Mem 6222

Front 1

What type of technique for endotracheal intubation will often lead to damage to the soft tissue of the larynx or pharynx and dislocation of the arytenoid cartilage?

Back 1

Blind Technique

p. 1592

Hint 1

Tracheal injuries of intubation are MC in women, suspected because often the tube used is too big.

Front 2

T/F: Mucosal tears during intubation may present early with: immediate bleeding or subcutaneous emphysema, or late with septic shock.

Back 2

True

p. 1592

Front 3

T/F: There are many forms of complications in ET tubes themselves, kinking of the tube, patient biting the tube or even secretion collecting in the tube. Another source may actually be an over inflated cuff herniating into the end of the tube and obstructing the tube.

Back 3

True

p. 1592

Front 4

What are some patients that cannot be orally intubated after removal of a trach (2)?

Back 4

1. patients who have undergone laryngectomy
2. Patients who have tumors or scarring that would otherwise occlude the airway.

p. 1592*

Front 5

What defines the "size of the tracheostomy tube"

Back 5

The inner tube diameter

p. 1592
What are the size ranges in adults?
What are the size ranges in children?

Hint 5

Adults: 5-10 mm
Peds: 2.5-6.5

p. 1592

Front 6

The inner cannula of a tracheostomy tubes have a removable inner cannula, that allows for the clearance of secretions without removal of the tube from the trachea. However, pediatric tubes do not have these inner cannulas, why?

Back 6

Pediatric tracheostomy tubes do not have an inner cannula because the small inner diameter, so the entire tube has to be removed to be cleaned

p. 1592*

Front 7

Trouble changing a tracheostomy will depend on what two things?

Back 7

1. When the procedure was performed
2. Patient Anatomy

p. 1592

Front 8

If a tracheostomy is < ____ days old, the tract will not be mature and the manipulation may easily create___ ____ ____ within the soft titssue of the neck. In addition, a tract may easily collapse at any time in patients with obese necks or neck masses.

Back 8

< 7 days,
a false passage

p. 1593*

Front 9

You have changed the tracheostomy tube of a patient who reported to the ER. Utilizing the obturator device to place this, because you know that this minimizes the damage to the soft tissue. After successfully placing the tube, which must you do quickly and why?

Back 9

Must remove the obturator from the tracheostomy, and place the inner cannula. As long as the obturator is in place, this is a solid object that obstructs breathing.

p. 1593*

Front 10

You have placed the patient in the supine position, with a towel under the shoulder to visualize the trach, you remove the old tube and suction, and now have clean stoma. The posterior wall of the trach is easily visualized. The procedure is going well, you gentley insert the new trachestomy tube, but then while doing so meet resistence. What happened?

Back 10

The tube has hit the cartilaginous wall. Remove the tube, reexamine stoma and try again. If again resistance, try a smaller tube. HOWEVER, a smaller tube is also shorter, and may not be long enough for the patients neck.

p. 1594*

Front 11

Patient has an accidental decannulation of their tracheostomy, the tube has been out for several hours. What needs to happen prior to tube insertion?

Back 11

Dilation of the stoma may be needed prior to insertion of catheter.

p. 1594*

Front 12

Secretions can sometimes form what is called a ball-valve obstruction within a tracheostomy tube. What is this?

Back 12

With respirations, the secretions will collect so that air is able to get in, but not out.

p. 1594

Front 13

What patients CANNOT be orally intubated?

Back 13

Laryngectomy

p. 1594*
- the only access to the tracheo-bronchial tree in laryngectomy patients is through the tracheostoma in the neck.

Front 14

How are layngectomy patients distinguished from tracheostomy patients?

Back 14

Hx and PE, and by the fact that laryngectomy patients are unable to vocalize or breath when the laryngectomy tube is occluded.

p. 1594*

Front 15

A patient is brought by EMS, appears in respiratory distress, with hx of tracheostomy tube. The nursing home reported that they thought it had dislodged, but when they examined it, it appeared to be in place. RT is at the bedside and attempts to suction it, with no luck. Why is the patient in respiratory distress with a trach that appears in place, but is not accommodating the suction?

Back 15

Because the tracheostomy tube is dislodged from the trachea, and is now inside just the neck. It is likely compressing on the trach with its limited space, making it even harder to breathe. Because it is inside subcutenous space, in lieu of the trachea, it will not receive the suction device.

p. 1594
What do you then do?

Hint 15

Remove the whole tracehostomy. Call ENT, but if airway not maintained, intubate.

Front 16

What are 3 common afflictions of those with tracheostomies, which are MC caused by: Staphylococcus Aureus, Pseudomonas, and Candida?

Back 16

1. stomal infection
2. Tracheitis
3. Bronchitis

p. 1594

Front 17

What is a rare, but life-threatening complication of tracheostomy?

Back 17

Tracheoinnominate artery fistula


p. 1594

Hint 17

caused by:
- tip of the trachea cannula against the innominate artery
- cuff from innappropriately high pressured cuffs/overinflation.

Front 18

A patient presents to the ER with Hemoptysis and hx of Tracheostomy placed ~3 weeks ago. What is the most serious concern

Back 18

Tracheoinnominate artery fistula

p. 1595

Hint 18

Approximately 50% of patients may present with a sentinel arterial bleed or hemoptysis.

p. 1595*

Front 19

A patient is brought to you via EMS. He had been provided zofran, for nausea after 1 day of scant hemotpysis, which increased today- more significant. Patient has a host of comorbid conditions, a PEG and Trach tube- placed <4 weeks ago. By the time he is presented he is in apparent respiratory distress and bleeding profusely, leaning forward on EMS gurney, to guard airway and has his own suction. What do you do for the hemorrhage?

Back 19

Firs thing- inflate the cuff in an attempt to tamponade the bleed at the likely formed tracheoinnominate artery fistula bleed. (this is successful in 85% of the cases, but is temporizing for surgery).

p. 1595*

Hint 19

However, if this does not work:
1. applyed anterior pressure on the tube, while slowly withdrawing.
2. No relief, then remove the device and place an ET tube past the artery and inflate, to at least prevent further aspiration.
Stomal hemorrhage following this is then controlled with the use of digital pressure of the innonimate artery against the manubrium. This should then be maintained enroute to the OR

p. 1595- Oh! And call ENT/Pulmonary- someone

Front 20

What can occur weeks to months following decannulation of a tracheostomy, and 2/2 mucosal necrosis and subsequent scarring; and is associated with: dyspnea, wheezing, stridor, and inability to clear secretions?

Back 20

Tracheal Stenosis

p. 1595

Front 21

T/F: Laryngotracheal stents and their associated tracheostomy tubes should only be removed by surgeons familiar with the devices and their placement.

Back 21

True

p. 1596*

Hint 21

see p. 1596, figure 242-7 for an image of laryngotracheal stent placement in relation to the tracheostomy tube

Front 22

What is the MC complication associated with tracheoesophageal prosthetic valves?

Back 22

leakage- either around the valve or through the lumen

p. 1596

Hint 22

Another complication is aspiration of the valve or valve extrusion. Aspiration can lead to: cough, dyspnea with discomfort, as well as respiratory distress.

Front 23

If a tracheoesophageal prosthesis is dislodged, how long before the puncture tract closes? How is it maintained?

Back 23

24-48 hrs to close

Foley or rubber catheter to maintain patency

p. 1596

Front 24

You want to place a catheter to maintain the patency of laryngotracheal puncture tract, but a colleague reminds you to ask how old it is, why?

Back 24

Should not be placed if site is less than 2 weeks, this can create a false passage.

p. 1597*

Front 25

You have a patient with hx of laryngectomy and tracheostomy; you want to provide an emergent airway and know it has to go through the stoma. What is something to keep in mid?

Back 25

Do not advance tube too far- as the carina may only be 4-6 cm from the tracheostoma.

p. 1597*

Front 26

What is lithium approved for (2)?

Back 26

- BiPolar Disorder
- Acute Mania

p. 1211

Front 27

What are 3 of the more common reasons for lithium toxicity?

Back 27

1. Unintentional overdose
2. Intentional overdose
3. Impaired renal clearance

p. 1211

Hint 27

75-90% of patients who are treated for lithium over the long term develop toxicity at some point during their therapy.

Front 28

What elements are removed from both intracellular and extracellular sites by lithium?

Back 28

1. Sodium
2. Potassium
3. Magnesium
4. Calcium

p. 1211

Front 29

Why is it that lithium has an adverse effect on the myocadial electrical conduction?

Back 29

Cause of the effect it has on sodium ions and the sodium-potassium pump

p. 1211

Front 30

T/F: Lithium has been known to prevent NorEpi reuptake, as well as increase release of serotinin and has been implicated in serotinin syndrome when combined with like therapies.

Back 30

True

p. 1211

Front 31

Which of the two drugs below are associated with a major drug interaction when mixed with Lithium?
- Haloperidol
- ACEI/ARB's
- CCB's
- Methyldopa
- Benzo's
- Sibutramine (Meridia)
- Lasix
- Bumex

Back 31

- Haloperidol
- Sibutramine (Meridia)

The others cause moderate interactions
- p. 1211, Table: 175-1

Front 32

A patient you admitted to the ICU after using vecuronium for an intubation is still sedated- beyond the time you estimated. As you are reflecting on her case, she was an individual in respiratory distress. No surgical hx, NKDA, Hx of bipolar, for which she took lithium, but her levels were appropriate. What is the reason for the prolonged state ( assuming every lab, PE and tox screening, etc was NML).

Back 32

Lithium will prolong the neuromuscular blockade of succinylcholine, vecuronium, and pancuronium; when given in long term lithium patients.

p. 1212*

Front 33

T/F: Lithium is bound to plasma proteins.

Back 33

False

p. 1212

Front 34

T/F: The distribution into and out of the brain is rapid with lithium, so levels correlate with serum levels.

Back 34

FALSE!
- actually, the distribution is slow into and out of the CNS- so serum and CNS levels do NOT match

p. 1212

Hint 34

Actually the difference can be 2-3 times

Front 35

A patient was provided hemodialysis for lithium overdose, a known SI attempt. Following the treatment the patient remains altered. Serum levels show improvement, what is going on?

Back 35

There is a slow movement out of the CNS. Serum levels do NOT predict central nervous system levels and do not precisely correlate with clinical symptoms.

p. 1212*

Front 36

T/F: There is scant, but possible hepatic involvement with lithium.

Back 36

FALSE: lithium is excreted unchanged in the urine and has NO hepatic involvement.

p. 1212

Front 37

The common adverse effects of lithium are: hand tremor, polyuria, rash. Why polyuria?

Back 37

Because of the loss of urine concentrating ability. In fact, this is the MC cause of drug induced Nephrogenic Diabetes Insipidus

p. 1212

What does a worsening hand tremor mean?

Hint 37

Developing Toxicity

Front 38

What are the Neurologic SE's associated with lithium (5)?

Back 38

1. memory loss
2. decreased concentration
3. fatigue
4. ataxia
5. dysarthria

- all this can improve with cessation

Hint 38

SEE Table 175-2 for the spectrum of side effects associated with lithium

Front 39

What are some common reasons for precipitating the development of lithium toxicity?

Back 39

1. Renal Failure
2. Volume Depletion: diuretic use, vomiting, diarrhea, diaphoresis, decreased oral intake
3. hyperthermia/neuroleptic malignant syndrome
4. infection
5. CHF
6. DM
7. Pre-Existing Cerebral Pathology
8. Surgery
9. Cirrhosis

p. 1213, Table 175-3

Front 40

10% of patients with severe lithium toxicity die. What from?

Back 40

Respiratory and Cardiovascular Collapse

p. 1213

Front 41

What grade of lithium level is MC associated with the following clinical features:

N/V, Tremor, hyperreflexia, ataxia, aggitation, muscle weakness

Back 41

Grade I

Serum level: 1.5-2.5mEq/L

p. 1213

Front 42

What grade of lithium level is MC associated with the following clinical features:

Stupor, Muscle Rigidity, hypertonia, and HoTn

Back 42

Grade II

Serum level: 2.5-4.0 mEq/L

p. 1213

Front 43

What grade of lithium level is MC associated with the following clinical features:

Coma, Seizures, Myoclonus, Cardiovascular Collapse

Back 43

Grade III

Serum level: >4.0 mEq/L

p. 1213

Front 44

T/F: Acute lithium toxicity is known for causing more GI than Neuro sxs.

Back 44

True

p. 1213

Front 45

Does serum concentration correlates better with degree of toxicity and prognosis in acute or chronic lithium use.

Back 45

Chronic. Remember, it takes time to cross the CNS
(acute lithium toxicity is MC GI sxs)

p. 1213

Front 46

You have a patient who is having a seizure, following a known lithium toxicity, ie. overdose. You provide Ativan like a crazy person, no relief. You then decide that the individual needs phenobarb or general anesthesia, when a friend suggests using phenytoin. What do you say?

Back 46

NO!!!
Phenytoin is unlikey to stop seizure from the lithium, because it decreases renal excretion.

p. 1213*

Front 47

When is whole-bowel irrigation in lithium toxicity recommended?

Back 47

When it is a known or suspected case of sustained release lithium

p. 1213

Front 48

What is the rule of thumb for acute ingestion of sustained release lithium, even if serum levels are NML.

Back 48

Admission

p. 1214

Front 49

What four things are barbituates MC used for?

Back 49

- seizure d/o's
- procedural sedation
- anesthesia induction
- occasionally used as an acute or chronic pain adjunct

p. 1214

Front 50

T/F: Barbituates are readily distributed throughout the body to most of the tissues, crossing the blood brain barrier and placenta, but spares the breast milk.

Back 50

False, all is true except the end. Barbituates cross into breast milk as well as the tissues, BBB, and the placenta.

p. 1214

(BBB=blood brain barrier)

Front 51

Where are most barbituates metabolized?

Back 51

Liver, CYP450


p. 1214

Front 52

Because of the action barbituates have on the CYP450, what medications will often has an accelerated metabolism?

Back 52

- oral contraceptives
- anticoagulants
- corticosteroids

p. 1214

Front 53

What does mild and moderate barbituate intoxication closely resemble?

Back 53

EtOH intoxication or other sedative hypnotic toxicity

p. 1215

Hint 53

Some common features that increase with increasing doses:
- ataxia
- drowsiness
- disinhibition
- slurred speech
- mental confusion

Front 54

What are the MC vital sign abnormalities seen in barbituate overdose?

Back 54

1. hypotension
2. respiratory depression
3. hypothermia

p. 1215

Hint 54

FYI: abnormal temperature control as well as respiratory depression is a centrally controlled phenomenon, and the hypotension is a result of decreased vascular tone.

