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Renal 2 > Toxicology: Slide 91 > Flashcards

Toxicology: Slide 91 Flashcards

1
Q

What is the most frequent cause of patients presenting to the ER with AMS?

A

Ethanol poisoning

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2
Q

What are common sources of ethanol?

A

Aftershave, cough preparations, glass cleaners, hair spray, disinfectants, mouthwash, paint stripper, perfumes, rubbing alcohol, beverages

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3
Q

What is anion gap?

A

Na - HCO3- Cl

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4
Q

What is a normal anion gap?

A

10-14 (12)

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5
Q

What toxins can cause a large anion gap?

A 
M: Methanol
U: Uremia
D: DKA (alcohol ketosis, starvation ketosis, ketoacidosis, acetoacetic acid, beta hydroxybutryric acid)
P: Phenformin, metformin
I: Isoniazid, iron, inborn errors of metabolism
L: Lactic acidosis, metformin
E: Ethylene glycol
S: Salicylates
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6
Q

What is wood alcohol, produced via distillation of hardwood?

A

Methanol

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7
Q

What are sources of methanol?

A

Shellac, paint thinner, rubber goods, synthetic textiles, gas line antifreeze, printing solutions, windshield washing solution, carburetor fluid

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8
Q

Where can you normally find methanol?

A

In saliva and expired air

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9
Q

Where is dietary methanol found?

A

Fruits and veggies (as free alcohol, methyl esters of fatty acids, or methoxy groups on polysaccharides such as pectin)

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10
Q

What is a food additive that can be converted to methanol?

A

Aspartame (NutraSweet)

-Ability to convert is really low

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11
Q

Describe methanol?

A

Colorless
Distinctive odor
Bitter taste

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12
Q

Does methanol distribute throughout the whole body?

A

Yes

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13
Q

What is responsible for toxicity in methanol poisoning?

A

Formate (it’s major metabolite)

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14
Q

How is methanol absorbed?

A

All routes (rapidly from GI tract with a peak in 30-60min)

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15
Q

How much methanol can cause blindness?

A

4mL

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16
Q

How much methanol can cause death?

A

15mL

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17
Q

What other route of methanol ingestion is associated with toxicity?

A

Inhalation of vapors

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18
Q

What is the main route of methanol metabolism?

A

Via oxidation by alcohol dehydrogenase

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19
Q

What is another route of methanol metabolism?

A

Through expired air

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20
Q

How much of methanol is metabolized to formic acid and formaldehyde?

A

40%

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21
Q

What is formaldehyde converted into and what is the clinical significance of this?

A

Formic acid- 1/2 life is 1-2 minutes and it is non-detectable

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22
Q

Is the metabolism of methanol faster than ethanol?

A

NO… it is 5 times slower than ethanol

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23
Q

What system regulates methanol metabolism in each species?

A

Folate systems

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24
Q

What species are susceptible to methanol poisoning and why?

A

Monkeys and humans

- Absence of large amounts of formate to be metabolized

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25
Q

What is the rate limiting step in methanol metabolism?

A

Availability of folic acid

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26
Q

What deficiency makes a patients more susceptible to methanol intoxication?

A

Folate deficiency

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27
Q

What 3 things do you consider in presentation of methanol poisioning?

A
  1. Amount of food in stomach
  2. Quality of ethanol consumed
  3. Quantity of methanol consumed
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28
Q

How many more times toxic is formic acid than methanol?

A

6 times

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29
Q

What 3 things is formic acid responsible for in methanol poisioning?

A
  1. Metabolic acidosis
  2. Anion gap
  3. Ocular toxicity
    - CAUSES MULTISYSTEM PROBLEMS
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30
Q

What are the main toxicities discussed from formic acid?

A

Visual, CNS, GI, Mild inebriation, long latent period, metabolic acidosis

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31
Q

What are the visual symptoms associated with formic acid?

A
  1. Diminished sensation of light
  2. Reduced central vision
  3. Photophobia
  4. Blurred vision
  5. Retinal edema
  6. Hyperemia of optic discs
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32
Q

What are the visual disorders associated with formic acid?

A
  1. Retinal edema develops over 2-4 days and persists up to 2 weeks
  2. Pupils may be dilated and sluggishly reactive
  3. Severe damage: Optic atrophy (late finding)
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33
Q

What are the CNS symptoms seen with formic acid?

A
  1. Cephalgia
  2. Dizziness
  3. Seizure
  4. Stupor
  5. Coma
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34
Q

What neurological abnormalities are seen with formic acid?

