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Pharma 2nd semester > Toxicology > Flashcards

Toxicology Flashcards

1
Q

give two possible mechanisms for specific antidotes and their example

A
  1. binding of poisons- chelators
  2. inhibition of distribution -methemoglobin-producers in cyanide intoxication
  3. inhibition of the formation of toxic metabolites- ethanol
  4. promoters of detoxification- acetylcysteine
  5. competitive inhibitors- naloxone
  6. agents promote regeneration of target cells- cholinesterase inhibitors
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2
Q

what does ‘ABCDEF’ stand for in the management of a poisoned patient?

A 
A- airway protection
B- ventilation
C- treatment of arrhythmias 
D- hemodynamic support
E- treatment of seizures
F-correction of temperature, metabolic abnormalities
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3
Q

types of decontamination

A

gastrointestinal
eye (for at least 20 min)
skin
body cavity evacuation

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4
Q

how do we perform whole bowel irrigation?

A

via gastric tube

6-8 liter of isosmotic physiological electrolyte solution (containing polyethylene glycol)

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5
Q

when do we not do a bowel surge (with sorbitol)?

A

in case of paralytic ileus

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6
Q

types of gastrointestinal decontamination

A
  1. induction of emesis
  2. gastric lavage
  3. whole bowel irrigation
  4. bowel purge
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7
Q

what do we use for induction of emesis?

A

syrup of ipecac

apomorphine (rarely)

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8
Q

which type of patients you should not induce emesis?

A

patients who are:

  1. unconscious
  2. poisoned with corrosive agents (acid,base)
  3. poisoned with petroleum distillate (risk of aspiration!)
  4. poisoned with convulsant
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9
Q

which type of patients you should not do gastric lavage?

A
  1. poisoned with corrosive agents (acid,base)
  2. poisoned with petroleum distillate (risk of aspiration!)
  3. poisoned with convulsant
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10
Q

what is the risk in forced diuresis?

A

risk of lung edema and electrolyte disturbance

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11
Q

what are the ways to eliminate poison through the GI?

A
  1. multiple-dose activated charcoal (“gut dialysis”)

2. cholestramine in digitalis intoxication (decreases the absorption

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12
Q

what are the ways to eliminate poison through the kidney?

A
  1. forced diuresis- loop diuretics, mannitol, infusion

2. alteration of urinary pH

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13
Q

which compounds easily removed by dialysis?

A

water-soluble, low molecular mass, don’t bind very strongly compounds
examples- alcohol, antibiotics, heavy metals, benzodiazepines

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14
Q

which compounds can be removed by hemoperfusion?

A

DOB
digoxin
organophosphates
barbiturates

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15
Q

complication in plasmapheresis

A

thrombocytopenia

microembolism

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16
Q

which compounds can be removed by plasmapheresis?

A 
carbamazepine 
lithium
methanol
metformin
phenobarbital
theophylline
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17
Q

how do we perform neutralization?

A
  1. alkali -therapy ( 5% NaHCO₃, 2%Na lactate)
  2. specific antitoxins
  3. antibodies
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18
Q

what are chelators?

A

organic compounds that function as chemical antagonists and used for the treatment of heavy metal poisoning

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19
Q

how is Dimercaprol given?

A

always IM

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20
Q

how is Dimercaprol excreted?

A

by the kidney (6-8 hours)

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21
Q

what is the advantage of Dimercaprol?

A

good permeability

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22
Q

therapeutic indication of Dimercaprol

A
  1. arsenic poisoning
  2. mercury poisoning
  3. Lead Poisoning (with EDTA)
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23
Q

special indication for Dimercaprol

A

encephalopathy (can enter the neurons)

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24
Q

side effects of Dimercaprol

A 
nausea, vomiting 
hypertension
tachycardia
fever, pain
thrombocytopenia
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25
Q

therapeutic indication of succimer

A

arsenic poisoning
mercury poisoning
lead- but not with encephalopathy

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26
Q

side effects of succimer (DMSA) and unithiol (DMPS)?

A

nausea, vomiting, diarrhea

better tolerated than dimercaprol

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27
Q

How is succimer and unithiol (DMPS) given?