Front 55

What is the cause of early death in barbituate overdose?

Back 55

respiratory arrest and cardiac collapse

p. 1215

Front 56

Why are serum barbituates levels in the treatment of an acute overdose deemed not very useful?

Back 56

They are not reliable because they do not reflect brain barbituate concentrations and may underestimate the clinical condition of the patient in the setting of polydrug.

p. 1215

Front 57

How are the following treated in the barbituate overdose/toxic patient
a. HoTn
b. hypothermia

Back 57

a. fluids, if that fails go with vasopressors
b. hypothermia, provide active rewarming measures

p. 1215

Front 58

When considering barbituate overdose, when does one consider multi-dose activated charcoal?

Back 58

only when they have taken a life threatening dose of phenobarbital

p. 1215

Hint 58

Typical dose of Multi-Dose Activated Charcoal:
50-100 gms PO followed by 12.5 to 25 gms PO every 4 hrs

Front 59

Why is force diuresis not recommended in barbituate overdose?

Back 59

Risk of sodium, fluid overload and a lack of proven efficacy

Front 60

Which has better responses in the treatment of phenabarbital overdose urine alkalinization or multi-dose activated charcoal?

Back 60

Multi-Dose Activated Charcoal (MDAC)

p. 1215

Front 61

T/F: Urine alkalinazation is not effective for shorter acting barbituates.

Back 61

True

P. 1216*

Front 62

What is the only barbituate overdose that is known to have any benefit with: hemodialysis, hemoperfusion, and hemodiafiltration

Back 62

Phenobarbitol

p. 1216*

Front 63

Following mild to moderate barbituate overdose, what is the time duration, in hours, that a patient should typically have evidence of improvement in Neuro function and Vitals to be considered for d/c to home?

Back 63

6-8 hrs

p. 1216

Front 64

What can manifest as minor symptoms: anxiety, restlessness, depression, insomnia, anorexia, N/V, muscle twitching, abdominal cramping, and sweating. Major symptoms may include: psychosis, hallucinations, delirium, generalized seizures and hyperthermia, and cardiovascular collapse.

Back 64

Barbituate Abstinence Syndrome

p. 1216

Front 65

What are the six major pharmacologic effects of Benzo's?

Back 65

1. sedative
2. hypnosis
3. anxiolytic
4. amnestic
5. anticonvulsant
6. muscle relaxer

p. 1216

Front 66

What is the MC benzo for procedural sedation as well as for general anesthesia 2/2 to its short duration of action?

Back 66

Midazolam (Versed)

p. 1216

Front 67

Secondary to varying degrees of Benzo pharmacologic profiles, some agents have a more profound sedative or hypnotic effect and may be more toxic in overdoses. What two are most likely to do this?

Back 67

1. Aprazolam (Xanax)
2. Flunitrazepam (Rohypnol)

p. 1216

Front 68

T/F: Benzo's are well absorbed from the GI tract.

Back 68

True

p. 1216

Front 69

T/F: All IM injections of Benzo's are unpredictable.

Back 69

False
- "With the exception of Midazolam (Versed) and Lorazepam (Ativan), all other benzo's are unpredictable absorption following IM injection".

p. 1216

Front 70

How long is the onset of action for midazolam and lorazepam following IV administration?

Back 70

1-5 minutes

p. 1216

Front 71

Benzo's are lipid soluble. What happens when lipid solubility of the agent is increased?

Back 71

It diffuses more rapidly across the blood brain barrier.

p. 1216

Front 72

The prominent manifestations of bezo toxicity: somnolence, dizziness, ataxia, slurred speech, confusion, general impairment of intellectual function. Coma can occur. In what 4 groups of people can this be MORE pronounced?

Back 72

1. elderly
2. infants and children
3. protein deficient persons
4. hepatic disease

p. 1218

Front 73

What are the three benzo's most commonly associated with anterograde amnesia?

Back 73

1. Lorazepam (Ativan)
2. Midazolam (Versed)
3. Triazolam (Halcion)

p. 1218

Front 74

What is the diluent in parenteral preparations of diazepam and lorazepam that can cause severe metabolic acidosis, nephrotoxicity, and hyperosmolar states when infused at doses >1 mg/kg/d for an extended period of time.

Back 74

Propylene Glycol

p. 1218

Hint 74

Toxicity requires hemodialysis

Front 75

Bezo labs are not generally ordered, as there are great risks for false positives and negatives. How long can a short acting and long acting benzo "pop" positive in the urine?

Back 75

- short acting for 3 days
- long acting for 30 days

p. 1218

Front 76

Many toxicologists suggest that there is minimal benefit to the use of flumazenil in the ER. Plasma elimination half life is approximately 1 hr- but variable and depends on the dose of flumazenil and the Benzo administered. However, what is one of the risks of using flumazenil and long acting benzo?

Back 76

Recurrent Benzo toxicity may result once the effects of flumazenil has worn off ~ 1 hour.

p. 1218*

Front 77

What is the dose of flumazenil that can be provided IV?

Back 77

0.2 mg IV


(to max 3 mg)

p. 1218

Front 78

What are the 6 contraindications to flumazenil use?

Back 78

1. Overdose to unknown agent
2. Susptected or known physical dependence on Benzo's
3. Suspected cyclic antidepressant overdose
4. Coingestion of seizure inducing agents
5. Known seizure d/o
6. Suspected increased intracranial pressure

p. 1218

Front 79

Why is flumazenil contraindicated in patients with suspected elevation of intracranial pressure, such as occurs with severe head injury?

Back 79

Because of its adverse effects on cerebral hemodynamics

p. 1219*

Front 80

T/F: There is good clinical evidence to support 6 hours as the appropriate time to observe a patient following benzo overdose.

Back 80

False, while we most commonly observe for a period of 6 hrs and feel this is safe, but there is no literature to validate appropriate time limit.

p. 1219

Front 81

What non-benzo, sedating therapy, causes suppression of the central nervous system serotoninergic activity and enhancement of dopaminergic and possibly noradrenergic activity?

Back 81

Buspar

p. 1219

Hint 81

Start dose is 5 mg tid, max dose is 60 mg tid

Metabolized MC in the liver, it is excreted MC renally

Front 82

What are some common SE's of Buspar?

Back 82

- sedation
- GI: discomfort, vomiting and dizziness
- in therapeutic dosing, does not cause psychomotor depression and is NOT associated with abuse or withdrawal

p. 1220

Front 83

T/F: Buspar has been associated with serotonin syndrome.

Back 83

True

p. 1220

Front 84

What two medications that are not approved by the FDA for insomnia, tho used for this, one is a centrally acting muscle relaxer and the other is an anxiolytic; schedule schedule III the other is a schedule IV.

Back 84

1. Carisprodol (muscle relaxer, schedule III)
2. Meprobamate (anxiolytic, schedule IV)

p. 1220

Front 85

You have a patient who appears to have ingested a medication that she had was originally provided for muscle relaxation. But she has a hx of SI and took a ton of it. She is obtunded, bradycardic, lungs sound wet; however, she has MYOCLONIC jerking- which appears unique to this particular medication. What has this patient taken?

Back 85

Carisoprodol

p. 1220

Front 86

What non-benzo sedative is associated with the formation of a gastric bezoar as well as a prolonged coma (secondary to the retained drug w/in the stomach), with the ingestion of a large number of tablets.

Back 86

Meprobamate


p. 1220*

Front 87

T/F: Meprobamate and carisoprodol have been associated with significant potential for abuse and dependence. Withdraw symptoms may include: tremor, anxiety, insomnia, and anorexia- which occurs MC w/in 12-48 hrs.

Back 87

True

p. 1220

Front 88

T/F: When a patient overdoses on EtOH- chloral hydrate may be used as a competitive antagonist, for alcohol dehydrogenase.

Back 88

FALSE!!! Actually the results are synergistic when chloral hydrate is given with EtOH, it is actively metabolized by EtOH dehydrogenase; because of this there is a decreased metabilism of Ethanol, which elevates the serum levels of EtOH as well as chloral hydrate. BAD!

p. 1220
Called "knock-out drops" or "Mickey Finn"

Front 89

What non-benzo sedative at therapeutic levels results in mental status depression, but intact airway and respiratory reflexes?

Back 89

Chloral Hydrate

p. 1220

Front 90

What is associated with a "pear-like odor"- and is considered to be a diagnostic clue of drug associated complications (Non-Benzo sedative)?

Back 90

Choral Hydrate

p. 1220

Front 91

What should be used to treat the ventricular arrythmias associated with chloral hydrate?

Back 91

B-adrenergic Blockers

p. 1220*

Hint 91

Arrythmias MC associated with Chloral Hydrate:
- PVC's
- Ventricular Fibrillation
- Torsades de pointes
- asystole

Front 92

What drug called "Liquid ecstacy", "Georgia Home Boy", "G", and "Grievous Bodily Harm" was originally designed to be used for IV anesthesia, but is more commonly used to build muscle mass, tx depression, anxiety, and cholesterol lowering.

Back 92

GHB (gamma-hydroxybutyrate)

p. 1221

Hint 92

Minimal protein binding and readily crosses the blood brain barrier and placenta. Has a steep dose response curve. Additionally, patients waking suprisingly quickly, MC after 6 hrs in the absence of coingestions

Front 93

GHB is associated with withdrawal syndromes, characterized by two distinct phases. What are they?

Back 93

1. First Stage: insmonia, confusion, GI distress, anxiety and tremor. (MC 2 hrs after last dose in those who habitually use)
2. Second stage, tachycardia, HTN, diaphoresis and tremor, confusion and hallucinations and paranoia (MC w/in 2-3 days)

p. 1221

Front 94

Melatonin is an endogenous hormone that is secreted by the pineal gland. Subtype 1 receptor is in the hypothalamic nucleus, Subtype 2 receptor is in the retina, subtype 3 is largely unknown. What medication is FDA approved for the treatment of insomnia and is highly selective agonist of subtype 1 and 2?

Back 94

Ramelteon (Rozarem)

p. 1221

Front 95

You have a patient who has high BP, you are treating with verapamil. He came to see you about a cough. You discovered a PNA, and treated him with Levaquin. While there he asks if you were going to give him a rx for the sleeping problem he talked to you about months ago, you had mentioned rozarem. Is there any risks.

Back 95

Relative risks. The absorption of rozarem is generally rapid, however, will increase in serum concentrations in the presence of: Flouroquinalones as well as verapamil.

p. 1221

Front 96

T/F: There is a risk of both dependency and abuse, as well as withdrawal, when using rozarem.

Back 96

False, none of that!

p. 1221

Front 97

Zolpidem (Ambien), Zaleplon (Sonata), and Zopiclone all impair psychomotor activity, create intolerance and dependence, and withdrawal. Which of the three creates less of the tolerance and withdrawal?

Back 97

Zaleplon (Sonata)

p. 1222*

Hint 97

- has shorter onset and halflife- this is believed to be the reason for this...

Front 98

T/F: Routine use of flumazenil is recommended for OD in non-benzo sedative overdose.

Back 98

FALSE!!! Not recommended at all. Supportive care only

p. 1222*

Hint 98

Remember: Ventricular arrythmias caused by chloral hydrate is treated with: Beta-adrenergic blockers.

Front 99

Aside from EtOH, what is the MC used psychoactive substance abused by young people?

Back 99

Marijuana

p. 1238

Front 100

When hallucinogenics are used, what is the most common type of hallucination?

Back 100

Visual Hallucinations (though they can be any type)

p. 1238

Front 101

Hallucinations caused by hallucinogens are vivid and real to the individual. More common are "illusions" than hallucinations. In what way are these manifested to an observer?

Back 101

- alterations in mood, heightened suggestibility. Individuals will often experience distortions in body image, distortion in the passage of time, and increased intensity of ANY emotions that they experience at the time of use.

p. 1239

Front 102

What is one of the most potent psychoactive compunds around?

Back 102

LSD

p. 1239

Hint 102

- agonist of serotonin
- rapidly absorbed, < 30 minutes, lasts 8-12 hours

Front 103

Physiologic effects of LSD are more commonly seen prior to the psychedelic effects. MC these are facial flushing, mild gastric distress, piloerection, increased muscle tension, and hyperreflexia. While seizures and severe life threatening combinations are rare, what will MC happen with an overdose of LSD?

Back 103

Coma, respiratory arrest, hyperthermia, and coagulopathy

p. 1239

Front 104

What is a dysphoric reaction or "bad trip" with LSD?

Back 104

When an individual feels panic attacks, extreme paranoia, acute psychotic reactions, and depressive reactions.

p. 1239

Hint 104

Psychedelic effects of LSD are MC perceived as pleasurable or horrifying, and are contingent on the user's prevailing mood as well as their environmental factors (setting).

Front 105

What is hallucinogen persisting perception disorder?

Back 105

Used to be called flashback- a debilitating maladay in which a patient experiences chronic perceptual distortions reminiscent of the drug induced state, accompanied by panic and anxiety (LSD hx)

p. 1239

Front 106

If someone is having a dysphoric rxn brought on by their LSD use, why is haloperidol considered a second line agent, only to be used if benzo's are not helping?

Back 106

Because there is a theoretic risk of lowering seizure threshold.

p. 1239

Front 107

What is a naturally occuring hallucinogenic compound found in at least three genera of mushrooms, especially Psilocybe genus?

Back 107

Psilocybin

p. 1239
WHAT IS THIS STRUCTUALLY SIMILAR TO?

Hint 107

LSD

Front 108

What happens to the potency of psilocybin-containing mushrooms when cooked or dried?

Back 108

Nothing, the potency is not affected by these things.

p. 1239
However, what is different from these mushrooms and those that are MC sold on the streets?

Hint 108

Hallucinogenic mushrooms from the streets are often non-psychoactive in nature, but instead have been adulterated with LSP or PCP.

Front 109

T/F: In spite of being labeled a schedule I drug by the USFDA, there are some medical therapeutic benefits to the use of hallucinogenic mushrooms.

Back 109

FALSE, there is no medical benefit to hallucinogenic mushroom use

p. 1239

Front 110

What drug has sxs set in with in 30 minutes, lasting 4-6 hrs, with hallucinogenic effects that are less than LSD- though similar. MC: mydriasis, tachycardia, hyperreflexia, and N/V. Some serious medical conditions of hyperthermia, rhabdo, and renal failure have also occurred?

Back 110

Psilocybin

p. 1239

Front 111

What is the hallucinogenic alkaloid found in the Mexican Peyote Cactus, a small spineless cactus that grows in SW USA and N. Mexico.

