Medication Error Flashcards

1
Q

Medication Error

A

NCCMERP: “Any PREVENTABLE event that may lead to inappropriate medication use or patient harm while medication is in control of the healthcare professional, patient, or consumer”

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2
Q

Adverse drug event (ADE)

A

Patient harm from drug exposure (an ADE can occur in the absence of a medication error)
- Non preventable

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3
Q

Preventable ADE

A

Medication error that reach the patient and cause harm (50% of all ADE)

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4
Q

Potential ADE

A

Medication error that does not cause harm (did not reach the patient or just good luck)

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5
Q

Adverse drug reaction (ADR)

A

A non preventable ADE( no medication error occurred but patient still experienced harm from drug exposure)
- Called side effect

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6
Q

FDA classification for ADEs (IND safety reporting during clinical trials)

A

Life threatening ADE: Places the patient at immediate risk of death
Serious ADE: Result in
– Patient death
– life threatening ADE
– Hospitalization or prolongation of existing hospitalization
– Persistent or significant incapacity or substantial disruption of normal daily life
– Congenital anomaly or birth defect
Suspected ADE: There is a possibility that the drug caused adverse event
Unexpected ADE: Any ADE, regardless of severity that is
- Not included in the investigator Brochure (IB)
- Not described in the IB as occurring at the observed specificity or severity
- Not consistent with the risk information in IB or general investigational plan

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7
Q

Significant of ADEs

A

ADEs during Transitions of Care:
- Medication adherence may suffer
- Medication may have been stopped, replaced, or added during hospitalization
- Poor healthcare provider communication and follow up exacerbates these problem
- Hospital readmission: ADR-related 20%, ADE-related 13%
ADEs in children:
- Dosing errors most common (93.2%)-Wrong amount of liquid measured
If you decrease medical errors => 30 days readmission rates decrease

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8
Q

NCCMERP medication error classification

A
  • Two third of ADEs are preventable
  • 40% are the result of negligence
    This is the fault of the system as most of the time they are understaffed and overworked
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9
Q

What causes medication errors

A

Medication selection and procurement
- Drug shortage or recall (get mixed up)
- Expired or adulterated drug(light get into drug)
- Ordered wrong product, strength or dilution
Improper drug storage
- Failure to refrigerate, protect from light
Ordering and transcribing
- Wrong drug, dose frequency of admistration or duration of therapy prescribed (18.5%)**
-Missed drug allergy or DDI
Transcribing
- Medication order interpreted incorrectly (25.5%)**
Preparation and dispensing
- Failure to select, package, label,….
Administration
- Failure to give the medication at all - Missed does (25.6%)**
- Failure to administer the drug to the right patient, at the right time, in the right dose
- Any discrepancy in administration from the prescriber direction or hospital guidelines
Monitoring
- No proper follow up for effect and potential ADEs

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10
Q

Pharmacist Patient Care Process Model

A
  • Collect: medication/medical/social history
  • Assess:
    – Each medication, adherence, access
    – Health and functional status, risk factors, cultural factors, health literacy
    – Immunization status, need for preventive care
  • Plan: Develop individualized patient-centered care plan
  • Implement: in collaboration with other healthcare professionals
  • Monitor, evaluate and follow up
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11
Q

ISMP list of confused drug names

A

LASA medication
Tips:
- Use brand and generic name on prescription and label
- Include indication on prescription
- Prevent LASA medication from appearing consecutively on CPOE screens
- Change appearance of lookalike names to highlight dissimilarities

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12
Q

Personalized Medicine

A
  • Pharmacogenetics: Focuses on individual genes
  • Pharmacogenomics: Focuses on the individual patient entire genome and how it affect the patient response to a drug
  • Genotype: Complete genetic make up of an individual: Knowledge of the genotype can be used to optimize pharmacotherapy in that individual patient
  • Phenotype: Observable traits of an individual patient
    – Largely determined by genotype, other traits by environment or a combination
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13
Q

