Toxicology Flashcards
(174 cards)
1
Q
give two possible mechanisms for specific antidotes and their example
A
- binding of poisons- chelators
- inhibition of distribution -methemoglobin-producers in cyanide intoxication
- inhibition of the formation of toxic metabolites- ethanol
- promoters of detoxification- acetylcysteine
- competitive inhibitors- naloxone
- agents promote regeneration of target cells- cholinesterase inhibitors
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
3
Q
types of decontamination
A
gastrointestinal
eye (for at least 20 min)
skin
body cavity evacuation
4
Q
how do we perform whole bowel irrigation?
A
via gastric tube
6-8 liter of isosmotic physiological electrolyte solution (containing polyethylene glycol)
5
Q
when do we not do a bowel surge (with sorbitol)?
A
in case of paralytic ileus
6
Q
types of gastrointestinal decontamination
A
- induction of emesis
- gastric lavage
- whole bowel irrigation
- bowel purge
7
Q
what do we use for induction of emesis?
A
syrup of ipecac
apomorphine (rarely)
8
Q
which type of patients you should not induce emesis?
A
patients who are:
- unconscious
- poisoned with corrosive agents (acid,base)
- poisoned with petroleum distillate (risk of aspiration!)
- poisoned with convulsant
9
Q
which type of patients you should not do gastric lavage?
A
- poisoned with corrosive agents (acid,base)
- poisoned with petroleum distillate (risk of aspiration!)
- poisoned with convulsant
10
Q
what is the risk in forced diuresis?
A
risk of lung edema and electrolyte disturbance
11
Q
what are the ways to eliminate poison through the GI?
A
- multiple-dose activated charcoal (“gut dialysis”)
2. cholestramine in digitalis intoxication (decreases the absorption
12
Q
what are the ways to eliminate poison through the kidney?
A
- forced diuresis- loop diuretics, mannitol, infusion
2. alteration of urinary pH
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
14
Q
which compounds can be removed by hemoperfusion?
A
DOB
digoxin
organophosphates
barbiturates
15
Q
complication in plasmapheresis
A
thrombocytopenia
microembolism
16
Q
which compounds can be removed by plasmapheresis?
A
carbamazepine lithium methanol metformin phenobarbital theophylline
17
Q
how do we perform neutralization?
A
- alkali -therapy ( 5% NaHCO₃, 2%Na lactate)
- specific antitoxins
- antibodies
18
Q
what are chelators?
A
organic compounds that function as chemical antagonists and used for the treatment of heavy metal poisoning
19
Q
how is Dimercaprol given?
A
always IM
20
Q
how is Dimercaprol excreted?
A
by the kidney (6-8 hours)
21
Q
what is the advantage of Dimercaprol?
A
good permeability
22
Q
therapeutic indication of Dimercaprol
A
- arsenic poisoning
- mercury poisoning
- Lead Poisoning (with EDTA)
23
Q
special indication for Dimercaprol
A
encephalopathy (can enter the neurons)
24
Q
side effects of Dimercaprol
A
nausea, vomiting hypertension tachycardia fever, pain thrombocytopenia
25
therapeutic indication of succimer
arsenic poisoning
mercury poisoning
lead- but not with encephalopathy
26
side effects of succimer (DMSA) and unithiol (DMPS)?
nausea, vomiting, diarrhea
| better tolerated than dimercaprol
27
How is succimer and unithiol (DMPS) given?
orally
| DMPS also parenteral
28
what is penicillamine used for?
Copper intoxication--->Willsons disease
| Rheumatoid arthritis- not used anymore
29
adverse effects of penicillamine
hypersensitive reactions
long term treatment--> autoimmune reactions (drug-induced lupus, drug-induced hemolytic anemia)
B6 vitamin depletion
30
what is EDTA used for?
lead poisoning
| * can remove lead from the bone
31
adverse effects of EDTA
Nephrotoxicity (rare)
32
what is deferoxamine used for?
iron poisoning
| hemochromatosis
33
how is EDTA given?
slow IV infusion for 5 days
34
how is Deferoxamine given?
