CHAPTER 450 POISONING AND DRUG OVERSE Flashcards

(178 cards)

1
Q

it refers to the development of dose-related adverse effects following exposure to chemicals, drugs, and other xenobiotics

A

poisoning

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2
Q

age prone to poisioning

A

<6 years old

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3
Q

major reason for increased number of poisoning deaths

A

opoids

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4
Q

unintentional exposures include

A
improper use of chemicals at work or play
label misleading
product mislabel
mistaken identification
unlabeled chemicals
uninformed self medication
dosing errors
elderly
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5
Q

most common reported reason for intentional poisoning

A

recreational use of ethanol

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6
Q

pharmaceutical agent most often implicated in fatal poisoning

A

acetaminophen

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7
Q

leading cause of death from poisoning

A

carbon monoxide

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8
Q

correct diagnosis established by

A

history, physical examination, routine and toxicologic laboratory evaluations and clinical course

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9
Q

history includes:

A
time
route
duration 
circumstances 
the name and dose
chemical involved
the time of onset
nature and severity of symptoms
time and type of first aid used
medical and psychiatry history
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10
Q

if the px is confused or comatose suspect?

A

history of psychiatry problems
recent changes of economic and relationship status
work with chemicals

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11
Q

what is body packing or body stuffing

A

ingesting or concealing drugs in the body cavity

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12
Q

relevant information may be available from

A
family 
friends
paramedics
police
pharmacist
physicians 
employers
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13
Q

it focuses the vital signs, and the systems

A

physical examination

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14
Q

neurologic status includes the:

A

documentation of the neuromuscular abnormalities such as dyskinesia, dystonia, fasciculations, myoclonus, rigidity and tremors

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15
Q

examine the eye for:

A

nystagmus and pupil size and reactviity

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16
Q

examine the abdomen for:

A

bowel activity and bladder size

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17
Q

examine the skin for:

A
burns
bullae
color
warmth
moisture
pressure sores
puncture marks
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18
Q

what to do when history is unclear?

A

examine all the orifices for the presence of chemical burns, and drug packets

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19
Q

it also provide important diagnostic clues

A

odor of breath
vomitus
color of the nails and skin and urine

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20
Q

how to diagnose a poisoning in cases of unknown etiology

A

relies on pattern recognition

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21
Q

how to detect pattern recognition to diagnose poisoning in unknown etiology

A

first: assess the pulse, blood pressure and respiratory rate and temperature and neurologic status and characterized the overall physiologic state as stimulated, depressed, discordant or normal
second: identify the pathophysiologic patterns or toxic syndrome (toxidrome)
third: identify the particular agent involved by looking at the unique poison specific physical or ancillary test abnormalities

