Tox Flashcards
(271 cards)
1
Q
Reasons to use and dont use flumazenil in benzo od
A
Only when no benzo dependence and patient hasn’t taken any other substance in addition to benzo.
Risk of withdrawal sx and seizures
2
Q
Flumazenil is especially contraindicated in
A
P w increased intracreamical pressure, closed head injury, taking TCA, epilepsy (inc risk of seizures)
3
Q
AEs of benzos in therapeutic doses
A
Slurred speech
Ataxia
Sedation
4
Q
Benzo withdrawal sx
A
HT, tachy, tremoulosnes, seizures, low grade fever, delirium
5
Q
What benzos are not detected in blood tests
A
midazolam, chlordiazepoxide, and flunitrazepam
6
Q
GHB moa
A
Neuroinhibitory + inc gaba b and dopa
7
Q
Mild GHB intoxication
A
Slurred speech
Disinhibition
Euphoria
Mild lethargy
8
Q
Moderate GHB intoxication
A
CNS and mild respiratory depression
Agitation when stimulated
Myoclonus
9
Q
Severe GHB intoxication
A
Unresponsive coma Miosis Bradycardia Mild hypotension Seizures Respiratory depression and apnea
10
Q
Short acting iv barbs
A
methohexital, thiopental, hexobarbital, pentobarbital
11
Q
Short acting oral barbs
A
secobarbital and butabarbital oral
12
Q
Patient has nystagmus, a bit slurred speech, a bit ataxia, seems somnolent and confused (dec GCS?), what drug might he have been taking
A
Mild to moderate overdose of barbs
13
Q
Barb severe overdose, what will be seen on: Echo: BT machine: Counting RR: Thermometer: Glucosometer: When talking to p:
A
Echo: Dec contractility BT machine: HoT Counting RR: Dec Thermometer: Dec Glucosometer: Dec! In many p! When talking to p: Coma or close to coma
14
Q
What may enchange elimination of phenobarbital?
A
urinary alkalization
Administer 1 to 2 mEq/kg (2 to 3 ampules in an adult) of bicarbonate IV initially followed by an infusion of 3 ampules of sodium bicarbonate mixed in 1 liter of D5W given at 1.5 to 2 times maintenance fluid rates.
Goal urine pH is 7.5 to 8. Do not allow serum pH to exceed 7.55.
Follow urine pH, serum pH and serum potassium carefully. Add potassium chloride to IV bicarbonate if the serum potassium is low.
15
Q
Observation criteria phenobarbital
A
Over 8 mg/kg
16
Q
An iminostilbene derivative with a tricyclic structure
A
Carbamazepine
17
Q
Carbamazepine effect on cyp 450
A
Enhances it
18
Q
Some medications that decrease elimination of carbamazepine
A
Erythromycin, isoniazid, propoxyphene
19
Q
Sx of od carbamazepine
A
Hallucinations Blurred vision Drowsiness Slurred speech Ataxia Nausea, vomiting Tremors Seizures Oliguria Bullous skin formations
Ocular
Mydriasis
Nystagmus
Ophthalmoplegia
Cardiovascular
Tachycardia
Hypotension
Neurologic
Ataxia
Slurred speech
Dystonia, myoclonic activity
Varying degrees of CNS agitation to depression progressing to coma
Seizures, headache, confusion, and athetosis
Increased or decreased deep tendon reflexes
Respiratory depression, apnea
Delayed gastric emptying, abdominal pain
Oliguria, urinary retention
20
Q
Therapeutic level of carbamazepine
A
4-12 mg/L,
21
Q
Carbamazepine effect on heart
A
May give AV-block due to interference with purkinjae and HIS
22
Q
DDx of carbamazepine overdose
A
- alcohol and other psychoaktive substance abuse
- anticholinergic toxidrome
- antidepressant toxicity
- lithium
-
other antiepileptic drugs toxicity (VPA, Phenytoin) - Neuroleptic Malignant Syndrome
-
encephalitis - sintus bradycardia
23
Q
What to do when QRS is wider than 100ms in carbamazepine poisoning
A
Administer Sodium Bicarbonate
24
Q
Valproate effect on cyp450
A
Slows it down
25
Cimentidine and ranitidine effect of valproic acid
Increase function by inhibitiong hepatic metabolism
26
Drugs that may slow down the gi absorption of valproate
Opiates and antihistaminsae
27
Valproate od sx
Unspecific, N/V, CNS, confusion and dec GCS
28
Important dangerous ae of valproate od that may occur after 72 h
Cerebral edema (due to hyperammonemia)
29
Aliphatic HCs
Linear hydrocarbons (alkanes, eses, ines)
30
Aromatic HC like benzene is used for
Solvents such as glue and paint
31
Most commonly ingested hydrocarbons
gasoline, chlorofluorocarbon propellants, motor oils, lighter fluid/naphtha, lamp oil, and mineral spirits
32
Acute systemic effects of hydrocarbons
```
Arrythmia
CNS depression
Seizures
Hepatic necrosis
Acute renal tubular necrosis
```
33
Pulmonary effects of HCs
- Causes aspiration
- Causes pneumonia by direct toxic effect of parenchyma, and injury t type II cells causing collapse,
- As a concequense, hemorrhagic alveoli's
- Inflammation, hemorrhage, edema, brachial necrosis, vascular necrosis
34
CNS effects of HCs
- Direct
- Hypoxia
- Hypercarbia (sniffing from bag)
Long term:
- White matter atrophy
- Peripheral neuropahty
- Blurred vision
- Sensory impairment
- Muscle atrophy
- Parkinsonism
35
Hepatotox of HCs
Cl is the worst
Carbon tetrachloride!
