Final Exam Flashcards
1
Q
Only ________ Black widows are Dangerous.
A
Female
2
Q
Primary toxin released from Black widows is?
A
Alpha-Latrotoxin
3
Q
What is the result of Alpha-Latrotoxin released by black widow’s?
A
Releases neurotransmitters
- ACh
- Norepinephrine
- Dopamine
- Glutamate
- Enkephalins
4
Q
Black widow bite produces what type of lesion?
A
Target Lesion
5
Q
Black widow venom is a ________ toxin.
A
Nerve
6
Q
Clinical Signs of Black Widow bite: (5)
A
1) Muscle Spasm
2) Painful Rigidity of Abdomen
3) Chest Tightness
4) Increased body temp
5) Localized Swelling
7
Q
First aid for black widow bite:
A
Clean the wound & apply ice
8
Q
Most effective treatment of black widow bite?
A
Anti venom “Lyovac” (Latrodectus
9
Q
What is the goal of Black Widow Bite treatment?
A
Stop muscle spasms
10
Q
How to identify the Brown recluse spider:
A
- Has 3 pairs of eyes
- “Fiddle back spider” / “Violin spider”
11
Q
Are Males or Females toxic (Brown Reclluse Spider)?
A
Both, but female has more venom
12
Q
What enzyme is the toxin in Brown recluse spiders?
A
Spingomyelinase D Enzyme
13
Q
What does Spingomyelinase D Enzyme cause in the body from the brown recluse spider?
A
1) Binds to cell membrane -> Chemotaxis
2) Attracts PMN’s -> Tissue Destruction
14
Q
What is the spreading factor of a brown recluse spider bite?
A
Hyaluronidase
15
Q
Clinical signs of a Brown Recluse spider bite:
A
- Bull’s Eye Lesion
- Red area that turns into a sore
16
Q
Medical treatment used for a brown recluse spider bite:
A
Dapsone (a leukocyte inhibitor)
17
Q
Aggression in Bees is triggered by _____ and they attack ______ colors.
A
CO2; dark
18
Q
Main peptides & proteins in bee venom:
A
1) Peptide 401
2) Apamin
3) Melittin
19
Q
Primary Enzymes in bee venom:
A
Phospholipase A2 & Hyaluronidase
20
Q
How many bee stings does it take to illicit allergic death?
A
One
21
Q
Clinical signs of a bee sting: (6)
A
1) Renal failure
2) Rhabdomyolysis
3) Optic neuritis
4) Atrial flutter
5) Hepatic dysfunction
6) Respiratory. Distress
22
Q
How do you remove a bee’s stinger from the skin?
A
Scrape it off. Squeezing can release more venom from the sac.
23
Q
Yellow Jackets do not have __________ _____________ so they can sting you ____________ ________.
A
Barbed Stingers; Multiple times
24
Q
Major Venom components of a yellow jacket (wasp): (5)
A
1) Phospholipase
2) Hyaluronidase
3) Cholinesterase
4) Mastoparans
5) Amines
25
Local clinical signs of a wasp sting: (4)
1) Redness
2) Edema
3) Erythema
4) Pruritis
26
Systemic clinical signs of wasp sting: (8)
1) Anaphylaxis
2) Hemolysis
3) Renal failure
4) encephalopathy
5) hepatotoxicity
6) optic neuritis
7) Hyperkalemia
8) Rhabdomyolysis
27
Math the disease to its carrier:
1) RMSF
2) Lyme Disease
3) Bubonic Plague
- Ixodes Tick
- Dermacentor Tick
- Fleas
1) RMSF. Dermacentor Tick
2) Lyme Disease. Ixodes Tick
3) Bubonic Plague. Fleas
28
The Black Legged tick (Deer tick) transmits:
Borrelia Burgdorferi & Lyme Disease
29
Brown dog tick transmits:
Rhipicephalus Sanguineus
30
What has the most active venoms of the “Hymenoptera”?
Ants
31
How do ants deliver their venom?
They bite, then move the stinger down
32
Field ant venom is high in ___________.
Formic Acid
33
Fire ant venom is a necrotizing ___________, and does what?
Alkaloid; that inhibits Sodium, Potassium & ATPase pumps in postsynaptic neuromuscular junctions.
34
What species has become the most lethal known venom of any animal in the New World?
Harvester Ant Venom
35
Systemic clinical signs of fire ant venom: (3)
1) Seizures
2) Intravascular Coagulopathy
3) Rhabdomyolysis
36
General care for Ant bites:
- Topical corticosteroids
- Antihistamines
- Camphor
37
What is used to denature Formic Acid from ant bites?
NaOCl
38
MC location of Poisonings
92.7% at a residence
39
What percent of poisonings occur in children younger than __________-.
50.9% / Six years
40
56% of poisoning fatalities occurred in what age group?
20-49 year olds
41
MC route of exposure for poisonings:
Oral Ingestion 70%
42
What is the primary agent responsible for fatalities?
Analgesics
43
MC reason for exposure to poisonings & %
Unintentional (83.8%)
44
Most poisonings occur at what time?
At home just before meal time
45
More people die in the US from ________ than from ____________.