IV or IM
35
Adverse effects of Deferoxamine
idiosyncraic reactions
ARDS
neurotoxicity
36
route of absorption of Arsenic?
respiratory and GI tract
37
where can we find Arsenic?
industry, agriculture (insecticides), wood preservatives
38
pharmacodynamics of Arsenic
inhibition of enzymes via sulfhydryl binding
39
distribution of Arsenic
soft tissues- first of all, liver and kidney, later skin hair and nail
40
Clinical presentation of acute Arsenic poisoning?
gastroenteritis-->severe diarrhea "rice water stool"
hypovolemic shock
arrhythmias
CNS symptoms
weeks later: ascending peripheral neuropathy
months later: transverse white striate on the nails.
41
Clinical presentation of chronic Arsenic poisoning?
weakness
peripheral neuropathy (socking-glove pattern)
skin changes- hyperkeratosis, hyperpigmentation
anemia
general cachexia
42
treatment of acute Arsenic poisoning
gut decontamination
intensive supportive care- fluid electrolytes
Dimercaprol chelation
43
treatment of chronic Arsenic poisoning
Dimercaprol chelation
44
Mercury source of intoxication
elemental mercury- manufacture of electrical equipment, paint products
mercury salts- disinfectants
45
the major route of absorption of mercury
elemental mercury- respiratory tract (inhalation)
mercury salts- GI and skin
organic Hg- Gi, skin and respiratory tract
46
distribution of mercury
soft tissues. first the kidney
| methylmercury reaches the brain
47
elimination of mercury by the...
kidney
48
Clinical presentation of acute Mercury poisoning?
elementary- pulmonary edema
salts-hemorrhagic gastroenteritis --> hypovolemic shock
acute tubular necrosis
49
Clinical presentation of chronic Mercury poisoning?
neuropsychiatric disturbance
| acrodynia (in children)- painful erythema in the extremities
50
therapy of acute Mercury poisoning
supportive care
inhalation (elementary): succimer and dimercaprol chelation
"mer" in Mercury
51
therapy of chronic Mercury poisoning
succimer chelation
| unithiol chelation
52
why we shouldn't use dimercaprol in chronic mercury poisoning?
it redistributes mercury to the CNS!
53
what is Minama disease and what does it cause?
Methyl-mercury poisoning
mainly CNS effects-paraesthesia, ataxia, coma, death
prenatal exposure--> mental retardation
54
Lead source of intoxication
```
occupational
environmental (batteries, paints, ceramics)
```
55
the major route of absorption of Lead
respiratory, GI, skin (organic)
*crosses the placenta
56
pharmacodynamics of lead
inhibits enzymes in porphyrine synthesis
interferes with the action of cations like Ca, Fe
alters the structure of membranes and receptors.
57
distribution of lead
first it binds to erythrocytes-->then soft tissues (liver &CNS) --> bones (can stay for 20 years in the bones)
58
elimination of Lead via the
kidney
59
Clinical presentation of acute Lead poisoning?
encephalopathy
acute abdominal pain (paralytic ileus)
hemolytic anemia
*rare
60
Clinical presentation of chronic Lead poisoning?
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)
61
Treatment of acute Lead poisoning
supportive care
| first dimercaprol and 4 hours later EDTA IV
62
Treatment of chronic Lead poisoning
EDTA IV infusion for 5 days, then PO succimer
*EDTA removes lead from the bones
63
major effects of organic lead (tetraethyl lead)
CNS effects
64
therapy of tetraethyl lead
decontamination from the skin
symptomatic treatment
chelators are not effective!
65
characteristics of carbon monoxide
colorless, odorless, no irritation
| lighter than the air
66
pharmacodynamics of carbon monoxide
affinity to hemoglobin is 300 times stronger than oxygen
67
symptoms of acute carbon monoxide poisoning
<50%--> headache, nausea, dizziness, weakness
>50% --> increased respiration and pulse, seizures, coma
>60%--> respiratory failure, death
68
symptoms of chronic carbon monoxide poisoning
headache, ataxia, insomnia, Parkinson- like symptoms
69
therapy of carbon monoxide poisoning
100% oxygen or
carbogen mix- 95 % O₂, 5% CO₂
or hyperbaric oxygen??
