Toxicology

Question 1

Treatment for hypoglycemia

Answer 1

Dextrose

Question 2

First medication given to an unconscious patent?

Answer 2

Dextrose

Question 3

Treatment for comatose patient who is an alcoholic?

Answer 3

Thiamine, glucose-metabolism cofactor in the brain

Question 4

Treatment for opioid OD?

Answer 4

Narcan: counter the effects of opioid overdose, such as heroin or morphine specifically the life-threatening depression of the central nervous system, respiratory system, and hypotension secondary to opiate overdose

Question 5

Treatment for Benzodiazepine OD?

Answer 5

Flumazenil

Question 6

Risk of using Flumazenil for benzo OD?

Answer 6

can cause seizures

Question 7

Use of IPECAC?

Answer 7

NO longer used, damages esophagus and didn’t prove to be helpful

Question 8

Use of Gastric Lavage?

Answer 8

ONLY use if OD is life threatening and its within 30 m of ingestion

Question 9

Use of activated charcoal?

Answer 9

Absorbs toxins, but canNOT be used for lethargic or unconscious patients

Question 10

Use of sorbitol?

Answer 10

NO longer used, did speed up GI tract

Question 11

Whole bowel irrigation use?

Answer 11

speed the passage of undissolved iron tablets through the GI tract, long-lasting tabs, lithium

Question 12

Poison control Number

Answer 12

800-222-1222

Question 13

First thing seen in Aspirin OD blood

Answer 13

elevated INR and PTT

Question 14

How early can one check the Tylenol level?

Answer 14

4 hours

Question 15

tylenol metabolism

Answer 15

95% by liver (sulfonation and glucuronidation), cytochrome P450, kidney

Question 16

PT

Answer 16

measure of thrombin in people on coumadin

Question 17

PTT

Answer 17

measure of thrombin in people on heparin

Question 18

EKG changes in Tylenol OD

Answer 18

U waves, flattened T waves, QT prolongation

Question 19

Tylenol metabolism in OD

Answer 19

liver (sulfonation and glucuronidation) pathway becomes saturated quickly and majority is metabolized by cytochrome P450

Question 20

Tylenol + P450 –>

Answer 20

NAPQI

Question 21

NAPQI + glutathione

Answer 21

renal excretion

Question 22

NAPQI with glutathione stores at < 30%???

Answer 22

NAPQI + proteins –> hepatic cellular death

Question 23

If patient ingested Tylenol within the hour, treatment would be?

Answer 23

charcoal

Question 24

Reasons for low levels of glutathione?

Answer 24

trauma, infection, toxins, (alcoholics, AIDS have low glut)

Question 25

4 Stages of Tylenol OD? Stage 1:

Answer 25

24h - minimal signs or symptoms, malaise, nausea, vomitting

Question 26

4 Stages of Tylenol OD? Stage 2:

Answer 26

48-72 hr, Most will recover even without treatment from here,
RUQ pain, elevated LFT’s

Question 27

4 Stages of Tylenol OD? Stage 3:

Answer 27

72-96 hrs, Fulminant liver failure
Coagulopathy, Encephalopathy
Renal failure, Metabolic acidosis

Question 28

4 Stages of Tylenol OD? Stage 4:

Answer 28

Complete recovery if survival of stage 3

Question 29

Nomogram

Answer 29

serum [Tylenol] v. time post-OD, need for liver transplant

Question 30

Nomogram is ineffective for

Answer 30

extended release or multiple ingestions

Question 31

4 hour Tylenol test can be used until

Answer 31

36 h

Question 32

Treatment for Tylenol OD

Answer 32

charcoal (w/in 1 h), NAC/mucomyst (by 8h its 100% effective)

Question 33

NAC/mucomyst works by

Answer 33

reversing NAPQI to acetominophen

Question 34

Is Tylenol/acetominophen toxic?

Answer 34

NO, it’s metabolites are

Question 35

Stage 4 Tylenol OD if no treatment with stage 3

Answer 35

day 4: 57-80% fatal, cerebral edema, hemorrhage, shock, ARDS, sepsis, MSOF

Question 36

Is Aspirin/ASA toxic?

Answer 36

Yes, metabolites are not

Question 37

ASA toxicity thrives in a ________ (produces more nonionized salicylate molecules)

Answer 37

acidic state

Question 38

ASA causes metabolic acidosis via

Answer 38

uncoupling of oxidative phosphorylation as well as uncoupling of the Krebs cycle

Question 39

ASA causes initially

Answer 39

respiratory alkalosis

Question 40

ASA causes initially respiratory alkalosis via

Answer 40

respiratory rate increases via direct effects on brain

Question 41

Once patient tires from increased RR,

Answer 41

respiratory acidosis follows

Question 42

ASA increases pulmonary vascular permeability

Answer 42

causing Non cardiogenic pulmonary edema

Question 43

Heroine can cause

Answer 43

causing Non cardiogenic pulmonary edema

Question 44

Bleeding ____ complication if acute OD

Answer 44

rare

Question 45

ASA is ototoxic

Answer 45

+tinnitus, reversible, correlated to ASA levels

Question 46

**Acute ASA OD Clinical Findings:

Answer 46

n/v, tinnitus, sweating, hyperventilating, metabolic acidosis, respiratory alkalosis

Question 47

Rumack-Mathew Nomogram

Answer 47

Acetominophen OD

Question 48

Chronic ASA OD Clinical Findings:

Answer 48

normal ASA serum level, neurobehavioral symptoms

Question 49

Dome nomogram

Answer 49

ASA/Aspirin OD

Question 50

Treatment for ASA OD

Answer 50

Charcoal, Acid/Base correction, hydration, Golytely, Urine alkalinization

Question 51

How does Urine alkalization work?

Answer 51

ASA is acidic, so alkalinizing the urine increases the output of ASA

Question 52

ASA OD that does not respond to treatment may need

Answer 52

dialysis if ARDS and pulmonary edema are present