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Pharm II > FINAL-TOX > Flashcards

FINAL-TOX Flashcards

1
Q

mechanism(s) of CO toxic action on the body

A

CO has 220 times greater affinity for Hgb compared to O2

CO + Hgb = carboxyhemoglobin which can not carry O2

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2
Q

tx for CO2

A

Administer high-flow oxygen with face mask or endotracheal tube

Arterial blood sample for blood gases and CO level

If CO > 50%, then hyperbaric oxygen chamber may be required

Monitor ECG for cardiac arrhythmias
Anticonvulsant drugs if seizures occur
CO CNS damage may be subtle and could last for years

Fetus vulnerable to CO, hyperbaric oxygen therapy may be required based on mother’s blood gases and CO level

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3
Q 
pathphys of organophosphates ( 
like..
	Malathion
 	Parathion
 	Diazinon
 	Fenthion
 	Dichlorvos
 	Chlorpyrifos 
 	Ethion
A

Inactivate AChE irreversibly by phosphorylating serine hydroxyl group into a covalent bong

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4
Q

clinical presentation of an overdose or exposure organophosphates

A

Cholinergic excess
- SLUDGE: salivation, lacrimation, urination, defecation, gastric emptying
- BBB: bradycardia, bronchorrhea, bronchospasm
- Respiratory insufficiency
- Nicotinic effects: fasciculation, paralysis
- Cardiac arrhythmias
Intermediate syndrome
- Bulbar, respiratory, proximal muscle weakness
Organophosphorus Agent-Induced Delayed Peripheral Neuropathy

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5
Q

treatment for organopsphosphate poisoning

how does this tx work

Can use Pralidoxime (2 PAM) which regenerates AchE through hydrolysis of the phosphorylated Ach-organophosphate complex.

A

atropine, scopolamine (also used for motion sickness), pralidoxime (2-PAM)

atropine for up to a month every day may be required (following overdose, nerve gas in war etc)

Atropine competes with Ach for binding sites on the muscarinic receptor and reverses the effects of excess Ach

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6
Q

atropine is the cure for what type of poison

yes maisa this card is fixed

A

mushroom poioning

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7
Q

signs of mushroom poisoning toxicity

A

rapid or delayed (weeks)
Signs of toxicity consistent with muscarinic (Ach) excess.

DUMBELS: diarrhea, sweating, miosis, nausea and urinary urgency.

Muscarine is a potent acetylcholine (Ach) agonist. Muscarine receptors in numerous organs stimulated by muscarin

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8
Q

: HA myalgia, severe CNS disturbance, and severe abd pain in a painter.
think

A

lead poisoning

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9
Q

how can lead enter the body

A

absorbed via the respiratory and GI tract.

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10
Q

DX tests for lead poisoning

A

calcium disodium
basophilic stippling indicates inhibition of enzyme
.

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11
Q

Tx for lead poisoning

A

chelating agent Ca EDTA or BAL should be considered

” Chelator works by forming two bonds with the metal ion preventing it from binding to tissue proteins and permitting rapid excretion

If the tube is purple it has sodium EDTA

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12
Q

The most common form of lead poisoning is

A

Inorganic lead

Ceramic dishware not intended for food use (

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13
Q

manifestations of lead poisoning other than CNS effects ( anorexia, fatigue, malaise, headache, developmental delay in children, coma and death)

A

“saturnine gout” (Lead inhibits ion transport and excretion in the kidney)

Lead induces “lead colic” a spasmodic contraction of the smooth muscles in the intestines.

Gingival lead lines caused by lead combining with the sulfur produced by oral bacteria. Lead sulfide deposits along the gum line.

Bone is the major storage site for lead with slow release into the circulation for years.

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14
Q

6 characteristics of an ideal chealtor

A
  1. water soluble
  2. resistant to biotransformation
  3. distributed into storage sites where metal is being sequestered.
  4. forms nontoxic complex with the metal.
  5. easily excreted in the urine and/or bile.
  6. low affinity for essential elements (calcium, zinc etc).
    - focuses on lead
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15
Q

BAL tx is most effective in what type of toxicity

A

BAL is more effective in complexing free metals and will not release metals bound to enzymes.

can lead to renal toxicity

beware of peanut sensitivity

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16
Q

ADE of BAL tx for metal poisoning

A

Most patients respond with up to 50 mm Hg rise in blood pressure.
Nausea, vomiting, headache, burning sensation of the lips, tingling of the hands.
Causes hemolytic anemia in patients with G6PD deficiency of their red cells.