for brain edema- glucocorticoids, mannitol
acidosis- alkali therapy
70
classify the hydrocarbons
1. Aliphatic:
- Saturated
- unsaturated
- halogenated
2. Aromatic:
- benzine and benzene derivatives
- nitro and amino derivatives
- decoupling drugs
- phenol
71
route of intoxications of saturated aliphatic HC
inhalation of vapor--> aspiration!
ingestion of liquid
"glue sniffing" --> abused drug
72
symptoms of saturated aliphatic HC poisoning
acute- irritation of the mucosa, ventricular arrhythmia
| chronic- tolerance, pulmonary effects
73
therapy of saturated & unsaturated aliphatic HC poisoning
symptomatic
no emesis
no gastric lavage (risk of aspiration)
74
where can we find saturated aliphatic HC inducing intoxication?
Gasoline, kerosene, petroleum distillates
75
name 2 saturated aliphatic HC
CH₄-- methane
C₂H₆-- ethane
Cn increases--> CNS depressant increases
76
how does saturated aliphatic HC cause ventricular fibrillation?
Sensitization of myocardium to NE
77
name 2 unsaturated aliphatic HC
C₂H₄-- ethylene
C₂H₂-- acethylene
inhalational anesthetics
Cn increases--> CNS depressant increases
78
which has stronger effects- saturated or unsaturated HB?
unsaturated
79
route of intoxications of unsaturated aliphatic HC
inhalation of vapor--> aspiration!
| ingestion of liquid
80
are Halogenated aliphatic HC lipid soluble?
extremely lipid-soluble
--> more toxic than non-halogenated
81
where can we find Halogenated aliphatic HC?
used as solvents and in cooling systems
82
symptoms of Halogenated aliphatic HC
```
CNS depression
cardiotoxicity
kidney and liver impairment
when inhaled--> lung edema
skin- 1-3 degree frostbite
```
83
therapy of Halogenated aliphatic HC poisoning
symptomatic
| alkali therapy in case of acidosis
84
what is the lethal dose of Carbon tetrachloride (CCl₄)?
20-30ml
85
symptoms of Carbon tetrachloride (CCl₄)
```
starting effects: irritation of mucosa, CNS depression, ventricular fibrillation (sudden death)
delayed effects (1-2 days later): hepatorenal syndrome, toxic hepatitis, ATN
```
86
treatment of Carbon tetrachloride (CCl₄)
symptomatic (gastric lavage, paraffin oil, active charcoal)
87
what is chloroform (CHCl₃)
halogenated aliphatic HC
strong narcotic
not used due to its hepatotoxicity
88
routes of intoxications of Benzene, toluene, xylene (Aromatic HC)?
Skin, GI, lungs
89
elimination of Benzene, toluene, xylene
via lung and kidney
90
symptoms of Benzene, toluene, xylene poisoning
acute--> narcosis, seizures, coma, arrhythmia
| chronic-->CNS, liver and kidney damage, bone marrow suppression
91
therapy of aromatic hydrocarbons
gastric lavage and purgation with cooking oil
| activated charcoal
92
symptoms of phenol poisoning
topically: local anesthetic effect -->serious necrosis without pain
orally: necrosis on the mucosa
systemic effects: CNS (seizures, coma)
93
absorption of Nitrobenzene and Aniline
GI, skin, lung
94
what is the lethal oral dose for Nitrobenzne?
2-3ml
95
symptoms of Nitrobenzene (C₆H₅ NO₂) poisoning?
acute- irritation of the mucosa (vomiting, spasm), CNS depression, methemoglobinemia, hemolysis
chronic- anemia, hemolytic icterus, CNS disturbance
96
therapy for Nitrobenzene (C₆H₅ NO₂) and Aniline (C₆H₅ NH₂) poisoning
reduction of methemoglobinemia
| orally--> milk, oil
97
what symptom is seen first in acute Aniline poisoning?
euphoria
98
what is DNP?
Dinitrophenol
| aromatic hydrocarbon
99
what is the lethal dose of Dinitroortocresol (DNOC)?
