Pharm S2B3 - Toxicology 4

Front 1

What are the symptoms of Iron toxicity?

Back 1

1. severe GI irritation
2. Inflammation
3. Necrosis & hemorrhage (mucosal block is destroyed) resulting in hypotension
4. Metabolic acidosis
5. Shock

"While pumping IRON, I had severe GI problems, started bleeding into my GI & went into Shock. I also had Metabolic Acidosis from working so hard from pumping all that Iron"

Front 2

What is the treatment strategy for Iron toxicity?

Back 2

1. Lavage only within the 1st hour after ingestion
2. administer DEFEROXAMINE parenterally (this may cause Histamine release)
3. treat symptomatically & support vital signs

Front 3

Where is Cadmium found? What are the symptoms of toxicity?

Back 3

Tobacco & batteries

1. Kidney
2. Lung
3. Cardiovascular
4. Immune
5. Carcinogen

Front 4

What symptoms does Manganese toxicity cause?

Back 4

Parkinson's like syndrome

**no chelator available

Front 5

What is Calcium Disodium Edetate used to chelate?

Back 5

1. Lead
2. Zinc
3. alternate choice for other metals

Front 6

What are the possible toxic effects of Calcium Disodium Edetate? How can these be avoided?

Back 6

1. Renal Damage
2. EKG abnormalities

*2 places where both Ca++ & Na+ are heavily used

-use less than 50 mg/kg/day
-urine flow must be maintained
-therapy should not exceed 5-7 days
-Do not used H2Na2EDTA, since it will bind Calcium & cause hypocalcemia

Front 7

What is Dimercaprol (BAL) used to chelate?

Back 7

1. Arsenic
2. Lead
3. Gold
4. Inorganic Mercury

Front 8

What are the toxic effects of Dimercaprol (BAL)?

Back 8

1. CNS disturbance
2. Cardiovascular disturbance = may produce shock due to capillary damage

*DIEmerCapillaries = shock from capillary damage

Front 9

What do you not want to co-administer or prevent a patient from taking when taking Dimercaprol (BAL)? Why?

Back 9

Iron b/c BAL-iron complex is toxic

Front 10

How is Dimercaprol used?

Back 10

1. usual course for metal poisoning is 7-14 days by deep IM injection

2. can be used with virtually complete Renal shutdown

Front 11

What are the uses of Penicillamine?

Back 11

1. Copper Chelator (alternate antidote for other metals, ie gold)
2. Wilson's disease
3. Rheumatoid Arthritis

Front 12

What are the toxic effects of Penicillamine? (3)

Back 12

1. Nephrotic Syndrome
2. Pyridoxine deficiency (B6)
3. Transient Eosinophilia

Front 13

When is Penicillamine contraindicated?

Back 13

Children or Adults with Chronic Renal Insufficiency

Front 14

Lead chelator similar to Dimercaprol but can be given orally? What is the most common side effect of this drug?

Back 14

Succimer = used for lead intoxication that is not that severe (lower conc.'s of lead)
-Calcium Disodium EDTA is used for higher conc.'s

GI disturbance

Front 15

Metal chelator used specifically to chelate Iron

Back 15

Deferoxamine

**can only be given Parenterally
-IM, IV

Front 16

What are the toxic effects of Deferoxamine? (2)

Back 16

1. Rapid infusion may induce shock via HISTAMINE release
-as do Vancomycin, Morphine, & d-Tubocurarine

2. Long-term therapy may cause Ocular damage

Front 17

How is Deferoxamine used?

Back 17

Oral dose is effective in binding Iron in the GI tract, but you must remove it by lavage or emesis b/c Deferoxamine-iron complex is more absorbable than iron itself

IV infusion is preferred

Front 18

What are the 2 types of methemoglobin Inducing Agents?

Back 18

Direct acting agents = Nitrites

Indirect acting agents = Aminophenols = converted to metabolites which, in vivo, oxidize Hemoglobin (Fe2+) to Methemoglobin (Fe3+)

Front 19

What is a Carboxyhemoglobin producing agent?

Back 19

Carbon Monoxide

Front 20

List 2 Cytochrome Oxidase Inhibitors

Back 20

1. Hydrogen Cyanide

2. Hydrogen Sulfide

Front 21

What are the symptoms of Methoglobinemia cause by Nitrites?

Back 21

1. Chocolate-colored blood
2. Hypotension
3. Hypoxia & Cyanosis
4. Convulsions
5. Coma
6. Respiratory failure

Front 22

What is the treatment for Methoglobinemia?

Back 22

Methylene Blue = converted Methoglobin back to Hb thru its effect on an intraerythrocytic enzymatic reducing mechanism

Front 23

When does Methylene Blue not work?

Back 23

In patients who are Glucose-6-Phosphate Dehydrogenase deficient
-can't make NADPH, which is needed to reduce Methylene Blue

Front 24

Odorless & colorless gas that is the greatest single cause of lethal poisonings in the USA

Back 24

Carbon Monoxide

Front 25

Describe Carboxyhemoglobin percentage in Non-smokers, Smokers, & auto exhaust

Back 25

Non-Smokers = 1%

Smokers = 5-10%

Auto exhaust = 4-7%

Front 26

What is the mechanism of toxicity of Carbon Monoxide?

Back 26

1. CO has a 200 times greater affinity for Hb than O2 & Carboxyhemoglobin cannot transport oxygen

2. Impairs the ability of Oxy-hemoglobin to give-up its oxygen to peripheral tissues = Left Shift

Front 27

What are the symptoms of Carbon Monoxide poisoning?