Back 111

Mescaline

p. 1240

Front 112

T/F: A much weaker hallucinogen, but similar to LSD, Mescaline, has some restricted legal use by the Native American Church.

Back 112

True

p. 1240

Front 113

What is "bitter" tasting hallucinogen, that causes significant uncomfortable physical side effects w/in 1 hour of ingestion. Commonly include: N/V, abdominal discomfort, diaphoresis, dizziness, nystagmus, ataxia, and HA- which improve in about 2 hrs after use.

Back 113

Peyote

p. 1240
- What is death from the Mescaline MC caused from?

Hint 113

Being an idiot when hallucinating (ie. Aberrant behavior)

Front 114

What is a synthetic phenylethylamine derivative structurally similar to amphetamines and mescaline?

Back 114

MDMA

p. 1240
- what is the MC street name for MDMA?

Hint 114

Ecstacy

- also called: "love drug", "club drug"- 2/2 unique effects on mood and intimacy

Front 115

The acute response to ecstacy lasts 4-6 hrs; and what are the experiences?

Back 115

- euphoria
- inner peace
- enhanced sociability
- verbosity
- and heightened sexual interest.

p. 1240

Hint 115

Common Side effects:
- mydriasis
- tachycardia and hypertension
- Nausea
- jaw tension
- bruxism
- xerostomia
- tension aches
- ataxia

Front 116

T/F: MDMA is MC accociated with hallucinations.

Back 116

False, MC it is associated with enhanced sensory effects, but rarely (if ever) is it associated with hallucinations

p. 1240

Front 117

What are some of the adverse effects associated with large doses of MDMA use?

Back 117

- severe hypertension
- intracranial hemorrhage
- hyperthermia
- hyponatremia
- fatal arrythmias

p. 1240

Front 118

What is the most frequently cited causes of death from MDMA?

Back 118

- hyponatramia and hyperthermia, which can lead to fatal arrythmias

p. 1240

Front 119

What is the pattern of MDMA toxicity manifested by (5)?

Back 119

1. hyperthermia
2. seizures
3. DIC
4. rhabdomyolysis
5. renal failure

p. 1240

Front 120

What is the neurotransmitter most effected by MDMA?

Back 120

Serotonin

p. 1240

Hint 120

In fact, combining this with SSRI or like agent can cause a severe reaction, consider that toxicity from MDMA manifests sxs similar to Serotinin Syndrome

Front 121

What are the long term affects from the neurotoxic injury from repeated use of MDMA?

Back 121

Long term functional consequences are: long lasting cognitive impairment including mood dysfunction and memory impairment, diminshed learning ability, and depression

p. 1240

Front 122

20 y/o brought by EMS, found unconscious, BP: 160/98, HR: 150, RR: 22 Temp: 104. Labs: CK 2200, BMP, Sodium 118, Potassium: 6.0 Chloride: 102 CO2: 24, BUN: 18 CR: 1.2, Glucose: 64. HCG: negative, UA: + blood and proteins dipstick, neg RBC's on micro. CXR and remainder of labs pending. She was out with friends who dumped her at the fire house and then bolted...what do you think is the source?
THis is important, cause a friend recognizes that the CK is through the ruff and wants to give her fluids and bring the BP down. What is something to keep in mind?

Back 122

1. MDMA (Ecstacy)
2. She is fluid overloaded, hence the hyponatramia, correction of this should be cautious, esp since this is overhydration more than anything. Hypertonic saline, judiously...look up. Temp is important, rapid cooling is important, and can prevent increases in morbidity and mortality. AVOID betablockers. THis is similar to sympathomimetics- unapposed alpha...bad!

p. 1240

Hint 122

- if needed, consider Benzo, Benzo, Benzo...when this does not work, consider then propofol.

Generally speaking Hypertonic saline: 100-200 mL/hour x 1-2 hours

Front 123

What hypnotic agent is structurally similar to ketamine?

Back 123

PCP

p. 1240

Hint 123

- dissociative anesthetic agent, however, it is also a hallucinogen, depressent, and stimulant...
But differs from other hallucingens in that it clouds senses not enhances them. Because of its mixed association, recognition of intoxication can be challenging

Front 124

Routes of administration of PCP?

Back 124

- Powdered (Angel Dust) combined with: tobacco, marijuana, and other vegatable matter and smoked
- ingested orally
- intransally insufflated
- injected IV

p. 1241

Front 125

What does one need to examine in the presence of PCP intoxication?

Back 125

- r/o occult trauma
- r/o rhabdo
- r/o hypoglycemia

p. 1241

Hint 125

- multi-organ failure, rhabdo, hypoglycemia, HTN, intracebral hemorrhage, hyperthermia causing hepatic necrosis have all been reported

Front 126

Cops bring a 40 y/o jackass to the ED. He is combative, violent and agitated. Even vitals are hard to obtain. Cops tell you he is a known PCP junky and this is the way they find him. He is putting up one heck of fight. What is the preferred restaining method for this joker?

Back 126

Pharmacologic restraint

- the fighting against staff and restraints worsens rhabdomyolysis.

p. 1241

Front 127

What can be smoked or ingested, lasting for approximately 2-4 hours, with sxs that include: drowsiness, euphoria, heightened sensory awareness, paranoia, and distortions of time and space and feelings of unreality?

Back 127

Marijuana

p. 1241

Front 128

16 y/o schmuck is observed with mildly tachycardic, injected conjunctiva, impaired motor coordination.+ orthostatic HoTn. You guess he also has bronchodilation. No hx of EtOH use. What is it?

Back 128

Marijuana

p. 1241

Hint 128

impairment in motor skills is common and is freqently a source for MVC's

Front 129

You are the pain manager of a patient. Contract does not allow for use of alternative drugs. Her rx profile is: Metoprolol, Simvastatin, protonix- because of her motrin, Morphine ER, and Norco. She recently had a UDS that was negative, except for marijuana. You call her out on it and she is shocked, she never touches that stuff. Could she be telling the truth?

Back 129

Yes, she is on motrin and protonix, these can lead to false +

motrin, naprosyn, protonix and HIV med: efavirenz

p. 1241

Front 130

What is Bufotoxin?

Back 130

Psychosubstances found in the venom, skin, and eggs of many toads.
- this is extracted from the toads parotid gland

p. 1241-1242

Front 131

What are the features of acute toxicity to Bufotoxins?

Back 131

Abdominal pain, vomiting (as well as salivation), sympathomimetic effects (increased HR and BP), features similar to cardiac glycoside toxicity (hyperkalemia, bradycardia, AV block, ventricular tachycardia, v-fib, and sudden death).


p. 1242

Front 132

What does the following resemble:

Morning Glory

Back 132

LSD

p. 1242

Front 133

What does the following resemble:

Nutmeg

Back 133

Anticholinergic, except that the pupils are miotic

p. 1242

Front 134

What does the following resemble:

Jimson Weed

Back 134

Anticholinergic

p. 1242

Front 135

What does the following resemble:

Ketamine and Dextrmethorphan

Back 135

PCP

p. 1242

Front 136

A 12 y/o kid is brought to you with anxiety, palpitations, and c/o CP. Admits to taking some kinda otc medications. Seem uncomfortable and at times delirious. What did he take

Back 136

Dextramethorphan

p. 1242

Front 137

An elderly patient was consuming an energy drink, when he felt chest discomfort and sensation of palpitations that did not stop. Monitor shows atrial fibrillation. States this happened when drinking tea in the past too, what drug class is this caused by?

Back 137

Methylxanthines

- in this case: Theobroma cacao, commeliathea.

p. 1256

Front 138

Caffeine is a methylxanthine and structural analog to what?

Back 138

Adenosine

p. 1256
- Read next card!

Hint 138

REMEMBER! What adenosine, also called adenocard does!!!!! (Thinking about this should make your heart stop for a second).
However, caffeine work to antagonize the effects of adenocard

Front 139

What is the most commly used psychoactive drug in the world and the ONLY one that can be legally purchased by children?

Back 139

Caffeine

p. 1256

Hint 139

Many energy drinks use Guarana- which contains relatively HIGH concentrations of caffeine!!!! YUP! look at the back of the monster...caffeine and guarana...it's like concentrated + extra concentrated.

Front 140

What are the routes of administration for caffeine?

Back 140

- PO
- IV
- PR
- IM
- SC

p. 1256

Front 141

T/F: Methylxanthines are rapidly absorbed, cross the blood brain barrier, placenta, as well as the breast milk.

Back 141

True

p. 1256

Front 142

What type of drug is Theophylline?

Back 142

Methylxanthine

p. 1256

Front 143

Who is Theophylline MC used for today (tho not in the US)?

Back 143

Those with debilitating bronchospastic diseases

p. 1256

Front 144

What is the underlying pathophysiology of Methylxanthines?

Back 144

Adenosine antagonism, increased endogenous adrenergic stimulation and at toxic levels, phosphodiesterase inhibition.

p. 1256

Front 145

What are the four main organ systems involved in methylxanthine toxicity?

Back 145

1. GI
2. Cardiovascular
3. Neurologic
4. Metabolic

p. 1257

Hint 145

TABLE 186-5

p. 1257

Front 146

The neurologic effects of methylxanthine are often severe and include HA, tremor and seizure. Methylxanthine induced seizures are often refractory to tx, why?

Back 146

Because it normally inhibits CNS excitatory neurotransmitter release and are refractory to tx due to ability of methylxanthine to antagonize adenosine.

p. 1257

Front 147

What is the MC cardiovascular effect of the methylxanthine caffeine?

Back 147

Beta-adrenergic effects increase ionotropy and chronotropy, as well as vasodilation- HoTn and reflex tachycardia.

(But why, if caffiene is an analog to adenosine does it cause tachycardia? Because the caffeine blocks the adenosine receptors and prevents the nervous system from responding to it, preventing the slowing of the heart rate).

p. 1257-1258

Hint 147

Sinus Tach is MC with theophylline toxicity- as serum levels increase, cardiac arrythmias develop: MFAT and a-fib/flutter.

Front 148

What are the 3 metabolic derangements caused by methylxanthine toxicity?

Back 148

1. Hypokalemia
2. Hyperglycemia
3. Metabolic Acidosis

p. 1258

Hint 148

Hypokalemia- increase catecholamines...MC in acute overdoses

Front 149

Caffeine causes dependence and risk of withdrawal. How soon can this occur following cessation from chronic use? And what are the sxs?

Back 149

1. w/in 6-24 hrs
2. HA, fatigue are the MC sxs...Caffeine withdrawal HA"s are very debilitating and should be considered in all patients who show to the ED for evaluation

p. 1258

Front 150

T/F: Serum levels of theophylline correlate well with the level of toxicity.

Back 150

False.

p. 1258

Front 151

What is the best predictor of major theophylline toxicity acutely? What is the best predictor in chronic exposure?

Back 151

1. acutely: peak serum concentration
2. chronic: increased patient's age

p. 1258*

Front 152

What is the lethal dose of caffeine?

Back 152

An acute ingestion of 10 grams of caffeine is lethal

p. 1258

Front 153

Why is activated charcoal almost never useful in acute caffeine overdose?

Back 153

Because it is rapidly absorbed from the GI tract

p. 1258

Front 154

Why zofran preferred antiemtic in patients with caffeine overdose?

Back 154

Because the phenothiazines have the ability to lower the seizure threshold of the patient. (Safer)

p. 1258

Front 155

T/F: Hemodialysis is just as effective as hemoperfusion, and may be even safer, for the treatment of theophylline toxicity.

Back 155

True

p. 1259

Front 156

What are the two common rules for considering hemodialysis in methylxanthine-induced life threatening event?

Back 156

1. Seizure
2. severe arrhythmia
- also
3. after an acute ingestion, a symptomatic patient has serum levels > 90 mcg/mL
4. chronic toxicity patient has a serum theophylline level > 40 mcg/mL w/significant sxs or comorbidities.

p. 1259*

p. 1259

Front 157

T/F: Nicotine readily crosses the blood brain barrier and affects the central nervous system w/in seconds of inhalation when smoked.

Back 157

True

p. 1259

Hint 157

- Absoprtion across mucous membranes is takes longer than inhalation
- The half life of nicotine is variable, avg 2 hrs
- metabolism of nicotine is via the liver, CYP450
- Nicotine binds to Nicotinic Acetylcholine receptors throughout the body, including CNS, autonomic and neuromuscular systems. It also affects the aortic and carotid chemoreceptors.
- As an agonist, nicotine activates ion channels, leading to increased neuronal firing with release of neurotransmitters, including Ach, dopamine, glutamate, NorEpi, and Serotonin

Front 158

What are the systems MC affected by Nicotine overdose?

Back 158

1. GI system
2. Cardiovascular System
3. Neurologic System
4. Respiratory System

p. 1259

Front 159

It has been more than 1 hour since a person was exposed to toxic levels of nicotine. What sxs might they possess?

Back 159

GI: diarrhea
Cards: Arrythmia, bradycardia, and HoTn
Neuro: Hypotonia, Seizure, and Coma
Respiratory: Hypoventilation, Apnea

p. 1259

Front 160

A mother walked into a room where she thinks her child ate 3 cigarette butts (~1 intact cigarrette). She called you immediately, what can you tell her?

Back 160

Her child has 90% chance of developing sxs of exposure; on avg this will occr within 30 minutes, needs to get tx- now.

p. 1239

Front 161

T/F: Activated charcoal is recommended following nicotine exposure.

Back 161

False: sxs that develop GI wise are N/V...making aspiration risk too great.

p. 1239

Front 162

T/F: Diuretics can cause a depletion in potassium as well as sodium; additionally, responsible for calcium regulation.

Back 162

True

p. 1273

Front 163

How do diuretics have an impact on calcium regulation?

Back 163

1. inhibition of Vit D synthesis, thus decreased absorption in the gut
2. increased renal absorption of calcium

The net result is actually calcium retention, possibility of hypercalcium.

p. 1273

Hint 163

FYI: Loop diurectics actually cause a loss of magnesium as well as calcium...
Amongst other things...

Front 164

An individual attempted to commit suicide by overdosing on her spironolactone, what is the biggest risk to the patient with this medication and those in the entire class of the medications?

Back 164

Hyperkalemia

p. 1273

Front 165

What are the clinical manifestations of excessive diuresis?

Back 165

1. Hypotension
2. Tachycardia
3. Electrolyte abnormalities
4. Generalized weakness.

p. 1273

Front 166

What electrolyte disturbance caused by diuretics is suggested by wide QRS as well as peaked T waves?

Back 166

Hyperkalemia

p. 1273

Front 167

What electrolyte disturbances can be caused by diuresis and can cause prolonged QT?

