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Therapeutics P3 Spring > Toxicology > Flashcards

Toxicology Flashcards

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1
Q

What are the first 3 things to do when a patient ODs

A

Stabilization
Exposure
Assessment

stabilization-

ABC management (airway, breathing, circulation (BP))

Oxygenation

Vital signs

IV access

Exposure-
Medications/illicit substances
doses
time of ingestion
Family/EMS report
Pill count

Assessment
- Physical exam
-Labs
- APAP/salicylate concentartions
- EtOH/ toxic alcohol panel
- decontamination
- antidote

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2
Q

What are some toxidromes we look at when looking at OD patients

A

Alpha and beta adrenergic
Anticholinergic
Sedative/hypnotic
Serotonin
Sympathomimetic

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3
Q

What are some anticholinergic symptoms in OD

A

Blind as a bat
Hot as hades
mad as a hatter
dry as a bone
red as a beet

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4
Q

What are some meds seen in urine drug screen

A

Amphetamines
Barbiturates
BZDs
Cannabinoids
Cocaine]
Opioids
Phencyclidine

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5
Q

What are some calculations helpful in OD

A

Anion gap- (Na+ + K +)- (Cl + HCO3)
Gap present if greater than 14

Osmolar gap
(2x NA+) + (BUN/2.8) + (glu/18) + (EtOH/4.6)
Gap is present if greater than 10

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6
Q

What are some positives and negatives about activated charcoal

A

Positive-
decreases time related problems (binds toxin before incorporation into blood stream. not useful more than a couple of hours after OD)

absorbs most toxins

Negative
- difficult administration
- should not be administered if airway is unprotected

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7
Q

Dosing of activated charcoal

A

1-2 gm/kg ABW or 50-100 gm in adults

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8
Q

What is whole bowel irrigation (polyethylene glycol) used for in toxicology? Dosing?

A

Iron, sustained release products, lithium

1 L to 2 L per hour in adults

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9
Q

What is hemodialysis used for in toxicology

A

Effective for
alcohol
Lithium
Salicylates
Theophyline

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10
Q

What is the biggest antidote for acitaminopehn

A

NAT (N acetylcyctine)

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11
Q

for salicylates (aspirin), what are some things to evaluate when evaluating toxicology

A

Anion gap (mixed acid base disorder), early respiratory alkylosis (hyperventilation)

Electrolyte distrubances (Hypokalemia, hypo/hypernatremia)

Salicylate concentrations ( mild toxicity- tinnitus, dizziness)
Severe toxicity (CNS effects)

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12
Q

salicylate toxicity signs and symptoms

A

N/V
Tinnitus and diaphoresis
Decreased GI motility
Altered mental status
seizures
Hyperventilation

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13
Q

General management strategies for salicylate toxicity

A

Stabilization (ABC management, oxygenation, Vital signs, IV access, CNS respiratory depression), Oxygenation, vital signs, IV access, CNS/respiratory deression

Exposure
Med/illicit substances
Dose(s)
Time of ingestion
Family/EMS report
Pill count

No changes with stabilization and exposure

Assessment
activated charcoal if willing and within 1-2 hours
Fluid will help eliminate via urine (use KCL as we see hypokalemia and to counteract it)
Use sodium bicarb
Hemodialysis

MAke sure RR matches what the patient was on before intubation, if we put them on normal RR, they may retain more of the acid and it may be lethal.

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14
Q

MOA of sodium bicarb in salicylate toxicity

A

They alkalyze the urine

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15
Q

Indication of sodium bicarb

A

serum salicylate level > 30mg/dl
Anion gap metabolic acidosis
altered mental status

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16
Q

dosing of sodium bicarb

A

1 to 2 mEq/Kg (50-100 mEq) IV push over 1 to 2 mins

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17
Q

What to monitor on sodium bicarb

A

Serum PH 7.5-8 (mae sure you dont send them into alkylosis)
Elevtrolytes (potassium, calcium)

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18
Q

sedatives (BZDs) toxicity signs and symptoms

A

CNS depression
Respiratory depression
Hypotension
Bradycardia

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19
Q

General management of sedative toxicity (BZDs)

A

Similar stabilization and exposure

Activated charcoal
EtOH/toxic alcohol panel
Apap/salicylate concentration
Flumazenil

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20
Q

What drug stops BZD toxocity

A

flumazenil

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21
Q

MOA of flumazenil

A

Competes with BZDs at BZD binding site of GABA complex

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22
Q

dosing of flumazenil

A

0.2 mg IV push

can induce withdrawal symptooms (N/V, agitation)