A
  1. Seizure, stupor, coma
  2. WBC and xanthochromia in CSF
  3. Extrapyramidal movement disorder (survivors of severe poisoning can get permanent damage to putamen)
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35
Q

What is indicative of a poor prognosis in pt. poisoned with formic acid presenting with seizure, stupor and coma?

A

Sign of increased ICP: Bradycardia, HTN, Dilated nonreactive pupils

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36
Q

What GI symptoms are seen with formic acid?

A

Nausea, vomiting, severe abdominal pain

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37
Q

What GI effects are seen with formic acid?

A
  1. 50% nausea vomiting (persistent and violent)
  2. 66% severe colicky abd. pain
  3. Elevated amylase
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38
Q

In methanol poisoning (formic acid) so blood levels correlate with symptoms?

A

NO… poor correlation

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39
Q

What levels of formic acid/methanol are considered toxic?

A

Peak levels greater than 50mg/dL

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40
Q

What should treatment of methanol poisoning be directed at?

A

Correcting the severe acidosis, then removing methanol and it’s metabolites

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41
Q

What can be done to treat methanol poisioning?

A
  1. Bicarb therapy (Continuous infusion of 5% NaHCO3, 2-3 mEq/kg with frequent monitoring of blood gasses)
  2. Folic acid: 1mg/kg q 4 hours x 6 doses
  3. Dialysis
  4. Ethyl alcohol therapy
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42
Q

Where do you find ethylene glycol?

A

SOLVENTS: Detergents, Paints, Lacquers, Drugs, Dyes, Hydraulic brake fluid, Polishes, Cosmetics, Glycerine substitute in enemas, Preservative in juices, Early medicinals, Radiator Antifreeze (95%), Brake fluid (70-95%), Coolant (95%), Windshield deicer (50%)

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43
Q

Why is ethylene glycol used as a solvent?

A

Because it has a high boiling point and can depress the freezing point of solutions

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44
Q

Describe ethylene glycol?

A

Sweet taste, aromatic odor (like liquers), low cost, substitute for alcohol, half like of 3 hrs

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45
Q

How does ethylene glycol poison?

A 
Via  ingestion
 (can't poision by inhalation due to high boiling point and low vapor pressure, and it isn't absorbed through skin)
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46
Q

What is the lethal dose of ethylene glycol?

A

100mL

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47
Q

How is ethylene glycol metabolize?

A

Metabolized in liver by alcohol dehydrogenase, then by aldehyde dehydrogenase

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48
Q

What acids are produced via ethylene glycol metabolism?

A

Glycoaldehyde, glycolic acid, glyoxylic acid, formic acid

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49
Q

What is a minor metabolite of ethylene glycol that contributes to organ damage?

A

Oxalic acid

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50
Q

What is a prominent feature of oxalic acid?

A

Oxalate crystalluria: Calcium oxalate precipitates in kidney, myocardium, brain, pancreas, and there is a link between oxalate precipitation and development of tubular necrosis

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51
Q

How does ethylene glycol poisoning present?

A

Like alcohol poisoning with 3 stages of acute toxicity

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52
Q

What are the 3 stages of acute toxicity with ethylene glycol poisoning?

A
  1. CNS
  2. Cardiopulmonary
  3. Renal
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53
Q

When does CNS stage of ethylene glycol poisoning occur?

A

30 min to 12 hours

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54
Q

What are the signs of CNS stage of ethylene glycol poisoning?

A

Intoxicated patient, no odor of alcohol, nausea and vomiting, metabolic acidosis, crystalluria, myoclonus, seizure, death, coma

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55
Q

When does the cardiopulmonary stage of ethylene glycol poisoning occur?

A

12-24 hours

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56
Q

What are the signs of the cardiopulmonary stage of ethylene glycol poisoning?

A

Tachypnea, tachycardia, HTN, pulmonary edema, cyanosis, bronchopneumonia, cardiac enlargement

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57
Q

When does the renal stage of ethylene glycol poisoning occur?

A

36-48 hours

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58
Q

What are the signs of the renal stage of ethylene glycol poisoning?

A

Crystalluria, costovertebral angle tenderness, acute tubular necrosis with oliguria, renal filure

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59
Q

What is measured to diagnose ethylene glycol intoxication?