Back 27

Headache, dizziness, stupor = primarily due to progressive brain anoxia

Carboxyhemoglobin is CHERRY RED = victims may have bright red, healthy-looking mucous membranes

Front 28

What is the treatment strategy for Carbon Monoxide poisoning?

Back 28

1. terminate exposure immediately
2. administer O2 by best means available
3. avoid respiratory stimulating drugs including Carbon Dioxide
4. DO NOT give Methylene Blue
5. treat symptoms & support vital signs
6. Only Severe Poisoning = Hyperbaric oxygen

Front 29

What are the Mild, Moderate, Severe, & Extreme clinical symptoms of CO poisoning?

Back 29

Mild = presence of symptoms, but w/ no loss of conscioussness, normal mental status, no cardica abnormalities, & no underlying conditions

Moderate = mild confusion, but no loss of conscioussness

Severe = loss of conscioussness, syncope, neurologic abnormalities (seizures), cardiac ischemia, arrhythmias

Extreme = Coma, respiratory failure, Acute MI, sustained Hypotension

Front 30

What things can complicate CO poisoning?

Back 30

1. Pregnancy
2. Coronary Artery Disease
3. Pulmonary disease
4. Significant Anemia
5. Children
6. Geriatric patients

Front 31

Colorless gas with a penetrating odor resembling that of Almonds

Back 31

Cyanide

Front 32

What is the mechanism of toxicity of Cyanide?

Back 32

Complexes with ferric iron of Cytochrome Oxidase & produces cellular anoxia by inhibiting Oxygen utilization in the Mitochondria

*one of the most rapid acting poisons & death can occur very rapidly after exposure

Front 33

What are the symptoms of Cyanide poisoning?

Back 33

1. Dizziness
2. Headache
3. Hypotension
4. Unconsciousness
5. Convulsions
6. Respiratory failure

Front 34

What is the treatment strategy for Cyanide poisoning?

Back 34

1. must be RAPID

2. Sodium Nitrite or Amyl Nitrite = forms Methemoglobin which competes with Cyanide ion for Cytochrome Oxidase
-Cyanide is converted to Thiocyanide by RHODANESE

3. administer Sodium Thiosulfate immediately after Nitrite administration
-limiting cofactor in Rhodanese reaction

4. Give artiricial respiration with 100% oxygen

5. treat symptoms & support vital signs

Front 35

What is the role of Rhodanese in Cyanide poisoning?

Back 35

CN- + S (thiosulfate) -> SCN- (Thiocyanide) which is excreted

Front 36

How is Hydrogen Sulfide poisoning treated?

Back 36

same as Cyanide poisoning

Front 37

What are the particles that are in Air Pollution?

Back 37

Carbon Monoxide = 52%
Sulfur Dioxide = 15%
Hydrocarbons = 12%
Particulate Matter = 10%
Nitrogen oxides = 6%

Front 38

Describe "EAST COAST" Air Pollution

Back 38

Reducing type of Air Pollution
-Most dangers (vs. W coast)
-SO2 & Smoke from coal
-Cardiac & Respiratory toxicity

Front 39

Describe "West Coast" Air Pollution

Back 39

Oxidizing Type of Air Pollution
-from Automotive exhaust
-causes Lung irritation (bad for people with Asthma or COPD)

Front 40

What particles can cause Silicosis?

Back 40

particles of free crystalline forms of Silica less than 5 micrometers in diameter are most important in causing Silicosis

Airborn particles may also play a role in promoting carcinogenesis

Front 41

What are the symptoms in the 3 stages of Silicosis?

Back 41

1st Stage: dyspnea & shortness of breath; discomfort

2nd Stage: weakness, respiratory impairment

3rd Stage: total disability; expirations are prolonged & difficult; induces a predisposition to TUBERCULOSIS; pt usually dies of RIGHT HEART FAILURE

Front 42

What occupations commonly lead to Silicosis? What is the treatment?

Back 42

Miners, Glass manufacturers, Stone Cutters

Symptomatic & supportive

Front 43

What can exposure to Asbestos fibers lead to?

Back 43

1. Linear fibrosis of the lungs
2. Pleural adhesions & calcifications
3. Tumors

Front 44

What multiplies the risk of Lung Cancer in Asbestos exposed people?

Back 44

Cigarette Smoking

Front 45

What are the symptoms of Asbestos exposure?

Back 45

1. Dyspnea
2. Respiratory impairment & disability
3. Bronchogenic Carcinoma (most common CA) & Pleural Mesothelioma (rare)

Front 46

Naturally occuring, radioactive gas which cannot be seen or smelled that can be found in basements of homes

Back 46

Radon

Front 47

What are the symptoms of Radon toxicity?

Back 47

1. increased risk of Lung Cancer

2. Risk of lung CA due to Radon exposure is multiplied when the person is a Smoker

Front 48

List the Bioterrorism Category A Agents

Back 48

1. Anthrax
2. Smallpox
3. Plague
4. Botulism
5. Tularemia
6. Viral Hemorrhagic Fevers

Front 49

List the Chemical Terrorism agents that are vessicant/blister agents

Back 49

Nitrogen Mustards
Sulfur Mustards
Lewisite

**spreading mustard on your skin gives you blisters

Front 50

List the Chemical Terrorism Pulmonary agents

Back 50

Ammonia
Chlorine
Phosgene

Front 51

What are the 2 Chemical terrorism Nerve agents

Back 51

Sarin

Soman