A

orally

DMPS also parenteral

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28
Q

what is penicillamine used for?

A

Copper intoxication—>Willsons disease

Rheumatoid arthritis- not used anymore

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29
Q

adverse effects of penicillamine

A

hypersensitive reactions
long term treatment–> autoimmune reactions (drug-induced lupus, drug-induced hemolytic anemia)
B6 vitamin depletion

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30
Q

what is EDTA used for?

A

lead poisoning

* can remove lead from the bone

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31
Q

adverse effects of EDTA

A

Nephrotoxicity (rare)

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32
Q

what is deferoxamine used for?

A

iron poisoning

hemochromatosis

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33
Q

how is EDTA given?

A

slow IV infusion for 5 days

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34
Q

how is Deferoxamine given?

A

IV or IM

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35
Q

Adverse effects of Deferoxamine

A

idiosyncraic reactions
ARDS
neurotoxicity

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36
Q

route of absorption of Arsenic?

A

respiratory and GI tract

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37
Q

where can we find Arsenic?

A

industry, agriculture (insecticides), wood preservatives

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38
Q

pharmacodynamics of Arsenic

A

inhibition of enzymes via sulfhydryl binding

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39
Q

distribution of Arsenic

A

soft tissues- first of all, liver and kidney, later skin hair and nail

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40
Q

Clinical presentation of acute Arsenic poisoning?

A

gastroenteritis–>severe diarrhea “rice water stool”
hypovolemic shock
arrhythmias
CNS symptoms

weeks later: ascending peripheral neuropathy
months later: transverse white striate on the nails.

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41
Q

Clinical presentation of chronic Arsenic poisoning?

A

weakness
peripheral neuropathy (socking-glove pattern)
skin changes- hyperkeratosis, hyperpigmentation
anemia
general cachexia

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42
Q

treatment of acute Arsenic poisoning

A

gut decontamination
intensive supportive care- fluid electrolytes
Dimercaprol chelation

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43
Q

treatment of chronic Arsenic poisoning

A

Dimercaprol chelation

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44
Q

Mercury source of intoxication

A

elemental mercury- manufacture of electrical equipment, paint products
mercury salts- disinfectants

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45
Q

the major route of absorption of mercury

A

elemental mercury- respiratory tract (inhalation)
mercury salts- GI and skin
organic Hg- Gi, skin and respiratory tract

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46
Q

distribution of mercury

A

soft tissues. first the kidney

methylmercury reaches the brain

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47
Q

elimination of mercury by the…

A

kidney

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48
Q

Clinical presentation of acute Mercury poisoning?

A

elementary- pulmonary edema
salts-hemorrhagic gastroenteritis –> hypovolemic shock
acute tubular necrosis

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49
Q

Clinical presentation of chronic Mercury poisoning?

A

neuropsychiatric disturbance

acrodynia (in children)- painful erythema in the extremities

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50
Q

therapy of acute Mercury poisoning

A

supportive care
inhalation (elementary): succimer and dimercaprol chelation
“mer” in Mercury

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51
Q

therapy of chronic Mercury poisoning

A

succimer chelation

unithiol chelation

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52
Q

why we shouldn’t use dimercaprol in chronic mercury poisoning?

A

it redistributes mercury to the CNS!

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53
Q

what is Minama disease and what does it cause?

A

Methyl-mercury poisoning
mainly CNS effects-paraesthesia, ataxia, coma, death
prenatal exposure–> mental retardation

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54
Q

Lead source of intoxication

A 
occupational
environmental (batteries, paints, ceramics)
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55
Q

the major route of absorption of Lead

A

respiratory, GI, skin (organic)

*crosses the placenta

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56
Q

pharmacodynamics of lead

A

inhibits enzymes in porphyrine synthesis
interferes with the action of cations like Ca, Fe
alters the structure of membranes and receptors.

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57
Q

distribution of lead

A

first it binds to erythrocytes–>then soft tissues (liver &CNS) –> bones (can stay for 20 years in the bones)

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58
Q

elimination of Lead via the

A

kidney

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59
Q

Clinical presentation of acute Lead poisoning?