A

Serum electrolytes, arterial blood gas, urinalysis, wood’s lamp examination, serum calcium and phosphorous concentration, serum osmolality, and osmolar gap

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60
Q

When does a rise in osmolar gap occur and why in ethylene glycol poisoning?

A

Early, when unmetabolized ethylene glycol is present in serum

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61
Q

Is serum calcium high in ethylene glycol poisoning?

A

NO, it’s low because of precipitation of calcium by oxalate

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62
Q

What is going on with anion gap in ethylene glycol poisoning?

A

Anion gap metabolic acidosis noted early

Large anion gap

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63
Q

When do you see a rise in the osmolar gap in ethylene glycol poisoning?

A

Occurs early when unmetabolized ethylene glycol is present in serum and is metabolized yielding a rise in glycolic acid levels (may not be present late in course)

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64
Q

What does the rise in the anion gap seen in ethylene glycol poisioning correspond to?

A

Amount of glycolic acid (osmolar gap may not reflect this)

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65
Q

What is seen under Wood’s Lamp evaluation show in ethylene glycol poisoning?

A

Examination of urine or emesis may show fluorescence from the fluorescein coloring added to most ethylene glycol antifreeze

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66
Q

What is the treatment for ethylene glycol poisioning?

A

SAME AS METHANOL.

  1. Bicarb therapy (Continuous infusion of 5% NaHCO3, 2-3 mEq/kg with frequent monitoring of blood gasses)
  2. Folic acid: 1mg/kg q 4 hours x 6 doses
  3. Dialysis
  4. Ethyl alcohol therapy
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67
Q

Where can cardiac glycosides come from?

A

Oleander (A flowering subtropical or trobical shrub for hedges)

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68
Q

What ares of oleander plants are toxic?

A

WHOLE THING

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69
Q

What age groups is most commonly poisoned by cardiac glycosides and why?

A

Kids- Stems are used as skewers for outdoor picnics

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70
Q

What other way can cardiac glycosides poison?

A

Smoke: Boiling or drying doesn’t inactivate the toxin

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71
Q

What are the effects of cardiac glycosides?

A
  1. Positive inotropic action

2. Negative chronotropic action

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72
Q

What does positive inotropic action cause?

A

Increased force of contraction… acts by slowing the SA node impulse formation, ehnances intra-atrial conduction, increases the rate of spontaneous depolarization

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73
Q

What does negative chronotropic action cause?

A

Slows conduction velocity reflected by slowing the heart rate due to increased vagal tone, prolonged refraction periods of the AV node and bundle of his

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74
Q

What are digitalis and digitoxin made from?

A

Foxglove or digitalis purpurea

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75
Q

What types of drugs are digitalis and digitoxin?

A

Cardiac glycosides

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76
Q

What % of digoxin is absorbed via the GI tract?

A

60-85%

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77
Q

What % of digoxin is excreted unchanged by kidneys?

A

85%

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78
Q

What is the renal excretion of digoxin proportional to?

A

GFR

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79
Q

After oral administration was is the time to onset of action and peak?

A

30-120 min and peaks in 3-8 hours

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80
Q

How does digoxin work?

A

It exerts a positive inotropic effect on cardiac muscle by impairing active transport of Na ions (remember, when a neuron is depolarized by a few mV, the permability of the membrane is altered making it more permeable to Na)

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81
Q

Since digoxin impairs active transport of Na ions, what is the effect on Na and Ca?

A

-Increased intracellular Na, and this causes an influx of Ca

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82
Q

By causing an influx of Ca, what effect does digoxin have an myocadial contraction?

A

Increased Ca perpetuates increased actin/myosin interactions increasing force of myocardial contraction

83
Q

What is the effect of digoxin causing myocardium to not be able to extrude the Na gained or recover the K lost in each AP?

A

Slower conduction velocity and increase in spontaneous depolarization

84
Q

What are the 5 areas of clinical manifestations for digoxin poisoning?

A
  1. GI
  2. CNS
  3. Psychiatric
  4. Visual
  5. Cardiac
85
Q

What are the GI symptoms seen with digoxin poisoning and what are they thought to be from?

A

Anorexia, nausea, vomiting

GI symptoms frequent in acute/chronic toxicity and thought to be due to stimulation in medulla

86
Q

What are the CNS symptoms seen with digoxin poisoning?

A

These are most common manifestations: Cephalgia, fatigue, malaise, drowsiness, generalized muscle weakness, irritability, vertigo, dizziness, syncope, apathy, lethargy, opisthotonus, and seizures

87
Q

What are the psychiatric symptoms seen with digoxin poisoning?