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22
Q

most reliable prognosticator of poor outcome in poisoning from stimulants

A

temperature elevation

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23
Q

what are the 4 physiologic state

A

stimulated
depressed
discordant
normal

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24
Q

stimulated physiologic state is characterized by

A

increased pulse, bp rr, temp and neuromuscular activity

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25
stimulated physiologic state reflects the
symphathetic, anticholinergic or hallucinogen poisoning or drug withdrawal
26
feature of all stimulants and is most marked in anticholinergic poisoning since the pupillary reactivity relies on muscarinic control
mydriasis
27
anticholinergic syndrome is characterized by:
hot dry flushed skin decreased bowel sounds urinary retention other: diaphoresis, pallor and increased bowel activity with nausea, diarrhea
28
findings that suggest sympathetic poisoning
increased vital signs and organ ischemia
29
selective alpha adrenergic stimulants such as decongestants can cause
reflex bradycardia
30
selective beta-adrenergic stimulants such as asthma therapeutics can cause
hypotension
31
ergot alkaloids can cause
limb ischemia
32
phencylidine and ketamide can cause
rotatory nystagmus
33
cocaine can cause
delayed cardiac contraction
34
what do seizures suggest
sympathetic etiology
35
state characterized by mixed vital signs and neuromuscular abnormalities
discordant physiologic state
36
cause of depressed physiological state
functional sympatholytics (agents that decrease cardiac function and vascular tone) cholinergic such as muscarinic and nicotinic agents opiods sedatives
37
feature that is most pronounced in opiods and cholinergic poisoning
miosis
38
other clues that may suggest physiologic depressed state
``` cardiac arrhythmias conduction disturbances mydriasis nystagmus seizures ```
39
what can cause arythmias and conduction disturbances
``` antiarrhythmias calcium channel blocker digitalis glycosides propoxyphene cyclic antidepressants ```
40
what can cause mydriasis
tricyclic antidepressants and some antiarrhymics, meperidine and diphenocylate atropine such as lomotil
41
what can cause nystagmus
sedative hypotics
42
what can cause seizures
cholinergic agents propoxyophene cyclic depressants
43
physiologic state characterized by decreased pulse, bp, rr, and temp and neuromuscular activity
depressed physiologic state
44
cause of normal physiologic state
non-toxic exposure psychogenic illness poisoning of toxic time bombs that are slowly absorbed and slowly distributed and require metabolic activation
45
laboratory result most common in advanced methanol, ethylene glycol and salicyate intoxication
increased anion gap metabolic acidosis
46
what happens when there is increased blood levels of bromide, calcium, iodide, lithium or magnesium
abnormally low anion gap
47
a difference of >10 mmol per liter between serum osmality suggests the presence of low molecular weight solute such as acetone, alcohol , glycol, and ether, or sugar
a difference of >10
48
ketosis suggest of
acetone, iso alcohol, salicylate poisoning or alcoholic ketoacidosis
49
hypokalcemia suggest of
beta-adrenergic blocker, caffeine, diuretics, theophylline, toleune
50
hyperkalcemia suggest of
poisoning of alpha adrenergic agonist beta adrenergic blocker cardiac glycosides fluoride
51
hypocalcemia suggest of
ethylene glycol fluoride oxalate poisoning
52
result of ECG in px poisoned with alpha adrenergic agonist, beta blockers, calcium channel blockers and cholinergic agents
bradycardia and atrioventricular block
52
QRS and QT interval prolongation is caused by
hyperkalemia antidepressants membrane active drugs
53
ventricular tacycardia suggests
poisoning with cardiac glycosides fluorides membrane active drugs
54
radiologic result in px with posoining of carbon monoxide, cyanide and opiods
pulmonary edema
55
aspiration pneumonia is common in px with
coma seizures petroleum distillate aspiration
56
what can be used to rule out and confirm suspected poisoning
toxicologic analysis
56
what can be used to rule out and confirm suspected poisoning
toxicologic analysis
57
screening test that should not be used because it cannot confirm the exact identity of the detected substance
rapid qualitative hospital-based urine test
58
useful for diagnostic purposes
response to antidotes
59
resolution of altered mental status and abnormal vital signs within minutes of IV administration of dextrose, naloxone, or flumazenil is diagnostic of
hypoglycemia opoid poisoning benzodiazepine intoxication
60
grade of physiologic stimulation that is anxious, irritable but the vital signs are normal with diaphoresis with flushing and pallor, mydriasis and hyperflexia sometimes present
grade 1 physiologic stimulation
61
grade of physiologic stimulation that is agitated may have confusion or hallucinations but can converse and follow commands but the vital signs are mild to moderately increased
grade 2 physiologic stimulation
62
