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Tox > Tox > Flashcards

Tox Flashcards

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

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2
Q

Flumazenil is especially contraindicated in

A

P w increased intracreamical pressure, closed head injury, taking TCA, epilepsy (inc risk of seizures)

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3
Q

AEs of benzos in therapeutic doses

A

Slurred speech
Ataxia
Sedation

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4
Q

Benzo withdrawal sx

A

HT, tachy, tremoulosnes, seizures, low grade fever, delirium

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5
Q

What benzos are not detected in blood tests

A

midazolam, chlordiazepoxide, and flunitrazepam

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6
Q

GHB moa

A

Neuroinhibitory + inc gaba b and dopa

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7
Q

Mild GHB intoxication

A

Slurred speech
Disinhibition
Euphoria
Mild lethargy

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8
Q

Moderate GHB intoxication

A

CNS and mild respiratory depression
Agitation when stimulated
Myoclonus

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9
Q

Severe GHB intoxication

A 
Unresponsive coma
Miosis
Bradycardia
Mild hypotension
Seizures
Respiratory depression and apnea
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10
Q

Short acting iv barbs

A

methohexital, thiopental, hexobarbital, pentobarbital

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11
Q

Short acting oral barbs

A

secobarbital and butabarbital oral

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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

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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
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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.

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15
Q

Observation criteria phenobarbital

A

Over 8 mg/kg

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16
Q

An iminostilbene derivative with a tricyclic structure

A

Carbamazepine

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17
Q

Carbamazepine effect on cyp 450

A

Enhances it

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18
Q

Some medications that decrease elimination of carbamazepine

A

Erythromycin, isoniazid, propoxyphene

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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

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20
Q

Therapeutic level of carbamazepine

A

4-12 mg/L,

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21
Q

Carbamazepine effect on heart

A

May give AV-block due to interference with purkinjae and HIS

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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
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23
Q

What to do when QRS is wider than 100ms in carbamazepine poisoning

A

Administer Sodium Bicarbonate

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24
Q

Valproate effect on cyp450

A

Slows it down

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25
Q

Cimentidine and ranitidine effect of valproic acid

A

Increase function by inhibitiong hepatic metabolism

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26
Q

Drugs that may slow down the gi absorption of valproate

A

Opiates and antihistaminsae

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27
Q

Valproate od sx

A

Unspecific, N/V, CNS, confusion and dec GCS

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28
Q

Important dangerous ae of valproate od that may occur after 72 h

A

Cerebral edema (due to hyperammonemia)

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29
Q

Aliphatic HCs

A

Linear hydrocarbons (alkanes, eses, ines)

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30
Q

Aromatic HC like benzene is used for

A

Solvents such as glue and paint

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31
Q

Most commonly ingested hydrocarbons

A

gasoline, chlorofluorocarbon propellants, motor oils, lighter fluid/naphtha, lamp oil, and mineral spirits

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32
Q

Acute systemic effects of hydrocarbons

A 
Arrythmia 
CNS depression 
Seizures
Hepatic necrosis 
Acute renal tubular necrosis
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33
Q

Pulmonary effects of HCs

A
  • 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
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34
Q

CNS effects of HCs

A
  • Direct
  • Hypoxia
  • Hypercarbia (sniffing from bag)
    Long term:
  • White matter atrophy
  • Peripheral neuropahty
  • Blurred vision
  • Sensory impairment
  • Muscle atrophy
  • Parkinsonism
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35
Q

Hepatotox of HCs

A

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

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36
Q

Problem with methylene chloride

A

Its metabolized by cup 450 to CO

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37
Q

HC effect on heart

A

Makes it more sensible for catecholamines -more risk for tachyarryhtmias and sudden cardiac death

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38
Q

HC effect on GI

A

Vomiting 1/3 and diarrhea

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39
Q

What HC is the worst for kidney

A

Aromatic toluene from chronic occupational -> distal renal tubular acidosis (collecting duct can’t excrete acid) -> anion gap acidosis