A

Amnesia, aphasia, confusion, disorientation, delirium, hallucinations, impaired memory

88
Q

What is affected more in digoxin poisoning, cones or rods (effects on retina)

A

CONES

89
Q

If cones are more affected in digoxin poisoning, what kind of vision is more affected, color or black and white?

A

COLOR: Objects appear yellow or green, less commonly brown, red, blue or white

90
Q

What other visual symptoms are seen with digoxin poisoning?

A

Blurred vision, photophobia, halos, borders on objects

91
Q

What are the cardiac effects seen in digoxin poisoning?

A

Every known cardiac dysrhythmia (most frequent and most dangerous SE)

92
Q

What are the 7 things associated with increased likelihood of digoxin toxicity?

A
  1. Age of patient*
  2. Degree of heart disease*
  3. Electrolyte disturbance: Hyperkalemia, hypomagnesemia, and hypercalcemia
  4. Hypoxia
  5. Hepatic disease
  6. Renal disease
  7. Antibiotic therapy (erythromycin or tetracycline)
93
Q

What is the lethal dose of cardiac glycosides?

A

20-50 times the usual daily maintenance dose

94
Q

What is a common cause of digoxin toxicity discussed?

A

Patients who have certain anaerobic bacterial infections of the colon…The organism reduces the lactone ring of the glycoside requiring large doses to acheive adequate levels of digoxin… Once you treat this with eythromycin or tetracycline, the digoxin levels will rise acute because the bacteria are gone and not inhibitng digoxin anymore

95
Q

What is the treatment for digoxin poisoning?

A
  1. Supportive

2. Digibind

96
Q

What is digibind?

A

A FAB fragment of an antibody directed towards digoxin that inactivates it

97
Q

How does digibind work?

A

It shortens the elimination time

The affinity of FAB for digoxin is greater than that for digoxin to the Na/K ATPase

98
Q

When do you use FAB?

A

It is reserved for life threatening situations

99
Q

What else can digibind bind to?

A

Digitoxin and oleander

100
Q

Describe salicylate poisoning in children and adults?

A

Children: Accidental ingestion
Adults: Intentional overdose

101
Q

What has caused the reduction in accidental ingestions in children?

A

Safety lids on containers and restricting dose in flavored aspirin

102
Q

What are the 3 main effects of salicylate?

A
  1. Antipyretic: Acts by altering response of hypothalamus to pyrogen
  2. Anti-inflammatory: Inhibits synthesis of prostaglanding which prevents sensitization of pain receptors
  3. Platelet aggregation inhibitor: By donating acetyl group to platelet membrane
103
Q

What is the normal half life of salicylic acid and what is the half life in overdose?

A

Normal is 2-4 hours, in overdose it can be greater than 20 hours

104
Q

What levels of salicylate are associated with adverse systemic effects?

A

Greater than 30

105
Q

Is the absorption of salicylic acid quick?

A

Yes, it is rapid and can have measurable serum concentrations in 15-30 minutes

106
Q

When does clinical toxicity and peak plasma levels appear in salicylic acid poisoning?

A

May not appear for 12 hours or more

107
Q

Why do large doses of apirin (salicylate) cause rising levels of salicylate for as long as 24 hours?

A

Inhibits gastric emptying resulting in delayed absorpion

108
Q

Where is salicylate metabolized?

A

Principally in the liver

109
Q

Can you see renal excretion of salicylic acid?

A

Yes, renal excretion of unmetabolized drug occurs: Renal excretion is usually under 19% at low doses, but can account for greater than 50% at high doses or in overdoses if urine pH is properly adjusted

110
Q

What are the 8 toxicities seen with salicylic acid poisoning?

A
  1. CNS stimulation of respiration
  2. Pulmonary edema
  3. Hyperpyrexia secondary to uncoupling of oxidative phosphorylation
  4. Electrolyte disturbance and dehydration
  5. Altered glucose metabolism through inhibition of enzymes in Kreb’s cycle
  6. Clotting disorder
  7. Gastrointestinal irritation and bleeding
  8. Acute renal failure
111
Q

What two acid-base disturbances are seen with salicylic acid poisoning?

A
  1. Respiratory alkalosis

2. Metabolic acidosis

112
Q

When do you see respiratory alkalosis in salicylic acid poisoning and what does this result in?