Back 167

1. hypocalcemia
2. hypomagnesemia
3. hypokalemia

p. 1273

Front 168

Explain the difference in alpha1 and alpha 2 receptors? ie. what effect on the body...

Back 168

Stimulation of the alpha 1 adrenergic receptor: work on peripheral veins and arteries causing vasoconstriction

stimulation of the alpha 2 adrenergic receptors: work in the CNS and peripheral nervous system. There is a inhibition in the release of catecholamine, that in turn promotes vasodilation and HoTn.

p. 1275

Front 169

What is the most ideal pressor agent when exccsive response from alpha blocker.

Back 169

Phenylephrine (Neo-Synephrine)

p. 1275

Front 170

What is the most commonly used alpha2 blocking agent?

Back 170

Clonidine

p. 1275

Front 171

What can be used in a patient who is experience opioid withdrawal to ameliorate the sxs associated with this?

Back 171

Clonidine

p. 1275

Front 172

A peds patient is presented: bradycardic, hypotensive, bradypneic and hypothermic. Pupils are miotic, otherwise NML PE- no evidence of trauma or pathonomonic for dz. MOP states that she does not know what happed, they found a bottle of grandpas pills for his BP next to the child but does not want to believe this is related. A friend leans in during the assessment and says "I thought it was opioid ingestion..." Close, what BP med presents the same way?

Back 172

Clonidine.

p. 1275

Front 173

While ABC's are the priority in toxic ingestion, including those who took clonidine, which the effects can actually last for days, what is a medication that may help as well?

Back 173

High dose Narcan, should not be considered a failure until greater than 10 mg IV have been provided

p. 1275

Front 174

A patient has had HTN inspite of the clonidine ingestion/toxicity. A colleague wishes to give a BP lowering agent, you tell him to wait if not too high, why?

Back 174

Because the HTN could give way to HoTn.

p. 1275

HOLY CRAP! You were right, hypotensive. But now your patient is really hypotensive. Now what?

Hint 174

Crystalloid should be enough to treat.

But if HTN was to be treated, as suggested in the earlier scenario, it should be with nitroprusside, so it can be immediately d/c'd.

p. 1275

Front 175

How does angiotensin II increase BP?

Back 175

- increasing aldosterone
- increasing response to catecholamines
- acting as a direct vasoconstrictor

p. 1275

Hint 175

ARBS: produce vasodilation and increase renal salt elimination.

Front 176

ARBS have never resulted in HoTn. Yet, they can cause_____, which MC occurs in renal patients.
ACEI are thought to slow diabetic glomerulonephropathy, as well as improved _____ ventricular fxn when administered after MI.

Back 176

1. Hyperkalemia

2. Left

p. 1275

Front 177

What is the most consequential adverse effect associated with ACEI and ARBS?

Back 177

Angioedema

p. 1275*

Front 178

What is one sure way to differentiate angioedema from allergic anaphylaxis?

Back 178

Uritcaria

p. 1276

Front 179

What is the best predictor of the need for intubation, airway intervention, following acute angioedema?

Back 179

Swelling of the oral cavity (oropharynx) and tongue

p. 1276

What is the most ideal means of intubation?

Hint 179

Nasotracheal intubation...but by anesthesia.

Front 180

What is the safest recommendation following an ARB/ACEI associated angioedema?

Back 180

Discontinue the frick'n med man!

p. 1276*

Hint 180

Now you know there is not a single test question out there that will ever be this easy!

Front 181

What is the effect that hydralazine has on the system?

Back 181

Arteriole smooth muscle relaxer

p. 1276

Front 182

A patient has been on hydralazine for an extended period of time. She then reports feelings of joint aches, fever. During this examination you notices that the heart sounds are faint, muffled. You obtain a CXR and EKG. Rad shows cardiomegaly and the EKG shows electrical alternans- what is going on, is it because of her medication- why.

Back 182

She is developing a lupus syndrome reaction to the hydralazine, believed to be sparked by autoantibodies. It is likely because she has been on a high dose for extended period of time. D/c the medications, and provide NSAID for improvement.

p. 1276

Front 183

T/F: Minoxidil is actually a potent vasodilator, generally used for resistent cases of HTN.

Back 183

True

p. 1276

Front 184

Why should crystalloids be used and pressor agents avoided when treating Minoxidil and Hydralazine overdose patients?

Back 184

Because severely poisoned patients may have coronary ischemia
If one is needed, use NeoSynephrine- almost pure alpha agonist.

p. 1276

Front 185

What affect does nitroprusside have on the vessels of the body?

Back 185

Dilates both arterial and venous muscles

p. 1276

Front 186

It is ideal when providing Nitroprusside not to exceed 2-5 mcg/kg/min, why?

Back 186

Because if you go too high, you can cause cyanide toxicity

p. 1276

Front 187

You just received a patient from a colleague who was started on a nitroprusside gtt. The order was for 2 mcg/kg/min, but was entered at a rate of 10 mcg/kg/min. The patient is beginning to crash- what do you do?

Back 187

Stop the drip and provide sodium thiosulfate.

p. 1276

Hint 187

This individual progressed from lactic acidosis to cardiovascular collapse.

Front 188

You are covering the ICU one day and are taking care of a patient who was noted to have cyanide toxicity from the nitroprusside secondary to a medical clerical issue. The sodium thiosulfate is still going, after 5 days. The patient is notibly more somnolent and c/o nausea. It is noted by you that the rate of the infusion has been unchanged, in spite of the labs reflecting a declining renal function. What is happening?

Back 188

Thiocyanate Toxicity (from the Sodium Thiosulfate)


p. 1276
What are the two most important predictors of toxicity?

Hint 188

1. rate of infusion (rate of production)
2. rate of excretion (renal function)

p. 1277

Front 189

T/F: Therapeutic levels have not been established for Second Generation Anticonvulsants, but serum levels are useful in defining toxicity.

Back 189

False

p. 1277

Hint 189

First generation anticonvulsants had a high likelihood of toxicity, so serum levels were important. However, Second generation anticonvulsants have very little potential to cause serious toxicity in an overdose (it's uncommon)

Front 190

What is a primary anticonvulsant therapy for partial and generalized tonic-clonic seizures. It is very useful in the treatment of non-drug induced status epilepticus in conjunction w/rapidly acting anticonvulsants. It also has been used in the setting of head trauma, as well as management of some chronic pain syndromes. Death from overdose is unlikley and supportive care is all that is needed.

Back 190

Phenytoin

p. 1277

Front 191

Phenytoin deaths are most commonly related to what two causes/sources?

Back 191

1. IV administration
and
2. Hypersensitivity reaction

p. 1277

Front 192

IV phenytoin has poor solubility in water. What are the vehicles for the parenteral formulation that are linked to toxicity of this agent? (2)

Back 192

1. 40% propylene glycol
2. 10% ethanol

p. 1277

Front 193

What agent, a prodrug of phenytoin, was made to improve phenytoin effects and minimize its associated toxicity risks?

Back 193

Fosphenytoin

p. 1277

Front 194

How does phenytoin exert its anticonvulsant effect?

Back 194

By blocking voltage sensitive and frequency dependent sodium channels in an inactive state- similar to local anesthesia

p. 1277

Hint 194

- it limits the ability of the neuron to fire trains of action potentials, therefore suppressing repetitive neuronal activity

Front 195

Why is it necessary to obtain serial serum readings for phenytoin in light of suspected oral overdoses?

Back 195

Absorption after oral ingestion slow, variable, and often incomplete.

p. 1277*

Hint 195

Of note, even among different preparations the concentration is different, and the peak level of concentration is variable: 3-12 hours.

Front 196

What anticonvulsant therapy is more than 90% protein bound in the blood stream: to albumin.

Back 196

Phenytoin

p. 1278

Front 197

What of phenytoin is responsible for the drug's clinical effect and toxicity, bound or unbound fraction of the drug?

Back 197

unbound

p. 1278

Therefore, what groups of individuals would be more likely to suffere these adverse outcomes?

Hint 197

1. Neonates
2. elderly
3. Pregnant women
4. individuals with uremia
5. hypoalbuminemia
6. hyperbilirubinemia
7. individuals taking drugs that may displace phenytoin from the binding site: ASA, valproate...etc.

Front 198

The metabolism of phenytoin is dose dependent, but where is it metabolized?

Back 198

Liver

p. 1278

Front 199

Why does IV administration of phenytoin carry the greatest risk of toxicity?

Back 199

2/2 to the constituents of the parenteral vehicle: propylene glycol as well as ethanol.

p. 1278*

Front 200

What is the most serious rxn following IV administration of phenytoin (aside from extravasation at the IV site as well as tissue necrosis)?

Back 200

Cardiac Toxicity

- ex: bradycardia, HoTn, and asystole

p. 1278

Front 201

T/F: cardiotoxicity has been observed following oral administration of phenytoin.

Back 201

False- it has never been reported...almost invariably associated with IV administration.

p. 1278

Front 202

Associated with the following sxs: nystagmus, nausea and vomiting, ataxia, dysarthria, choreoathetosis, opisthotonos, and neurologic depression or excitation, what route of phenytoin is MC associated with this acute overdose?

Back 202

Oral Administration

p. 1278

Front 203

Occurring within the first few months of taking phenytoin, what, if it occurs, will manifest as: fever, skin rashes, blood dyscrasias, and hepatitis?

Back 203

Hypersensitivity Reaction

p. 1278

Front 204

A patient was having a seizure and provided anticonvulsant. Shortly after this broke, and became lucid again, c/o "itching down in my taint!". What drug causes this?

Back 204

IV Fosphenytoin

- perineal pruritis

p. 1278

Front 205

T/F: Fosphenytoin does not cause cardiotoxicity, because it does not possess the dilutents of which it is an analog for: propylene glycol and ethanol.

Back 205

False!! While it does not possess these dilutents, it still can cause cardiotoxic effects.

p. 1278-1279

Hint 205

- effects of these dilutents: enhanced vagal tone, Compound has been shown to cause: coma, seizures, circulatory collapse, ventricular dysrrythmias, AV node depression, and HoTn. Additionally, hyperosmolarity, hemolysis and lactic acidosis.

Front 206

The symptoms associated with the following phenytoin level:

< 10

Back 206

Usually No sxs

p. 1279, table 191-3

Front 207

The symptoms associated with the following phenytoin level:

10-20

Back 207

Occasionally nystamus

p. 1279, table 191-3

Front 208

The symptoms associated with the following phenytoin level:

20-30

Back 208

Nystagmus

p. 1279, table 191-3

Front 209

The symptoms associated with the following phenytoin level:

30-40

Back 209

Ataxia, Slurred Speech, nausea and vomiting

p. 1279, table 191-3

Front 210

The symptoms associated with the following phenytoin level:

40-50

Back 210

Lethargy, Confusion

p. 1279, table 191-3

Front 211

The symptoms associated with the following phenytoin level:

> 50

Back 211

Coma and Seizures

p. 1279, table 191-3

Front 212

You are examining a patient following administration of phenytoin. You observe a forced lateral gaze nystagmus. Does this imply anything?

Back 212

The first initial sign of toxicity

p. 1279

- however, the absence of this does not mean the absence of toxicity.

Hint 212

However, as toxicity progresses: confusion, coma, and apnea.

Front 213

You are working in the ER on a night shift when a patient is brought to you in Status Epilepticus...posessing tonic, clonic jerking for more than 5 minutes w/o a break, was provided phenytoin. Shortly after this, the patient possessed EKG changes, prolonged QT, widened QRS, and altered ST segment changes. Why?

Back 213

This is showing signs of cardiac toxicity, which is common with pheytoin. In this case however, it is likely 2/2 the infusion rate being too fast.

p. 1279

Front 214

What should be done in the case of IV infusion of phenytoin and the development of cardiotoxic effects?

Back 214

D/c the phenytoin and begin crystalloid infusion.

p.1279
- table 191-5

Front 215

T/F: Pheytoin toxicity has been associated with peripheral neuropathy as well as urinary incontinence.

Back 215

True

p. 1279
- table 191-5

Front 216

T/F: Hemodialysis is not often regarded as useful for the treatment of phenytoin toxicity.

Back 216

True...because phenytoin is protein bound, but in overdose cases it can be considered useful in coingestions.

p. 1280

Front 217

T/F: Phenytoin induced metabolic acidosis needs correction, and is done to decrease the free phenytoin fraction. Providing activcated charcoal (1gm/kg) w/in first 24 hrs may help.

Back 217

True

p. 1280

Front 218

A friend of yours is turning patients over to you. His last patient is a young lady who took a butt load of phenytoin, and in spite of this appears well. He reports to you that it was a family misunderstanding, and he feels good about letting her go 2/2 to the patient's NML serum level x 1. Disregarding the apparent gross negligence with an SI psych patient, do you plan to do anything different after your now former friend leaves?

Back 218

Yes, re-examine her making your own decisions, and repeating serial phenytoin levels.
2/2 to the long erratic absoprtion of phenytoin after oral overdose, the decision to d/c or medically clear a patient for psych eval CANNOT be based on one serum level (cleared for psych eval, not released to home)

p. 1280**

Front 219

Is cardiac monitoring necessary after isolated oral ingestion of phenytoin?

Back 219

No

(we'll still do it, but there is no cardiotoxic effects with oral overdosing, if cardiac tox effects, consider something else)

p. 1280*

Front 220

What anti-convulsant drug inhibits sodium channels and interferes with muscarinic Ach receptors, nicotinic Ach receptors, N-Methyl-d-aspartate receptors, and CNS adenosine receptors. Relieves neuropathic pain by blockade of synaptic transmission in trigeminal nucleus. It also possesses anticholinergic, anti-arrhythmic, anti-depressant, sedative, and neuromuscular-blocking properties. It has effects that may lead to SIADH. Also induces CYP450...

Back 220

Tegratol (Carbamazepine)

p. 1280

Hint 220

Absorption is slow, 8-12 hrs.

Front 221

T/F: Tegretol, unlike pheytoin, does not protein bind.

Back 221

False, while it does not bind as much, ~80%, it still is protein bound.

p. 1280

Front 222

Carbamazepine is converted to a compund by CYP450 to an active metabolite which is responsible for the toxicity. What is it?

Back 222

Epoxide

p. 1280

Front 223

Tegretol has a delayed an erratic absoprtion. With a crescendo-decrescendo clinical course. What are the clinical manifestations of acute toxicity?

Back 223

1. coma
2. acute respiratory failure
3. ataxia
4. nystagmus
5. miosis
6. mydriasis
7. ileus
8. bowel obstruction
9. hypertonicity
10. increased DTR's
11. dystonic reactions
12. anticholinergic toxidromes

p. 1280

Front 224

Though rare, what are two anti-convulsant therapies that can lead to seizures in overdoses?