Make free radicals -> bind metabolites -> both bind liver enzymes and nucleic acids -> lipid per oxidation (electrons stolen and cell membranes destroyed) -> necrosis
Typically cbentrilobular
36
Problem with methylene chloride
Its metabolized by cup 450 to CO
37
HC effect on heart
Makes it more sensible for catecholamines -more risk for tachyarryhtmias and sudden cardiac death
38
HC effect on GI
Vomiting 1/3 and diarrhea
39
What HC is the worst for kidney
Aromatic toluene from chronic occupational -> distal renal tubular acidosis (collecting duct can't excrete acid) -> anion gap acidosis
40
Hx of HC
```
What agent
Route
Amount
Time
Any other substances
Vomiting or coughing before hospital
Attemts of treatment before hospital?
```
41
kerosene and other aliphatic hydrocarbons smell like
petroleum distillate odor
42
halogenated hydrocarbons smell
halogenated hydrocarbons
43
Vitals after HC
Fever and dec O2
44
HC effect on CBC
Initial leukocytosis
Eventualu aplastic anemia, risk of AML
45
Blood tests to take for HC
```
Metabolic
BUN
Cr
CK (rhabdo?)
Glu
Ele
Hepatic
Anion gap
```
46
What may be found in CXR after HC
Multiple small patchy densities with ill defined margins indicating aspiration pneumonia
May appear before sx, take XR at once
47
5 Ws
Who, What, When, Where, Why
48
Coma cocktail
O2, glucose, naloxone, dextrose, thiamine
49
Why observe
May have serious effects that are not apparent ant once
50
Important rule outs
ATOMIC
Alcohol
Trauma (CT)
Overdose
Metabolic distrurbance (electrolytes, glycose, thyroid, creatinine)
Infection (pneumonia, aspiration pneumonia sepsis, meningitis)
CO
51
PE
Undress p completely
Check for objects and substances
- Mental status
- Vital signs
- Pupils
- Bowel sounds (stimulation in alcoholic withdrawal, mushrooms, phosphor organic)
- Muscle, activity and coordination, tone, lead pipe,
- Skin
- Lungs
- Cardiovascular
52
When to be cautious about naloxone
Opioid addiction, multi-drug poisoning
53
Naloxone dose adutls
2 mg, repeat every 2 minutes until 10 mg
54
Naloxone infants and children under 5 years
0,1 per kg initially
55
Acetaminophen anti-dote
N-acetulcysteine
56
Beta blockers antidote
Glucagon
57
Ca channel blockers antidote
Iv Ca, insuline and glucose
58
Carbamates antidote
Atropine, pralidoxime
59
What is the effect of ipecac
It can induce emesis
| MOA: Irritation of stomach and chemotrigger zone in brain
60
When not to induce emesis
```
Generally never in hospital but also
Not in
- Dec mental status or seizures
- vomiting
- corrosive poisons
- volatile poisons
- Heart disease p
- Pregnant
- Hyrdrocarbons and other that are worse for lungs than gi
```
61
When to perform gastric leakage from HCs
Benzene, toluene, camphor, halogenated hydrocarbons, pesticides, heavy metals if more than 5ml/kg, eg 500 ml in 100 kg man
62
Charcoal indication
In general poor evidence but
- Multiple sunstances
- life threatening amount
63
Drugs that may benefit from multi dose charcoal
Phenobarbital
Carbamazepine
Aspirin
Theophylline
64
Charcoal is not effective for
```
cyanide
mineral acids
caustic
organic solvents, hydrocarbons
metals (iron, lithium, mercury, lead)
ethanol, methanol, ethylen glicol, isopropranol
```
65
Poisins that mainly cause death by airways
Carbamate, pesticides, hydrocarbons, solvents, petrol
66
Contraindication for alkaline diuresis
Renal failure
67
Is acidification of urine done?