Grade of physiologic stimulation that is delirious, unintelligible speech, uncontrollable motor hyper-activity moderately increased vital signs and tachyarrhythmias are possible
grade 3 f physiologic stimulation
63
grade of physiologic stimulation that is in coma, seizures and in cardiovascular collapse
grade 4 physiological stage stimulation
64
grade of depressed if the px is awake, lethargic or sleeping but arousable by voice or tactile stimulation and able to converse and follow commands but may be confused
Grade 1 physiologic depression
65
grade of physiologic depression if the px responds to pain but not to voice can vocalize but not converse with the spontaneous motor activity present with brainstem reflexes intact
grade 2 physiologic depression
66
grade of physiologic depression that is unresponsive to pain, spontaneous motor activity absent with brainstem reflexes depressed, motor tone, respirations and temperature decreased
grade 3 physiologic depression
67
grade of physiologic depression that is unresponsive to pain, flaccid paralysis, brainstem reflexes and respirations absent with cardiovascular vital signs decreased
grade 4 physiologic depression
68
what are the treatment goals for poisoning and drug overdose
``` support of vital signs prevention of further poisoning absorption enhancement of poison elimination administration of specific antidotes prevention of re-exposure ```
69
what is the highest priority in the pre-toxic phase?
decontamination and treatment are solely based on history and pe
70
when history is not obtainable and poison is causing delayed toxicity what is the appropriate best thing to do?
blood and urine samples were sent for toxicologic screening and quantitative analysis
71
what is toxic phase
interval between the onset of poisoning and its peak effect
72
management during toxic phase
based on laboratory and clinical findings
73
when does the effect of overdose manifested
begin sooner and peak later and last longer than they do after a therapeutic dose
74
what is the first priority
resuscitation and stabilization
75
what to give in px with altered mental status that has come and seizures
intravenous glucose naloxone thiamine
76
measures that enhance the decontamination of salicylates
urinary alkanization
77
enhance decontamination in metals
chelation therapy
78
what is the goal of supportive therapy
maintain the physiologic homeostasis until detoxification is accomplished and to prevent and treat secondary complications
79
indications for admission in intensive care unit
patients with severe poisoning (coma, respiratory depressionm hypotension, cardiac conduction abnormalities, cardiac arrythmias those needing close monitoring
80
respiratory care to prevent aspiration of gastrointestinal contents especially in those with CNS depressions and seizures
endotracheal intubation
81
respiratory care for px with respiratory depression or hypoxemia and for facilitation of therapeutic sedationn or paralysis of patients in order to prevent or treat hyperthermia, acidosis and rhabdomyolysis associated with neuromuscular hyperactivity
mechanical ventilation
82
oxygenation and ventilation is best determined by
pulse oximetry and arterial blood gas analysis
83
not a reliable indicator for the need of intubation
gag reflex
84
if the px hypotension is unresponsive to volume expansion and appropriate next step is?
treatment with norepinephrine and epinephrine and high dose dopamine
85
what should be considered in px with severe but reversible cardiac failure
intraaortic balloon pump counterpulsation | venoarterial or cardiopulmonary perfusion techniques
86
treatment for sympathetic hyperactiviity
benzodiazepine
87
treatment for anticholinergic posoining
physostigmine
88
treatment for ventricular arrhythmia
sodium bicarbinate lidocaine phenytoin
89
treatment in px with torsades de pointed and prolonged QT intervals
magnesium sulfate and overdrive pacing
90
treatment for severe cardiac glycoside poisoning
magnesium and anti digoxin antibodies
91
seizures caused by excessive stimulation of catecholamine receptors is treated with
agents that enhance GABA activity such as benzodiazepine and barbiturates
92
seizures caused by isoniazid are treated with
pyridoxine
93
what is contraindicated in toxicologic seizures
phenytoin
94
serotonergic receptor overstimulation is serotonin syndrome is treated with?
cyproheotadine
95
the average time from ingestion to presentation of adults
>3 hours
96
the average time of ingestion to presentation of children
>1 hour
97
preferred method of gastrointestinal decontamination that has fewer contraindications and complications
activated charcoal
98
mechanism of action of charcoal
the charcoal adsorbs ingested poisons within the gut lumen allowing the charcoal toxin complex to be evacuated in stool
99
what compounds that are not well absorb in charcoal
charged ionized chemicals such as mineral, acid, alkalis, and highly dissociated salts of cyanide, fluoride, iron, lithium and other inorganic compounds
100
side effects of charcoal
nausea, vomiting, and diarrhea or constipation and prevents the absorption off orally administered therapeutic agents
101
complications of charcoal