Suicides; Homicides
46
Standard treatment for poisonings: (4 steps)
1) ABC’s
2) Support the patient
3) Protect the Airway
4) Give Activated Charcoal
47
Top 3 substances involved in human exposures & their percentages:
1) Analgesics - 11.7%
2) Cosmetics & personal care products - 9.2%
3) Cleaning substances - 9%
48
MC substance involved in PEDIATRIC poison exposures:
Cosmetics & Personal care products (13.4%)
49
Definition of Toxicology
The study of poisons
50
Definition of Hazard:
Likelihood an event will occur based on how the product is packaged, formulated or its accessibility
51
Definition of Risk:
Probability that an event will occur based on patient vulnerability
52
Definition of Toxic Substance
Poisons
53
Definition of Poison:
Any chemical substance which can cause harm
54
Definition of Antidote:
Remedy for counteracting a poison
55
What are the 3 types of Antidotes & what do they do?
1) Chemical: react to form harmless compound
2) Mechanical: prevents absorption
3) Physiologic: counteracts the effects
56
Emergency actions for non-specific poisons include: (4)
1) Symptomatic? -> Call 911
2) Maintain airway
3) Vital signs
4) Supportive care
57
MOI of Carbon Monoxide poisoning:
1) CO binds to Hb creating Carboxyhemoglobin
2) Impairs O2 delivery to tissues
3) Especially affects Heart & Brain
4) Causes Cellular Hypoxia
58
Signs & Symptoms of Carbon Monoxide Poisoning: (3)
1) Depend on % of CO-Hb levels in blood
2) Cherry red blood is Pathognomic
3) Pt. Is NOT Cyanotic
59
Mild Clinical grading of Carbon Monoxide Poisoning Symptoms: (4)
1) Headache
2) nausea/Vomiting
3) Dizziness
4) Flu-Like symptoms
60
Moderate Clinical grading of Carbon Monoxide Poisoning Symptoms: (6)
1) Confusion/Slow thinking
2) SOB
3) Blurred vision
4) Tachycardia & Tachypnea
5) Ataxia
6) Weakness
61
Severe Clinical grading of Carbon Monoxide Poisoning Symptoms: (7)
1) Palpitations/Chest Pain
2) Drowsiness
3) Disorientation
4) Hypotension
5) Syncope
6) MI
7) Pulmonary Edema
62
Antidote for Carbon Monoxide Toxicity:
100% Oxygen
63
MC route of exposure for Heavy Metal toxicity:
Oral (secondary is inhalation of fumes)
64
Heavy metal toxicity is expressed _____________ because of their ability to bind one or more __________ of __________ ____________ __________ which then _____________ the enzyme system.
Biologically; Ligands; Biologic Enzyme Systems; Inactivates
65
Antidote for heavy metal poisonings:
Chelating agents
66
Chelating Agents ___________ inactivate heavy metal poisons.
Chemically
67
Chelates are ____________ and are excreted by the __________.
Water-soluble; kidneys
68
Example of Chelating agent & what it is used for:
Calcium Disodium (EDTA); lead toxicity
69
Calcium Disodium (EDTA) as a chelating agent can cause:
- Renal issues
- Fever
- Dermatitis
70
What is the most significant of the heavy metal poisonings?
Lead
71
What is the most critical aspect of diagnosing lead poisoning?
Pt. History
72
What is the most important chronic environmental illness affecting modern children?
Lead poisoning
73
What organ is the most concerned in lead poisoning?
the Developing brain
74
Lead Poisoning in children produces long-term problems with: (3)
1) Learning
2) Intelligence
3) Earning Power
75
Adults with lead poisoning have problems with: (3)
1) Depression
2) Aggressive Behavior
3) Antisocial Behavior
76
Males with lead poisoning have…
Lower sperm counts
77
Females with lead poisoning have…
Increased incidence of miscarriage and smaller babies
78
Clinical Features of Plumbism (Acute Lead Intoxication) (7)
1) Colic
2) Metallic taste in mouth
3) Vomiting, diarrhea or constipation
4) Increased thirst
5) Hemolysis
6) Oliguria
7) Paresis and Paresthesia
79
Other health effects of Lead poisoning: (6)
1) Slow growth/development
2) anorexia
3) renal damage
4) drowsiness
5) paralysis
6) premature birth
80
Signs & Symptoms of chronic lead poisoning: (5)
1) Burtonian Line
2) basophilic stippling
3) Anemia
4) Colic, diarrhea, vomiting
5) muscle weakness
81
Chronic lead toxicity can cause increased density at the ____________ of ___________ bones.
Metaphyses; Tubular (growing)
82
Lead lines are MCly seen in what 2 bones?
Proximal Fibula & Distal Ulna
83
What abnormality in lead poisoning is seen in the Distal femur?
Erlenmeyer Flask Appearance
84
Lead Palsy results in: (2)
1) Wrist Drop (radial)
2) Foot drop (common fibular)
85
Treatment for acute lead intoxication: (4)
1) Induce vomiting
2) Give cathartics
3) Give proteins (milk, egg. White)
4) Chelating Agents
86
Treatment for Chronic Lead toxicity:
Chelating agents
87
Iron toxicity is seen mostly in __________.
Children
88
MOI of Iron toxicity: (6)
1) occurs. When iron levels > binding capacity of transferrin
2) damages tissue by Direct Corrosive Effects
3) Injures Blood vessels
4) Hepatocellular Death via Hemochromatosis
5) Metabolic Acidosis
6) Coagulation issues
89
Iron is irritating to the _______ _________.
gastric mucosa
90
Once absorbed, iron is taken up by what cells?