No, the risk of rhabdo makes it not worth it
68
LIpid rescue is used for
Good for lipophilic substances
- TCA
- CCBs
- BBs
- Cocaine
- Anti-convulsants
- Anti-depressants
- Organic solvents
- Bio-weaponds
- Bupivacaine
69
Toxins that may require hemodialysis
```
Ethylene glycol
Lithium
Methanol
Salicylates
Theophylline
VPA
Phenobarbital
```
70
Whats in common?
```
Ethylene glycol
Lithium
Methanol
Salicylates
Theophylline
VPA
Phenobarbital
```
May require hemodialysis
71
Major groups of new psychoactive substances
Depressant
Stimulant
Hallucinogenic
Synhtethic cannabinoids
72
Other name of ephedrone
Scientific: Methcathinone
(made from oxidation of ephedrine)
MCat
73
Methcathinone effect
```
Similar to amphetamine
Psychoactive stimulant
Dopamine rey-take inhibitor
Confusion to psychosis
Euphoria
Lack of appetite
Forgetting to drink
Locomotor activity
Hypertension
```
74
Methyldioxyprovalerone (MDPV) MOA
NDRI (norepie and dopa reuptake inhibitor)
Similar to ritalin but 4 times more potent
75
Short term effects of MDPV
Basically SNS activation
| Alterness and awareness
76
High doses of MDPV cause
Psychosis and panic
Lack of sleep
Addiction
Sexual desire
77
Long term effects of MDPV
Comedown syndrome
| Postural hypotension, depression, lethargy
78
"Spice" moa
Cannabonoid agonist
79
Treatment in spice
Usually monitoring and hydration is enough, maybe benzos
80
What can be given to counteract on psychotic effects on the heart, to reduce risk of arrhythmia
Benzos
81
Pestisides include
Active biological substance and something to carry it, often a HC
82
Major deadly pesticides
Organophosphorius (endosulphan)
Aluminium phosphide
Paraquat
83
Some examples of organophosphates
Chlorpyrifos, parathion, dimethoate, fenthoin
84
Sx of organophosphate poisoning
1 Acute cholinergic crisis
2 Intermediate syndrome
3 Delayed polyneuropathy
85
Organophosphates MOA
Inhibit AChH, (by binding in a way thats hard to reverse)
86
Dimethyl vs diethyl
Dimethyl is fast, diethyl is fast (Bort act on reactivation of ACHE
87
Organophosphates cause __ syndrome
Muscarinic syndrome (and also nicotinic)
88
Sx nicotinic syndrome
Fasciculations, muscle cramps, fatigue, paralysis, tachycardia, HT
89
ECG changes after organophosphates
Small vintage (peak to peak QRS under 5 in limb or 10 in precordial)
ST-T changes
Prolonged QT
VES ++
90
Possible reasons for intermediate syndrome of organophosphate poisoning
toxin-induced myonecrosis
combined pre- and postsynaptic impairment of
neuromuscular transmission
downregulation or desensitization of postsynaptic ACh receptors after prolonged ACh stimulation
91
What is intermediate syndrome of organophosphate poisoning
Occurs a couple of days after
initial weakness of neck flexion
respiratory muscle weakness and respiratory failure
cranial nerve palsies (typically III, IV, VI, VII and X)
proximal muscle weakness of extremities
92
Ginger paralysis syndrome
= delayed effects of organophosphate poisoning
- neuropathy
- waekness
- Peronality changes
- Pancreatitis
93
When use atropine in OP poisoning
HR under 80, HoT under 80 systolic ++
| high HR not contraindication
94
Pralidoxime and obidoxime are
ACHE reactivates
95
Advantage of glycopyrrolate for reversal of OP poising
No CNS effect
96
aldicarb, benomyl, carbaryl, carbendazim, carbofuran, propuxur, triallate are
carbamates
97
Carbamates differences from OPs
Also affect pseudocholinesterase BChE
Reversible
Less CNS effect
98
What are OCs
Organochloride pesticides
Chloridated cyclic hydrocarbons
99
DDT, BHC (benzene) and lindane are
OCs
100
Lindane effect on heart
Histologic alteration of LV wall
101
OC moa
- Depolarize nerves
- Dicoordinate GABA
- Predispose to arrythmias
102
OC sx
Many, CNS and seizures are most important
103
Cholestyramine may be useful in
Biliary-fecal excretion of OC
104
Pyrethins and pyrethroids use
Mosquito and scabies
105
Pyrethins and pyrethroids moa
Na channels
106