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40
Q

Hx of HC

A 
What agent
Route
Amount 
Time 
Any other substances
Vomiting or coughing before hospital 
Attemts of treatment before hospital?
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41
Q

kerosene and other aliphatic hydrocarbons smell like

A

petroleum distillate odor

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42
Q

halogenated hydrocarbons smell

A

halogenated hydrocarbons

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43
Q

Vitals after HC

A

Fever and dec O2

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44
Q

HC effect on CBC

A

Initial leukocytosis

Eventualu aplastic anemia, risk of AML

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45
Q

Blood tests to take for HC

A 
Metabolic
BUN 
Cr
CK (rhabdo?) 
Glu 
Ele 
Hepatic
Anion gap
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46
Q

What may be found in CXR after HC

A

Multiple small patchy densities with ill defined margins indicating aspiration pneumonia

May appear before sx, take XR at once

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47
Q

5 Ws

A

Who, What, When, Where, Why

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48
Q

Coma cocktail

A

O2, glucose, naloxone, dextrose, thiamine

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49
Q

Why observe

A

May have serious effects that are not apparent ant once

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50
Q

Important rule outs

A

ATOMIC
Alcohol
Trauma (CT)
Overdose
Metabolic distrurbance (electrolytes, glycose, thyroid, creatinine)
Infection (pneumonia, aspiration pneumonia sepsis, meningitis)
CO

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51
Q

PE

A

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
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52
Q

When to be cautious about naloxone

A

Opioid addiction, multi-drug poisoning

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53
Q

Naloxone dose adutls

A

2 mg, repeat every 2 minutes until 10 mg

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54
Q

Naloxone infants and children under 5 years

A

0,1 per kg initially

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55
Q

Acetaminophen anti-dote

A

N-acetulcysteine

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56
Q

Beta blockers antidote

A

Glucagon

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57
Q

Ca channel blockers antidote

A

Iv Ca, insuline and glucose

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58
Q

Carbamates antidote

A

Atropine, pralidoxime

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59
Q

What is the effect of ipecac

A

It can induce emesis

MOA: Irritation of stomach and chemotrigger zone in brain

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60
Q

When not to induce emesis

A 
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
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61
Q

When to perform gastric leakage from HCs

A

Benzene, toluene, camphor, halogenated hydrocarbons, pesticides, heavy metals if more than 5ml/kg, eg 500 ml in 100 kg man

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62
Q

Charcoal indication

A

In general poor evidence but

  • Multiple sunstances
  • life threatening amount
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63
Q

Drugs that may benefit from multi dose charcoal

A

Phenobarbital
Carbamazepine
Aspirin
Theophylline

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64
Q

Charcoal is not effective for

A 
cyanide
mineral acids
caustic 
organic solvents, hydrocarbons
metals (iron, lithium, mercury, lead) 
ethanol, methanol, ethylen glicol, isopropranol
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65
Q

Poisins that mainly cause death by airways

A

Carbamate, pesticides, hydrocarbons, solvents, petrol

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66
Q

Contraindication for alkaline diuresis

A

Renal failure

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67
Q

Is acidification of urine done?

A

No, the risk of rhabdo makes it not worth it

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68
Q

LIpid rescue is used for

A

Good for lipophilic substances

  • TCA
  • CCBs
  • BBs
  • Cocaine
  • Anti-convulsants
  • Anti-depressants
  • Organic solvents
  • Bio-weaponds
  • Bupivacaine
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69
Q

Toxins that may require hemodialysis

A 
Ethylene glycol
Lithium
Methanol
Salicylates
Theophylline
VPA
Phenobarbital
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70
Q

Whats in common?

Ethylene glycol
Lithium
Methanol
Salicylates
Theophylline
VPA
Phenobarbital
A

May require hemodialysis

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71
Q

Major groups of new psychoactive substances

A

Depressant
Stimulant
Hallucinogenic

Synhtethic cannabinoids

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72
Q

Other name of ephedrone

A

Scientific: Methcathinone
(made from oxidation of ephedrine)

MCat

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73
Q

Methcathinone effect

A 
Similar to amphetamine 
Psychoactive stimulant 
Dopamine rey-take inhibitor 
Confusion to psychosis 
Euphoria 
Lack of appetite 
Forgetting to drink 
Locomotor activity 
Hypertension
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74
Q