A

Early: Secondary to stimulating the CNS respiratory center in the medulla resulting in tachypnea and hyperpnea… this leads to decreased pCO2, increased pH, and respiratory alkalosis

113
Q

When do you see metabolic acidosis in salicylic acid poisoning and what does this result in?

A

Develops secondary to accumulation in organic acids, may not occur until 12-24 hours post ingestion

114
Q

What 3 things are seen in uncoupling of oxidative phosphorylation due to salicylic acid poisoning?

A
  1. Failure to produce ATP (increases O2 consumption and decreased CO2 production, which increases heat production)
  2. Dissipated heat (temps of 105-107)
  3. Increases tissue glyclysis and peripheral demand resulting in hyperglycemia or hypoglycemia (can increase cerebral glycolysis selectively depleting CNS glucose stores
115
Q

What effect is seen in the blood due to salicylic acid and why?

A

Coagulopathy because salicylates decrease production of factor VIII, raising the PT

116
Q

What is seen secondary to vitamin K dependent synthesis of factor VIII in salicylic acid poisoning?

A

Hypothrombinemia

117
Q

What 3 things happen as a result of hypoprothombinemia due to salicylic acid poisoning?

A
  1. Decreased platelet adhesiveness which remains for the life of the platelet which is 7-10 days resulting in increased bleeding time
  2. Increased capillary fragility
  3. Decreased platelet production
118
Q

What are the signs and symptoms of salicylic acid toxicity?

A
  1. Hyperpnea in association with vomiting, confusion, lethargy, fever, coma, seizures
  2. Tinnitus
  3. Hyperpyrexia
  4. Disorientation, coma, and seizures (ominous findings suggesting serious OD)
119
Q

When and why would you use a salicylate nomogram?

A

Can be used for acute ingestion of salicylates beginning 6 hours post ingestion with single ingestions
Can be helpful in deciding need for hospitalization or type of therapy

120
Q

What is the treatment for salicylic acid poisoning?

A

NONE… symptomatic and supportive care

121
Q

What are the uses for acetaminophen

A

anti-pyritic

Analgesic

122
Q

What is the role of the kidney in acetaminophen metabolism

A

Small amount excreted, otherwise unchanged

123
Q

Describe the time period and symptoms associated with Phase I of Acute Acetominophen intoxication

A 
Occurs in 30 mins-4 hours
Anorexia
Nausea
Vomitting
Diaphoresis

An important feature of this phase is that there are no specific symptoms to indicate how serious the intoxication may become.

124
Q

Describe the time period and symptoms associated with Phase II of Acute Acetominophen intoxication

A

Occurs in 24-72 hrs

Liver function abnormalities
Right upper quadrant pain.

In general, the elevations of serum transaminase concentrations do not correlate well with the clinical outcome.

125
Q

Describe the time period and symptoms associated with Phase III of Acute Acetominophen intoxication

A

3-5 ays post intox

Jaundice 
coagulopathy
hypoglycemia
encephalopathy
renal failure
myoccardiopathy

May be signs of hepatic necrosis: jaundice, hypoglycemia, encephalopathy.
Coagulopathy: may be severe and include DIC and bleeding diathesis.
Liver enzymes peak during this phase

126
Q

Describe the time period and symptoms associated with Phase IV of Acute Acetominophen intoxication

A

7-8 days post into

Abnormalities return to normal or you go straingh tin the shitter (Liver failure and death.)

127
Q

What are factors to consider when deciding if acetaminophen ingestion may lead to liver toxicity in a patient

A 
Amount ingested
History of emesis
Time from ingestion
Age of patient
Serum concentration in relation to nomogram
128
Q

What is the MOST important variable when predicting liver fox ?

A

Serum concentration (#1)

You must also determine the approximate time of ingestion

129
Q

What is the mechanism of action of N-Acetylcysteine(Mucomyst) ? (Acetominophen antidote)

A

N-acetylcystine supplies sulfhydryl groups to the toxic intermediary allowing elimination through nontoxic routes

130
Q

Besides giving N-acetylcystine, what treatment options are available for acetaminophen fox?

A

Emesis or Gastric lavage
Activated Charcoal

Supportive care:
Neomycin enema (reduces liver tox)
Fresh frozen plasma
Vitamina K
Glucose
131
Q

Organophosphates/Carbamates are considered what kind of molecules ?

