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SUMPHARM > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What is the typical route of exposure for carbon monoxide?

A

Inhalation. Released from running cars.
50%! in blood lethal
Typical levels Non-smoker: 1% Smoker: 5-10%

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2
Q

What is the clinical presentation of a carbon monoxide overdose?

A
  1. Psychomotor impairment
  2. Headache and tightness temporal area
  3. Confusion and vision
  4. Tachycardia, tachypnea, syncope
  5. Deep coma, convulsions, shock, and respiratory failure. –> Symptoms worsen as % CO increases.
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3
Q

What is the mechanism of toxic action of CO in the body?

A

binds tightly to the oxygen-binding sites of Hgb –> reducing the transfer of oxygen to tissues. *Organs with the highest oxygen demand affected: brain, heart, and kidneys.

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4
Q

If a patient with a possible CO exposure has a normal O2 saturation, are they likely okay?

A

Pulse oximetry cannot distinguish between CO-Hgb and O2-Hgb.

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5
Q

What is the treatment of CO exposure/overdose?

A

Removal from exposure and high-flow oxygen via face mask or ET tube
short period of time- risks ARDS.
hyperbaric chamber, pregnant women or pts with CO > 50%.

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6
Q

Will the CNS effects from CO overdose resolve with treatment?

A

Most resolve, but some subtle effects can last for years.

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7
Q

What are examples of organophosphate pesticides?

A

Farm- crop duster- Parathion, malathion, trichlorfon

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8
Q

What are examples of toxic nerve gases?

A

warfare: Soman, sarin, tabun-

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9
Q

What is the mechanism of toxic action of organophosphate pesticides and nerve gas?

A

Inhibition of AchE –> excess Ach at the motor end plate nicotinic receptors –> paralysis –> respiratory failure.

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10
Q

What is the clinical presentation of an overdose to organophosphate pesticides and nerve gas?

A
  • Paralysis
  • Miosis, blurry vision
  • bradycardia
  • Bronchial constriction, increased secretions
  • N/v/d
  • Relaxation of urinary sphincters, bladder wall contraction –> urinary frequency/urgency.
    DUMBELS!-anticholinergic
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11
Q

How is organophosphate or nerve gas poisoning treated? How does this work?

A

Atropine –> blocks Ach receptors. *1-2mg every 5-15mins until atropine effects appear –> dry mouth, etc. Atropine qd up to a month may be required.

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12
Q

If atropine is not available, what other medication can be used to treat organophosphate or nerve gas poisoning?

A
  1. Pralidoxime (2PAM) –> regenerates AchE through hydrolysis of the phosphorylated Ach-organophosphate complex.
  2. Scopolamine –> Ach blocker.
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13
Q

What are the two groups of mushrooms that can elicit toxic overdose/poisoning?

A
  1. Rapid onset type: amanita muscaria

2. Delayed-onset type: amanita virosa and phalloides.

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14
Q

What is the mechanism of the toxic action of amanita muscaria mushroom poisoning on the body? What symptoms will this cause?

A

Potent Ach agonist –> rapid onset of DUMBELS sxs (diarrhea, urinary frequency, miosis/muscle weakness, bronchospasm, bradychardia, emesis, lacrimation, and salivation/sweating).

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15
Q

What is the treatment of Amanita muscaria mushroom poisoning?

A

Atropine (parenteral).

**Sxs typically resolve completely.

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16
Q

What is the MOA of amanita virosa or Amanita phalloides (death caps) poisoning?

A

binds to RNA polymerase in liver hepatocytes –> shuts down protein synthesis in the liver –> liver failure.
Sx N/V-, followed by hepatic and renal cellular injury.

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17
Q

What is the treatment of amanita virosa or amanita phalloides?

A

NONE

TX- liver transplant, BUT fatal.

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18
Q

What is the typical route of exposure for lead overdose?

A

Occupational or environmental -batteries, glass, pigment paints, plastics, and ceramics, old buildings, herbal medicines.
Respiratory (MC) and GI tracts.
>10 ug/dL.

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19
Q

How long does lead stay in the body?

A

Decades!! Distributes into RBCs and into the bone -> major storage site.

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20
Q

What are major sources of childhood lead poisoning?

A

Pica: eating non-foods.