A

encephalopathy
acute abdominal pain (paralytic ileus)
hemolytic anemia

*rare

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60
Q

Clinical presentation of chronic Lead poisoning?

A

blood- anemia (microcytic), the appearance of basophilic stippling in the RBC (diagnostic clue)
GI - constipation, “gingival lead lines”
CNS- adults–> peripheral neuropathy- weakness of the extensors (wrist drop) . children–> minimal brain dysfunction
bones- children–> growth retardation (lead deposits in the epiphysis)

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61
Q

Treatment of acute Lead poisoning

A

supportive care

first dimercaprol and 4 hours later EDTA IV

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62
Q

Treatment of chronic Lead poisoning

A

EDTA IV infusion for 5 days, then PO succimer

*EDTA removes lead from the bones

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63
Q

major effects of organic lead (tetraethyl lead)

A

CNS effects

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64
Q

therapy of tetraethyl lead

A

decontamination from the skin
symptomatic treatment

chelators are not effective!

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65
Q

characteristics of carbon monoxide

A

colorless, odorless, no irritation

lighter than the air

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66
Q

pharmacodynamics of carbon monoxide

A

affinity to hemoglobin is 300 times stronger than oxygen

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67
Q

symptoms of acute carbon monoxide poisoning

A

<50%–> headache, nausea, dizziness, weakness
>50% –> increased respiration and pulse, seizures, coma
>60%–> respiratory failure, death

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68
Q

symptoms of chronic carbon monoxide poisoning

A

headache, ataxia, insomnia, Parkinson- like symptoms

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69
Q

therapy of carbon monoxide poisoning

A

100% oxygen or
carbogen mix- 95 % O₂, 5% CO₂
or hyperbaric oxygen??

for brain edema- glucocorticoids, mannitol
acidosis- alkali therapy

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70
Q

classify the hydrocarbons

A
  1. Aliphatic:
    - Saturated
    - unsaturated
    - halogenated
  2. Aromatic:
    - benzine and benzene derivatives
    - nitro and amino derivatives
    - decoupling drugs
    - phenol
71
Q

route of intoxications of saturated aliphatic HC

A

inhalation of vapor–> aspiration!
ingestion of liquid
“glue sniffing” –> abused drug

72
Q

symptoms of saturated aliphatic HC poisoning

A

acute- irritation of the mucosa, ventricular arrhythmia

chronic- tolerance, pulmonary effects

73
Q

therapy of saturated & unsaturated aliphatic HC poisoning

A

symptomatic
no emesis
no gastric lavage (risk of aspiration)

74
Q

where can we find saturated aliphatic HC inducing intoxication?

A

Gasoline, kerosene, petroleum distillates

75
Q

name 2 saturated aliphatic HC

A

CH₄– methane
C₂H₆– ethane

Cn increases–> CNS depressant increases

76
Q

how does saturated aliphatic HC cause ventricular fibrillation?

A

Sensitization of myocardium to NE

77
Q

name 2 unsaturated aliphatic HC

A

C₂H₄– ethylene
C₂H₂– acethylene
inhalational anesthetics

Cn increases–> CNS depressant increases

78
Q

which has stronger effects- saturated or unsaturated HB?

A

unsaturated

79
Q

route of intoxications of unsaturated aliphatic HC

A

inhalation of vapor–> aspiration!

ingestion of liquid

80
Q

are Halogenated aliphatic HC lipid soluble?

A

extremely lipid-soluble

–> more toxic than non-halogenated

81
Q

where can we find Halogenated aliphatic HC?

A

used as solvents and in cooling systems

82
Q

symptoms of Halogenated aliphatic HC

A 
CNS depression 
cardiotoxicity 
kidney and liver impairment 
when inhaled--> lung edema
skin- 1-3 degree frostbite
83
Q

therapy of Halogenated aliphatic HC poisoning

A

symptomatic

alkali therapy in case of acidosis

84
Q

what is the lethal dose of Carbon tetrachloride (CCl₄)?

