochrome C oxidase inhibition… it binds to HEME in the porphyrin ring (making Fe3+ again) in this form it is unable to release oxygen! Symptoms = rapid onset arrythmia and headache Source = burning plastics (smoke inhalation)

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3
Q

At what %’s of COHb would you expect certain symptoms?

A

0-10% = nothing 20% = headache 20-30% = rapid fatigue/irritable/defective memory 30-40% = weakness/vomiting/dizzy/ataxia 40-50% = severe ataxia, loss of sphincter tone 50-60% = coma, convulsions, tachycardia >60% = death

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4
Q

characteristics of dioxin

A

-planar configuration -stable in envt and in body -highly lipid soluble (accumulates in fat… slowly eliminated!… NOT susceptible to cyp450)

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4
Q

MOA of Carbon Monoxide Poisoning

A

CO increases the “apparent affinity” of Hb for O2… requiring a very low pO2 to unload O2 at tissues… as a result, those with CO poisoning have cherry red blood!

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4
Q

Name 2 vulnerable populations to changes in COHb%

A

1) pts with coronary artery disease (cannot compensate by increasing blood flow to heart vessels… so they require well-oxygenated Hb especially with exertion) 2) fetus – just like their Hb has a higher affinity than the mother for O2, it is also much higher for CO (which is why smoking pregnant moms probably have lower wt. babies/ increase risk of stillborn due to CO exposure)

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5
Q

MOA of Iron poisoning, sources, and antidote

A

Source = dietary or frequent blood transfusions MOA = lipid peroxidation (superoxide is typically made in presence of free Fe2+) Antidote = Deferoxamine chelator (binds free Fe2+)

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6
Q

Treatment of Pb poisoning

A

Supportive = mannitol diuretics Chelation therapy = CaNaEDTA or succimer

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7
Q

term for any substance foreign to body (poisonous or not)

A

xenobiotic agent

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8
Q

Which drugs can cause toxicity in a cell-selective manner?(2 of em)

A

Thalidomide (given to pregnant moms) caused reduction in long bones (usually humerous) specifically days 35-50 of pregnancy MPTP – street drug that selective kills dopaminergic neurons resulting in a parkinson-like syndrome

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9
Q

Why are infants more susceptible to nitrite poisoning… and how do they typically get it? (ie from doing what?)

A

They get it from drinking well-water that has nitrATES… but their stomache pH is less acidic so bacteria can live there to reduce nitrATES to nitrITES (this doesn’t typically happen in adults)

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9
Q

Talk about lead Absorption, distribution, and elimination

A

Abs: easily passes into alveoli… children absorb it much better in the GI vs adults! Distrib: soft tissue first (liver and kidney), binds RBCs, the works its way into bone Elim: half-life=1-2 months! *NOTE acute toxicity is very rare…

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10
Q

Name 3 mechanisms protecting against reactive oxygen species like superoxide

A

1) superoxide dismutase: changes O2- —>H2O2 2) glutathione peroxidase: change H2O2 —> H20 3) glutathione reductase: change GSSG back to GSH by using NADPH

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10
Q

What are the 3 most important factors in determining COHb%

A

1) concentration of CO 2) duration of exposure 3) respiratory rate (canary in a coal mine to test for CO)

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11
Q

Are pts with cyanide poisoning cyanotic?

A

No! the heme binds oxygen and can’t release it so it looks red

13
Q

Name 4 important ways to increase elimination of absorbed poisons

A

1) forced diuresis – furosemide and mannitol 2) adjust urinary pH 3) Hemodialysis – pass blood over semi-permeable membrane to remove toxins 4) Hemoperfusion – pass blood over adsorbent charcoal to remove toxicant agent

14
Q

What is the use of activated charcoal during acute poisoning?

A

acts as an adsorbent to “soak-up” any un-absorbed poison in the GI

15
Q

MOA of benzopyrene

A

requires metabolism to an epoxide (just like aflatoxin)… where it will bind guanine… the result is “BP-G” is recognized as an “A” which will then bind T in later replication resulting in mutations and potentially cancer *acts as an initiator in the 2 step model of carcinogenesis

17
Q

discuss MOA of ethanol

A

physical interaction with CNS and alters membrane fluidity

19
Q

any poisonous material is termed

A

toxicant

20
Q

Ipecac is used to induce vomiting (emesis)… but what are 6 scenarios where use of ipecac is contraindicated?