Liver cells
91
What 2 things does mitochondrial poison do?
1) Disrupts electron transport chain
2) Inhibits oxidative Phosphorylation
92
Stage 1 of Iron toxicity signs: (3)
- Acute GI corrosive effects
- Hematochezia
- Melena
93
Stage 2 of Iron Toxicity signs: (1)
Sometimes called Latent/Quiescent period
1) Resolution of GI symptoms
94
Stage 3 of Iron Toxicity Signs: (2)
1) Recurrance of GI hemorrhage
2) Death is common in this stage
95
Stage 4 of Iron toxicity Signs: (2)
1) Gastirc Outlet Obstruction
2) Pyloric Stenosis
96
What time does each stage of Iron Toxicity occur (post-ingestion)?
1: 30 min-6 hours
2: 6-24hrs
3: 12-48hrs
4: 4-6 weeks
97
Chronic Iron Toxicity is associated with: (5)
1) Pigmented Hepatic Cirrhosis
2) Diabetes Mellitus
3) Hyperpigmentation of the Skin
4) Hemosiderosis
5) Hemochromatosis
98
Treatment for Chronic Iron Toxicity: (4)
1) Induce vomiting
2) Activated Charcoal (NO HELP)
3) Transport
4) Chelators like Deferoxamine
99
Mercury toxicity can be caused by:
Dental Amalgam Fillings
100
What type of mercury passes through the placenta and maternal exposure can lead to spontaneous abortion or retardation?
Methylmercury
101
What vaporizes easily at room temperature?
Elemental mercury (Quicksilver)
102
What type of mercury is found in thermometers, amalgams & manometers?
Elemental mercury (Quicksilver)
103
Clinical Signs of elemental (quicksilver) toxicity: (5)
1) Pulmonary symptoms
2) Fever/chills
3) Dyspnea
4) lethargy/confusion
5) can be misdiagnosed as parkinson’s/alzheimers
104
Treatment for elemental (quicksilver) toxicity:
ABC’s, O2 & Chelation
105
2 routes of exposure for Inorganic Mercury (mercurial salts) toxicity:
1) Oral
2) GIT
106
Source of Inorganic Mercury (mercurial salts) Toxicity: (2)
1) Disc batteries
2) Mercurous Chloride
107
Signs & Symptoms for Inorganic Mercury (mercurial salts) Toxicity:
1) Ashen gray mucous membranes
2) Severe abdominal pain
3) Hematemesis
4) Loose Teeth
5) Renal tubular necrosis
108
Treatment for Inorganic Mercury (mercurial salts) Toxicity:
ABC’s & Chelation therapy
109
Organic mercury (methyl mercury) results from ingestion of:
Contaminated food such as
- Shell fish
- Tuna
- Shark
110
How long does Organic mercury (methyl mercury) remain in your body after ingestion?
4-6 weeks
111
Where is Organic mercury (methyl mercury) eliminated in the body?
Bile
112
What must occur in the body before symptoms arise with Organic mercury (methyl mercury) toxicity?
Target enzymes and depletion of these enzymes (days to weeks before symptoms)
113
Clinical presentation of Organic mercury (methyl mercury) toxicity: (6)
1) Visual disturbances
2) Ataxia
3) Hearing loss
4) Mental deterioration
5) Muscle Tremors
6) Paralysis
114
What is Thimerosal?
Organic Mercurial Compound with 49.6% Ethyl Mercury
115
What was formerly used as a preservative in pediatric vaccines to prevent bacterial contamintion?
Thimerosal
116
Thimerosal is ________ soluble and eliminated through the _________.
Water; Urine
117
How fast is Ethyl Mercury eliminated from the body?
3-6x faster than the environmental form “methyl mercury”
118
What is the 1/2 life of ethyl mercury compared to Methyl mercury in infants who have been given vaccines?
Ethyl: 6-8 days
Methyl: 45 days
119
What type of vaccines still have mercury in them today?
Multi-dose vial flu shots (Fluzone, Sanofi Pasteur & Fluvirin)
120
Thimerosal (Ethyl Mercury) Diagnosis is based on: (2)
1) Pt. History & clinical signs
2) Urinary Mercury levels greater than 20-25 ug/L
121
Treatment for Acute Thimerosal (Ethyl mercury) toxicity:
Same as any poison
122
Treatment for Chronic Thimerosal (Ethyl mercury) toxicity:
Chelation therapy (BAL)
123
What heavy metal is a natural element found in soil & minerals?
Arsenic
124
What heavy metal commonly contaminates well water?
Arsenic
125
What heavy metal is tasteless and resembles sugar?
Arsenic
126
Arsenic exposure is typically (3 things):
1) Suicidal
2) Homicidal
3) Occupational
127
You may be exposed to Arsenic by slowly…
1) taking in small amounts in food, water or air
2) breathing in sawdust or burning arsenic-treated wood
128
Food sources of Arsenic: (4)
1) Rice Products (Baby foods)
2) Ground water
3) Apple & Grape juice
4) Red wine
129
MOI of Arsenic:
Inhibition of Sulfhydryl enzymes replaced by Phosphate molecules in high energy compounds
130
What type of arsenic is a carcinogen & what type of cancer results?