85
Q

symptoms of Carbon tetrachloride (CCl₄)

A 
starting effects: irritation of mucosa, CNS depression, ventricular fibrillation (sudden death)
delayed effects (1-2 days later): hepatorenal syndrome, toxic hepatitis, ATN
86
Q

treatment of Carbon tetrachloride (CCl₄)

A

symptomatic (gastric lavage, paraffin oil, active charcoal)

87
Q

what is chloroform (CHCl₃)

A

halogenated aliphatic HC
strong narcotic
not used due to its hepatotoxicity

88
Q

routes of intoxications of Benzene, toluene, xylene (Aromatic HC)?

A

Skin, GI, lungs

89
Q

elimination of Benzene, toluene, xylene

A

via lung and kidney

90
Q

symptoms of Benzene, toluene, xylene poisoning

A

acute–> narcosis, seizures, coma, arrhythmia

chronic–>CNS, liver and kidney damage, bone marrow suppression

91
Q

therapy of aromatic hydrocarbons

A

gastric lavage and purgation with cooking oil

activated charcoal

92
Q

symptoms of phenol poisoning

A

topically: local anesthetic effect –>serious necrosis without pain
orally: necrosis on the mucosa
systemic effects: CNS (seizures, coma)

93
Q

absorption of Nitrobenzene and Aniline

A

GI, skin, lung

94
Q

what is the lethal oral dose for Nitrobenzne?

95
Q

symptoms of Nitrobenzene (C₆H₅ NO₂) poisoning?

A

acute- irritation of the mucosa (vomiting, spasm), CNS depression, methemoglobinemia, hemolysis
chronic- anemia, hemolytic icterus, CNS disturbance

96
Q

therapy for Nitrobenzene (C₆H₅ NO₂) and Aniline (C₆H₅ NH₂) poisoning

A

reduction of methemoglobinemia

orally–> milk, oil

97
Q

what symptom is seen first in acute Aniline poisoning?

98
Q

what is DNP?

A

Dinitrophenol

aromatic hydrocarbon

99
Q

what is the lethal dose of Dinitroortocresol (DNOC)?

100
Q

where is DNP used?

A

in the chemical industry

*used in the past as weight loss agent

101
Q

where is DNOC used?

A

in the agriculture?

102
Q

routes of poisoning of DNP and DNOC?

A

inhlation
skin
GI

103
Q

what is the main mechanism of action in aromatic hydrocarbons poisoning? (DNP, DNOC)?

A

increased energy converts to heat

104
Q

symptoms of acute DNP &DNOC poisoning?

A 
hyperpyrexia
dehydration--> ↓BP
HR↑ 
Dyspnea
cyanosis
anoxia
lung edema
105
Q

symptoms of chronic DNP &DNOC poisoning?

A 
weight loss
fever
kidney, liver, heart impairment
bone marrow function
hemolytic anemia
106
Q

therapy of acute DNP &DNOC poisoning?

A 
decontamination (lavage, emesis, washing the skin)
cold batch
O₂ inhalation
0.9% NaCl
glucose infusion
107
Q

what is forbidden to give in formaldehyde poisoning?

A

Sulfonamides

can cause RF

108
Q

what are formaldehyde and metaldehyde?

A

Aldehydes :)

109
Q

what is the lethal dose of metaldehyde?

A

4g for adults

0.1-0.5 g for children

110
Q

where is metaldehyde used?

A

as fuel cubes and pesticides

111
Q

what is the therapy of formaldehyde poisoning?

A

drink milk, water
gastric lavage
alkalization
hemodialysis

112
Q

Symptoms of metaldehyde poisoning?

A 
GI: hemorrhagic gastritis 
severe CNS effects: ↑ muscle irritability
muscle rigidity
seizures
respiration stops
113
Q

therapy of metaldehyde

A 
gastric lavage 
induction of emesis
activated charcoal
purgation
symptomatic treatment--> maintaining BP
114
Q

when do the symptoms of methanol intoxication begin?

A

8-30 hours later

115
Q

what are the symptoms of methanol intoxication?

A 
metabolic acidosis--> respiratory failure
abdominal pain (pancreatic damage) 
blindness
116
Q

therapy of methanol intoxication and divalent glycols poisoning?

A 
ethanol! 10g/hr IV
or
orally 20-30mk every 3-4 hours
alkalization, hemodialysis
fomepizole- alcohol dehydrogenase inhibitor IV

*Ca IV in case of muscle spasm in DG poisoning

117
Q

what are diethylene glycol and ethylene glycol?