Variability in drug metabolism

A
  • Genetic factors: gene ployophism such as mutation, insertion, deletion, separation and gene duplication
  • Epigenetic factors: chemical modification in gene activity that DO NOT change DNA sequence
  • Age
  • Gender
  • Ethnicity
  • Disease: Liver disease, Kidney disease, Acute viral infection
  • Environmental factors
    – Cigarette smoking(CYP450IA2), coffee, alcohol
    – Drug administration(drug interaction) herbal
  • Exposure to DDT or gasoline fumes
  • Dietary factors (charbroiled beef, grapefruit juice (inhibit drug metabolizing enzyme)
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14
Q

Drug metabolism

A

Introduces or expose a FG
- Most reaction catalyzed by CYP450 enzymes
Covalent linkage between FG on the parent compound with glucuronic acid, sulfate, glutathione
- Lead to more rapid excretion
Pgp (drug efflux pump)
- Active in liver and small intestine (ABCB1-drug transporter)

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15
Q

Example: 6-MP (mercaptopurine)

A

6-Mercaptopurine (6-MP) (Biomarker-TPMT): FDA approved labeling**
- Purine antagonist used to treat childhood acute lymphoblastic leukemia (ALL) and (off label adult or childhood inflammatory bowel disease)
- TPMT IMs and PMs are predisposed to severe 6-MP toxicity
- Consider alternative in known PMs due to risk fatal bone marrow suppression

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16
Q

6-MP and TPMT activity

A

6-TGNs– both therapeutic and toxic effect
3 competing metabolic pathways
- Inactivation to 6-thiouric acid in gut wall and liver (oral bioavailability 16%)
- Inactivation (B and T cells) to 6 methylmercaptopurine (6-MMP) by (TPMT)
- Activation intracellular to 6-thioguanine nucleotides (TGNs) in 4 steps
1. to (6-TIMP) by (HGPRT)
2. 6-TIMP to (6-MMPR) by TPMT
3. Conversion of 6-MMPR to 6-TXMP by IMPDH
4. Activation of 6-TXMP to 6-TGNs by GMPS
if you have TPMT (mutation) then you can ignore the second pathway instead they focus on the third pathway

17
Q

6-MP metabolism and TMPT polymorphisms

A

Homozygous (EM): More inactive 6-MMP, less 6-TGNs
- Normal dose (1.5mg/kg/d)
Heterozygous (IM): relatively more 6-TGNs (more side effects) due to less inactivation to 6-MMP
- 30 to 70% of normal dose
Homozygous (PM)-(poor metabolism): little to no TPMT activity, no 6-MMPs, potentially fatal myelotoxicity due to high levels of 6-TGNs
- Start with 10-fold lower daily dose given 3 times weekly instead of daily
- For nonmalignant conditions, consider alternative treatment

18
Q

Tricyclic antidepressant (TCAs)

A

Nortryptiline(Biomarker-CYP2D6): FDA approved labeling
- PMs-Higher than expected blood levels of all tricyclic antidepressants (TCAs) (off label manage crone’s disease, inflammatory valve disease)**
- Certain drugs inhibit CYP2D6 activity (normal metabolizer can resemble PMs) - (contain polymorphism)
- Monitor TCA blood levels when TCA co administer with known CYP2D6 inhibitor

19
Q

TCA metabolism and CYP2D6

A

Phenotype:effect
UM: Increased rate of TCA metabolism*, Lower plasma conc. can increase risk of therapeutic failure
- Avoid TCAs due to potential lack of efficacy
- If needed then consider a higher starting dose
EM: Normal Metabolism
- Normal recommend started dose
IM: Decreased Rate of TCA metabolism, Higher plasma conc. can lead to increase risk of side effect
- Consider 25% reduction of recommended starting dose
- Use TDM
PM: Greatly reduced TCA metablism, higher risk of side effect
- Avoid TCA due to potential side effect
- If needed consider 50% reduction of recommended starting dose
- Use TDM

20
Q

Pharmacogenomic related drug label warning

A

Currently 433