Trivalent Arsenic; lung & skin cancer
131
What is the most toxic form of Arsenic?
Trivalent Arsenic
132
Where can Trivalent Arsenic be recovered from on the body?
Skin, Hair & Nails
133
Clinical presentation of Acute Arsenic Poisoning: (5)
1) Profuse diarrhea (rice water stool)
2) Garlic odor to breath
3) Dark urine
4) Vertigo, shock & death
5) Hemolysis
134
What types of cancer are increased with Arsenic poisoning?
Lung, Bladder/Kidney & Liver
135
Clinical Signs of Chronic Arsenic Toxicity: (5)
1) Palmar and Plantar hyperkeratosis (skin bumps)
2) Anemia (milk & roses complexion)
3) Gangrene Feet ( Blackfoot disease)
4) Anorexia/GI Symptoms
5) Encephalopathy
136
Diagnosis of Arsenic toxicity:
Urine sample = most reliable
> 200 ug/L is abnormal
137
Treatment for arsenic toxicity: (2)
1) Support airway, breathing & circulation
2) Chelation therapy
138
What is Chlorella?
From Algae: natural immune stimulant and has a high affinity for heavy metals
139
What foods aid in the removal of heavy metals?
Garlic, Onions & cilantro
140
What are the 3 MC alcohol poisonings:
1) Ethanol
2) Isopropanol
3) Methanol
141
Acute intoxication with any alcohol can result in: (4)
1) Coma
2) Respiratory depression
3) CV collapse due to CNS depression
4) aspiration of vomitus
142
Ethanol is what type of alcohol?
Aliphatic
143
Ethanol is found in: (4)
1) aftershaves, cologne, perfumes
2) mouthwash
3) OTC meds
4) alcoholic beverages
144
Ethanol is a direct ______ ___________ which causes decreased _________ & ___________ levels.
CNS depressant; Motor & Consciousness
145
Ethyl Alcohol is also known as:
Grain alcohol
146
Ethyl alcohol is derived from:
Fermentation of sugars in fruits, cereals and vegetables
147
What is the “proof” of Ethyl alcohol?
100 proof = 50% alcohol
148
When the stomach is empty, peak levels of Ethanol absorption occurs at?
30-90 minutes (total absorption can take 6 hours)
149
Metabolism of ethanol is carried out by the?
Liver
150
What liver enzymes metabolize ethanol?
1) Alcohol dehydrogenase
2) aldehyde dehydrogenase
3) MEOS (5%, but increases to 25% in alcoholics)
151
Nonhabituated patients metabolize how much ethanol per hour?
13-25 mg/dL/h
152
What is the primary source of ingested Ethanol?
Alcoholic beverages
153
Associated problems with ethanol ingestion include: (4)
1) Hypoglycemia
2) head trauma
3) carbon dioxide narcosis
4) hypoxia
154
How do. You calculate BAC?
[0.8 ml 90% ethanol / kg body weight = BAC]
220 lb Male -> 100 kg Male -> 80ml or a little less than 3 ounces of 90% or 180 proof or 6 beers = BAC of 0.08%
155
Long term effects of ethanol toxicity: (5)
1) Hepatic Cirrhosis
2) Esophageal cancer
3) pancreatic cancer
4) Wernicke’s syndrome
5) B vitamin deficiencies/malnutrition
156
Treatment for ethanol toxicity:
1) keep pt. From injury inf themselves
2) protect airway
3) Disulfuram blocks acetaldehyde dehydrogenase causing build up of aldehyde
157
Methyl alcohol is AKA:
Wood alcohol
158
Sources of Methanol:
- Cleaning fluids, solvents, paints
- Windsheild washer fluid
- Moonshine
159
What is the fatal dose of Methanol?
30-240ml
160
MOI of the metabolism of methanol:
Methanol -> Formaldehyde -> Formic Acid -> CO2 +H20
161
What alcohol has a profound metabolic acidosis and blindness associated with it?
Methanol
162
What does Methanol do to the eye? (7)
Formic acid inhibits cytochrome oxidase in the fundus.
- disrupts axoplasmic flow
- swelling of axons
- optic disc edema
- blurred vision
- yellow spots
- snowstorm vision
- photophobia
163
What type of respiration is seen in Methanol toxicity?
Kussmaul’s respiration (tachypnea & dyspnea)
164
Treatment of methanol ingestion: (4)
1) ETHANOL
2) Fomepizole (anti oil)
3) airway/breathing support
4) folic acid
165
Isopropyl is AKA:
Rubbing alcohol
166
What is the 2nd MCly consumes alcohol?
Isopropyl
167
What is the lethal dose of isopropyl?
240ml
168
Clinical presentation of Isopropyl toxicity:
1) Headache, dizziness
2) ataxia, nystagmus
3) abdominal pain, hematemesis
4) might have fruity breath
169
Isopropanol is metabolized to acetone by _____
ADH
170
Treatment for Isopropyl toxicity: (3)
1) gastric lavage
2) activated charcoal
3) airway support
171
What alcohol is a clear, colorless, odorless, viscous fluid with a bittersweet aftertaste?
Ethylene glycol
172
What is the source of ethylene gylycol?
Antifreeze
173
Is ethylene glycol toxic?