Methyldioxyprovalerone (MDPV) MOA

A

NDRI (norepie and dopa reuptake inhibitor)

Similar to ritalin but 4 times more potent

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75
Q

Short term effects of MDPV

A

Basically SNS activation

Alterness and awareness

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76
Q

High doses of MDPV cause

A

Psychosis and panic
Lack of sleep
Addiction
Sexual desire

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77
Q

Long term effects of MDPV

A

Comedown syndrome

Postural hypotension, depression, lethargy

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78
Q

“Spice” moa

A

Cannabonoid agonist

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79
Q

Treatment in spice

A

Usually monitoring and hydration is enough, maybe benzos

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80
Q

What can be given to counteract on psychotic effects on the heart, to reduce risk of arrhythmia

A

Benzos

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81
Q

Pestisides include

A

Active biological substance and something to carry it, often a HC

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82
Q

Major deadly pesticides

A

Organophosphorius (endosulphan)
Aluminium phosphide
Paraquat

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83
Q

Some examples of organophosphates

A

Chlorpyrifos, parathion, dimethoate, fenthoin

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84
Q

Sx of organophosphate poisoning

A

1 Acute cholinergic crisis
2 Intermediate syndrome
3 Delayed polyneuropathy

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85
Q

Organophosphates MOA

A

Inhibit AChH, (by binding in a way thats hard to reverse)

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86
Q

Dimethyl vs diethyl

A

Dimethyl is fast, diethyl is fast (Bort act on reactivation of ACHE

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87
Q

Organophosphates cause __ syndrome

A

Muscarinic syndrome (and also nicotinic)

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88
Q

Sx nicotinic syndrome

A

Fasciculations, muscle cramps, fatigue, paralysis, tachycardia, HT

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89
Q

ECG changes after organophosphates

A

Small vintage (peak to peak QRS under 5 in limb or 10 in precordial)

ST-T changes

Prolonged QT

VES ++

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90
Q

Possible reasons for intermediate syndrome of organophosphate poisoning

A

 toxin-induced myonecrosis
 combined pre- and postsynaptic impairment of
neuromuscular transmission
 downregulation or desensitization of postsynaptic ACh receptors after prolonged ACh stimulation

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91
Q

What is intermediate syndrome of organophosphate poisoning

A

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

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92
Q

Ginger paralysis syndrome

A

= delayed effects of organophosphate poisoning

  • neuropathy
  • waekness
  • Peronality changes
  • Pancreatitis
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93
Q

When use atropine in OP poisoning

A

HR under 80, HoT under 80 systolic ++

high HR not contraindication

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94
Q

Pralidoxime and obidoxime are

A

ACHE reactivates

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95
Q

Advantage of glycopyrrolate for reversal of OP poising

A

No CNS effect

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96
Q

aldicarb, benomyl, carbaryl, carbendazim, carbofuran, propuxur, triallate are

A

carbamates

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97
Q

Carbamates differences from OPs

A

Also affect pseudocholinesterase BChE

Reversible

Less CNS effect

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98
Q

What are OCs

A

Organochloride pesticides

Chloridated cyclic hydrocarbons

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99
Q

DDT, BHC (benzene) and lindane are

A

OCs

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100
Q

Lindane effect on heart

A

Histologic alteration of LV wall

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101
Q

OC moa

A
  • Depolarize nerves
  • Dicoordinate GABA
  • Predispose to arrythmias
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102
Q

OC sx

A

Many, CNS and seizures are most important

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103
Q

Cholestyramine may be useful in

A

Biliary-fecal excretion of OC

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104
Q

Pyrethins and pyrethroids use

A

Mosquito and scabies

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105
Q

Pyrethins and pyrethroids moa

A

Na channels

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106
Q

Pyrethins and pyrethroids sx and tx

A

Not supersevere, usually supportive

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107
Q

Paraquat is __ and may be mistaken for __

A

Bypyridyl herbicide

Cola

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108
Q

Bipryidyl herbicides MOA

A

Free radicals destroy cell membrane, worst for liver, kidney and lung

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109
Q

Paraquat typical sx

A

Hemorragic pumonary edama, ARDS, fibrosis

110
Q

Diquat typical

A

To cns, like like parkinson or brain stem infarction

111
Q

Paraquat oral ingestion sx

A

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
Q

Dx of paraquat and diquat

A

Add salt and look for color in urine

113
Q

Tx in bipyridayl herbicides

A

All the normal stuff and immunosupression

Careful with O2 (free radicals)