Pyrethins and pyrethroids sx and tx
Not supersevere, usually supportive
107
Paraquat is __ and may be mistaken for __
Bypyridyl herbicide
Cola
108
Bipryidyl herbicides MOA
Free radicals destroy cell membrane, worst for liver, kidney and lung
109
Paraquat typical sx
Hemorragic pumonary edama, ARDS, fibrosis
110
Diquat typical
To cns, like like parkinson or brain stem infarction
111
Paraquat oral ingestion sx
Just think that cells are dying everywhere
```
Liver failure
Hepatic failure
Ventricarular arrhythmia and arrest
CNS depression or seizures
Pulmonary hemorrhage
Prorgressive pulmonary firbosis
Rhabdo
```
Diquat is same, but generally more CNS and less other
112
Dx of paraquat and diquat
Add salt and look for color in urine
113
Tx in bipyridayl herbicides
All the normal stuff and immunosupression
Careful with O2 (free radicals)
114
2,4-D (2,4-dichlorophenoxyacetic acid), dichloroprop, mecoprop, are
Chlorophenoxyacetic herbicides
115
Chlorophenoxyacetic herbicides moa
Damage cell membranes and ruins oxidative phosphorylation by disrupting of acetylcoenzyme A
116
Sx of Chlorophenoxyacetic herbicides
- Intravascular volume loss -> hypovolemia
- Hypertonia and reflex
- CNS depression and respiratory depression
117
Alkaline diuresis effect on herbicide?
Yes
118
Dinitrophenols mechanism
Shuttling of protons
119
Dinitrophenols sx
Marked increase in metabolism:
Everything goes up
Severe:
All the normal organ problems, cns, lints, heart, kidney, liver
Methemeglobinemia anemia
Yellow skin, stool and urine
120
Yellow skin, stool and urine is seen in
Dinitrophenols
121
Glyphosate moa
Not sure, combination with other active ingredients
122
Glyphosphate sx
GI burns,
hyperthermia
Metabolic acidosis ++
123
Tx Glyphosphate
All the normal
ENdoscopy to look for burns
Correct acidosis and hydrate well
124
Symptoms of metallobisdithiocarbamates poisoning:
irritation and alcohol dehydrogenase inhibition
125
Antidote for ethanol glycol and methanol
Fomepizol (and ethanol)
126
Heavy metal antidote
Chealating drugs
127
Iron antidote
Deferoxiamine
128
Isoniazid antidote
Pyridoxime
129
TCA antidote
NaHCO3, alkanization to open fast sodium channels, dec cardiac effects
130
Cyanide antidote
Hydroxycobalamin
131
Methyl mercury in concentrated in
NS, and RBCs
132
Organomercurials legal?
Banned in many countries because of toxicity
133
Organomercurials sx
Acrodynia
| Slurred speech, hearing, vision, balance etc
134
Essential part of organomercurail management
Chealation (DMSA etc)
135
Dialysis in organomercurials
May be necessary in addition to chelation, even low doses are life threatening
136
-tyltin are
Organotins
137
Organothins moa
Seveal mitochonrihal enzymes, problems w oxidative phosphorylation
138
Organothins sx
Hepatomegaly and liver ennymes
| Hyperexitability, LOC and other CNS
139
Thallum fast
No, CNS effects can take a week;
Lethargy, paresthesia, ataxia ++
Alopecia takes 2 w
140
Thallum on gi
Bloody diarrhea, salivation
141
Aphemtaimine and cocain time to reach urine
3 days indicate decreasing dose elimination phase, not increasing (roughly)
142
Chronic weed user will have evidence in urine
1 months after
143
What can be given to increase fecal excretion of thallum
potassium ferric ferrocyanide (Prussian blue)
144
Warfarins moa
Inhibit 2,7,9,10
Direct capillary damage
145
CT
Take in cocaine, brain hemorrhage
146
Antidote for warfarin
Vit K1, not K3 and K4
147
Superwarfarins onset and duration
48 h - several months
148
Contraindication for gastric levage
No agreement from patient, even if uncoucious and life life threatening
149
Aluminium phosphide MOA
Taken up in mucos membrane, PH3 gas made -> Inhibits cyt c -> ROS -> cell damage
150
Metabolism of AP
In liver to phosphine which is also toxic
151
Gastric leakage size
36 french, very large, not normal size, 45 com long
152
Contraindication of gastric leavage
Uncorporative
Non-toxic dose (few pills)
Hydrocarbons only if intubates!