Not by itself, but its metabolites are highly toxic
174
Ethylene glycol combines with calcium to form:
Calcium oxalate crystals
175
Lethal dose of ethylene glycol:
100ml
176
What happens in the body with ethylene glycol toxicity? (3)
Tissue destruction
- precipitation of calcium oxalate in tissues
- especially renal cortex
- severe metabolic acidosis
177
Phase 1 Clinical presentation of Ethylene Glycol toxicity:
- Inebriated
- nauseated
- vomiting
- ataxia
- no alcohol smell on breath
178
Phase 2 Clinical presentation of Ethylene Glycol toxicity:
- tachycardia/elevated BP
- pulmonary edema/tachypnea
- cardiac failure
- calcium oxalate crystals deposited in vascular tree, lungs & heart
179
Phase 3 Clinical presentation of Ethylene Glycol toxicity:
- flank pain
- costovertebral angle tenderness
- Oliguric acute renal failure
180
Time frame for Phases 1-3 of Ethylene glycol toxicity (after ingestion)
1: 30-12hrs
2: 12-24hrs
3: 24-72hrs
181
Diagnoses of Ethylene glycol toxicity: (4)
1) drunk with NO alcohol smell on breath
2) Calcium oxalate crystals in urine
3) renal failure
4) Kussmaul’s Respiration
182
What enzyme converts Ethylene Glycol into Oxalic Acid?
Alcohol Dehydrogenase
183
Ethylene Glycol toxicity treatment: (4)
1) Treat acidosis
2) Ethyl alcohol
3) Thiamine
4) Water-soluble vitamin B complex
184
Corrosive vs. Caustic (denotes a ________ substance)
Corrosive: ACIDIC
Caustic: ALKALINE
185
MOI of Acids:
[Denature proteins]
- Coagulative necrosis
- tough leathery eschar or coagulum
186
What is the MCly involved organ in acid toxicity?
Stomach
187
If a pt. Has ingested an acid…
ANY ingestion constitutes a medical emergency
188
If acid has come in contact with the skin or eyes…
Flush with water. Remove jewelry & contacts & wash with soap
189
Do you give water to someone who has swallowed an acid?
NO it will have an exothermic reaction. Do not induce vomiting & maintain airway
190
Clinical concerns with acid ingestion:
1) perforation after 3rd or 4th day as eschar sloughs
2) gastric obstruction may develop over 2-4 week period
3) upper GIT hemorrhage
191
What is more common acid or alkali toxicity?
Alkali
192
MC alkali agents that cause toxicity:
Ammonia & Sodium Hydroxide
193
Most cases of alkali toxicity are what age group?
Children under 5
194
MOI of alkali toxicity:
1) Liquefactive necrosis -> tissue injury
2) cell death from emulsification of membranes
195
What tissue are most severely injured with alkali toxicity?
Squamous epithelial cells of oropharynx & esophagus
196
Alkali burns to the skin appear:
Yellow, soapy & soft
197
Clinical concerns for alkali toxicity: (5)
1) Edema
2) Erythema
3) Ulceration
4) Necrosis
5) Perforation
198
What can you give orally to a pt. With alkali toxicity?
Milk, water or egg whites
199
Mixing bleach with acid or alkali cleaning or ducts releases:
Chlorine gas
200
Petroleum Distillates are produced from
Fractional distillation of crude petroleum
201
Major threat of Hydrocarbon toxicity is:
Aspiration Pneumonitis (vomiting increases this risk)
202
When aspirated (in hydrocarbon toxicity), petroleum distillates…
Inhibit surfactant causing alveolar collapse -> hypoxemia
203
Signs & Symptoms of pulmonary involvement in hydrocarbon toxicity: (4)
1) coughing, gasping, choking
2) gasoline breath
3) Rales & wheezes on auscultation
4) Hemoptysis & pulmonary edema
204
Signs & Symptoms of CNS involvement in hydrocarbon toxicity: (3)
1) Dyspnea
2) syncope
3) cuddles cardiac death
205
What should you NOT do with hydrocarbon toxicity?
DO NOT induce vomiting as it increases the risk of aspiration pneumonitis
206
What you SHOULD do in hydrocarbon toxicity:
Maintain airway & support respiration
207
Sources of alkali toxic substances: (6)
1) Drain cleaners
2) oven cleaners
3) swimming pool
4) dishwasher detergent
5) disc batteries
6) soaps & bleach
208
what is the most extensively used illicit drug?
Weed
209
What is the active ingredient in weed?
Tetrahydrocannabinol (THC)
210
Where in the plant is the highest concentration of THC found?
Leaves and flowering tops
211
An average joint contains how much THC?
15-30mg
212
Weed has how many active chemicals?
Over 400
213
What drug is used to treat nausea and vomiting associated with chemo therapy?
Dronabinol (Marino)
214
Where is weed excreted in the body?
15-50% in the urine & feces
215
Weed detection is done by measuring…
Urine levels of THC carboxylic acid
216
What effect does weed have in the body?
- Binds to cannabinoid receptors CB1 & CB2
- Potentiates receptors causing brain to forget experiences
217
Cannabinoid Receptors are mostly located where? Where are ther very few?