A

Acetylcholinesterase inhibitors

They stop the breakdown of ACh (not good in the heart, leads to dangerous bradycardia)

132
Q

List 4 Carbamate drugs

A

Edrophonium, neostigmine, physostigmine, pyridostigmine

133
Q

What diseases are carbamates often used to treat ?

A

Myasthenia Gravis
Glaucoma
SVT
Antidote for Anti-Cholinergic Poisoning.

134
Q

What are Organophosphates used for ?

A

Insecticides (flea collars, ant traps, fly paper.

135
Q

how are organophosphates absorbed into the body ?

A 
ALL ROUTES 
Absorbed from all routes
Transcutaneous
Gastrointestinal tract
Conjunctiva
Respiratory tract
136
Q

How are carbamate absorbed ?

A

Orally or topically through the eye

137
Q

What occurs as a consequent of organophosphate exposure ?

A

Stimulates autonomic nervous system, skeletal muscle, and CNS

138
Q

Which is more easily reversed Organophosphates or Carbamates ?

A

carbamates

Shorter duration of action
Lower toxicity
Don’t cross the blood brain barrier well

139
Q

What is the characteristic odor associated with organophosphate us ?

A 
Garlic smell (usually retain the odor on their breath, in there vomitus, or in their feces for several days.
)
140
Q

At low doses do the Muscarinic or Nitcotinic symptoms of ACh poisoning predominated ?

A

Muscarinic

At high doses, nicotinic predominates

141
Q

SLUG BAM

Muscarinic Effects

A

Salivation
Lacrimation
Urination
GI upset

Bradycardia, bronchoconstriction, bowel movement
Abdominal Cramps
MIosis (constriction of the pupil)

142
Q

Nicotinic effects

M
T
W
tH
F
A 
M- Mydriasis (pupils dilate)
T- Tachycardia
W- Weakness
tH- Hypertension/Hyperglycemia
F- Fasciculation
143
Q

Consider if you are aware that a patient is taking carbamates but there is CNS involvement. What should you think ?

A

Mixed Carbamate, organophosphate (or other toxin)

144
Q

What is the main cause of death with Organophosphates

A

Respiratory Failure

bronchospasm, increased bronchial secretions, decreased respiratory muscle strength(paralysis), pulmonary edema in addition to AV blocks

145
Q

Describe Intermediate Syndrome in organophosphate poisoning ?

A

24-96 hours after poisoning

Paralytic symptoms which can last as long as 18 days and effects respiratory muscles, proximal limbs, and neck flexors

Apnea that may require Intubation

NON RESPONSIVE TO ATROPINE OR PRALIDOXIME

146
Q

What is the main treatment for the muscarinic effects of /Organophosphate poisoning ?

A

Atropine

Atropine: AChR antagonist (binds to the receptor but doesn’t cause depolarization)

147
Q

When would you not wanna give atropine to a patient with muscarinic poisoning ?

A

Do not give atropine in presence of cyanosis as it may produce V. fib in the face of hypoxia

148
Q

What would you give to ameliorate the Nicotinic effects of acetylcholine fox ?

A

Pralidozime

Reverses AChEsterase inhibition

149
Q

List some things that contain cyanide

A

Insecticides
Rodenticides
Silver polish
Used in extraction of gold and silver from ores
Used in chemicals to remove hair from hides
Used in manufacture of plastics
Ciggarettes :Smokers with 2.5 times more than nonsmokers
Pits and seeds of plum, peach, pear, apple, apricot, cherry, almond

150
Q

Describe the mechanism of action for cyanide poisoning

A

Cyanide binds to iron in hemoglobin yielding cyanohemoglobin which can’t transport oxygen

It also inhibits the final step of oxidative phosphorylation, thereby inhibiting cellular respiration and production of ATP (Cytochrome Oxidase)

151
Q

Is CN rapidly absorbable ?

A

YES VERY

Cell membranes are highly permeable to it

152
Q

Which enzyme metabolized Cyanide to Thiocyanate by conjugating CN and Thiosulfate (Thiocyanate is inert and harmless) ?

A

Rhodanase

80% of detox occurs via this rout

153
Q

What vitamin is cyanide incorporated into ?

A

Hydroxycobalamine (B12)

154
Q

What patients are at high risk for CN poisoning ?

A

lab technicians, chemists, pharmacists, physicians. Industrial accidents or fires.

155
Q

What is the characteristic odor produced by cyanide ?

A

Characteristic musty quality that resembles bitter almonds or macaroons

Cannot be detected by 20-40% of people

156
Q

What does venous blood look like in CN poisoning and why ?