1g
100
where is DNP used?
in the chemical industry
| *used in the past as weight loss agent
101
where is DNOC used?
in the agriculture?
102
routes of poisoning of DNP and DNOC?
inhlation
skin
GI
103
what is the main mechanism of action in aromatic hydrocarbons poisoning? (DNP, DNOC)?
increased energy converts to heat
104
symptoms of acute DNP &DNOC poisoning?
```
hyperpyrexia
dehydration--> ↓BP
HR↑
Dyspnea
cyanosis
anoxia
lung edema
```
105
symptoms of chronic DNP &DNOC poisoning?
```
weight loss
fever
kidney, liver, heart impairment
bone marrow function
hemolytic anemia
```
106
therapy of acute DNP &DNOC poisoning?
```
decontamination (lavage, emesis, washing the skin)
cold batch
O₂ inhalation
0.9% NaCl
glucose infusion
```
107
what is forbidden to give in formaldehyde poisoning?
Sulfonamides
| can cause RF
108
what are formaldehyde and metaldehyde?
Aldehydes :)
109
what is the lethal dose of metaldehyde?
4g for adults
| 0.1-0.5 g for children
110
where is metaldehyde used?
as fuel cubes and pesticides
111
what is the therapy of formaldehyde poisoning?
drink milk, water
gastric lavage
alkalization
hemodialysis
112
Symptoms of metaldehyde poisoning?
```
GI: hemorrhagic gastritis
severe CNS effects: ↑ muscle irritability
muscle rigidity
seizures
respiration stops
```
113
therapy of metaldehyde
```
gastric lavage
induction of emesis
activated charcoal
purgation
symptomatic treatment--> maintaining BP
```
114
when do the symptoms of methanol intoxication begin?
8-30 hours later
115
what are the symptoms of methanol intoxication?
```
metabolic acidosis--> respiratory failure
abdominal pain (pancreatic damage)
blindness
```
116
therapy of methanol intoxication and divalent glycols poisoning?
```
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
what are diethylene glycol and ethylene glycol?
Divalent glycols
118
where can we find Divalent glycols?
used as solvents, lubricants, antifreeze substance
| car cooling system (?)
119
symptoms of divalent glycols poisoning
Anuria! (kidney damage)
CNS
acidosis
liver damage
120
what do Inocybe- type mushrooms contain that make them poisonous?
muscarine (alkaloid)
121
what are the symptoms of mushroom poisoning (Inocybe type)?
parasympathomimetic effects
| extreme diarrhea
122
therapy of mushroom poisoning (Inocybe type)?
atropine 1-2mg every 30 min
123
what do the mushrooms "Amanita muscaria" and "Amanita pantherina" contain?
muscarine
muscaridine
muscimol (GABAa agonist)
ibotenic acid
124
what are the symptoms of Amanita muscaria and pantherina poisoning?
```
salivation
sweating
vomiting
diarrhea
atropine intoxication: restlessness, hallucinations
```
125
what is the therapy of Amanita muscaria and pantherina poisoning?
symptomatic
| NO ATROPINE!
126
what does Amanita phalloides (death cup) contain?
amatoxins (toxic polypeptides):
amantin𝝰
phalloidin
127
what type of mushrooms have rapid onset?
Inocybe
Amanita muscaria
Amanita pantherina
128
what type of mushrooms have delayed onset?
Amanita phalloides
129
is Amanita phalloides toxic?
high lethality because of hepatotoxicity
130
symptoms of Amanita phalloides
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
treatment of Amanita phalloides
supportive (no antidote)- protection of liver and kidney, forced diuresis, hemoperfusion, glucocorticoids
high dose G-penicillin, silibinin, N-acetylcysteine
132
what is the mechanism of action of cyanide?
lactic acidosis and cytotoxic hypoxia
133
symptoms of cyanide poisoning
hyperpnea
coma
asphyxia
convulsion
134
Therapy of cyanide poisoning
1. formation of methemoglobin!
| 2. give EDTA
135
routes of acid intoxication
oral, skin, eye, inhalation
136
symptoms of acid intoxication
```
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
therapy of acid intoxication
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
which therapy shouldn't do in acid intoxication
emesis induction
| gastric lavage
139
what happens in Oxalic acid intoxication?