Many: (Cognition & movement affected)
Basal Ganglia, Hippocampus, Cerebellum
Few: (Heart & lungs)
Lower brain stem
218
Acute effects of Weed usage: (7)
1) Sinus tachycardia
2) Orthostatic hypotension
3) Elevated BP
4) Increased Myocardial Oxygen demand
5) Short-term memory impairment
6) Xerostomia
7) Rhinitis
219
Treatment for acute intoxication of weed:
Place pt. In a dark room & treat symptoms accordingly
220
Weed compromises the ability to ______ and ____________ _____________ which can last for ________ or ___________.
Learn; Remember Information
Days; Weeks
221
In a 2019 study of 129 college students, what skills were impaired by those who smoked weed?
Attention, Memory & Learning
222
Therapeutic effects of smoking weed: (6)
1) Antitumor effect
2) Antiemetic
3) Appetite stimulant
4) Analgesic
5) Anxiolytic
6) Sleep Wake
223
Weed usage can lead to what conditions? (4)
1) Chronic bronchitis episodes
2) Increased risk of MVA
3) Decreased birth weight
4) Increased schizophrenia risk
224
MOI of Cocaine:
- Causes central and peripheral blockage of the re-uptake of catecholamines
- Blocks sodium channels (local anesthetic)
- Buildup of Dopamine in the SYNAPSE
225
Cocaine is classified as a
Stimulant-benzoylmethylecgonine
226
What drug was formerly used in rhinoplasty?
Cocaine
227
What is the serum half life of cocaine?
30-80 minutes
228
What plant are opiates derived from?
Poppy plant
229
Examples of Opiates (3)
Oxycodone
Hydrocodone
Fentanyl
230
What drug has a high risk of Respiratory depression?
Opiates
231
What are the classic signs of an opioid overdose?
The classic triad:
1) Pinpoint Pupils
2) Unconsciousness
3) Respiratory Depression
232
CNS effects of Opiates: (3)
1) Respiratory depression
2) sedation/ euphoria
3) nausea & vomiting
233
CVS effects of Opiates: (2)
1) Peripheral dilation
2) Hypotension/Brady cardia
234
GI Effects of Opiates: (3)
1) Decreased motility
2) Contipation
3) Miosis
235
What drug is used as treatment for Opiate overdose? What is it?
Naloxone (opioid receptor antagonist)
236
What is the most abused & most rapidly acting Opiate?
Heroin
237
Heroin is extracted from what plant?
Seed pod of poppy plants
238
Mexican Heroid is also known as
Black tar
239
Buprenorphine is sold under the name ________, and used to treat ___________ ____________.
Subutex; Opioid Addiction
Methadone (Dolophine) is also used
240
Most sedatives/hypnotics stimulate:
GABA
241
MCly used Sedatives/hypnotics are:
Benzodiazepines (one of the most frequent prescribed drugs in the world)
242
Examples of Benzodiazepines: (6)
1) Xanax
2) Librium
3) Valium
4) Dalmane
5) Versed
6) Halcion
243
Adverse effects of Benzodiazepines (8)
1) Over-sedation
2) Effects combined w/ other CNS depressants
3) Disinhibition
4) Depression
5) Cognitive impairment
6) Pregnancy adverse effects
7) Abuse
8) Tolerance/dependence/withdrawal
244
Signs & Symptoms of Serotonin Syndrome:
“MADAMS TIPS”
- Mental status change
- Agitation
- Diarrhea
- Ataxia
- Myoclonuc
- Shivering
- Tremor
- Increased Reflexes
- Pyrexia
- Sweating
245
Serotonin Syndrome is the result of excess:
5-HT
246
Drugs that can create serotonin syndrome:
1) SSRI’s
2) NSSRI’s
3) Cocaine, Amphetamines, Codeine
4) Dextromethorphan
247
Ephedrine & Pseudoephedrine were originally obtained from:
Ephedra Mahuang
248
MOI of amphetamines:
Cause the release of catecholamines at the neuron PRESYNAPTIC terminal
249
Long-term effects of Crystal meth use:
1) brain damage
2) weight loss
3) tooth decay “meth mouth”
4) formication (bugs crawling on skin)
250
Treatment for amphetamine overdose: (3)
1) activated charcoal
2) DO NOT induce vomiting
3) maintain & support airway
251
Match the following:
1) Spathiphyllum spp. - Poinsetta
2) Philodendron spp. - Holly
3) Toxicodendron radicals. - Peace lilly
4) Nerium oleander. - Philodendron
5) Ilex spp. - Pokeweed, Inkberry
6) Euphorbia pulcherrima. - Oleander
7) Phytolacca americana. - Poison Ivy
1) Spathiphyllum spp. (6) Poinsetta
2) Philodendron spp. (5) Holly
3) Toxicodendron radicals. (1) Peace lilly
4) Nerium oleander. (2) Philodendron
5) Ilex spp. (7) Pokeweed, Inkberry
6) Euphorbia pulcherrima. (4) Oleander
7) Phytolacca americana. (3) Poison Ivy
252
What does Demulcent therapy consist of?
Ice cream, Milk & Egg whites
253
General management of a plant poisoned Patient (4)
1) Observe Patient
2) Demulcent Therapy
3) Activated Charcoal
4) Cathartics (remove remaining material)
254
What aspect of pokeweed is the most toxic?
Roots & leaves (fruit = mild)
255
What is the toxic principle of pokeweed?