153
AP severe dose sx
ARDS, cardiac arrhythmias, liver and
| renal failure, convulsions, coma and death
154
AP sx
symptoms usually develop within 30 min of ingestion
GI – severe epigastric pain, repeated vomiting, diarrhoea
circulation – hypotension, tachycardia, toxic myocarditis, arrhythmias, ST-T changes, subendocardial infarction
respiration – cough, dyspnoea, cyanosis, pulmonary oedema, ARDS
metabolic acidosis, intravascular haemolysis
typically, patients remain conscious till the late stages
155
AP tx
gastric lavage with potassium permanganate (
156
Zink phosphide smell
Rotten fish
157
CCBs bradycardia
Atropine
158
Clinical features of zinc phosphide poisoning:
similar to those of AP but slower in onset (slower release of
phosphine)
early symptoms – nausea, vomiting, thirst, tightness in the chest, excitement, agitation
pulmonary oedema, ECG changes, shock, oliguria
convulsions, coma
hepatotoxicity
metabolic acidosis, hypocalcaemia, thrombocytopenia
159
Barium conpouncds MOA
Interfere w sodium-potassium pump -> changes in cell membrane permeability -> paralysis of muscle s
160
Barium conpouncds sx
Interfere w muscle cell membrane!
repeated vomiting, abdominal pain
tightness of the muscles of the face and neck, muscle tremors
loose motions, anxiety, convulsions, perioral paraesthesia that spreads to other parts of the body, ascending quadriparesis with respiratory muscle involvement, difficulty in breathing
cardiac arrhythmias – wide-complex tachyarrhythmias, ectopics, ventricular tachycardia, ventricular fibrillation, prolonged QTc interval, prominent U waves
hypokalaemia (obs! )
161
What not to give in barium compounds
Mg sulphate
162
Mulluscicides kill
Snails
163
Low Vd and low protein binding its good for
Hemodyalysis
164
Quetiapine goode for hemodialysis?
No, high protein binding and liver rather than kidney elimination
165
Hemodialysis pro
Very small particles compared to the other
166
Hemoperfusion moa
Use charcoal or cuisine, should be larger particles, but can take larger amount then hemodialus
Can take larger size like plasma proteins
167
Hemofiltration
Particle size in between hemodialysis and hemoperfusion, can not take plasma proteins and things bound to them
168
Hemodialysis mechanism
Diffusjon
Hemofilter w semipermeable membrane, dialysite
169
Inducation for hemodialysis
Absolute:
Must have taken drug and drug must fit for hemorrhages (small partible low vd low protein binding)
Clinically necessary
170
Hemodialysis used for
```
Alchohols
Lithium
Salisylates
Theophylline
Valproate
```
171
Benefits of hemodialysis
Correct acidosis and other metabolic problems
Can treat kidney failure with hypervolemia
172
Methaldehyde moa
The mechanism of metaldehyde toxicity is not well understood:
harmful effects are mediated by a mechanism similar to its sister compound acetaldehyde (?)