A

It is bright red just like arterial blood due to the poor 02 utilization

157
Q

Lee-Jones tests done on gastric aspirate and can detect as little as 50 mg of ingested cyanide. What can skew this test ?

A

Salicylates

Cause a similar color change

158
Q

AMyl Nitrite Pearls (administered through positive pressure mask) is one of the two antidotes for CN poisoning. What is this drugs mechanism of action ?

A

forms methemoglobin which is capable of binding cyanide in the plasma and effectively competes with cyanide already bound to cytochome oxidase

159
Q

What is the second antidote for CN poisoning ? What is the mechanism of action ?

A

IV Sodium Nitrite
forms methemoglobin which is capable of binding cyanide in the plasma and effectively competes with cyanide already bound to cytochome oxidase

160
Q

Which drug can cause methhemoglobin to convert CN into Thiocyanate (inert) ?

A

Sodium thiosulfate therapy (must be in form of methemoglobin, however.)

161
Q

In which patients must you be careful when administering Nitrite therapy for CN poisoning, as high doses will cause methhemoglobinemia ?

A

Children

162
Q

Traditionally mortality due to iron poisoning reached 50%, today is is around 5%. Why ?

A

Desferoxamine (iron chelating agent.)

163
Q

Who is most at risk for iron poisoning ?

A

Children (eat iron tablets on accident)

164
Q

What form of iron is absorbed by a rate limiting transport mechanism ?

A

Ferrous (Fe 2+)

165
Q

What is the carrier ion for Iron (Ferrous) ?

A

Ferritin ( oxidizes Ferritin back to Fe 3+, Ferric)

166
Q

Why is eliminating iron in he body difficult ?

A

No effective physiologic mechanism for iron excretion which is a fact of great importance in iron intoxication.

167
Q

what dose of elemental iron is considered in the toxic range /

A

20-60 mg/kg

168
Q

what dose of iron is considered in the lethal range ?

A

60-180 mg/kg

169
Q

Why are higher doses of iron more likely to cause tox. ?

A

Destruction of the mucosal barrier in the GI –> Increased iron absorption.

170
Q

Describe Phase I of iron fox ?

A 
Within 30-120 mins: 
Vomiting
Hematemesis
Abdominal pain
Diarrhea
Lethargy
Shock 
Hypotension
Metabolic acidosis
171
Q

Describe Phase II of iron fox ?

A

2-24 hrs

“Recovery”
Apparent response to therapy

172
Q

Describe Phase III of Iron fox ?

A

12-48 hrs

Metabolic Acidosis
Shock
coma

173
Q

Describe Phase IV of Iron fox ?

A

2-4 days

Hepatic necrosis
Bleeding Diathesis

174
Q

Describe Phase V of Iron Tox /

A

2-4 weeks

Gastrointestinal
Gastric scarring
Pyloric stenosis
Achlorhydria
Hepatic cirrhosis
CNS abnormalities
175
Q

What are the main diagnostics symptoms for iron tox ?

A

Vomitting up pill fragments

Bloody diarrhea (black stool also) and hematemesis

Lethargy/comotose/shock

176
Q

What might you see on X-ray in someone who has early iron tox ?

A

PILLS !

177
Q

At what biochemical point does iron become toxic ?

A

when the concentration exceeds the total iron binding capacity

Once plasma transferrin saturated the iron is distributed into cells and causes damage

178
Q

What is the normal serum iron level for an adult ? Child ?

A

Adult : 50-150 ug/dl

Child: 40-100 ug/dl

179
Q

What is the normal TIBC levels of iron ?

A

1/3rd saturated under normal conditions and ranges from 300-450 ug/dl

180
Q

Could you give a patient with iron tox dialysis ?

A

No. Dialysis and diuresis is ineffective .

181
Q

Why might gastric lavage be ineffective agains iron fox ?

A

Iron tends to clump together

182
Q

How is deferoxamine administered ?

A

IV

183
Q

What is the mechanism of action for deferoxamine ?

A

Chelates iron and this complex(ferrioxamine)is stable and soluble in water, and is readily excreted by the kidneys

184
Q

100 mg of deferoxamine can bind how much iron ?

A

8-9 mg of elemental iron

185
Q

Describe the dosing rate for deferoxamine ?

A

IV administration is preferred route continueous infusion 10-15 mg/kg/hour. Decrease rate to 5 mg/kg/hr after 4-6 hours

Maximum dose 6 grams in 24 hour period or 80 mg/kg in children

186
Q

What occurs to the urine during deferoxamine use ?