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21
Q

What are the 2 general types of lead? Which is most commonly associated with overdose?

A
  1. MC-Inorganic lead: lead chloride, lead sulfide-

2. Organic lead: ethyl lead. Very rare ,banned for use in antiknock gasoline.

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22
Q

What is the mechanism of toxic action of lead in the body?

A
  1. inhibits Hgb synthesis –> severe anemia VIA: Lead binding to ALA-dehydratase enzyme
  2. inhibits pyramidine 5’ nucleotidase —> inhibiting the removal of RNA needed for a RBC to become mature —> basophilic stippling (stipple brush) of cells.
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23
Q

What symptoms occur with lead poisoning?

A
  • CNS: anorexia, fatigue, headache, mental retardation, coma, and death.
  • Spasmodic contraction of the smooth muscle of the intestines
  • Gingival lead lines- blue green border of gums
  • Lead lines in the hyperdense metaphysis, distal femur and distal/proximal tibia.
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24
Q

What is the treatment of lead poisoning?

A
  • British Anti-Lewisite : BAL
  • Ca EDTA
    Chelation agents: grab, forms ring around, Water soluble, Easily excreted in the urine and/or bile., Low affinity for essential elements (calcium, zinc, etc
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25
Q

In what patients must you be cautious with when giving BAL?

A

peanut allergy!
glass container- IM inj.

MOA: formation of a stable SH-metal bond that is then excreted in the urine.

ADE:N/v, headache, burning sensation of the lips, tingling of the hands. Hemolytic anemia in those with G6PD deficiency. Renal toxicity if tubular urine is very acidic.

26
Q

What is the MOA,ADE of Ca EDTA? Route of administration?

A

MOA: Binds divalent metals (lead, arsenic). Administered IM or IV.

ADE: Renal damage, fever, chills, n/v.

27
Q

What are the 2 endogenous cannabinoids?

A

Arachidonoyl glycerol and anandamide.

28
Q

What is marijuana’s active substance?

A

Tetrahydrocannabinol (THC)

29
Q

What is the IRON admin and OD antidote? Who at risk?

A

Ferrous Iron Fe2
Deferoxamine-chelator
Children-most look like candy and in previtamins

30
Q

What is the clinical presentation of a THC overdose/exposure?

A

YOUR HIGH

  • Euphoria, relaxation, feeling of well-being, grandiosity, time doesn’t exist
  • Visual distortion, drowsiness, coordination, memory
  • Increased appetite, reduced nausea, DEC intraocular pressure (glaucoma), relief of chronic pain.
31
Q

What are the withdrawal symptoms of THC?

A

ADE: DEPENDENCE.

*premature birth.Restlessness, irritability, mild agitation, insomnia, GI

32
Q

What 2 cannabinoids are FDA approved?

A

Dronabinol and Nabilone. **Treat chemotherapy induced nausea.

33
Q

What is the mechanism of toxic action of THC?

A

Binds to presynaptic cannabinoid (THC) receptors —> inhibition of excitatory glutamate or enhancement of GABA.

34
Q

What is the effect of cannabinoids on those with lung disease?

A

No evidence of effect. No decreased lung function or increase in asthma.

35
Q

What drugs are screened for in the urine?

A
  1. Amphetamines
  2. Barbiturates
  3. Benzodiazepines
  4. THC
  5. Cocaine *benzoylecgonine metabolite
  6. Opioids (morphine, propoxyphene)
  7. PCP
36
Q

What are 6 reasons for urine drug screening?

A
  1. Workplace monitoring.
  2. Forensic (medical legal)
  3. Criminal justice (parole monitoring)
  4. Psychiatric
  5. US Gov contracts, research grants
  6. Professional license renewal (airline pilots)

Screening is based on immunoassay technology, and results are given immediately. clinically.
Confirmation testing is used in medical-legal,

37
Q

What are cut off levels in regards to urine drug screening?

A

amount of the drug that must be present in the blood to elicit a positive on a urine screen.
**This is to avoid accidental/environmental exposures **Cut off levels are different

38
Q

What does it mean to adulterate a urine screening?

A

Add another chemical to the urine I.e. Visine added to urine with THC will increase the THC binding to the glass container.

39
Q

What is the percentage blood alcohol level on someone with a blood level of 510 mg/dL?