decrease of the inhibitory GABA activity in the brain convulsions
173
Metaldehyde sx
Symptoms of acute metaldehyde poisoning:
onset after acute ingestion is generally within 1-3 h
traces amounts – salivation, facial flushing, fever, abdominal cramps, nausea, vomiting
up to 50 mg/kg – drowsiness, tachycardia, spasms, irritability
50-100 mg/kg – ataxia, increased muscle tone
100-150 mg/kg – convulsions, tremor, hyperreflexia
150-200 mg/kg – muscle twitching
about 400 mg/kg – coma, death (generally secondary to CNS depression and consequent respiratory failure)
174
Methaldehyde tx
- Gastic leavage and charcoal
- Supportive
- N-acetylcystein may help liver and kidney
175
Albumin dialysis
Idea is to eliminate protein bound, very expensive, main indication is liver failure, eg APAP toxicity, alcoholic liver,
176
DEET is
Diethyltoluamide
177
DEET acute poisoning
hypotension, respiratory depression
CNS toxicity:
behavioural disorders, restlessness, irritability
headache, ataxia
rapid loss of consciousness, seizures
sometimes flaccid paralysis and areflexia
178
Symptoms of cutaneous exposure to EDB (ethylene dibromide)
ulcerations
conjunctivitis
gastrointestinal and mucosal irritation
CNS irritation and depression
179
Symptoms of oral ingestion of EDB:
vomiting, diarrhoea, burning in the throat soon
after ingestion (features may last for 1-3 days)
ulceration of the mouth and throat
tremors, CNS depression, altered consciousness hypotension
oliguria
jaundice
uncommon features – pulmonary oedema, muscle necrosis, hyperthermia
180
tropane alkaloids
atropine, scopolamine, and hyoscyamine
181
Plants that contain alkaloids
Datura species (jimson weed, angel's trumpet, thorn apple)
Hyoscyamus niger (henbane)
Atropa belladonna (deadly nightshade)
Mandragora officinarum (mandrake)
182
Benzos safe
Not really when alone, but synergic w alcohol and not good in combinations
183
Datura use
Resuse pain, dilate bronchioles
184
Tropane alkaloids moa
Anticholinergic
185
Important to remember about tropane alkaloids
Gastric emptying is slowed and dose in blood may continiue to increase for up to 48 days
186
Remember about flumazenil
Last short, may only gain consciousness for some minutes, but good to ask what they took
Has some diagnostic purpose
Rather intubate than give continilous doses of flumazenil
Careful if there might be dependence!! (Strong withrawl syndrome, and seizures)
187
Benzos elimination
Nothing can be done to enhance it
188
Barbituates vs benzos (or thiopental?)
Barbituates cause deeper coma, more respiratory depression and more cardiotox
189
Carbamazepine is structurally similar to
TCAs
190
Kinetics of carbamazepine
Large Vd
Unpredictable absorption
Needs to be monitored
191
Pathyphyys of carbamazepine
Opening of sodium channels
192
Carbamazepine metabolite
Metabolized by CYP450
Very active metabolite
Cause autoincudtion after long use, need to increase the doses eventually
193
Clinical course of carbamazepine
Therapeutic window is very narrow 4-11 mg/L!
Theoretically conscious but nystagmus, tremors, vomiting etc
Large doses give cholinolytic delirium (like in alcohol)
Cardiac depression and HoT, many CNS, alcohol like
Next stage will give Resp dec
Cholinergic properties, urinary retention (needs to have urinary catheter)
Skin changes that may give TEN syndrome
DRESS
Bind nucleic acids
194
Ddx of carbamazepine
Other cholinergic
Antihistaminic
TCA
Alcohol withdrawal
195
Electrolytes in carbamazepine
Hyponatremia (connected w effect on ADH)
196
Charchoal in carbamazepine
Yes, but exclutde ileus first!!
197
What to do if widening of QRS in carbamazepine
Give saline
198
Less toxic HC
Solid
199
Aspiration hazard HCs
Turprentine, gasoiline, keraosene, minral seed oil
200
Tropane alkaloids sx
```
Dry mucous membranes and skin
Dysphagia and dysarthria
Photophobia
Blurred vision
Tachycardia
Urinary retention
initial signs and symptoms may be followed by hyperthermia, confusion, agitation, combativeness, seizures, coma, and death.
amnesia regarding events following ingestion of tropane alkaloids is common.
```
201
Tropane alkaloids mnemonic
The mnemonic "red as a beet, dry as a bone, blind as a bat, mad as a hatter, and hot as a hare" is useful to remember the anticholinergic toxidrome.
202
Can atropine etc be tested in blood?
No, but in urine
203
Lab tests for ethanol
ABG
| AG & OG
204
60 year old patient with asthma, ER, severe N/V, abdominal pain, seizures, mild agitation, tremors? severe tachycardia with hypotension, tachypnea. Lab: hypokalemia with hyperglycemia?. You expect
Theophylline gives
- Hyperglycemia
- Hypokalemia
- (Hypercalcemia)
- (Hypophosphatemia)
- N/V pain, diarrhea
- Tremors, restlessness, agitation
- Seizures
- Tachycardia
- Hypotension
- Tachypnea
205
Amphetamine overdose sx
- Exitation
- Tachycardia w hypotension and tachypnea is possible
Not really any GI sx
206
Physostigmine prehospital?