114
Q

2,4-D (2,4-dichlorophenoxyacetic acid), dichloroprop, mecoprop, are

A

Chlorophenoxyacetic herbicides

115
Q

Chlorophenoxyacetic herbicides moa

A

Damage cell membranes and ruins oxidative phosphorylation by disrupting of acetylcoenzyme A

116
Q

Sx of Chlorophenoxyacetic herbicides

A
  • Intravascular volume loss -> hypovolemia
  • Hypertonia and reflex
  • CNS depression and respiratory depression
117
Q

Alkaline diuresis effect on herbicide?

A

Yes

118
Q

Dinitrophenols mechanism

A

Shuttling of protons

119
Q

Dinitrophenols sx

A

 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
Q

Yellow skin, stool and urine is seen in

A

Dinitrophenols

121
Q

Glyphosate moa

A

Not sure, combination with other active ingredients

122
Q

Glyphosphate sx

A

GI burns,
hyperthermia
Metabolic acidosis ++

123
Q

Tx Glyphosphate

A

All the normal
ENdoscopy to look for burns
Correct acidosis and hydrate well

124
Q

Symptoms of metallobisdithiocarbamates poisoning:

A

irritation and alcohol dehydrogenase inhibition

125
Q

Antidote for ethanol glycol and methanol

A

Fomepizol (and ethanol)

126
Q

Heavy metal antidote

A

Chealating drugs

127
Q

Iron antidote

A

Deferoxiamine

128
Q

Isoniazid antidote

A

Pyridoxime

129
Q

TCA antidote

A

NaHCO3, alkanization to open fast sodium channels, dec cardiac effects

130
Q

Cyanide antidote

A

Hydroxycobalamin

131
Q

Methyl mercury in concentrated in

A

NS, and RBCs

132
Q

Organomercurials legal?

A

Banned in many countries because of toxicity

133
Q

Organomercurials sx

A

Acrodynia

Slurred speech, hearing, vision, balance etc

134
Q

Essential part of organomercurail management

A

Chealation (DMSA etc)

135
Q

Dialysis in organomercurials

A

May be necessary in addition to chelation, even low doses are life threatening

136
Q

-tyltin are

A

Organotins

137
Q

Organothins moa

A

Seveal mitochonrihal enzymes, problems w oxidative phosphorylation

138
Q

Organothins sx

A

Hepatomegaly and liver ennymes

Hyperexitability, LOC and other CNS

139
Q

Thallum fast

A

No, CNS effects can take a week;
Lethargy, paresthesia, ataxia ++

Alopecia takes 2 w

140
Q

Thallum on gi

A

Bloody diarrhea, salivation

141
Q

Aphemtaimine and cocain time to reach urine

A

3 days indicate decreasing dose elimination phase, not increasing (roughly)

142
Q

Chronic weed user will have evidence in urine

A

1 months after

143
Q

What can be given to increase fecal excretion of thallum

A

 potassium ferric ferrocyanide (Prussian blue)

144
Q

Warfarins moa

A

Inhibit 2,7,9,10

Direct capillary damage

145
Q

CT

A

Take in cocaine, brain hemorrhage

146
Q

Antidote for warfarin

A

Vit K1, not K3 and K4

147
Q

Superwarfarins onset and duration

A

48 h - several months

148
Q

Contraindication for gastric levage

A

No agreement from patient, even if uncoucious and life life threatening

149
Q

Aluminium phosphide MOA

A

Taken up in mucos membrane, PH3 gas made -> Inhibits cyt c -> ROS -> cell damage

150
Q

Metabolism of AP

A

In liver to phosphine which is also toxic

151
Q

Gastric leakage size

A

36 french, very large, not normal size, 45 com long

152
Q

Contraindication of gastric leavage

A

Uncorporative
Non-toxic dose (few pills)
Hydrocarbons only if intubates!