A

Colors it pink (iron oxidizing, like rust)

Continue treatment until pink color of urine has disappeared and the patient is asymptomatic

187
Q

What are the indication for chelation therapy ?

A

When iron exceeds TIBC capacity(iron level greater than TIBC)or if serum iron 350 mg/dl or greater

Serious signs of toxicity without any measurements

188
Q

What is the mechanism of action for anti-cholinergics ?

A

They block ACh from binding to its receptor

(the muscarinic site or postganglionic cholinergic nerve ending

189
Q

What are some types of Anti-ACh agents ?

A 
Antihistamines
Antiparkinsonian agents
Antipsychotic agents
Belladonna alkaloids
Opthalmic solutions
Plants
Tricyclic antidepressants
190
Q

What are specific Anti-ACh drugs ?

A 
Brompheniramine
Diphenhydramine
Promethazine(phenergan)
Hydroxyzine(visteril)
Meclazine(antivert)
Scopolamine(dramamine)
Benzotropine(cogentin)
Orphenadrine(norflex
Atropine (not on the list, but seriously it is one)
191
Q

What is the memory tool for symptoms causes by anti-cholinergics ?

A 
Hot as a Hare 
Blind as a bat ( causes mydriasis)
Dry as a bone  (anhydrous)
Red as a beet (
Mad as a hatter (crazzzyy)
192
Q

List the peripheral symptoms associated with Anti-cholinergic poisoning ?

A

Dilated unreactive pupils (ACh causes constriction)
Blurred vision
Vasodilation and flushing
Dry Skin (ACh –> sweat gland secretion)
Hyper-reflexia
Hypertension
Decreased bronchial, pharyngeal, nasal and salivary secretions
Urinary Retention (ACh causes trigone constriction
Decreased Bowel motility (ACh –> bowel motility)

193
Q

What occurs to the CNS during Anti-ACh tox. ?

A

Initially stimulation, followed by depression.

194
Q

What are the CNS manifestations of Anti-ACh tox. ?

A

Acute psychosis: disorientation, incoherence, confusion, hallucinations(typically visual, but auditory or tactile),delusions, paranoia

Abnormal Speech
Ataxia,incoodination
agitation and restlessness 
Hyperpyrexia
Severe memory impairment.

Somnolence
Weakness
Coma
Seizures

195
Q

What should you for ventricular ectopy in patients with Anti-ACH toxicity ? Why ?

A

Lidocaine

Many the anticholinergics have a quindine like action so the use of procanamide, quinidine or disopyramide should be avoided.

196
Q

What can you give for psychosis in patients with Anti-ACh

A

Valium

(avoid phenothiazines ie thorazine, phenergan, compazine, prolixin, mellaril, stelazine)because they have anticholinergic effects

197
Q

What is the main treatment for patients with anti-ACh toxicity ?

A

Anti-Cholinesterase Inhibitors (Carbamates like the ‘Stigmines’

Physostigmine(antilirium)

Mestinon(pyridostigmine)

Tensilon(edriphonium)

Neostigmine(prostigmie)

198
Q

What is the best treatment for Anti-ACh toxicity, since it can cross the BBB and reverse CNS effects ?

A

Physostigmine

199
Q

What are the indications for Physostigmine use ?

A

Extreme delirium or agitation who may inflict injury on themselves

Hemodynamically significant sinus tachycardia or SVT

Repetitive or long lasting seizures

Extreme hyperthermia unresponsive to mechanical cooling

COMA is not an indication for use

200
Q

Describe the dosage for Physostigmine in Adults and children ?

A

1-2 mg IV in adults

.5mg or .02 mg/kg IV in children

201
Q

What is the half life of physostigmine ?

A

90 minutes ! , therefore, may need to use repeated doses for longer acting anticholinergics

202
Q

What are the contraindications to physostigmine ?

A

Absolute: Mechanical obstruction of gastrointestinal or genitourinary tracts

Relative: Diabetes, glaucoma, asthma, heartblock, coronary artery disease, gangrene, peptic ulcer disease, and ulcerative colitis

203
Q

Wht is the difference between TCA/SSRI toxicity and Anti-ACh ?

A

Usually lead to tachycardia, drowsiness, dry mouth. (Much like anti-cholinergics)
Main difference is cardiac symptoms, QT prolongation.

Renal 2 (10 decks)

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