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23
Q

What to use in caution when using flumazenil

A

Cation in patients with seizures (as we treat seizures with BZDs and they will not work if flumazenil is in their symptoms)

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24
Q

tricyclic antidepressants indication

A

Bed wetting
Depression
Insomnia
Migraines
Neuropathy

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25
Name tricyclic antidepressants
Amitriptyline Desipramine Doxepin Imipramine Nortriptyline
26
what drug has one of the hivhest risk of lethal drug overdoses
amitriptyline
27
PK of TCAs
Large Vd Rapid absorption from GI tract (anticholinergic effect may slow down GI motility)
28
What are some things we worry about in TCAs
-Anticholinergic activity -Alpha receptor blockade -Serotonin, norepinephrine and dopamine inhibition - sodium and potassium channel blockade - CNS and respiratory depression
29
TCAs toxicity signs and symptoms
Seizures, anticholinergic symptoms and prolonged QRS most common hypotension altered mental status
30
What are the different risks of different QRS values
QRS>100 msec- increased risk of seizure activity QRS>150- increased risk of cardiac arrythmias Metabolic acidosis- promotes unbinding of drug from proteins
31
alpha receptor blockade of TCA lead to what side effect
Hypotension
32
general management strategies of TCAs OD
Stabilization and exposure similar Assessment- Vasopressor (norepinephrine, epinephrine) may be used in seizure management of QRS>100, sodium bicarb used if metabolic acidosis.
33
MOA of sodium bicarb in RCA? Indications
Increases sodium gradient of poisoned sodium channels. indications - QRS interval > 100 msec - TCA induced arrhythmias or hypotension - Metabolic acidosis
34
When to dx sodium bicarb in TCA poisoning
QRS < 100 resolution of ECG abnormalities hemodynamically stable
35
Name some typical and atypical antipsychotics
Typical- Haloperidol, fluphenazine, chlorpromazine, thioridazine, Perphanazine Atypoical- Aripiprazole, clozapine, olanzapine, paliperidone, ziprasidone
36
What are the different side effects seen with 1st gen and 2nd gen antipsychotics
First gen- D2 antagonism (most likely to have more side effects) 2nd gen- 5HT2A/D2 antagonism
37
Antipsychotic signs and symptoms
-QT prolongation (magnesium used to treat) -Tachycardia -Hypotension -Extrapyramidal symptoms -Neuroleptic malignant syndrome (NMS) -Sedation
38
for atypical antipsychotics, when do we see roxicity symptoms, peak symptoms? Duuration?
Symptoms are typically seen within 1-2 hrs of ingestion Peak symptoms in 4-6 hrs Duration is roughly 12-48 hrs
39
Antidotes for EPS seen in antipsychotic OD
Benztropine 2 mg IM Diphenhydramine 1-2 mg/kg IV/IM, 50 mg PO
40
Advantages of benztropine and diphenhydramine when treating EPS
Benztropine has longer half life and diphenhydramine has oral dosing
41
What is the mains symptom we are worried about after ingestion of antipsychotics
Neuroleptic malignant synrome
42
Explain NMS? When does it occur? Who does it usually occur in? How long does it continue?
Hyperpyrexia up to 108 f with altered mental status (delirium or coma) and lead pipe muscular rigidity occurs 3-9 days after initiating therapy or adding second agent More often in less than 40 year old males Continues for 5-10 days
43
What drugs cause 84% of NMS
Haloperidol, depot fluphenazine or chlorpromazine use
44
What is NMS death caused by
Death is secondary to rhabdomyelosis, renal failure, CV collapse, respiratory failure, arrhythmias or thromboembolism
45
NMS tx
Dx offending agent rapid external cooling BZDs Dantrolene (reverses malignant hyperthermia) Bromocriptine (If we need PO)
46
What is serotonin syndrome? What are the symptoms? How fast does it occur?
Serotonin syndrome is a toxic hyperserotonergic state. Excessive stimulation of post synaptic receptors in the CNS triad of symptoms - Altered mental status - Autonomic instability - Neuromuscular abnormalities within 6 hrs of an increase in percipitating medication
47
serotonin syndrome treatment
Dx offending agent BZDs Aggressive cooling Cyproheptadine
48
main differences in serotonin syndrome and NMS
Fever lasts less than 24 hours and lower limbs and more affected than upper limbs in serotonin syndrome NMS has higher fever lasing longer than 24 hours and diffuse lead pipe rigidity
49
What meds cause serotonin syndome