153
Q

AP severe dose sx

A

ARDS, cardiac arrhythmias, liver and

renal failure, convulsions, coma and death

154
Q

AP sx

A

 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
Q

AP tx

A

gastric lavage with potassium permanganate (

156
Q

Zink phosphide smell

A

Rotten fish

157
Q

CCBs bradycardia

A

Atropine

158
Q

 Clinical features of zinc phosphide poisoning:

A

 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
Q

Barium conpouncds MOA

A

Interfere w sodium-potassium pump -> changes in cell membrane permeability -> paralysis of muscle s

160
Q

Barium conpouncds sx

A

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
Q

What not to give in barium compounds

A

Mg sulphate

162
Q

Mulluscicides kill

A

Snails

163
Q

Low Vd and low protein binding its good for

A

Hemodyalysis

164
Q

Quetiapine goode for hemodialysis?

A

No, high protein binding and liver rather than kidney elimination

165
Q

Hemodialysis pro

A

Very small particles compared to the other

166
Q

Hemoperfusion moa

A

Use charcoal or cuisine, should be larger particles, but can take larger amount then hemodialus
Can take larger size like plasma proteins

167
Q

Hemofiltration

A

Particle size in between hemodialysis and hemoperfusion, can not take plasma proteins and things bound to them

168
Q

Hemodialysis mechanism

A

Diffusjon

Hemofilter w semipermeable membrane, dialysite

169
Q

Inducation for hemodialysis

A

Absolute:
Must have taken drug and drug must fit for hemorrhages (small partible low vd low protein binding)
Clinically necessary

170
Q

Hemodialysis used for

A 
Alchohols 
Lithium 
Salisylates 
Theophylline 
Valproate
171
Q

Benefits of hemodialysis

A

Correct acidosis and other metabolic problems

Can treat kidney failure with hypervolemia

172
Q

Methaldehyde moa

A

 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
Q

Metaldehyde sx

A

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
Q

Methaldehyde tx

A
  • Gastic leavage and charcoal
  • Supportive
  • N-acetylcystein may help liver and kidney
175
Q

Albumin dialysis

A

Idea is to eliminate protein bound, very expensive, main indication is liver failure, eg APAP toxicity, alcoholic liver,

176
Q

DEET is

A

Diethyltoluamide

177
Q

DEET acute poisoning

A

 hypotension, respiratory depression

CNS toxicity:
 behavioural disorders, restlessness, irritability
 headache, ataxia
 rapid loss of consciousness, seizures
 sometimes flaccid paralysis and areflexia

178
Q

Symptoms of cutaneous exposure to EDB (ethylene dibromide)

A

 ulcerations
 conjunctivitis
 gastrointestinal and mucosal irritation
 CNS irritation and depression

179
Q

Symptoms of oral ingestion of EDB:

A

 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
Q

tropane alkaloids

A

atropine, scopolamine, and hyoscyamine

181
Q

Plants that contain alkaloids

A

Datura species (jimson weed, angel’s trumpet, thorn apple)

Hyoscyamus niger (henbane)

Atropa belladonna (deadly nightshade)

Mandragora officinarum (mandrake)

182
Q

Benzos safe

A

Not really when alone, but synergic w alcohol and not good in combinations

183
Q

Datura use

A

Resuse pain, dilate bronchioles

184
Q

Tropane alkaloids moa

A

Anticholinergic

185
Q

Important to remember about tropane alkaloids

A

Gastric emptying is slowed and dose in blood may continiue to increase for up to 48 days

186
Q

Remember about flumazenil

A

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
Q

Benzos elimination

A

Nothing can be done to enhance it

188
Q

Barbituates vs benzos (or thiopental?)

A

Barbituates cause deeper coma, more respiratory depression and more cardiotox

189
Q

Carbamazepine is structurally similar to

A

TCAs

190
Q

Kinetics of carbamazepine

A

Large Vd
Unpredictable absorption
Needs to be monitored

191
Q

Pathyphyys of carbamazepine

A

Opening of sodium channels

192
Q

Carbamazepine metabolite

A

Metabolized by CYP450
Very active metabolite
Cause autoincudtion after long use, need to increase the doses eventually

193
Q

Clinical course of carbamazepine

A

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
Q

Ddx of carbamazepine

A

Other cholinergic
Antihistaminic
TCA
Alcohol withdrawal

195
Q

Electrolytes in carbamazepine

A

Hyponatremia (connected w effect on ADH)

196
Q

Charchoal in carbamazepine

A

Yes, but exclutde ileus first!!