Back 224

Cabemezapine
and
Phenytoin

p. 1280

Front 225

Cardiac Arrhythmias are rare in this drug, but it is one of the few drugs that can cause:

Both QRS widening as well as seizures

what is it?

Back 225

Carbemezapine (Tegretol)

p. 1280

Hint 225

Labs in acute overdose: hyponatremia, hyperglycemia, and transient elevation of serum liver enzymes

Front 226

What serum level of Tegretol will be most commonly associated with a fatal outcome?

Back 226

60-80 mcg/mL

But, toxicity is dictated MC by the clinical course and PE of the patient

p. 1280

Front 227

What can be provided to a tegretol over dose patient if with in one hour of ingestion for overdose? After that 1 hour time? What about QRS widening on EKG?

Back 227

1. Activated charcoal
2. Hemodialysis
3. Sodium Bicarb

p. 1280

Front 228

What is the most frequent sign following ingestion/overdose/toxicity of valproate?

Back 228

- CNS depression- ranging from drowsiness to coma
- additionally: respiratory depression, HoTn, low serum glucose, low serum calcium, hypernatremia, hypophosphatemia, and anion gap metabolic acidosis...which may persist for days

p. 1281

Hint 228

- Believed to increase brain endogenous opioid levels
- Metabolized by the liver
- Peak serum concentrations: 4 hours

Front 229

You are examining a patient who has an elevated ammonia level, but no hx of liver failure (no reported hx of cirrhosis/EtOH abuse, etc). What can cause this?

Back 229

Valproate toxicity...

- increases renal production and inhibits hepatic metabolism.

p. 1281

Hint 229

- following acute overdose, cerebral edema has been seen.

Front 230

What serum concentration of valproate will likely induce a coma?

Back 230

> 800 mcg/mL


p. 1281

Front 231

You have a patient with a hx of overdose valproate and sxs c/w the following: lethargy, hyperammonemia, and hepatic dysfunction. Is there anything you can giver her?

Back 231

L-Carnitine 50 mg/kg/d

p. 1281

Front 232

T/F: Second generation anticonvulsants possess little toxicity in acute overdose, and most serious complications reported occur in cases of mixed ingestion.

Back 232

True

p. 1281

Front 233

What anticonvulsant can cause crystallization in the kidney's, crystalluria and hematuria and possibly acute renal failure and is treated with IV fluids.

Back 233

Felbamate (Felbatol)

p. 1281

Front 234

What anticonvulsant has indirect effects on calcium, has reported drug effects with cimetidine and antacids but no serious side effects.

Back 234

Neurontin

p. 1282

Hint 234

- half-life: 5-9 hours
- overdose: drowsiness, ataxia, N/V, MC resolves in 10 hrs.

Front 235

What new agent of anticonvulsant is similar to the older agents, but also has been associated with acute pancreatitis in overdose?

Back 235

Lamictal

p. 1282

Front 236

What newer anticonvulsant is associated with; 20-30 hr half-life, poor interaction with contraceptives and other anticonvulsant, promotion of renal stones? But generally is well tolerated.

Back 236

Topamax

p. 1282

Front 237

Match the following aliphatic compound hydrocarbons:
1. Short a. Liquid
2. Intermediate b. gas
3. long c. solids

Back 237

1. b...short chain aliphatic compunds are gases (methane, propane)
2. a....intermediate chain aliphatic compounds are liquids (solvents, oil and gas)
3. c...Long chain aliphatic comounds are solids (such as wax)

p. 1287

Front 238

What are the two MC toxic exposures of hydrocarbons?

Back 238

ingestion and inhalation

p. 1287

Front 239

What is huffing?

Back 239

When an individual places a solvent hydrocarbon soaked rag over their mouth and nose for inhalation euphoric effect

p. 1287

Front 240

What is bagging?

Back 240

When an individual places hydrocarbon in a bag (usually a plastic one) and repeatedly inhales deeply from the bag

p. 1287

Front 241

What is sniffing?

Back 241

When a hydrocarbon is inhaled directly into the nostrils

p.1287

Front 242

The toxic potential of a hydrocarbon depends on what 6 things?

Back 242

1. physical characteristics (viscosity, surface tension, and volatility)
2. chemical characteristics (aliphatic, aromatic or halogenated)
3. presence of toxic additives (pesticides or heavy metals)
4. routes of exposure
5. concentration of the substance
6. dose of the substance

p. 1287

Front 243

What characteristic contributes the most to the aspiration risk of a hydrocarbon?

Back 243

physical characteristic (such as the viscosity)

p. 1287

Front 244

Viscosity is defined as the resistance to flow. As viscosity decreases, what happens to the aspiration risk?

Back 244

Increases

p. 1287
- Read the next card!

Hint 244

Viscosity is measured in Soybolt Universal Seconds (SUS)

Front 245

Finish the following:
"Patients ingesting substances with viscosities of <____ SUS (ie. gasoline, kerosene, mineral seal oil, turpentine) are at greater risk for aspiration than those ingesting substances with viscosities >____ SUS (ie. diesel fuel, brease, mineral oil, wax, petroleum jelly).

Back 245

a. <60 SUS
b. >100 SUS

p. 1287*

Front 246

What is defined as "the creeping ability" of a hydrocarbon?

Back 246

Surface Tension


p. 1287

Hint 246

"Aspiration risk increases, as this decreases"

Front 247

What measures the ability of a substance to vaporize?

Back 247

Volatility

p. 1287

Hint 247

A compound that is high in volatility will evaporate easily, and MC has a low viscosity and surface tension.

Front 248

What is the risk associated with inhalation of a volatile hydrocarbon?

Back 248

results of systemic absorption and toxicity are great.

p. 1288

Front 249

What electrolyte abnormality is associated with Toluene?

Back 249

Hypokalemia

p. 1288

Front 250

A patient with known hydrocarbon exposure, c/o: coughing, choking, gasping, dyspnea, burning of the mouth. What do you suspect?

Back 250

Aspiration, likely pneumonitis

p. 1288

Hint 250

patients may also develop fever, >102.2, this is common 2/2 inflammatory response

Front 251

Patients with aspiration hx of hydrocarbon substance...what is true regarding the chest x-ray and onset of rad evidence?

Back 251

The initial radiograph in a symptomatic person may be NML and the asx patient may have an abnormal radiograph- sometime in the clinical course.

p. 1288*

Hint 251

MC: appear w/n 2-6 hrs
MC: Will often last for: 18-24 hrs
MC: b/l infiltrates at the bases

Front 252

What is the most acute worrisome cardiac complication associated with solvent abuse?

Back 252

sudden sniffing death syndrome

p. 1289

Front 253

What is sudden sniffing death syndrome?

Back 253

It is a catecholamine sensitization by the heart to hydrocarbons (esp halogenated), which results in ventricular arrythmias.

p. 1289

Hint 253

Other mechanisms of sudden death are: asphyxia, respiratory depression, and vagal inhibition.

Front 254

What are the signs of neurologic toxicity with hydrocarbons?

Back 254

- slurred speech
- ataxia
- lethargy
- coma

p. 1289

Front 255

What electrolyte abnormality is assocated with the abuse of airplane glue, plastic cement, and acrylic paint?

Back 255

Hypokalemia

p. 1289
Table 193-1, Toluene

Front 256

A 45 y/o shoe making worker reports chronic numbness and paresthesias in the extremities. States that he had been to his doctor and checked for DM, as well as Folate/B12 deficiency. + hx of Tob use 1 ppd x 2 yrs in his twenties. No EtOH use. No Drug use. Surgeries, Appendectomy when 12 y/o. Fhx: none for neurologic disease. PE reveals no focal neuro deficits, NML exam, except for sensation disturbance- endorsed by the patient. What do you think at this point is the problem?

Back 256

Hydrocarbon exposure.

p. 1290

Hint 256

n-hexane and n-butyl ketone

found in solvents in printing, shoe making, textile and furnitureindustries.

Front 257

What GI effects occur from hydrocarbon exposure?

Back 257

1. Nausea and vomiting
2. abdominal pain
3. loss of appetite

p. 1290

Hint 257

Hepatic toxicity- an occur with halogenated hydrocarbons.
Carbon tetrachloride can cause liver necrosis similar to APAP toxicity

Front 258

T/F: Most commonly, after exposure to hydrocarbons, liver enzymes will normalize with in 24 hours. Therefore it is impossible to go into cirrhosis.

Back 258

False- in acute setting liver enzymes will Normalize w/in 24 hours. However, long term exposure to carbon tetrachloride can result in cirrhosis and hepatomas.

p. 1290

Front 259

What results do chlorinated hydrocarbons (chloroform, carbon tetrachloride, and trichloroethylene) have on the kidney's?

Back 259

Nephrotoxic

p. 1290

Front 260

What effect does Toluene have on the kidney's?

Back 260

Renal Tubular Acidosis

p. 1290

Front 261

A middle age man reports with sxs of muscle weakness.
His labs reveal a NML anion gap, hyperchloremic acidosis, with a potassium of 1.9 , and a urine pH: >5.5; CK 2200. Seems to manifest sxs c/w borderline paralysis, with 1+ strength at best throughout. What hydrocarbon do you suspect?

Back 261

Toluene

p. 1290

Front 262

T/F: With regard to hematologic effects, patient's may come to the ED with lethargy, shortness of breath, and cyanosis. What do these sxs depend on?

Back 262

1. Route of exposure
2. Duration of exposure.

p. 1290

Front 263

T/F: Dermal exposure to hydrocarbons can result in toxicity. In fact, frost bite has occured with some agents.

Back 263

True:
frostbite with fluorinated agents

p. 1290

Front 264

T/F: Diagnosis of hydrocarbon toxicity is based on the results of serum specometry for hydrocabon disassociative properties.

Back 264

WHAT?!?! False, it is based on the composite picture:
1. hx
2. PE
3. bedside cardiac monitoring
4. Lab tests
5. CXR

- the composite picture

p. 1290

Hint 264

AMS:
- D-stick
- Ammonia
- Head CT
- LP

Front 265

What drug is contraindicated in the treatment of chemical pneumonitis from hydrocarbons?

Back 265

Steroids

p. 1291

Hint 265

because the drugs impair cellular immune response and increase the chance of bacterial superinfection
Yet prophylactic abx use has no proven benefit either

Front 266

How is hypotension managed following hydrocarbon exposure? What should be avoided?

Back 266

1. Fluids
2. Avoid catecholamines: dopamine, norEpi, and Epi= as these can precipitate a dysrrythmia, especially after exposure to halogenated hydrocarbons and aromatic hydrocarbons

p. 1291

Front 267

How soon are hydrocarbon induced dysrrythmias seen, particularly after inhalation.

Back 267

Very Soon following contact.

Hint 267

Avoid procainamide as well as amiodorone, as these can prolong QT interval

Front 268

When suspected contact/exposure to hydrocarbons, esp superficial/skin contact, what is one of the most important consideration in mitigating worsening events?

Back 268

Get patient completely undressed and washed with soap and water, to protect the patient and the staff.

p. 1291
- read next card**

Hint 268

There may be a role for GI decontamination w/in 1 hour after the ingestion of large amounts of hydrocarbons that are more likely to cause systemic toxicity if absorbed, such as halogenated hydrocarbons. However, for these cases there are no studies demonstrating benefit.

Front 269

How soon can a patient with hx of aspiration non-halogenated aliphatic hydrocarbons be d/c'd from the hospital?

Back 269

6-8 hrs of asx period.

p. 1291

Front 270

What are caustics?

Back 270

Substances that cause both functional and histologic damage on contact.

p. 1292
- this can be acid (<7) or alkali (>7) substances

Front 271

What are the three caustic exposure risks?

Back 271

1. unintentional (MC curious toddler/children)
2. intentional teen or adult ingestions with suicidal intentions
3. incidental (often occupational exposure)

p. 1292

Front 272

What is the MC alkali exposure reported by the American Association of Poison Control Centers?

Back 272

Bleach

p. 1292

Hint 272

MC the exposure is benign

Front 273

The pH, concentration, duration of contact, volume present, and titratable acid or alkali reserve determine the level of tissue injury. pH < 3 for acids and > 11 for alkali- tend to cause significant injury.
Solid caustic ingestion causes tissue injury where? Where as liquid caustics cause more tissue injury where?

Back 273

1. Solid caustics cause injury in the oropharynx and proximal esophagus
2. Liquid caustics often cause distal esophageal and gastric injury

p. 1292

Hint 273

Grading the esophageal mucosal injury requires endoscopy:
Grade 1: tissue edema and hyperemia
Grade 2: ulcerations and blisters and white exudates
A: non-circumferential
B: circumfirential
Grade 3: Burns that are deep ulcerations and necrotic lesions.

after initial injury, tissue healing begins in the 2 months after. Mild cases, normal esophageal function and tissue is restored. Severe cases, dense scar tissue resulting in stricture.

Front 274

What caustic type causes a deep tissue injury called liquefacation necrosis?

Back 274

Alkali Injuries

p. 1293
- Household bleach, pH of ~11; rarely causes significant injury. Industrial bleach, causes significant necrosis. For more on this, read this section in the book.

Front 275

What caustic type causes coagulation necrosis?

Back 275

Acids

p. 1293

Front 276

What results in high grade gastric injuries when ingested (2/2 pylorospasm and pooling) and a higher mortality rate, alkali or acid?

Back 276

Acid

p. 1293

Front 277

An individual has evidence of caustic ingestion, from hx and PE: oral and facial dribbling burns.

Reports: dysphonia, stridor, and respiratory distress, where is the injury?

Back 277

Laryngotracheal

p. 1293

Front 278

An individual has evidence of caustic ingestion, from hx and PE: oral and facial dribbling burns.

Reports: Dysphagia, odonophagia, epigastric pain, and vomiting, where is the injury?

Back 278

Gastric Tract

p. 1293

Front 279

T/F: Intentional ingestion of caustics are associated with higher grades of GI tract injuries, with or without clinically obvious signs.

Back 279

True

p. 1293

Hint 279

FYI: MC higher grades of injury will often have some initial sign/sx: stridor, drooling or vomit.

Front 280

What are the etiologies of shock in the caustic ingestion patient?

Back 280

- GI bleed
- complications of GI perforation
- volume depletion
- coingestants

p. 1293

Hint 280

Complete examination includes examination for:
1. peritoneal signs/evidence of hollow viscous injury
2. palpation of entire chest wall for subcutaneous emphysema
3. careful examination of the eyes and skin- splash injury, dribble injury

Front 281

What ancillary tests should be ordered in: intentional ingestion, strong alkali (ie, those with signs and sxs of significant injuries)?