mechanical obstruction of airway, aspiration, vomiting, and bowel obstruction and infarction caused by inspissated charcoal
102
when is charcoal not recommended
ingested corrosives because it will obscure endoscopy
103
what method is preferred for life-threatening poisons that cannot be treated with other method
gastric lavage
104
how is gastric lavage performed?
performed by sequentially administering and aspirating 5 ml of fluid per kilogram of body weight through a no.40 French orogastric tube (no. 28 for children)
105
preferred solute used in gastric lavage in infants
normal saline and tap water
106
the positon of px when doing gastric lavage to prevent aspiration
trendelenburg and left lateral decubitus
107
lavage absoprtion within 5 mins, 30 mins and 60 mins of ingestion
decreases as time lengthens
108
common complication of gastric lavage
aspiration
109
serious complication of gastric lavage
esophageal and gastric perforation and tube misplacement
110
contraindicated in gastric lavage
corrosive petroleum distillate ingestions because the risk of gastroesophageal perforation and aspiration pneumonitis compromised airway risk of hemorrhage or perforation due to esophageal or gastric pathology recent surgery px who refuse
111
emetogenic agent that is once used in decontamination but no longer used in decontamination
syrup of ipecac
112
chronic use of ipecac complications
electrolyte and fluid abnormalities, cardiac toxicity, and myopathy
113
another method for gastric decontamination that is performed by administering bowel cleansing solution that contains electrolytes and polyethylene glycol
whole bowel irrigation
114
whole bowel irrigation is appropriate in px with
ingested foreign bodies packets of ilicit drugs and heavy metals
115
salts given together with charcoals to promote the rectal evacuation of gastrointestinal contents
cathartics
116
side effects of cathartics
abdominal pain nausea occasional vomitting
117
complications of repeated doses of cathartics
severe electrolytes disturbances and excessive diarrhea
118
contraindications of cathartics
ingested corrosives and with preexisting diarrhea
119
when is dilution recommended
only after the ingestion of corrosives
120
technique used in rare situations such as ingestions of potentially toxic foreign bodies
endoscopic or surgical removal
121
initial treatment for for topical exposures
immediate copious flushing with water and saline
122
preferred for eye irrigation
saline
123
treatment for inhlational exposures
supplemental oxygen or fresh air
123
treatment for inhlational exposures
supplemental oxygen or fresh air
124
treatment for dermal decontamination
triple wash
125
removal of liquids in cavities such as vagina and rectum
irrigation
126
when is multiple-dose of charcoal therapy considered
ingestion of theophyline, phenobarbital, carbamazepine, dapsone and quinine
127
complications of multiple-dose charcoal therapy
intestinal obstructions, pseudo-obstruction and nonoccluisive intestinal infarction in px with decreased gastric motility
128
how urinary alkalinization works
ion trapping via alteration of urine ph may prevent the renal absorption of poisons that undergo excretion by glomerular filtration and active tubular secretion
129
what ions are trapped in the membrane
acidic are ionized and trapped in alkaline urine whereas basic become ionized and trapped in acid urine
130
urine alkalinization urine ph
ph >7.5 and urine output of 3-6 ml of body weight per hour by the addition of sodium bicarbonate to an IV solution
131
contraindication of urinary alkalinization
congestive heart failure, renal failure and cerebral edema
132
agents most amenable to enhance elimination bu dialysis
``` low molecular mass <500 high water solubility low protein binding small volumes of distirbutio (<1l) prolonged elimination (long half life) high dialysis clearance relative to total body clearance ```
133
when is dialysis considered
severe poisoning due to carbamazepine, ethylene glycol, isoprophyl alcohol, lithium, methanol, theophyline, salicylates and valproate
134
candidates for extracorporeal removal
px with severe toxicity whose condition deteriorates despite the aggressive supportive therapy, those with potentially prolonged irreversible or fatal toxicity, those with dangerous blood level of toxins, those who lack capability for self detoxification because of liver or renal failure and those with serious underlying illness or complication that will adversely affect recovery
135
how do antidotes work
counteract the effect of poisons by neutralizing them or by antagonizing their physiologic effect by activation of opposing nervous system activity, provision of competitive metabolic or receptor substance
136
how to prevent re-exposure
limit their access to poisions
137
fundamentals of supportive care in poisoning management
``` airway protection oxygenation/ventilatiom treatment of arrythmias hemodynamic support treatment of seizures correction of temperature and abnormalities correction of metabolic derangement prevention of secondary complications ```
138
fundamentals in prevention of further poisoning absoprtion