No
207
What is metabolized to acetone?
Isopropanol, reason why it cause keto acidosis
208
When is physostigmine used?
Only in the most severe cases of atropine poisoning
209
Physostigmine contraindications
```
TCA
Disopyramide
Quinidine
Procainamine
Cocaine or other making cardiac conduction abnormalities
```
Airway disease, intestinal obstruction, depolarization agents
210
Most toxic mushroom
Cyclopeptides
211
Orellanine
Nephrotoxic mushroom
212
Ibotenic acid and muscimol (A muscaria, A pantherina), also termed isoxazoles
Intoxication and jerking movements
213
Gyromitryn or monomethylhydrazine (Gyromitra mushrooms)
Hemolytic
214
Muscarine (Inocybe and Clitocybe mushrooms)
Cholinergic
215
Coprine (Coprinus atramentarius, inky cap)
Disulfiramlike reaction
216
Psilocybin (Psilocybe and Paneolus mushrooms, magic mushrooms)
Hallucinogenic
217
Allenic norleucine (Amanita smithiana)
Nephrotoxic
218
Amantia time for sx
6-12 hours after ingestion, may not realize the mushroom was the reason
219
Amantia phalloides moa
primarily alpha-amanitin, are responsible for the hepatic, renal, and encephalopathic effects.
interrupts the actin polymerization-depolymerization cycle and impairs cell membrane function.
Give very uncomfortable diarrhea
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Amatoxin
nhibits RNA polymerase II, therefore interfering with DNA and RNA transcription. The toxin mainly affects tissues with high rates of protein synthesis, including the liver, kidneys, brain, pancreas, and testes.
May take days
221
Amanita important indicator for prognosis
PT
222
Amatnina gastric levage
Can be done up to 12 h after (delayed gastric poisoning)
223
Amanita charcoal
GIve multiple dose
Must be given many times because it has hepatic circulation (absorbed in liver, excreted in bile, taken up again, back into liver etc, cycle needs to be stopped)
224
Neurologix sx of atropine
Agitation, confusion, hallusiationas
| Seizures, respiratory depression, coma
225
Bp after atropine
Incosistent high and low
226
Physostigmine dose
2mg repeated within hour
227
Contrainidation to physostigmine
(remeber will give PNS effects)
```
Astma
HT
DM
Gangrene
Obstruction
Reciving depolarizing drugs
```
228
Precations when giving physostigmine
Monitor heart
Have atropine ready in case of hypoxia from bronchoreha and bronchosmams
Uwaga fasiculations and muscle weakness (have patient lying down)
229
When give physostigmine
Only severe problems that can't be fixed in other way
- Seizure, hemodynamic or psychosis
230
Contraindicated drug when atropin intox
phenothiaziedes (antipsychotic that has anticholinergic properties)
231
How long sx free before set atropine p free(home from hospital)
6h
232
What mushrooms give cholinergic toxidrome?
ClitoCYBE
InoCYBE
some AMANTIIA
some BOLetus
233
Mnemonic cholinergic toxidrome
```
SLUDGE
Salivation
Lacromation
Urination
Diarrhea
GI distress
Emesis
```
234
What mushrooms give GABAergic syndrome
Anything containing muscimol
Amanita gemmata
Amanita muscaria (rød fluesopp)
Amanita pantherina (panter-fluesopp)
A kokeri
235
Ibotenic acid in mushrooms cause
Glumaminergic syndrome
236
Typical sx of mushrooms containing both isotonic acid and muscimol
Will result from increase in glutaminergic effects (NMDA, major excitatory) and in GABA effects (inhibitory)
HALLUSINATIONS
- Dysarthria
- Ataxia
- Muscle craps
- Everything from agitation to coma
237
What toxins are found in amanita mascara (rød fluesopp)
Muscarine (causing sludge but not very important)
Ibotenic acid and muscimpol (causing GABA and glumatminergic stimulation, hallusinctaions ++)
Does NOT!! contain cyclopeptide amatoxin with life threatening hapatotox!!!
238
-CYBE have
muscarine
239
Muscarine does not act on
Nicotonic, only M1 and M2, no muscle effect
Not on CNS!!
Act on POSTganglionec sm and glands
240
Muscarine vs Ach
Similar effects but longer half life because cholinesterase can't break it down
241
- euphoria, visual and religious hallucinations and feeling closer to nature have been reported.
- Visual hallucinations may include perceived motion of stationary objects or surfaces.