Back 281

1. VBG/ABG
2. CMP (electrolytes/liver enzymes)
3. CBC
4. Coags
5. ABO
6. Lactate
7. Upright CXR

p. 1293

Front 282

T/F: Caustic ingestions can cause an anion gap acidosis based on lactate production due to direct tissue injury or shock.

Back 282

True

p. 1293

Front 283

T/F: Acid ingestion can be associated with both severe anion gap and non-anion gap acidosis.

Back 283

True

p. 1293-1294

Front 284

What can be done to look for free air under the diaphragm (perf'd viscous), if the patient is unable to tolerate standing?

Back 284

- left lateral lying image
- consider also a chest CT

p. 1294

Front 285

What is the first priority in patient management following caustic ingestion?

Back 285

Airway mgt

p. 1294*

Hint 285

Caustic airways are to be regarded as difficult airways

Front 286

Why are blind nasotracheal intubations following caustic ingestion regarded as contraindicated?

Back 286

2/2 to the potential for exacerbating airway injury

p. 1294*

Front 287

What are the standard decontamination measures upon arrival of caustic exposure?

Back 287

- removal of soiled or soaked clothing/materials
- copious irrigation with towels and soap
- vomiting may re-expose the patient and the staff (address early and ensure staff has appropriate attire donned)

p. 1294

Front 288

T/F: Gastric decontamination with activated charcoal is an absolute contraindication in caustic ingestions.

Back 288

False, it is a relative contraindication

p. 1294*
Important too, next slide

Hint 288

- Caustics do NOT adhere to charcoal and may jeopardize adequate visualization during endoscopy
- However, appropriate in episodes of coingestion, which pose a risk of severe toxicity

Front 289

T/F: Syrup of ipecac, nasogastric tubes, and dilution/neutralization are contraindicated in the caustic ingestion patient.

Back 289

True

p. 1295*

Front 290

Central venous access may be necessary in the caustic ingestion, exposure patient; for the purposes of monitoring and resuscitation, or if massive amounts of calcium are needed for systemic toxicity of what agent?

Back 290

Hydroflouric Acid

p. 1295

Front 291

There has been much debate as to which caustic ingestions need endoscopy. It is generally accepted/agreed that which patients NEED EARLY endoscopy, because of their predisposition to such high grades of injury?

Back 291

Intentional (SI) exposure

p. 1295*

Front 292

When is early endoscopy performed in unintentional caustic ingestion/exposure in both adult and pediatric populations?

Back 292

When they possess obvious signs or sxs of injury such as stridor or significant oropharyngeal burns and/or vomiting, drooling, or food refusal, with or without oropharyngeal burns.

p. 1295*

Front 293

What is the purpose of endoscopy following caustic ingestion?

Back 293

Diagnostic

p. 1295

Front 294

When does tissue friability increase following caustic injury and become its worst (hence the reasoning for early endoscopy in the appropriate patient)?

Back 294

- Caustic Burns increase significantly at 24-48 hrs post-injury
- Maximal friability is days 5-14

p. 1295

Front 295

When is the ideal timeframe to perform endoscopy to avoid iatrogenic perforation in caustic ingestion?

Back 295

Ideally, within the first few hours, < 24 hours post ingestion, but not to exceed 24 hours post ingestion to avoid iatrogenic perforation

p. 1295*

Front 296

If an individual did not want to perform endoscopic evaluation of the esophagus following caustic insult, what other modalities are available?

Back 296

1. Abdominal CT
2. Serial Lactic Acid Measurements
3. Ultrasonography


p. 1295

Front 297

T/F: There is a gross inflammatory process from caustic ingestion that can be retarded by the use of 1 time high dose steroids.

Back 297

False, there has been no evidence to support consistent benefit, therefore systemic steroids cannot be recommended as a standard of care.

p. 1295

Hint 297

Additionally, prophylactic abx's are not recommended either, as their use was only recommended concurrently with steroids.

Front 298

What are the following an indication for:
- Large volume ingestions (>150 mL)
- signs of shock
- respiratory distress
- persistent lactic acidosis
- ascites
- pleural fluid

Back 298

surgical exploration

p. 1295-1296

Front 299

Alkali injuries are associated with morbidity and mortality from direct tissue necrosis. However, why is the risk with acid greater?

Back 299

Because their is not only tissue destruction but additional systemic toxicity.

the systemic toxicity:
- acid-base d/o
- hemolysis
- coagulopathy
- and renal failure

p. 1296

Front 300

How long should occular caustics be irrigated for?

Back 300

There is no set duration. However, MC it is recommended that the eyes be irrigated for 15 minutes and reassessed. Use nitrazine paper (pH paper) tp examine, normal is (7.4).

Front 301

What is the best irrigation solution to irrigate the eye following caustic contact?

Back 301

Normal Saline or Lactated Ringers.

p. 1296

Hint 301

Tap water is too hypotonic and can lead to edema

Front 302

What is regarded as the key principle of choice with regard to the irrigation of eyes following caustic contact?

Back 302

Not necessarily the choice of fluid as immediate, acute concern, but that the immediate and copius fluid application is a MUST!

p. 1296*

Front 303

You whatch as a friend is irrigating an occular injury from caustic insult. However, immediately following the 15 minutes of irrigation, your friend applies nitrazine and reads a pH~7.6. He says "completed" and walks out. Is this right?

Back 303

NO. You should hold the irrigation for enough time. THis was likely a false + and reflected more of the pH of the irrigation solution than of the eye.

p. 1296

Front 304

T/F: Most disc batteries pass through the GI tract w/o complications, as a FB.

Back 304

True

p. 1296

Front 305

MC GI injuries from disc batteries take place in the esophagus. Risks are greatest if the battery diameter is ____, of esophageal injury and impaction.

Back 305

> 15-20 mm

p. 1296

- when this is suspected, what do you do?

Hint 305

Obtain radiographs is a must. If in the airway: bronchoscopy is a must. If in the gastroesophageal junction and appears to be in the stomach, then follow up radiograph is a must and should be obtained in 24-48 hours...to ensure that the battery is passed the pylorus.

Front 306

Hydrofluoric Acid is a weak acid, so why is it a threat? (Most commonly to the upper extremities)

Back 306

The free fluride ion complexes with body calcium and magnesium, resulting in calcium chelation and cellular death.

p. 1297

Hint 306

FYI: inverse association between the onset of pain and the concentration, less concentration the longer the time to sxs- even up to a day after contact. > 50% contact, immediate pain

Front 307

A 22 y/o M c/o an b/l arm and chest pain from contact with solutions at work when a shelf fell over. He works as a glass etcher. Upon examination, there is some wounds with a white discoloration but are not on appearance c/w the patients report of pain...ie. Pain out of proporation to his expressed complaint. You order labs and have his wound irrigated. And provide pain mgt. As his labs are coming back that patient is reportedly going into V-fib. You provide 200J biphasic x 3 in between the CPR set, and even went to epi and Amiodorone, but have to call it. You go back to finish documenting the code and note a low Calcium, Magnesium, Elevated Potassium, Acidosis. What happened.

Back 307

Systemic Absorption from the contact burns from Hydrofluoric Acid.

p. 1297
NEXT SLIDE

Hint 307

Topical calcium gluconate gel was the appropriate therapy after irrigation and would have treated the pain as well as the Calcium deficiency

Front 308

If topical therapies of Calcium Gluconate are not helping a patient exposed to Hydrofluoric acid, and you want to provide this systemically, how would you do this?

Back 308

Intra-arterial Hydrofluoric Acid is most appropriate.

p. 1297

Front 309

You want to provide a hydrofluoric acid patient with intra-arterial calcium. Should Calcium Chloride be used?

Back 309

NO, it should be avoided as it can lead to skin necrosis and extravasation injury.

p. 1297

Front 310

What route of exposure to hydrofluoric acid has the highest mortality rate?

Back 310

Oral ingestion

p. 1297

Front 311

The vast majority of overdoses associated from antibiotics are from what cause?

Back 311

Iatrogenic

p. 1324

Front 312

What are the MC adverse effects seen with antimicrobials?

Back 312

- allergic reaction
- drug interactions
- secondary side effects
- toxic effects (rare)

p. 1324

Front 313

What age group incurs most of the drug overdoses from antibiotics?

Back 313

Neonates and infants, secondary to their small weight and mathematics

p. 1325

Front 314

What is the acute toxicity and treatment for the following:

PCN

Back 314

1. Seizures
2. Benzo's

p 1325

Front 315

What is the acute toxicity and treatment for the following:

Amoxicillin

Back 315

1. Crystalluria, hematuria and acute renal failure
2. IV hydration

p. 1325

Front 316

What is the acute toxicity and treatment for the following:

Cephalosporins

Back 316

1. Encephalopathy, seizures
2. Benzo's

p. 1325

Front 317

What is the acute toxicity and treatment for the following:

Chloramphenicol

Back 317

1. Cardiovascular collapse
2. Hemodialysis

Front 318

What is the acute toxicity and treatment for the following:

Flouroquinolones

Back 318

1. Seizures
2. Benzo's

p. 1325

Front 319

What is the acute toxicity and treatment for the following:

Macrolides

Back 319

1. Prolonged QT interval, Torsades De Pointes
2. Magnesium Sulfate

p. 1325

Front 320

What is the acute toxicity and treatment for the following:

Sulfonamides

Back 320

1. Methemoglobinemia
2. Methylene Blue

p. 1325

Front 321

What is the acute toxicity and treatment for the following:

Vancomycin

Back 321

1. "Red-Man Syndrome"
2. Slow/Stop infusion and consider antihistamines- esp if advances to allergic response

p. 1325

Front 322

What is the acute toxicity and treatment for the following:

Isoniazid

Back 322

1. Inhibition of gamma-aminobutyric acid synthesis and functional deficiency pyridoxine, seizures
2. Benzo's and Pyridoxine

p. 1325

Front 323

What is the acute toxicity and treatment for the following:

Quinine

Back 323

1. Na-K channel blockade, alpha-adrenergic antagonist, hypoglycemia, ototoxicity, and ophthamic toxocity
2. Multi-dose activated charcoal, sodium bicarb, dextrose and octreatide

p. 1325

Front 324

What is the acute toxicity and treatment for the following:

Chloroquine

Back 324

1. Seizures, QRS-complexes, and QT interval prolongation, HoTn, Hypokalemia
2. Epinephrine, Diazepam

p. 1325

Front 325

What is the acute toxicity and treatment for the following:

Primaquine

Back 325

1. Methemoglobinemia, hemolysis
2. Methylene Blue

p. 1325

Front 326

Patients who sustain an acute overdose from antibiotics, experience what?

Back 326

None, they MC remain asx

p. 1325

Front 327

Significant ingestion of what three antibiotics can result in severe toxicity?

Back 327

1. Isoniazid
2. Chloroquine
3. Quinine

p. 1325

Front 328

T/F: Unless there are contraindications, GI decontamination with activated charcoal is a MUST in those suspected of toxic ingestion of potentially dangerous antibiotics. Even multi-dose activated charcoal w/o sorbitol.

Back 328

True

p. 1325

Front 329

Hemodialysis and hemoperfusion are not useful for the treatment of most antiobiotic intoxicants, except for three agents. What are they?

Back 329

1. Dapsone
2. Chloramphenicol
3. Pentamidine

p. 1325

Front 330

What is the most toxic aminoglycoside?

Back 330

Neomycin

p. 1325

Front 331

What is the treatment for toxicity caused by aminoglycoside?

Back 331

Fluids/Hydration as well as monitoring of hearing and renal function

p. 1325

Hint 331

- Nephrotoxicity is associated with: age, decreased renal and liver function, as well as high/prolonged doses, high trough serum concentrations, and the presence of shock.

Front 332

What is the antimicrobial drug class, and list some of the drugs, with the greatest potential for toxic effects?

Back 332

Anti-malarials

- quinine
- primequine
- meflaquine
- chloroquine

p. 1325

Front 333

Why is quinine associated with cardiotoxicity: wide QRS, torsades, HoTn, syncope and sudden cardiac death?

Back 333

Because of the effect this has on sodium-potassium channel blockade

p. 1325

Hint 333

Ototoxic effects: tinnitus and deafness
Hypoglycemia

Front 334

What is one of the few drugs, when overdose/toxicity is suspected, where muti-dose activated charcoal is a must? What is another treatment?

Back 334

1. Quinine
2. sodium bicarb for wide QRS

Front 335

What can cause more profound HoTn than quinine overdose, is often accompanied by respiratory depression and hypokalemia, neurotoxicity. Decreased mortality has been demonstrated with early intubation, gastric lavage, deep sedation, as well as benzo's, vasoactive support?

Back 335

Chloroquine

p. 1325

Front 336

30 y/o M from Djibouti presents with hx of depression, and taking overdose of medications for TB, and has the following sxs: Nausea, AMS, and changes in walking approximately 30 minutes following suspected ingestion. As he is being brought in, he begins to seize. What is the medication?

Back 336

Isoniazid

p. 1326

Front 337

What are the three classic features of acute isoniazid overdose?

Back 337

1. seizure
2. metabolic acidosis
3. protracted coma

p. 1326*

Hint 337

Tx with B6, pyridoxine- 5 gms

Front 338

When should the diagnosis of isoniazid toxicity be considered?

Back 338

When a patient shows evidence of refractory seizures

p. 1326*

Front 339

T/F: Phenytoin is a last, but helpful resort in the tx of Isoniazid induced seizures.

Back 339

False, there is NO role. Additionally, there is little role for the use of sodium bicarbonate in the metabolic acidosis associated with acute isoniazid overdose.

p. 1326

Front 340

T/F: Encephalopathy, agitation, and absence seizures have been reported with ceftazidime, cefepime, and cefuroxime.

Back 340

True

p. 1326

Front 341

QT prolongation has been associated with Macrolides. Which macrolide has been associated with pancreatitis, when overdosed?

Back 341

E-mycin

p. 1326

Front 342

Retinol is absorbed from the gut, from Vitamin A, is then stored in the liver, and then forms part of the visual pigment in the eye. What is the recommended dose for males and females?

Back 342

Males 5000 units per day
Females 4000 units per day

p. 1320

Front 343

What forms the visual pigment of the eye, is important for the mucous secreting columnar epithelial cells, maintains bone growth, and maintains cellular membrane stability?

Back 343

Vitamin A/Retinols

p. 1320

Front 344

What are the symptoms of hypervitaminosis A?