Resinous material & a water soluble saponin
256
Clinical signs of Poke weed poisoning:
1) Burning sensation in the mouth
2) GI cramps
3) Vomiting, diarrhea
4) visual disturbances
5) Diaphoresis
6) Salivation
257
What do you have to do to prepare pokeweed correctly?
Boil the leaves twice
258
Treatment for pokeweed poisoning: (2)
1) Activated charcoal
2) Transport
259
Arum family plants contain:
Calcium Oxalate crystals
260
Members of the Arum family of plants (3)
1) Caladium
2) Dieffenbachia (dumbcane)
3) Philodendron
261
Where in the plant are calcium oxalate crystals found in the Arum family?
Stalk = most severe
But are located everywhere
262
Biting into an Arum family plant causes (3)
1) Pain & Irritation to mouth (salivation)
2) Edema
3) Choking
263
Treatment for Arum Ffamily plant poisoning:
Supportive care & Demulcent Therapy
264
Mistletoe berries contain
Tyramine & Phenylethylamine
265
Clinical Signs of Mistletoe poisoning:
1) Acute Gastroenteritis
2) Cardiovascular collapse
3) respiratory difficulty
4) nausea & vomiting
5) delirium & hallucinations
6) death
266
Treatment for Mistletoe poisoning:
Activated charcoal & transport
267
Are poinsettias toxic?
No, but they contain a latex sap leading to irritation of the mucous membranes
268
Treatment for poinsettia irritation:
Demulcent therapy
269
Cardiotoxic plants contain:
Cardiac Glycosides
270
Examples of Cardiotoxic plants:
Oleander, Azaleas & Lilly of the Valley
271
MOI of Cardiotoxic plants:
Bind to cell membrane & inhibit the Na/K pump
272
Clinical signs of Cardiotoxic Plant poisoning:
Heart block
Brady or Tachycardia
V-fib
273
Clinical signs of Oleander poisoning:
1) GIT irritation
2) abdominal pain & vomiting/Diarrhea
3) Hyperkalemia
4) AV Block / cardio genie shock
274
Treatment for Oleander Poisoning:
1) Induce Vomiting
2) Activated charcoal
3) Transport
275
What portion of poison ivy plant is toxic?
ALL; even smoke from burning it
276
What is the toxic principle found in poison ivy?
Oily Oleoresin called Urushiol
277
Clinical signs of Poison Ivy poisoning: (4)
1) contact dermatitis
2) blistering
3) inflammation
4) vesicle formation
278
Poison Ivy treatment: (5)
1) Epsom salt
2) Electronic itch stopper
3) Tecnu cleanser
4) corticosteroids
5) histamine blockers
279
Plants other than Poison ivy that contain Urushiol:
1) Cashew nut shells
2) mango tree
3) Ginkgo tree
280
Clinical signs of Capsicum Annuum “pepper pant”: (2)
GIT upset & Diarrhea
281
Treatment for Capsicum Annuum “pepper plant” poisoning:
Demulcent therapy
282
What are the MCly used insecticides in the world?
Organophosphates
283
What type of Insecticides are responsible for the most poisonings?
Organophosphates
284
MOI of Organophasphates:
Indirect acting Cholinomimetics (directly inhibit ACh)
ACh + ACHase -> Choline + Acetyl-ACHase
Acetyl-ACHase + H20 -> Acetic Acid + ACHase
OP + ACHase -> Phosphorylated ACHase
Phosphorylated ACHase + ACH -> No Reaction
285
The MOI reaction seen in Organophosphates is __________ and takes _________ for ACh levels to return to normal.
Irreversible; 4 weeks
286
What is the basic problem regarding ACH in Organophosphate toxicity?
ACHase is inhibited; therefore ACh accumulates at the POSTSYNAPTIC synapse over stimulating the Cholinergic receptors
287
Muscanaric Clinical features due to over stimulation of the cholinergic receptors….
Over stimulation of parasympathetic & sympathetic organs that are stimulated by ACh
288
Nicotinic Clinical features due to over stimulation of the cholinergic receptors….
Spastic paralysis of skeletal muscle in high levels
289
Parasympathetic over stimulation of muscarinic receptors in OP poisoning results in: DUMBELS Analogy
1) Diarrhea
2) Urination
3) Miosis
4) Bronchspasm, Bronchorrhea
5) Emesis
6) Lacrimation
7) Salivation
290
Over stimulation of the Sympathetic muscarinic receptors in OP poisoning can result in… (4)
1) Diaphoresis
2) Anxiety
3) Ataxia
4) Respiratory & Circulatory Collapse
291
Over stimulation of the Sympathetic Nicotinic receptors in OP poisoning can result in… (4)
1) Muscle Fasciculations
2) Muscle cramps
3) Seizures
4) Respiratory difficulty
292
In OP Poisoning, death is usually due to…
Respiratory failure
293
Chronic OP ingestion can cause… (3)
1) Proximal muscle weakness due to motor end plate degeneration
2) Axonal Degeneration
3) Peripheral neuropathy
294
How do you diagnose OP Toxicity?
Via RBC Cholinesterase levels
(10 mls of blood in a green top tube)
295
Treatment for OP Poisoning:
1) Activated charcoal
2) Remove clothing & wash w/ soap. Rinse with ethyl alcohol
3) Antidotes
296
What are the 2 antidotes for OP poisoning?