A

Divalent glycols

118
Q

where can we find Divalent glycols?

A

used as solvents, lubricants, antifreeze substance

car cooling system (?)

119
Q

symptoms of divalent glycols poisoning

A

Anuria! (kidney damage)
CNS
acidosis
liver damage

120
Q

what do Inocybe- type mushrooms contain that make them poisonous?

A

muscarine (alkaloid)

121
Q

what are the symptoms of mushroom poisoning (Inocybe type)?

A

parasympathomimetic effects

extreme diarrhea

122
Q

therapy of mushroom poisoning (Inocybe type)?

A

atropine 1-2mg every 30 min

123
Q

what do the mushrooms “Amanita muscaria” and “Amanita pantherina” contain?

A

muscarine
muscaridine
muscimol (GABAa agonist)
ibotenic acid

124
Q

what are the symptoms of Amanita muscaria and pantherina poisoning?

A 
salivation
sweating
vomiting
diarrhea 
atropine intoxication: restlessness, hallucinations
125
Q

what is the therapy of Amanita muscaria and pantherina poisoning?

A

symptomatic

NO ATROPINE!

126
Q

what does Amanita phalloides (death cup) contain?

A

amatoxins (toxic polypeptides):
amantin𝝰
phalloidin

127
Q

what type of mushrooms have rapid onset?

A

Inocybe
Amanita muscaria
Amanita pantherina

128
Q

what type of mushrooms have delayed onset?

A

Amanita phalloides

129
Q

is Amanita phalloides toxic?

A

high lethality because of hepatotoxicity

130
Q

symptoms of Amanita phalloides

A

two-phase symptoms:
early (8-24hr)–> emesis, diarrhea, shock, damage of the intestinal mucosa, liver, kidney
later (48hr later)- hepatotoxicity–>juandice, fulminant liver
toxic nephrosis

131
Q

treatment of Amanita phalloides

A

supportive (no antidote)- protection of liver and kidney, forced diuresis, hemoperfusion, glucocorticoids
high dose G-penicillin, silibinin, N-acetylcysteine

132
Q

what is the mechanism of action of cyanide?

A

lactic acidosis and cytotoxic hypoxia

133
Q

symptoms of cyanide poisoning

A

hyperpnea
coma
asphyxia
convulsion

134
Q

Therapy of cyanide poisoning

A
  1. formation of methemoglobin!

2. give EDTA

135
Q

routes of acid intoxication

A

oral, skin, eye, inhalation

136
Q

symptoms of acid intoxication

A 
necrosis of the skin
spasm of glottis 
coagulation in the esophagus & stomach-->pain-->shock
recurring emesis-->airway necrosis
perforation of the stomach--> peritonitis
acidosis 
anuria (kidney damage)
scabs formation
137
Q

therapy of acid intoxication

A

dilution of acid in the stomach -water, milk
oral anesthetics
morphine, atropine, glucocorticoids
drop infusion of 5% NaHCO₃ (treat the acidosis)
antimicrobial therapy (peritonitis may develop)

138
Q

which therapy shouldn’t do in acid intoxication

A

emesis induction

gastric lavage

139
Q

what happens in Oxalic acid intoxication?

A

tetany and cardiac depression
(Oxalate binds Ca in the blood)
anuria

140
Q

therapy of Oxalic acid intoxication

A

CaCl₂ oral
Ca gluconate IV
fluid infusion +enhanced diuresis
+therapy of acid intoxication

141
Q

what happens in base intoxication

A

liquefactive necrosis

tetany

142
Q

therapy of base intoxication

A

dilution of base in the stomach -water, milk
oral anesthetics
morphine, atropine, glucocorticoids
antimicrobial therapy (peritonitis may develop)
give Ca

143
Q

in what percent do we start having symptoms of Methemoglobin poisoning?

A

20% symptoms of hypoxemia

60-80% lethal

144
Q

how does methemoglobin or verdoglobin poisoning cause anuria?