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17
Q

Ca EDTA what type of metal poisoning would you not want to use it in

A

Ethylenediaminetetracetic acid
EDTA charged at physiological pH and does not enter cells.

Lead binds with high affinity. Not used for mercury due to poor binding in vivo.

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18
Q

tx for iron overdose

A

deferoxamine

deferasirox

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19
Q

CM of iron poisoning

A

Nausea, vomiting, abdominal cramps, constipation, epigastric discomfort.

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20
Q

Parenteral dose im, iv.
Isolated from Streptomyces pilosus.
Drug has high affinity for Fe and low affinity for calcium.

A

deferoxamine

Some allergic reactions are seen (rashes through anaphylaxis)

21
Q

drug name and ADE of the tx for iron overdose that cna be administered PO

A

deferasirox

GI disturbance and skin rash, low incidence ADRs.

22
Q

opioid overdose Tx

A

naloxone, naltrexone, methyl naltrexone

23
Q

opioid overdose CM

A 
analegesia
euphoria
sedation
resp depression
cough supression
miosis
tuncal rigidity
N/V
meperidine induces tachy
GI constipation
renal function
24
Q

which receptors fo canaboids act on

A

Bind to presynaptic cannabinoid receptors which results in inhibition of either excitatory glutamate or GABA.

25
Q

drugs commonly screened for

A 
Amphetamines
Barbiturates
Benzodiazepines
THC
BE (the thing that cocaine becomes)
Opiates (morphine)
PCP
Propoxyphene
26
Q

For legal action you use a ___ for drug testing

A

confirmation method (2-3 weeks for results)
Most used confirmation method GC/MS
All States require confirmation

27
Q

two synthetic analogs of THC

A

dronabinol and nabilone

28
Q

most used confirmation method

A

GC/MS

all states require confirmaton

29
Q

what are some Causes for False Pos/Negs:2

A 
Cross reacting other drugs with antb
Chemical interferences
Actual drug not abused
Dilution and/or substitution
Adulteration
30
Q

adulterants

A

adulterants: bleach, visine, urinaid, hoy soap

31
Q

elimination of ETOH

A

Alcohol is zero order eliminations like phenytoin and ASA

32
Q

converts ethanol into acetaldehyde

A

ADH

33
Q

Acetaldehyde is converted by ___ into acetate and acetate is turned into CO2 and H20

A

Acetaldehyde is converted by ALDH into acetate and acetate is turned into CO2 and H20

34
Q

asians have a deficiency in

A

” Genetic polymorphism in Asians because of deficiency in ALDH í feel sick

35
Q

how does disulfiram work

A

inhibits ALDH

36
Q

Ethanol acts by enhacing

A

GABA

EtOH does enhance GABA binding to GABAA receptors (sedative-hypnotic aspects to EtOH)

37
Q

Ethylene glycol how does it kill you

A

is converted by the same enzymes as alcohol but is eventually converted to oxalic acid because it leads to kidney failure

38
Q

Ethylene glycol Tx

A

flood body with alcohol and the body will metabolize and remove ethylene glycol which will not be metabolized because it will be blockes

39
Q

LFT w/ greatest sensitivity

A

GGT

40
Q

how does Naltrexone work for ETOH abuse

A

block opioid receptors (opioid receptor antagonist). Makes patient more tolerant to the “high” of EtOH, less inclined to drink more.

41
Q

Acamprosate

A

GABAa agonist and NMDA receptor antagonist

42
Q

Vitamin B1 is used for

A

alcohols as their absorption is impaired

deficiency is called Beriberi

43
Q

how does ETOH interact with APAP

A

increases biotransformation and increased production of toxic metabolite

44
Q

Ethylene Glycol phases

A

Excitation followed by CNS depression within a few hours.
At 4-12 hours severe metabolic acidosis from metabolites.
Oxalate crystals in kidney leads to renal failure.

45
Q

TX for ethylene glycol overdose

A

Administer EtOH or Fomepizole, treat for acidosis

46
Q

Tx for acetaminophen overdose

A

N-acetyl cysteine (NAC)

needed because GSH does not cross the BBB

47
Q

how does APA overdose work

A

glutathione is needed to make non toxic is needed to

overdose leads to depletition GSH and leads to liver toxicty

48
Q

antidote to benzo toxicity

A

flumazenil

flute-mase-nail

overdose leads to respiratory depression

49
Q

mechanism of benzo action

A

Benzo increase FREQUENCY of Cl channel opening by binding to GABA receptor (barbs keep gate open longer).

Pharm II (16 decks)

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