- psychosis
- sympathomimetic activity such as mydriasis and tachycardia.
Psilocybin-containing mushrooms
Inoles
Similar to LSD, act on serotonin recepotors
Do not treat fever its because of agitation
242
Toxins in A phalloides (grønn fluesopp)
Phalloidin (cyclopeptide toxin) and amatoxin
243
Phalloiding effect
Interrups actin polymerization-depolymerization cycle
244
Amatoxin effect
Inbibit RNA somtehing, high rate of prog sync means more effective
LIver, kidney, brian, pancreas, testes
245
Amantine absorbtion
In bile
246
Lethal dose of alfa amantidin
Under 0.1 mg / kg
247
Phalloidins if found in
Phalloides
verna
virosa
bisporigera
248
Amatinas stages
Stage I:
sudden onset of nausea, vomiting, watery diarrhea, and cramping abdominal pain occurs 6-12 hours after ingestion
Stage II:
clinical improvement occurs with supportive care
despite the resolution of symptoms, hepatic and renal damage is ongoing, which is evident by rising laboratory test values.
Stage III:
if discharged, patients may return to the hospital 2-6 days later with severe coagulopathy, renal failure, and encephalopathy.
249
Amantita sx
Related to hepatic failure and bleeding
Tachy and HoT
250
Amanita tx
Alkanization of unit first hours!
| silymarin/sylinibib
251
Indcuationf for new liver after amanita
Two-fold prolongation in PT, despite fresh-frozen plasma
Persistent hypoglycemia
Serum bilirubin levels of more than 25 mg/dL
Hiperammonemia
Grade III or grade IV hepatic encephalopathy
252
Coprinus atramentarius give what effect
disulfiram-like (the drug used for alcoholics to feel worse when then drink)
253
Disulfiram reaction
Hangover like
```
Flushing or blotching red rash (face, neck, thorax)(ASIAN FLUSH)
Sense of face and hand swelling
Diaphoresis (=sweathing)
Palpitations/chest pain
Dyspnea/hyperventilation
Nausea/vomiting
METALLIC TASTE
Headache
Vertigo/dizziness
Tingling PARESTHEISAS (perhaps due to hyperventilation)
Apprehension/sense of impending doom
Weakness
```
HT or HoT
254
Fomepizole
blocking alcohol dehydrogenase and formation of acetaldehyde.
255
MMH comes from
Gyromitra
256
Important to remember about MMh
It is also volatile
257
MMH neurotox MOA
pyridoxomine, importnatn enzymes, GAD
| -> GABA DEFICIENCY
258
Gyromitra sz
```
GI
Hematopoetic
JAUNDICE (hemolusus)
CYANOSIS (methemoglobinesiA)
HoT
P+ HEMOFEC
HEMOLYSIS
```
259
Tx seizures after gyromitra
Pyridoxine B6 (not benzo!)
260
Toxin in cortinarius species
Orellanine, NEPROTOXIC
proximal tubule!
and almost only there! (FA)
+ GI
261
APAP metabolism
90 percent of acetaminophen is metabolized in the liver to sulfate and glucuronide conjugates via sulfotransferase (SULT) and UDP-glucuronosyl transferases (UGT)
The remaining acetaminophen is metabolized via oxidation by the hepatic cytochrome P450 (CYP2E1, CYP1A2, CYP3A4 subfamilies) mixed function oxidase pathway into a toxic, highly reactive, electrophilic intermediate, N-acetyl-p-benzoquinoneimine (NAPQI)
262
Metabolism og NAQUI (the toxic metabolite of APAP)
By GSH to cysteine conjugates
263
the Rumack–Matthew nomogram,
was developed to estimate the likelihood of hepatic injury due to acetaminophen toxicity for patients with a single ingestion at a known time.
264
EtOH effect of APAP
Less toxicity w acute, more w chronic etOH
265
Factors increasing APAP toxicity
- Dose and acuity
- Age
- Chronic alcohol
- other drugs or herbs
- malnutrishion
266
APAP stage I
Unspecific, maybe maybe AST ALT
267
APAP stage II
After over 24 h, less sx, worse liver
268
APAP stage III
72 h, liver damage and lactic acidosis
269
Mech of lactic acidosis in APAP III
- Mitochondrial damage from NAPQI, and dysfunctional liver bad at clearance
270
BAd prognostic factor in APAP III
Lactate
271
Tx APAP
50 g charcoal first 4 h
N-acetulcysteine