A

***0.51%. Convert 100mg to blood level, move over 3 decimal!

40
Q

What is the translation of alcohol in Arabic? DX?

A

“Something subtle”

Liver disease, HTN, pancreatitis, seizures (alcohol withdrawal).

41
Q

What slows absorption of alcohol and metabolizes?

A

Food

LIVER-90% is biotransformed

42
Q

Ethanol has a zero-order biotransformation. What does this mean?

A

rate of biotransformation is independent of time and concentration. AKA adults remove 7-10g of ethanol per hour, no matter how much ingested.
APE- Ethanol, phenytoin, aspirin

43
Q

What part of alcohol breakdown gives the unfortunate symptoms of nausea, vomiting, facial flushing, dizziness, and headaches?

A

Acetaldehyde.
Asian population -genetic polymorphism for depleted ALDH —> build up of acetaldehyde after even a single drink —> major ADRs. Less alcholics in ASIA

44
Q

What is disulfiram?

A

agent to discourage alcohol use.

inhibits ALDH build up of acetaldehyde

45
Q

What is the progression of liver disease with alcoholism?

A

Alcoholic fatty liver (reversible) —>
alcoholic hepatitis (inflammation) —>
cirrhosis —> liver failure.

46
Q

What LFT is most specific to alcoholic liver damage?

A

Gamma glutamyltransferase (GGT)

47
Q

What is Wernicke-Korsakoff syndrome?

A

Thiamine (B1) deficiency most commonly due to alcoholism. —> ataxia, paralysis of external eye muscles, confusion, coma, death.

48
Q

What is the treatment of Wernicke-Korsakoff syndrome?

A

B1 supplements!

49
Q

How does alcohol cause drug-drug interactions?

A

Alcohol induces CYP450 enzymes responsible for biotransformation of acetaminophen. INDUCE turn on enzymes more, which will metabolize drug more, INC metabolites.
INHIBitors turn off enzymes which will INC drug concentration serum

50
Q

What is naltrexone?

A

Opioid antagonist antidote-

tolerant to the “high” of EtOH, makes them less inclined to drink.

51
Q

What is the treatment of methanol overdose?

A

IV EtOH to saturate alcohol DH and decrease MeOH metabolism. Then dialysis is used to remove the MeOH and formate metabolite.
OR can use Fomepizole to inhibit alcohol DH (but $$$).

52
Q

What are the 3 stages of toxicity of ethylene glycol?

A
  1. Excitation followed by CNS depression within a few hours.
  2. At 4-12 hours severe metabolic acidosis occurs from metabolites.
  3. OA late crystals in kidney leads to renal failure.
53
Q

How is ethylene glycol overdose treated?

A
  1. Administer EtOH IV OR Administer fomepizole ($4000/patient) 2. Treat for acidosis
54
Q

What drugs are used to treat alcohol withdrawal syndrome?

A

Benzodiazepines: PAMS- Chlordiazepoxide (prodrug that is converted into desmethyldiazepam)

  • Thiamine
55
Q

What is the mechanism of action of benzodiazepines?

A

GABA receptor agonists —> Inhibition, DEC neuron excitability.

  1. Sedation
  2. Hypnosis
  3. Anesthesia
  4. Muscle relaxation
  5. Pretreatment
56
Q

What is the reversal agent/antidote used in benzodiazepine overdose?

A

Flumazenil.

57
Q

What other drugs will Flumazenil also reverse the effects of?

A

Zolpidem, zaleplon, and eszopiclone —> the “z” drugs. **Does NOT reverse the barbiturates,

58
Q

What happens with long term use of benzodiazepines?

A

The active metabolites accumulate due to the long half-life.

59
Q

What is the toxic mechanism of action of acetaminophen?

A

toxic metabolite in the body *(NAPQI), which is transformed by *Glutathione in the body into a non-toxic metabolite.
We run out of glutathione (due to diet etc), NAPQI will destroy the liver.

60
Q

What is the antidote of acetaminophen?

A

N-acetylcysteine (NAC) W/ * Glucose IV —> restore proper blood glucose levels.

61
Q

Why can’t we give glutathione as an antidote for acetaminophen overdose?

A

not lipid soluble - can’t cross membranes

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