Back 344

- blurred vision
- appetite loss
- abnormal skin pigment
- loss of hair
- dry skin
- pruritis
- long bone pain- and increased incidence of bone fractures
- can also lead to pseudo tumor cerebri and hepatic failure

p. 1320

Front 345

The physiologic active form of Vitamin D is 1,25-dihydroxycholecalciferol, comes from what?

Back 345

Vitamin D3

p. 1321

Front 346

What aids vitamin D in absorption, and where is it absorbed?

Back 346

1. bile aids in absorption in Vitamin D, in the...
2. Jejenum, from the jejenum to portal circulation, reaching the liver and is hydroxalated (partially), then sent to the kidney for further hydroxylation. Then to the serum

p. 1321

Front 347

What is the average daily requirement of Vitamin D?

Back 347

400 IU

p. 1321

Front 348

The toxicity of hypervitaminosis D, with clinical findings of anorexia, nausea, abdominal pain, lethargy, weight loss, weight loss, polyuria, constipation, confusion and coma, is from what?

Back 348

Hypercalcemia

p. 1321

Front 349

What is the tx for Hypervitaminosis D?

Back 349

- d/c vitamin D
- d/c calcium intake
- monitor serum calcium levels
- Pamidronate disodium, a bisphosphanate, can be used too.

p. 1321

Front 350

What are the following foods rich with:
- wheat germ
- corn
- soybean
- sunflower seeds
- cod liver

Back 350

Vitamin E

p. 1321

Front 351

At high levels, what does effect does vitamin E have on platelet aggregation?

Back 351

Prohibits it (ie. prolongs bleeding time)

p. 1321

Front 352

A patient comes to see you, bleeding uncontrollably from her nose and oozing from her gums. She states that she had heart surgery a few months ago, takes toprolol, simvastatin, lisinopril, and predaxa, as well as MV and Vitamin E- which she just started at the recommendation of her friend. What do you think?

Back 352

The vitamin E prohibits platelet aggregation...pts ingesting large amounts of Vitamin E who are taking anti-coagulants should be observed closely for bleeding tendencies, those not taking anti-coagulants will rarely have coagulation difficulties, except neonates, who are more sensative to the effects of Vitamin E.

p. 1321*

Front 353

What two vitmains have a negative impact on Vitamin K absorption?

Back 353

1. High levels of Vitamin A
2. Vitamin E

p. 1321

Front 354

What vitmain is required for clotting factors?

Back 354

Vitamin K

p. 1321

Front 355

Megadoses of what vitamin can lead to: hemolytic anemia, kernicterus, and hemoglobinuria in premature infants and renal tubular degeneration, liver damage, hypothrombinemia, and petechial hemorrhages in adults?

Back 355

Vitamin K

p. 1321*

Front 356

Thiamine (Vitamin B1) is found in what foods?

Back 356

- fruits
- grains
- meats
- fish
- milk
- highest levels are found in pork products

p. 1321

Front 357

T/F: Though rare, when taken in at high levels thiamine can be toxic.

Back 357

False, your body does not store this...so, it is non-toxic

p. 1321

Front 358

A women reports to the ER after trying to commit suicide using her sisters bottle of Riboflavin...taking the whole thing. What do you do?

Back 358

What ever regular screening examination you do to have her admitted to Psych, there has never been a case of toxicity from this regardless of the amount.

p. 1321

Front 359

A patient is seen by you where you work part time, in a clinic, c/o sxs: cracked lips, redened togue, and eczema of face and genitals. What vitamin is this patient shy in?

Back 359

B2 Riboflavin

p. 1321

Front 360

What are the sxs associated with Niacin deficiency?

Back 360

- anorexia
- anxiety
- depression
- irritability
- weakness

p. 1322

Front 361

A child busted into his Dad's medicine cabinet to take a bunch of crap to get high. Instead he got a sensation that his face, neck and chest were burning, itching and reddening- with the red color being visible. He also c/o nausea, abdominal pain, diarrhea and a HA. Though likely intending something altogether different, what vitamin did this kid take?

Back 361

Niacin (B3)


p. 1322

Hint 361

concern with effects of the heart and liver enzymes in chronic use

Front 362

What effect can Vitamin B6 (Pyridoxine) deficiency have on an infant?

Back 362

- growth retardation
- weightloss
- hyperirritability
- convulsions
- anemia

p. 1322

Front 363

Vitamin B6 in doses that exceed ____ over several weeks can lead to nerve damage.

Back 363

>5 gms per day

p. 1322*

Front 364

What vitamin, that comes in many forms, is responsible for for the formation of amino acids and proteins?

Back 364

B12

p. 1322

Front 365

What vitamin deficiency has been associated with macrocytosis on CBC as well as hemolysis (elevated LDH), and neuro problems: symmetrical paresthesias of the hands and feet and decreased vibratory sensations.

Back 365

Vitamin B12 (pernicious anemia)

p. 1322

Front 366

T/F: B12 toxicity is rare, except for a pigment change in the skin that will clear with in 2 weeks of cessation.

Back 366

True

p. 1322

Front 367

A guy comes to see you following dietary changes and feeling depressed. States that he has been on a low calorie diet for "months". In spite of losing weight, his cholesterol continues to climb, he is losing his hair, has dry skin, worsening appetite (making the diet easier), and has been feeling depressed. TSH, CBC, and CMP NML. What vitamin is he deficient in?

Back 367

Biotin

p. 1322

Front 368

What is essential for DNA, RNA, and proteins; may reverse megaloblastic RBC's of pernicious anemia, but no impact on neurologic effects. Is found in green leafy veggies, yeasts and liver; and non-toxic in large doses?

Back 368

Folate

p. 1322

Front 369

What vitamin increases the absorption of Iron, and a deficiency will lead to: collagen, protein, and metabolism abnormalities. It is predominantly found in fruits and veggies and absorbed in the jejenum and ileum?

Back 369

Vitamin C

p. 1323

Front 370

T/F: Vitamin C is preserved in veggies and some fruits when heated, dried, or stored.

Back 370

False, all these forms of storage and preservation decrease vitamin C

p. 1323

Front 371

T/F: Vitamin C has been shown to produce attacks of gout and nephrolithiasis. intrarenal deposition of oxalate crystals has been reported to cause renal failure in patients with chronic high-dose ascorbate ingestion.

Back 371

True

p. 1323**

Front 372

High doses of Vitamin C can lead to diarrhea and abdominal pain that stop with cessation. What are two common false positive tests with this as well?

Back 372

1. False + guiac
2. False elevations in glucose

p. 1323

Front 373

T/F: THere is evidence to support the use of gingko for Dementia and Intermittent claudication, St John's Wort for depression, Kava for anxiety, and Saw Palmetto for BPH. Yet, these agents have some inherent side effects as well as potential for herb-drug interaction.

Back 373

True

p. 1323*

Front 374

Review Charts: pp. 1320-1324

Back 374

Tables 199-1, 199-3, 199-4, 199-5

Front 375

What are chemicals which posess three properties: 1. good conductor of heat and electricity 2. they are able to form cations 3. they can combine with non-metals through ionic bonds.

Back 375

Metals

p. 1308*

Front 376

What are the following metals:
- Berryllium
- Vanadium
- Cadmium
- Barium
- Osmium
- Mercury
- Thallium
- Lead

Back 376

Toxic Metals

p. 1308
- Which two metals are the most concerning for human poisoning?

Hint 376

Mecury and Lead

Front 377

What is the term for chemical elements with properties intermediate to metals and non-metals.

Back 377

Metalloids

p. 1308*
What are their two general properties?

Hint 377

1. they are semi-conductors of electricity
2. they form amphoteric oxides

Front 378

What are the following:
- boron
- silicon
- germanium
- arsenic
-antimony
- tellurium
- polonium

Back 378

Metalloids

p. 1308
- What is the most clinically significant metalloid?

Hint 378

Arsenic

Front 379

Exposure from metals and non-metals can come from three main sources, like what?

Back 379

1. the pure element
2. an organic (contains carbon) compound containing the element
3. an inorganic (does not contain carbon) compound containing the element

p. 1308

Front 380

There areas of the body MC affected by metals and metalloids are: neurologic, cardiovascular, GI, hematologic, and renal (protean manifestations). Why is it important to recognize an initial "index case" of metal poisoing when a metal source is enviromental or industrial?

Back 380

To keep others from being exposed

p. 1308*

Front 381

What is the MC chronic metal poisoning and remains a major environmental contaminant, esp in developing world?

Back 381

Lead

p. 1308
What are the routes of exposure MC?

Hint 381

Inhalation and/or Ingestion

Front 382

What elemental deficiencies can contribute to increased GI absorption of lead in children?

Back 382

- Calcium
- Iron
- Zinc
- Copper

p. 1309

Front 383

Bullets shot into muscle or bone are rarely a problem for lead toxicity. However, they do become a concern when located where?

Back 383

Within/Near body fluids: such as CSF and/or synovial fluid.

p. 1309

Front 384

Where is > 90% of the bodies lead stored?

Back 384

In the bone

p. 1309

Front 385

What impact does lead have on the CNS?

Back 385

1. Injuries to the astrocytes, microvasculature and damage to the blood brain barrier, cerebral edema, and increased ICP 2. decreased in memory and learning 3. alteration in calcium homeostasis, leads to spontaneous, uncontrolled neurotransmitter release
Peripheral nervous system: segmental demyelination, secondary axonal degeneration of mostly motor nerves

p. 1309

Front 386

What effect does lead have on cardiovascular system?

Back 386

1. HTN
2. atherosclerotic vascular disease

p. 1309

Front 387

What effect does lead have on hematopoietic system?

Back 387

interferes with porphyrin metabolism, ie. anemia. Microcytic anemia may not only be from Iron, but also from lead. Additionally, may cause hemolysis

p. 1309

Front 388

What effect does lead have on the kidney/renal system?

Back 388

Causes a Fanconi's Syndrome- rejection of amino acids, glucose, uric acid, bicarb and phosphate by the proximal tubules of the kidney, and a resultant Renal Tubular Acidosis.

p. 1309

Front 389

What toxic metal is MC associated with the peripheral nerve evidence of calssic "wrist drop", as well as absent DTRs, motor weakness and paresthesias, but spared sensory fxn?

Back 389

Lead exposure

p. 1309

Front 390

A patient is presented with c/o HA's, which make him very irritable, as well as memory difficulty. Additionally has had numbness and discomfort and weakness in extremities. No recent trauma and no recent/remote hx of intranial/axial surgeries. + ROS: abd pain/diarrhea, increased urination, decreased labido and low energy. VS: 190/98, HR: 88, RR: 10, Temp: 98.7, SaO2: 96% RA.
Shx: Works as a stain glass designer. No EtOH/Tob or Recreational drugs. Non-Married, no children.
PE: NML, except for appearance of uncomfortable M patient, no distress.
CT scan and CXR obtained at the desk: Negative. VBG: PH: 7.4, pCO2: 55, PO2: 65, HCO3: 16. Labs: UA: + Urate crystals. CMP: 140/3.8/110/16/40/1.7/60, ALT/AST: 190/145.
What is his problem?

Back 390

Chronic Lead toxicity

p. 1309

Front 391

What can cause encephalopathy, beginning as: seizures, coma and maybe delirium and/or mania in children?

Back 391

lead poisoning.

p. 1309

Front 392

What sxs of lead poisoning predominate in the acute setting? What about chronic?

Back 392

Acute setting: GI sxs
Chronic Setting: Neuro sxs

p. 1309

Front 393

What should you be suspicious of when a patient has the following:
1. abdominal pain
2. neurologic dysfunction
3. hemolytic anemia

Back 393

Lead poisoning

p. 1310**
Definately consider in children presenting with encephalopathy

Front 394

What is the single "best test" for evaluating lead toxicity?

Back 394

serum lead level.

>10 mcg/dL are elevated

p. 1310

Front 395

While the blood lead level is important, this takes time (sometimes days). Diagnostic studies in the ED therefore rely on what for evidence of lead exposure?

Back 395

evaluation of anemia and examination of radiographs

p. 1310*

Front 396

T/F: Basophilic stippling, from impaired clearing of RNA degradation products is a specific marker of lead toxicity.

Back 396

False, it is seen in lead tox for that indicated reason, but it is not specific for lead toxicity

p. 1310

Front 397

What are lead lines on long bone imaging of lead poisoning children?

Back 397

The areas of the bones where remodeling did not occur, it is NOT the deposition of lead in the bone

p. 1310

Front 398

What should be PROMPTLY instituted in the treatment of lead encephalopathy, even while waiting for serum lead levels?

Back 398

Chelation Therapy

p. 1310

Front 399

You have a kid who was going to go fishing with his dad. FOP reports that he had some lead anchors in the kit, but then they were gone. He believes that child swollowed them as a joke, he is concerned. You obtain radiograph and see them on the film, and they appear to be two medium to large anchors. What do you do? What if the abdominal film reveals "specks" of lead?

Back 399

- Large anchors= surgical removal
- small "flecks"= whole bowel irrigation with polyethelene glycol.

p. 1310

Front 400

Chelation dosing schedules are guided by: 1. serum levels 2. presence or absence of sxs 3. _____ of the patient.

Back 400

Age

p. 1310

Front 401

T/F: Side effects of chelation therapy, for lead toxicity, are common. It is important to have a toxicologist involved early.

Back 401

True

p. 1310

Front 402

Dimercaprol is a chelating agent used for lead toxicity, along with edetate calcium disodium. However, the diluent must be used with caution in what group of individuals?

Back 402

Peanut allergy....

the diluent contains peanut oil.

p. 1310*
What are the side effects of this agent?

Hint 402

- HTN
- fever
- pain
- sterile abscess at injection site
- nausea
- vomiting
- diarrhea
- abdominal pain
- HA
- lacrimation
- rhinorrhea
- hemolysis (G6PD deficiency)

Front 403

Some individuals fear that giving a chelating agent, such as edetate calcium disodium as an effective chealator will mobilize the lead stored in the bone. Edetate does not cross the blood brain barrier, what can be done to minimize this risk?

Back 403

Giving a chelating agent that can prevent this, while giving edetate calcium disodium, one that crosses the blood brain barrier: Dimercaprol.

p. 1311

Front 404

T/F: Edetate calcium disodium is the same as edetate disodium

Back 404

NO!!! Edetate disodium, is for the treatment of hypercalcemia. Edetate calcium disodium is used as a chelating agent in the treatment of lead toxicity.

p. 1311**

Hint 404

Mixing these up can be deadly

Front 405

T/F: Arsenic can be found in kelp, well water, and insecticide as well as rodenticides. It is well absorbed in the GI, respiraotry and parenteral routes. However, it is not absorbed well into intact and non-intact skin.