A

Hemolysis of RBCs–>methB or verdoglobin will block the nephrons–>ARF

145
Q

give 2 methemoglobin producing agents

A
  1. oxidizing agents: chlorates, perchlorates
  2. nitrates: sodium nitrite, nitroglycerin
  3. aromatic amino and nitro compounds- aniline, nitrobenzene, nitrophenol
  4. methylene blue, toluidine blue
146
Q

what bacteria can cause food poisoning?

A 
staphylococci
salmonellae
proteus vulgaris
E.coli
B. cereus
147
Q

symptoms of food poisoning

A

vomiting, gastroenteritis, fever, hypovolemia

148
Q

therapy of food poisoning

A

gastric lavage, activated charcoal
replacement of volume and electrolytes
Ab if needed

149
Q

lethal dose of Botulism

A

0.001-0.002mg/kg

150
Q

mechanism of action of Botulism

A

inhibit release of Ach

151
Q

what is the latency time of botulism?

A

long (12-36hrs)

152
Q

symptoms of botulism poisoning

A 
first diarrhea--> then paralytic ileus
ptosis 
dilation of pupils
salivation--> then secretion stops
aphasia-->aspiration--> pneumonia
bladder atony
paralysis of skeletal muscle (respiratory stop!)
153
Q

therapy for botulism poisoning

A

Antitoxin (A,B,E)
purging with castor oil +neostigmine
transfusion

154
Q

when does infant botulism occur?

A

3 weeks to 6 months of age

155
Q

what is the difference between adult and infant botulism intoxication?

A

infants ingest spores themselves ==> produce toxin in the intestines

156
Q

symptoms of infant botulism

A 
constipation
poor feeding 
weak cry
muscle weakness decreased reflexes 
paralysis
157
Q

duration of symptoms of infant botulism

158
Q

classify the insecticides

A
  1. chlorinated hydrocarbons
  2. botanical insecticides
  3. cholinesterase inhibitors
    - organophosphates
    - carbamates
159
Q

what is the mechanism of action of DDT?

A

in the liver: enzyme induction

inhibit the inactivation of Na channels–< enhanced irritability

160
Q

symptoms of DDT poisoning

A

CNS stimulation
tremor
muscle spasm
carcinogenic in the long run

161
Q

properties of DDT

A

lipid-soluble
poor oral absorption
potent CYP450 inducer!

162
Q

what does pyrethrum (botanical insecticide) cause?

A

by inhalation –> asthma attack

headache most common symptom

163
Q

what does rotenone (botanical insecticide) cause?

A

inhibit NADH-NAD transformation

by inhalation–> respiratory depression, epileptiform seizures

164
Q

mechanism of action of carbamates and OPS

A

reversible (car)
irreversible (OPS)
inhibition of cholinesterase

165
Q

mechanism of action of carbamates and OPS

A

reversible (car)
irreversible (OPS)
inhibition of cholinesterase

166
Q

symptoms of carbamates and OPS

A 
*from Ach accumulation
Salivation 
sweating 
diarrhea-->  shock 
bronchical constriction
167
Q

Therapy for carbamates or OPS poisoning

A

atropine!
1-2mg
OPS–> pralidoxime

168
Q

toxic ingredients of snake venom

A 
neurotoxic peptides 
cholinesterase inhibitors
cardiotoxins 
enhanced blood coagulation components 
protein inhibits coagulation 
ingredients with analgestic effect
169
Q

sucking snake poison from the wound would help?

A

no, it passes through the lymph not only the circulation

170
Q

symptoms of snake poisoning

A

painful swelling
lymphangitis
nausea, haematemesis, diarrhea
↓ temperature, ↓ BP

171
Q

therapy of snake poisoning

A 
calmness 
polyvalent antitoxins 
H1 blockers
glucocorticoids 
hydration
172
Q

toxic ingredients of Bee & wasp sting

A

peptides
histamine
enzymes
wasp–> serotonin, Ach

173
Q

symptoms of Bee & wasp sting

A

in case of high number of stings–> shock, hemolysis, kidney failure

hypersensitivity! anaphylactic shock

174
Q

therapy of Bee & wasp sting

A

anaphylactic shock–> epi

glucocorticoids

Pharma 2nd semester (49 decks)

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