197
Q

What to do if widening of QRS in carbamazepine

A

Give saline

198
Q

Less toxic HC

A

Solid

199
Q

Aspiration hazard HCs

A

Turprentine, gasoiline, keraosene, minral seed oil

200
Q

Tropane alkaloids sx

A 
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
Q

Tropane alkaloids mnemonic

A

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
Q

Can atropine etc be tested in blood?

A

No, but in urine

203
Q

Lab tests for ethanol

A

ABG

AG & OG

204
Q

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

A

Theophylline gives

  • Hyperglycemia
  • Hypokalemia
  • (Hypercalcemia)
  • (Hypophosphatemia)
  • N/V pain, diarrhea
  • Tremors, restlessness, agitation
  • Seizures
  • Tachycardia
  • Hypotension
  • Tachypnea
205
Q

Amphetamine overdose sx

A
  • Exitation
  • Tachycardia w hypotension and tachypnea is possible

Not really any GI sx

206
Q

Physostigmine prehospital?

A

No

207
Q

What is metabolized to acetone?

A

Isopropanol, reason why it cause keto acidosis

208
Q

When is physostigmine used?

A

Only in the most severe cases of atropine poisoning

209
Q

Physostigmine contraindications

A 
TCA
Disopyramide 
Quinidine 
Procainamine
Cocaine or other making cardiac conduction abnormalities

Airway disease, intestinal obstruction, depolarization agents

210
Q

Most toxic mushroom

A

Cyclopeptides

211
Q

Orellanine

A

Nephrotoxic mushroom

212
Q

Ibotenic acid and muscimol (A muscaria, A pantherina), also termed isoxazoles

A

Intoxication and jerking movements

213
Q

Gyromitryn or monomethylhydrazine (Gyromitra mushrooms)

A

Hemolytic

214
Q

Muscarine (Inocybe and Clitocybe mushrooms)

A

Cholinergic

215
Q

Coprine (Coprinus atramentarius, inky cap)

A

Disulfiramlike reaction

216
Q

Psilocybin (Psilocybe and Paneolus mushrooms, magic mushrooms)

A

Hallucinogenic

217
Q

Allenic norleucine (Amanita smithiana)

A

Nephrotoxic

218
Q

Amantia time for sx

A

6-12 hours after ingestion, may not realize the mushroom was the reason

219
Q

Amantia phalloides moa

A

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

220
Q

Amatoxin

A

nhibitsRNA 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
Q

Amanita important indicator for prognosis

A

PT

222
Q

Amatnina gastric levage

A

Can be done up to 12 h after (delayed gastric poisoning)

223
Q

Amanita charcoal

A

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
Q

Neurologix sx of atropine

A

Agitation, confusion, hallusiationas

Seizures, respiratory depression, coma

225
Q

Bp after atropine

A

Incosistent high and low

226
Q

Physostigmine dose

A

2mg repeated within hour

227
Q

Contrainidation to physostigmine

A

(remeber will give PNS effects)

Astma
HT
DM 
Gangrene
Obstruction
Reciving depolarizing drugs
228
Q

Precations when giving physostigmine

A

Monitor heart

Have atropine ready in case of hypoxia from bronchoreha and bronchosmams

Uwaga fasiculations and muscle weakness (have patient lying down)

229
Q

When give physostigmine

A

Only severe problems that can’t be fixed in other way

  • Seizure, hemodynamic or psychosis
230
Q

Contraindicated drug when atropin intox

A

phenothiaziedes (antipsychotic that has anticholinergic properties)

231
Q

How long sx free before set atropine p free(home from hospital)

A

6h

232
Q

What mushrooms give cholinergic toxidrome?