Back 405

False, the beginning is true, however, the last statement is not. It is well absorbed through non-intact skin

p. 1311

Hint 405

FYI: after absorption arsenic localizes to erythrocytes and leukocytes. W/in 24 hrs it is then distributed to liver, spleen, kidney, lung, GI tract, muscle, nervous system

Front 406

Does arsenic reversibly or irreversibly bind?

Back 406

Reversibly binds

p. 1311

Hint 406

Read: Pathophysiology of arsenic.

p. 1311. 1 paragraph

Front 407

An individual presents to you c/o N/V, diarrhea- that is perfuse and uncontrolled over last 10 minutes. He is tachycardic, hypotensive, tachypneic and appears toxic and is declining in front of you. You decide to intubate him and draw a rainbow of labs. EKG shows ST segment depression in the precordial leads. CXR with diffuse, patchy infiltrates, c/w gross pulmonary edema. basic panel reveals ARF. Just before he collapsed he said, "I think she's trying to kill me...I swear, I taste metal...she said die like the rat and roach you are...". WOW! What do you supposed she gave him?

Back 407

Arsenic (Acute Toxicity)

p. 1311

Front 408

Patient states that he was using some homeopathic crap over last month "and a lot of it", per a friend, and has developed HA, confusion, and personality changes. has numbness and "weird" sensations all over. EKG: QT prolongation, he has a cough and alveolar inflitrates, as well as rash, patches of hair loss and mee's lines. What is in the homepathic medicine that is jacking this guy up?

Back 408

Arsenic (he has a subacute toxicity)

p 1311

Front 409

What should be considered in a patient who ha hypotension of unknown etiology that was preceded by severe gastroenteritis?

Back 409

Arsenic toxicity

p. 1312*

Front 410

Definitive dx of acute arsenic poising depends on what finding?

Back 410

Elevated arseninc levels in a 24-hour urine collection

p. 1312*

Hint 410

- collected in metal free container after abstaining from a sea food diet for 5 days

Front 411

Why urine to check arsenic levels, why not blood?

Back 411

Owing to the rapid distribution of arsenic in the tissues

p. 1312

Front 412

What are the chief causes of death in arsenic toxicity, therefore of utmost importance in stabilization of arsenic toxicity?

Back 412

hypotension and dysrrythmias

p. 1312

Hint 412

Fluids and if needs be, pressors

Front 413

How is elemental mercury MC absorbed?

Back 413

Inhalation, as a vapor

p. 1313

Front 414

T/F: Absoprtion of elemental mercury is MC negligible, so that swallowing mercury contained in a glass thermometer (elemental mercury) does not produce adverse effects unless that tract is damaged.

Back 414

True

p. 1313**

Hint 414

Can also be absorbed dermally, slow absoprtion and delayed systemic toxicity after IM injections is reported
Crosses blood brain barrier...where it is trapped in the CNS

Front 415

Where are inorganic mercury salts MC deposited?

Back 415

In the kidney, causing renal failure

p. 1313

Hint 415

MC systems effected by Mercury: Renal, Neurologic and gastric

Front 416

What are the acute signs of elemental mercury inhalation, toxiciy?

Back 416

- SOB
- Fever
- chills
- cough
- nausea
- vomiting
- diarrhea
- metallic taste
- HA
- weakness
- blurred vision

p. 1313
- sometimes acute lung injury

Front 417

Patient c/o N/V/D- bloody stools, and metallic taste in his mouth. Oral mucosa has a graying color to it. What metal compound has he ingested?

Back 417

Inorganic Mercury Salts

p. 1313

Front 418

What is the following c/w:
GI: metallic taste, burning sensation in mouth, loose teeth, mucosal lesions, fissues and excessive salivation
Neuro: tremor, neurasthenia (depression, HA, diff w/concentration), erthism- easy blushing and extreme shyness.
Renal: reversible proteinuria, nephrotic syndrome
Additionally, may have pink disease- generalized rash, edema, erythema of the palms, soles and face, excessive sweating, fever, irritability, spleenomegaly, and hypotonia- MC pelvis and pec's

Back 418

Chronic Inorganic mercury toxicity

p. 1313

Front 419

What is erethism? What should it alert you to?

Back 419

1. Easy blushing and shyness
2. mercury toxicity

p. 1313

Front 420

What level of mercury in the 24 hr UA supports clinically meaningful mercury exposure?

Back 420

> 20 mcg/dL

P. 1313

Front 421

What is one of the treatment options from the effects of organic mercury toxicity>

Back 421

The patient has limited fxn from Ach, therefore Neostigmine may be appropriate

p. 1313

Front 422

T/F: Chelation therepy, after mercury exposure is useful in acute setting and less so with chronic.

Back 422

True

p. 1313

Front 423

T/F: Dimecaprol is contraindicated in methyl mercury poisoning owing to the potential for excaerbation of central neurologic sxs.

Back 423

True

p. 1313**
Succimer is generally well tolerated. (Severe and mild poisonings)

Hint 423

View Table 197-7, p. 1314

Front 424

What is defined by the US Occupational Safety and Health Administration to be any chemical that has been scientifically to be a health hazard (causes acute/chronic health effects) or physical hazard (combustible liquid/explosive).

Back 424

Hazardous chemical

p. 1315*

Front 425

Why are children "uniquely" sensitive to some chemical exposures?

Back 425

- Physiologically, they have increased respiratory exposure, as their minute volumes are higher, resulting in greater inhalation doses of airborne toxins.
- Airways are smaller, creating less room for inflammation and the clearing of secretions
- Dermal Absorption is increased, their skin is thinner and more permeable
- Dehydration risk is great from V/D.

p. 1315-1316

Front 426

What effect do the following toxins have, with regard to delayed manifestation of sxs?
- Chlorine
- Ethylene oxide
- Hydrofluoric Acid
- Hydrogen sulfide
- Methyl Bromide
- Nitrogen Oxides
- Paraquat
- Phosgene
- Phosphine
- Zinc Phosphide

Back 426

Pulmonary Edema

p. 1315, Table: 198-2

Front 427

A pregnant woman is brought to the ER following exposure to known industrial toxin. Are their any special provisions for her pregnancy

Back 427

NO, best interest for the baby is treating patient/effectively

p. 1315

Front 428

What are the three determinants of airborne agent toxicity?

Back 428

1. concentration of inhaled toxin
2. duration of exposure
3. whether the exposure occurred in an enclosed space

p. 1316
- What are some other influential factors?

Hint 428

1. vapor density
2. allergic or non-allergic bronchospasm
3. exertional state or metabolic rate of the victim
4, unique host susceptibility- such as RAD
5. hx of smoking
6. age

Front 429

Why, following respiratory toxin exposure, should there be a low threshold to intubate the patient?

Back 429

- because of the potential for sudden deterioration

p. 1316
- next slide

Hint 429

Look for evidence of this need"
- carbaceous sputum
- singed facial or nose hair
- soot around face
- stridor, retractions, cough in the right setting, tachypnea, wheezing and cyanosis
- etc.

Front 430

While in most cases prophylactic steroids and abx are not recommended for inhalation exposure to toxins, what one exposure is "possible exception" to the rule?

Back 430

Nitrogen Dioxide Exposure

p. 1316

Front 431

What chemical agent was originally used on WWI, responsible for 80% fatalities. No longer made in US military, but is in manfacturing and industry for use as a chemical precursor to: plastics, pharmaceuticals, dyes, polyurethane, and pesticides?

Back 431

Phosgene

p. 1316

Front 432

An friend of yours in on the phone and asks if he should be concerned. He just started working at a plant, when he heard an alarm go off, following an explosion and a "white cloud". He reported the smell of freshly mown hay and then felt irritation in his eyes, nose and throat...should he be concerned?

Back 432

yes, this is Phosgene

- go to hospital. Pulmonary edema is likely w/in 24 hrs.

p. 1316*

Front 433

A patient may delayed in onset of sxs following phosgene exposure, or may be immediate. If sxs of dyspnea and/or pulmonary edema set in w/in ____ hours, the prognosis is very poor.

Back 433

4 hours

p. 1316

Front 434

Why is rest mandatory as a part of the recovery from phosgene exposure?

Back 434

Because exertion is known to worsen sxs.

p. 1316

Front 435

What is the treatment for phosgene exposure?

Back 435

Supportive care.

p. 1316

Front 436

What chemical is MC utilized in labs, paper manufacturing, swimming pools, chemical distribution and municipal water treatment centers?

Back 436

Chlorine

p. 1317

Front 437

When dispensed, this agent has a pungent odor and and a dense, green, yellow gas...with plenty of warning properties associated with it. It causes central airway damage as well as pulmonary edema.
Immediately following contact: occular and upper airway irritation along with nausea and vomiting are common- even following mild exposure.

Back 437

Chlorine gas

p. 1317

Front 438

What do the following sxs mean, as they relate to chlorine exposure (esp w/in 6 hrs):
- coughing
- hoarseness
- pulmonary edema
- respiratory distress (in some cases)

Back 438

Severe Chlorine Exposure

p. 1317

Front 439

What causes a triphasic illnesses following exposure:
- dyspnea, FLS
- transient improvement
- worsening dyspnea- which heralds the onset of pulmonary edema 24-72 hrs after exposure.
Methemaglobinemia has been reported with this, and some propose the use of steroids and abx therapies as a part of the treatment.

Back 439

Nitrogen Oxides

p. 1317

Front 440

What do the following have in common as sources of metabolic toxin:
- burning of wool, plastics
- minining, photography, solvents
- Fumigants and fertilizers
- vermin extermination
- chemical labs
- medicines: Laetrile, sodium nitroprusside
- plants- seeds apricots
- cigarrete smoke
- vehicle exhausts

Back 440

Cyanide exposure

p. 1317

Front 441

Where does cyanide bind with a high affinity? Why does this matter?

Back 441

- ferric ion cytochrome3 portion of the cytochrome oxidase w/in mitochondria
- prohibits cellular respiration, even in the presence of O2. (those organs and tissue with high oxygen consumption are the most affected, first)

p. 1317

Hint 441

(FYI: Cassava Root- when not cooked risks great levels of Cyanide toxicity)

Front 442

There is a natural occurrence of cyanide in the body from foods, cigarettes (2.5 times higher levels than non-smokers), why is this a concern? Why do people get toxic?

Back 442

- It is cleaned out by the liver (by rhodanese)
- toxicity develops when this is rapidly overwhelmed

p. 1317

Front 443

Respiratory exposure to Cyanide, occurs quicky. When exposed to cyanide < 50 parts per million, what are the sxs?

Back 443

- restlessness
- anxiety
- palpitations
- dyspnea
- HA

p. 1317

Front 444

Respiratory exposure to Cyanide, occurs quicky. When exposed to cyanide > 50 parts per million, what are the sxs?

Back 444

- Severe dyspnea
- Coma
- Seizures
- Cardiac Dysrrythmias

- coma, cardiovascular collapse, and death may occur immediately on exposure to extremely high levels of cyanide

p; 1317

Front 445

To be lethal, how long must an individual be exposed to cyanide gas ~ 200 ppm?

Back 445

30 minutes

p. 1317

Front 446

To be lethal, how long must an individual be exposed to cyanide gas ~ 600-700 ppm?

Back 446

5 minutes

p. 1317

Front 447

Toxicity from cyanide ingestion is w/in minutes. A seriously poisoned pt manifests what sxs?

Back 447

1. confused
2. hyperventilating
3. hypotensive
4. bradycardic

p. 1317

Front 448

What toxin is associated with the smell of bitter almonds?

Back 448

Cyanide

p. 1318

Front 449

A patient is brought to the ER, dyspnic and appears to be in severe respiratory distress. Friend who called 9-1-1 reported the smell of almonds. You place the patient on high flow O2, of course, as well as monitor. What additional lab (s)- are directly useful? What is the cause of this patients respiratory disease (assuming NML/non-contributory health hx as well as no prior illnesses).

Back 449

- Cyanide levels, Lactate
- Cyanide exposure

p. 1318

Hint 449

MC: Lactate > 10 mmol/L
- all labs and hx support hypoxemia


FYI: Sources of Cyanide toxicity:
- Acetonitrile
- Amygdalin (Apricot pits)
- Nitroprusside

Front 450

Resuscitative measures in Cyanide exposure, initially, are very important: Oxygen, crystalloids, etc. Treating the acidosis with ventillation/oxygen is helpful. But why is sodium bicarb recommended?

Back 450

- It enhances the effect of nitriteand thiosulfate

p; 1318

Front 451

Amyl Nitrate for cyanide exposure is used for?

Back 451

Inhalation antidote, pending IV access...temporizing measure

p. 1318

Front 452

You have a patient with known cyanide exposure. She is comatose, bradycardic. You go to provide sodium thiosulfate, but a friend tries to stop you, reporting HoTn patient...was this a good save, or crap?

Back 452

Crap! HoTn in this particular patient is not a contrindication

p. 1318

Front 453

Why are nitrates so helpful for cyanide exposure?

Back 453

They cause a methemoglinemia...causing cyanide to bind more avidly to it than to ferric iron.

p. 1318

Front 454

When treating for cyanide toxicity, which is infused first, sodium nitrite or sodium thiosulfate?

Back 454

Sodium nitrite

-p. 1319

Hint 454

Read from Nitrites, p. 1318-1320

Front 455

T/F: Hyperbaric oxygen is appropriate for the tx of cyanide exposure.

Back 455

False...it is recommended for cyanide and carbon monoxide poisoning

p. 1319

Front 456

What is the dose for hydroxycobalamin? What is it used for?

Back 456

- 5 gms, (70 mg/kg), IV over 30 minutes.
- it is used for tx of cyanide- carries loss toxicity

p. 1319

Hint 456

Because of it's low toxicity and efficacy, hydroxycobalamin is thought to be ideal, when the dx of cyanide toxicity appears uncertain or in the cases where the induction of methemaglobinemia may be detrimental. SE's: HTN, reddish discoloration of the skin and mucous membranes. Anaphylaxis is rare!

Front 457

What has the smell of rotten eggs, is colorless, flammable gas. It is among the MC of fatal gas inhalation. Disrupts oxidatitve phsophorylation?

Back 457

Hydrogen sulfide

p. 1320

Front 458

Which agent is a chemical asphyxiant that possess irritative properties such that respiratory and occular irritation are common following exposure. In high concentrations, rapid LOC, seizures and death may occur in few breaths. Tx: High flow O2, decontamination and sodium nitrite.

Back 458

Hydrogen Sulfide

p. 1320