gastrointestinal decontamination such as gastric lavage, activated charcoal, whole bowel irrigation,dilution and endoscopic surgical removal and decontamination of other sites such as eye, skin and body decontamination
139
fundamentals in enhancement of poison elimination
multiple dose activated charcoal alteration of urine ph chelation extracorpeal removal
140
causes of stimulated physiologic condition
sympathetic such as sympathomimetics, ergot alkaloids, methylxanthines, monoamide oxidase inhibitors anticholinergics such as antihistamines, antipsychotics and belladona alkaloids, cyclic depressants and mushroom and plants
141
examples of sympathomimetics
a1 adrenergic agonist and b2 adrenergic agonist
142
mechanism of action of sympathomimetics
stimulation of central and peripheral sympathetic receptor directly or indirectly (release and inhibit release of norepi and dopamine)
143
mechanism of action of sympathomimetics
stimulation of central and peripheral sympathetic receptor directly or indirectly (release and inhibit release of norepi and dopamine)
144
clinical features of sympathomimetics
a1- reflex bradycardia | b- hypotension and hypokalemia
145
treatmen of sympathomimetics
phentolamine-severe hypertension | labetalol-hypotension and tacycardia
146
examples of ergot alkaloids
ergotamine methysergide bromocriptine pergolide
147
mechanism of action of ergot alkaloids
stimulation and inhibition of serotonergic and a adrenergic receptors simulation of dopamine receptors
148
clinical features of ergot alkaloids
formication and vasospasm with limb, myocardial and cerebral ischemia to gangrene and involuntary movements
149
treatment for ergot alkaloids
nitroprusside or nitroglycerine for vasopasm prazosin, captopril- limb ischemia dopamine for movement disorders
150
examples of methyxanthines
caffeine and theophylline
151
mechanism of action of methylxanthines
inhibition of adenosine synthesis and adenosine receptor antagonism stimulation of epi and norepi release inhibition of phosphodiesterase-increased intracellular cyclic adenosine and guanosine monophosphate
152
clinical features of methylxanthines
pronounced gastrointestinal symptoms | toxicity occur at lower drug level in chronic than in acute
153
treatment of methylxanthines
propranolol for tacycardia with hypotension | beta blocker for supraventricular or ventricular tacycardia
154
indications for hemoperfusion and hemodialysis
unstable vital signs seizures theophylline level of 80-100 after acute overdose and 40-60 with chronic exposure
155
example of monoamide oxidase inhibitors
phenelzine tranycypromine selegiline
156
mechanism of action of monoamine oxidase inhibitors
inhibition of monoamide oxidase resulting in impaired metabolism of endogenous catecholamines and exogenous sympathomimetic agent s
157
clinical feature of monoamine oxidase inhibitors
delayed and slowly progressive | terminal hypotension and bradycardia in severe cases
158
treatment of monoamine oxidase inhibitors
short acting agents such as nitroprusside and esmolol for severe hypotension and tacycardaia direct acting sympathomimetic: norepi and epi for hypotension and bradycardia
159
examples of anticholinergic agents
``` antihistamines antipsychotics belladonna alkaloids cyclic antidepressants mushrooms and plant s ```
160
examples of anti-histamines
diphenydramine doxylamine pyrilamine
161
mechanism of action of antihistamines
inhibition of central and postganglionic parasympathetic muscarinic cholinergic receptors
162
clinical features of anti-histamines
``` dry skin mucous membranes decreased bowel movements flushing urinary retention myoclonus picking activity ```
163
treatment of antihistamines
physostigmine for delirium and neuromuscular hyperactivity
164
examples of antipyschotics
chlorpromazine olanzapine quetiapine thioridazine
165
mechanism of action of antipsychotics
inhibition of alpha adrenergic dopaminergic histaminergic muscarinic and serotonegic receptors inhibit sodium, pottasium and calcium channles
166
clinical features of antipsychotics
miosis anticholinergic effects extrapyramidal effects tachycardia
167
treatment for antipsychotics
sodium bicarbonate for ventricular tachydysrhymias | magnesium, isoproterenol in torsades des pointes
168
examples of belladonna alkaloids
atropine hyoscyamine scopolamine
169
mechanism of action of belladonna alkaloids
inhibition of central and pots-ganglionic parasympathetic muscarinic cholinergic receptors
170
clinical features of belladonna alkaloids
``` dry skin mucous membrane decreased bowel sounds flushing urinary retention myoclonus picking activity ```
171
treatment for belladonna alkaloids
physostigmine
172
examples of cyclic depressants
amitriptyline dexopine imipramine
173
mechanism of action of cyclic depressants
inhibition of alpha adrenergic dopaminergic , histaminergic and muscaranic and serotonergic receptors inhibition of nore and epi inhibition of serotonin reuptake
174
clinical features of cyclic antidepressants
``` seizures tachycardia cardiac conduction delays anticholinergic toxidrome ```
175
treatment of cyclic depressants
hypertronic sodium bicarbonate