A

ClitoCYBE
InoCYBE
some AMANTIIA
some BOLetus

233
Q

Mnemonic cholinergic toxidrome

A 
SLUDGE 
Salivation
Lacromation
Urination
Diarrhea
GI distress
Emesis
234
Q

What mushrooms give GABAergic syndrome

A

Anything containing muscimol

Amanita gemmata

Amanita muscaria (rød fluesopp)

Amanita pantherina (panter-fluesopp)

A kokeri

235
Q

Ibotenic acid in mushrooms cause

A

Glumaminergic syndrome

236
Q

Typical sx of mushrooms containing both isotonic acid and muscimol

A

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
Q

What toxins are found in amanita mascara (rød fluesopp)

A

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
Q

-CYBE have

A

muscarine

239
Q

Muscarine does not act on

A

Nicotonic, only M1 and M2, no muscle effect

Not on CNS!!

Act on POSTganglionec sm and glands

240
Q

Muscarine vs Ach

A

Similar effects but longer half life because cholinesterase can’t break it down

241
Q
  • 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.
A

Psilocybin-containing mushrooms

Inoles

Similar to LSD, act on serotonin recepotors

Do not treat fever its because of agitation

242
Q

Toxins in A phalloides (grønn fluesopp)

A

Phalloidin (cyclopeptide toxin) and amatoxin

243
Q

Phalloiding effect

A

Interrups actin polymerization-depolymerization cycle

244
Q

Amatoxin effect

A

Inbibit RNA somtehing, high rate of prog sync means more effective

LIver, kidney, brian, pancreas, testes

245
Q

Amantine absorbtion

A

In bile

246
Q

Lethal dose of alfa amantidin

A

Under 0.1 mg / kg

247
Q

Phalloidins if found in

A

Phalloides
verna
virosa
bisporigera

248
Q

Amatinas stages

A

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
Q

Amantita sx

A

Related to hepatic failure and bleeding

Tachy and HoT

250
Q

Amanita tx

A

Alkanization of unit first hours!

silymarin/sylinibib

251
Q

Indcuationf for new liver after amanita

A

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
Q

Coprinus atramentarius give what effect

A

disulfiram-like (the drug used for alcoholics to feel worse when then drink)

253
Q

Disulfiram reaction

A

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
Q

Fomepizole

A

blocking alcohol dehydrogenase and formation of acetaldehyde.

255
Q

MMH comes from

A

Gyromitra

256
Q

Important to remember about MMh

A

It is also volatile

257
Q

MMH neurotox MOA

A

pyridoxomine, importnatn enzymes, GAD

-> GABA DEFICIENCY

258
Q

Gyromitra sz

A 
GI 
Hematopoetic
JAUNDICE (hemolusus) 
CYANOSIS (methemoglobinesiA) 
HoT
P+ HEMOFEC
HEMOLYSIS
259
Q

Tx seizures after gyromitra

A

Pyridoxine B6 (not benzo!)

260
Q

Toxin in cortinarius species

A

Orellanine, NEPROTOXIC

proximal tubule!
and almost only there! (FA)

+ GI

261
Q

APAP metabolism

A

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
Q

Metabolism og NAQUI (the toxic metabolite of APAP)

A

By GSH to cysteine conjugates

263
Q

the Rumack–Matthew nomogram,

A

was developed to estimate the likelihood of hepatic injury due to acetaminophen toxicity for patients with a single ingestion at a known time.

264
Q

EtOH effect of APAP

A

Less toxicity w acute, more w chronic etOH

265
Q

Factors increasing APAP toxicity

A
  • Dose and acuity
  • Age
  • Chronic alcohol
  • other drugs or herbs
  • malnutrishion
266
Q

APAP stage I

A

Unspecific, maybe maybe AST ALT

267
Q

APAP stage II

A

After over 24 h, less sx, worse liver

268
Q

APAP stage III

A

72 h, liver damage and lactic acidosis

269
Q

Mech of lactic acidosis in APAP III

A
  • Mitochondrial damage from NAPQI, and dysfunctional liver bad at clearance
270
Q

BAd prognostic factor in APAP III

A

Lactate

271
Q

Tx APAP

A

50 g charcoal first 4 h

N-acetulcysteine

Tox (1 decks)

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