1) Atropine
2) Pralidoxine (2-PAM Chloride) can reverse phosphorylation of AChE
297
What is the Most toxic OP?
TEPP (Tetraethyl Pyrophosphate)
298
Examples of OP’s: (3)
1) Chlorpyifos (Dursban)
2) Diazinion
3) Malathion
299
Carbamates are derived from:
Carbamic acid
300
What are Carbamates?
Reversible Cholinesterase Inhibitors
301
Difference between OP’s and Carbamates
Signs & Symptoms are similar, but Carbamates are more benign and shorter in duration.
Carbamates do not show CNS Signs
302
Treatment for Carbamates toxicity:
1) Activated charcoal
2) remove clothing & wash w/ soap. Rinse with Ethyl Alcohol
3) use antidotes (same as OP’s)
303
MOI for Organochlorines:
Inhibit GABA receptor and Prevent Cl- influx in the CNS
304
Organochlorides mainly affect:
CNS & CVS
305
Clinical presentation of Acute Organochloride toxicity: (6)
1) Nausea, vomiting
2) Seizures
3) Apprehension / confusion
4) Muscle twitching
5) Face paresthesias
6) respiratory failure
306
Clinical presentation of Chronic Organochloride toxicity: (7)
1) Anorexia
2) Hepato & Renal toxicity
3) CNS disturbances
4) skin irritation
5) weight loss
6) Paresis
7) Neoplasia
307
Treatment for Organochloride toxicity:
Protect airway, Activated charcoal, supportive care
308
What insecticide is derived from the flowers of Chrysanthmum?
Pyrethrum
309
Which insecticide has a very low mammalian toxicity?
Pyrethrum
310
Pyrethrum exposure can cause (5)
1) Nausea, vomiting
2) Hyperexcitability
3) allergic rhinitis
4) dermatitis
5) Asthma & cough
311
Treatment for Pyrethrum toxicity
Adam’s flea spray
312
Excessive topical use of DEET has been linked with
Toxic encephalopathy
313
Clinical features of DEET toxicity: (6)
1) Lethargy
2) Anxiety
3) Ataxia
4) Seizures, Coma
5) Irritant dermatitis
6) Conjunctivitis
314
What can you place in your basement to prevent insects? What does it contain that works?
Bois’d arc fruit (Horse apples)
Contains Elemol
315
What is the phone # for poison emergency?
1 (800) 222-1222
316
General approach to poison treatment:
- If victim has collapsed/not breathing call 911
- ABC’s: airway, breathing, cardiac
- Decontaminate the gut, clothing, skin
- Monitor vital signs
- Unconcious? -> Maintain Airway
317
If a poison victim is convulsing… (5)
1) DO NOT stick fingers in mouth
2) get them to the middle of the floor
3) remove constrictive clothing
4) keep stimuli to a minimum
5) Call 911
318
Child 1 swallow = ?
Adult 1 swallow = ?
Child -> 1 teaspoon
Adult -> 1 Tablespoon
319
3 ways to prevent absorption of a poison:
1) Gastric evacuation
2) Administer Absorbent
3) Catharsis
320
Syrup of Ipecac is a…
Emetic
321
Emetine & Cephaline are…
Syrup of Ipesac’s
322
Emetine works where in th body?
Systemically & locally. Has a cumulative toxic effect on the heart
323
What is Cephaline?
Direct GI irritant that is twice as potent as Emetine
324
Who should you give Syrup of Ipecac to?
- Only alert pt’s w/ gag reflex
- over 6 months old
325
Never repeat a dose of Ipecac more than _____________ after first administration
20 minutes
326
When should you NOT give Ipecac? (5)
1) At home
2) Pt. Is less than 1 year old
3) If oven cleaners, dishwasher detergent or other strong acids/bases (corrosives) have been taken
4) Kerosene, gasoline, paint thinner, furniture polish has been taken
5) Pt. Is Lethargic or Convulsing
327
What is “gastric lavage”?
Pumping the stomach
328
What does Ionized dieresis do?
Facilitates excretion of poisons that are eliminated through the kidneys
329
Once an absorbent binds to the poison is is excreted through…
The feces
330
Substances that are not well absorbed by Activated charcoal: (6)
1) Lithium
2) Strong acids/bases
3) Metals (iron, lead, arsenic, iodine)
4) Flourine & boric acid
5) Alcohols & Acetone
6) Hydrocarbons (petroleum distillates & pine oil)
331
What is the ratio for Activated charcoal to toxin?
10x Charcoal for the amount ingested
332
Contraindications for Activated Charcoal: (4)
1) Intestine obstruction
2) Injested strong acid or base
3) Constipated
4) If antidote was used (it will get absorbed as well)
333
What are cathartics?
Drugs that promote evacuation of the bowel
(Purgatives, laxatives)
334
4 Commonly used cathartics:
1) Sorbitol
2) Mannitol
3) Mg Sulfate
4) Mg Citrate
335
Orbital should not be used in
Children under 1 year old because it can lead to excess fluid loss
336
MOI of Cathartics:
Osmotic agents that stimulate GI motility
337
Contraindications for using Cathartics: (3)
1) Absent bowel sounds
2) CVD or Renal disease
3) Electrolyte Imbalance