tetany and cardiac depression
(Oxalate binds Ca in the blood)
anuria
140
therapy of Oxalic acid intoxication
CaCl₂ oral
Ca gluconate IV
fluid infusion +enhanced diuresis
+therapy of acid intoxication
141
what happens in base intoxication
liquefactive necrosis
| tetany
142
therapy of base intoxication
dilution of base in the stomach -water, milk
oral anesthetics
morphine, atropine, glucocorticoids
antimicrobial therapy (peritonitis may develop)
give Ca
143
in what percent do we start having symptoms of Methemoglobin poisoning?
20% symptoms of hypoxemia
| 60-80% lethal
144
how does methemoglobin or verdoglobin poisoning cause anuria?
Hemolysis of RBCs-->methB or verdoglobin will block the nephrons-->ARF
145
give 2 methemoglobin producing agents
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
what bacteria can cause food poisoning?
```
staphylococci
salmonellae
proteus vulgaris
E.coli
B. cereus
```
147
symptoms of food poisoning
vomiting, gastroenteritis, fever, hypovolemia
148
therapy of food poisoning
gastric lavage, activated charcoal
replacement of volume and electrolytes
Ab if needed
149
lethal dose of Botulism
0.001-0.002mg/kg
150
mechanism of action of Botulism
inhibit release of Ach
151
what is the latency time of botulism?
long (12-36hrs)
152
symptoms of botulism poisoning
```
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
therapy for botulism poisoning
Antitoxin (A,B,E)
purging with castor oil +neostigmine
transfusion
154
when does infant botulism occur?
3 weeks to 6 months of age
155
what is the difference between adult and infant botulism intoxication?
infants ingest spores themselves ==> produce toxin in the intestines
156
symptoms of infant botulism
```
constipation
poor feeding
weak cry
muscle weakness decreased reflexes
paralysis
```
157
duration of symptoms of infant botulism
2-6 weeks
158
classify the insecticides
1. chlorinated hydrocarbons
2. botanical insecticides
3. cholinesterase inhibitors
- organophosphates
- carbamates
159
what is the mechanism of action of DDT?
in the liver: enzyme induction
| inhibit the inactivation of Na channels--< enhanced irritability
160
symptoms of DDT poisoning
CNS stimulation
tremor
muscle spasm
carcinogenic in the long run
161
properties of DDT
lipid-soluble
poor oral absorption
potent CYP450 inducer!
162
what does pyrethrum (botanical insecticide) cause?
by inhalation --> asthma attack
| headache most common symptom
163
what does rotenone (botanical insecticide) cause?
inhibit NADH-NAD transformation
| by inhalation--> respiratory depression, epileptiform seizures
164
mechanism of action of carbamates and OPS
reversible (car)
irreversible (OPS)
inhibition of cholinesterase
165
mechanism of action of carbamates and OPS
reversible (car)
irreversible (OPS)
inhibition of cholinesterase
166
symptoms of carbamates and OPS
```
*from Ach accumulation
Salivation
sweating
diarrhea--> shock
bronchical constriction
```
167
Therapy for carbamates or OPS poisoning
atropine!
1-2mg
OPS--> pralidoxime
168
toxic ingredients of snake venom
```
neurotoxic peptides
cholinesterase inhibitors
cardiotoxins
enhanced blood coagulation components
protein inhibits coagulation
ingredients with analgestic effect
```
169
sucking snake poison from the wound would help?
no, it passes through the lymph not only the circulation
170
symptoms of snake poisoning
painful swelling
lymphangitis
nausea, haematemesis, diarrhea
↓ temperature, ↓ BP
171
therapy of snake poisoning
```
calmness
polyvalent antitoxins
H1 blockers
glucocorticoids
hydration
```
172
toxic ingredients of Bee & wasp sting
peptides
histamine
enzymes
wasp--> serotonin, Ach
173
symptoms of Bee & wasp sting
in case of high number of stings--> shock, hemolysis, kidney failure
hypersensitivity! anaphylactic shock
174
therapy of Bee & wasp sting
anaphylactic shock--> epi
| glucocorticoids