A

1) coma 2) convulsions 3) CNS stimulants 4) strong acids/bases 5) petroleum distillates 6) heart disease/pregnant

22
Q

Give 3 examples of receptor-ligand mechanism of toxicity

A

1) TCDD (dioxin) - Ah receptor 2) PCBs - Ah receptor 3) endocrine disruptors (DES) - Estrogen receptor

23
Q

DOC treatment for mercury poisoning

A

Succimer = chelator… hemodialysis can also be used

24
Q

any disease caused by a toxicant

A

toxicosis

25
Q

Name 6 organ-based symptoms of plumbism (chronic Pb poisoning)

A

GI: severe abdominal pain (lead colic) NeuroMusc: muscle weakness *wrist drop* CNS: ataxia, visual disturbances, projectile vomiting Hematologic: RNA aggregates in blood —> inhibit heme synthesis Renal: proteinuria, hematuria etc. Other: Gingival *“lead line” *

26
Q

MOA of dioxin (and also PCBs)

A

-diffuse across membrane -bind Ah receptor in cytosol (chaperone cleaves) -AhR + TCDD complex goes to nucleus to bind AhR Nuclear translocator -AhR + ARNT + TCDD complex acts as a transcription factor to alter gene expression

27
Q

Treatment for CO poisoning?

A

Pure 02… it will compete with CO for Hb… 100% t 1/2 = 45min versus normal air 4 hours

28
Q

Antidote for cyanide poisoning (2 parts)

A

1) TREAT with low dose nitrite… causes release of CN- 2) take care of free CN- by treating with thiosulfate to make much less toxic SCN- *an enzyme will convert methemoglobin Hb-Fe3+ back to Hb-Fe2+

29
Q

Mech #5 of toxicity = peroxidation of lipids… explain how this happens, give examples… and name one drug that induces this to happen

A

Free radicals beyotch! They typically occur from CCl3, as O2- (superoxide), or OH (hydroxyl radical)… Paraquat can induce free radical formation by stealing ONE electron from NADPH—>NADP+… to make O2- (superoxide)… this is known as initiation step… the O2- then goes on to steal a single electron from other things (like cell membrane) leading to oxidative stress and potentially toxicity

31
Q

MOA of aflatoxin

A

requires metabolism to active 3-membered ring with oxygen (epoxide)… in this form it will covalently bind cellular macromolecules… if it binds proteins it will result in hepatocyte death most likely… if it binds DNA it can cause mutations leading to cancer *inflammation exaggerates the response to the toxin

33
Q

Give and example of an endocrine disruptor that acted as an initiator for carcinogenesis.. and was given as a drug in the 1970’s to prevent miscarriages

A

diethylstilbestrol (DES)… the babies of those pregnant women went on to develop vaginal carcinoma at a unusually young age… because the initiator event was given to them in utero

34
Q

Mech #3 of toxicity = Interference with Energy production… name 3 that were covered in depth

A

1) Nitrites 2) Carbon Monoxide 3) Cyanide

35
Q

Which drugs can cause toxicity by activating gene transcription (2)

A

1) TCDD - Dioxin 2) PCB’s

37
Q

Mech #2 of toxicity is interference with excitable membranes = volatile organic solvents … give 6 examples of such chemicals and their resulting symptoms from toxicity

A

1) benzene = hematopoietic toxicity - aplastic anemia/leukemia 2) carbon tetrachloride = hepatotoxicity 3) methanol = RETINAL toxicity (blindness) 4) n-hexane = neurotoxicity 5) ethylene glycol ethers = reproductive toxicity 6) dioxane (not dioxin!) = resp. irritant

38
Q

How does nitrogen dioxide cause damage (2 ways)

A

1) by making HNO3 strong acid 2) acting as an oxidant (lipid peroxidation)

39
Q

Mech #4 of toxicity = binding to biomolecules… name 3 examples covered in depth

A

1) Acetaminophen 2) Afltoxin 3) Benzopyrene

40
Q

Which version of PCBs act as good and bad ligands for Ah receptor?

A

Coplanar PCB: meta, para substituted (high affinity!) Non coplanar PCB: ortho-substituted (not a good ligand)

41
Q

Explain normal vs. overdose of acetaminophen

A

Normally (therapeutic dose): 95% is conjugated, 5% is metabolized by cyp2E1 to NAPQI… glutathione then steps in to conjugate NAPDI to mercapturic acid to be excreted During overdose: a larger amount goes down the cyp2E1 pathway and glutathione stores run out… so NAPQI will conjugate with nearby cellular proteins or DNA resulting in hepatocyte death *keep in mind, drugs that induce cyp450’s like ethanol or phenobarbitol will also increase amount of NAPQI and a poor diet will decrease amount of glutathione available

42
Q

Will the patient look cyanotic with nitrite poisoning?

A

Yes!… blood will look chocolate brown rain

43
Q

MOA & Treatment of nitrite poisoning

A

MOA = Changes Hb-Fe2+ to Hb-Fe3+ (methemoglobin)… this form cannot carry oxygen so you get the chocolate brown blood Treatment = Methylene Blue… MB reductase1 will steal and electron from NADH and MB reductase2 will steal an electron from NADPH… either will result in Hb-Fe2+ again so oxygen can be carried

Pharm Exam 4 (3 decks)

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