Antidepressants (SSRIs, TCAs, SNRIs, trazodone, dextromethorphan) DIrect agonists (buspirone, lithium, sumatriptan) Increased release of serotonin (amphetamines, cocaine, mirtazapine, MDMA) Inhibitors of serotonin metabolism (linezolid, MAO)
50
Indicatiojn and monitoring of digoxin? When must it be drawn
Indicated for treatment of A Fib and HF. Monitored with serum concentrations due to narrow therapeutic index 6 hours after previous dose
51
How does digoxin work?
works by blocking Na/K ATPase exchange in cells. might cause hyperkalemia if it is in high levels
52
Digoxin toxicity signs and symptoms
Non cardiac- N/V, Abdominal pain, anorexia, confusion, vision changes Cardiac- Bradycardia, 2nd or 3rd degree heart block Arrhythmias Hyperkalemia
53
What are the different levels of K and their associated mortality levels
5-6.4 is 34% mortality > 6.4 is 90% mortality
54
Is hemodialysis effective with digoxin
NO
55
general management of digoxin toxicity
-dx digoxin -ABC management -obtain serum digoxin concentration -Monitor vital signs and ECG changes (arrhythmias, bradycardia) - administer activated charcoal (if ingested within 2 hrs) - consider administration of digibind
56
MOA of digibind
Binds free digoxin and tissue bound digoxin released during equilibrium state
57
indications of digibind
ventricular arrythmias, bradycardia, 2nd or 3rd degree heart block not responsive to tropine Hyperkalemia (>5.5) with s/s of toxicity serum dig> 10-15 Ingestion > 10 mg
58
How many mg of digoxin does each vial bind
Each vial binds approx 0.5 mg of dig
59
How do we calculate the number of digibind vials that we use based on serum digoxin levels
digibind vials= digoxin concentration x patients weight (kg) --------------------------------------------------- 100
60
How to calculate digoxin dose based on acute ingestion of known amount
Total body load (TBL)= mg digoxin ingested x 0.8 TBL/0.5 mg= # digibind bials to administer
61
does digoxin occur with acute or chronic therapy
BOTH
62
What do we think of digoxin concentrations in serum after digibind administration
Useless as it may be elevated as digibind is causing redistribution of digoxin from adipose tissue
63
What are some signs and symptoms seen in CCBs, BBs and both
CCBs- hyperglycemia, metablic acidosis, pulmonary edema, Ileus (SR) BBs- Hypoglycemia, bronchospasms Both- Hypotension, bradycardia, arrhthmias, cardiogenic shock, CNS depression
64
general management of CCB and BB toxicity
ABC management Monitor vital signs and ECG changes (arrhythmias, bradycardia) Administer activated charcoal (depending on time of presentation)
65
What are potential antidotes for BB and CCB toxicity
Atropine Calcium Glucagon High dose insulin therapy Vasopressor therapy
66
Atropine MOA? Dosing?
blocks parasympathetic activity to increase heart rate (for bradycardia) against CCB and BB 0.5-1 mg IV push readily available, but not usually effective in CCD and BB overdoses
67
calcium MOA against CCB and BB
Enters open voltage sensitive calcium channels to promote calcium release form sarcoplasmic reticulum resulting in myocardial contractility more effective in CCB overdose vs BB overdose
68
Who has more calcium, CaCl or Calcium gluconate
Calcium chloride has 3x more elemental calcium gluconate Calcium gluconate has less side effects
69
Vasopressor MOA and drugs
Norepinephrine and epinepherine binds beta receptors not occupied by BB as well as Gs receptors to eventually stimulate cAMP and calcium release to improve contractility
70
What do we use for vasodilatory shock? What do we use for cardiogenic shock
Vasodilatory shock- norepinephrine Cardiogenic shock- epinephrine If we want to increase HR and BP- epinephrine If we want to increase only BP- norepinephrine
71
glucagon MOA
stimulates contractility by bypassing beta receptors and binding to Gs receptors to activate conversion of ATP to cAMP
72
dosing of glucagon when using for BB or CCB OD
Adults- 3-10 mg IV bolus
73
What do we need to do when we give a patient glucagon
May need to pre medicate with ondansetron and add PRN regimen due to N/V with glucagon
74
MOA of high dose insulin therapy for CCB and BB OD therapy
MOA- increased inotropy and increased intracellular glucose transport
75
Dosing high dose insulin for CCB and BB OD
Insulin drip at 0.5 to 1 unit/kg/hr IV Dextrose at 0.5 gm/kg/hr IV
76
Monitoring with high dose insulin therapy for CCB and BB therapy
Improved contractility within 15-60 mins Goal glucose- 100-250 mg/dl serum electrolytes (glucose. potassium) every 1 to 2 hrs
77

Therapeutics P3 Spring (33 decks)

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