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CV Exam III > INTRODUCTIONTOPEDIATRICPHARMACOLOGY > Flashcards

INTRODUCTIONTOPEDIATRICPHARMACOLOGY Flashcards

1
Q

Of current FDA approved drugs, how many are approved for pediatric use?

A

less than 50%

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2
Q

What do you call the use of a medication for a non-FDA approved indication?

A

off label

60% ar ethis in peds

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3
Q

How do we determine pediatric drug doses for off-label use?

A

case series, trial

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4
Q

Commonly Used Age Definitions

A

Premature neonate
1 month to 1 year of age

Child
1 –11 years

Adolescent
12 –16 years

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5
Q

Commonly Used Weight Definitions

A

Extremely low-birth-weight (ELBW)

90thpercentile forGA

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6
Q

premature and low birth weight up

A

mortality

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7
Q

HISTORICALMISTAKES

Sulfonamide: kernicterus

A

Displaces bilirubin from protein-binding sites, bilirubin deposits in the brain, results in encephalopathy

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8
Q

HISTORICAL MISTAKES

Chloramphenicol: grey baby syndrome

A

Abdominal distension, vomiting, diarrhea, characteristic gray color, respiratory distress, hypotension, progressive shock

couldnt excrete

immature glucuronidating

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9
Q

HISTORICAL MISTAKES

A

Congenital abnormalities; also: polyneuritis, nerve damage, mental retardation

morning sickness and sleeping aid

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10
Q

OVERRIDING PRINCIPLE

A

Children are NOT just “little adults”

Cannot extrapolate dose from adult data based simply on body weight or surface area

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11
Q

Oral Drug Absorption

A

Gastric volume ↓

Gastric acid ↓ (gastric pH ↑)
Increased absorption of acid labile drugs (penicillin G, erythromycin) (goes from 6-8 to 1-3 unless premautre it stays high and some drugs arent being destroyed)
Decreased absorption of weakly acidic drugs (phenobarbital, phenytoin)
Extrauterine factors (nutrition) most likely responsible for initiating acid production

Transport of bile acids ↓

Gastric emptying ↓, intestinal transit time ↑

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12
Q

Intramuscular Drug Absorption

A 
Absorption inconsistent due to differences in:
Muscle mass
Poor perfusion (erratic blood flow)
Peripheral vasomotor instability
Insufficient muscle contractions

Sick, immobile neonates or those receiving paralytics may show reduced absorption rates

IM dosing reserved for emergencies or when IV sites inaccessible

Exception: phytonadione IV given at birth >slow release until dietary intake adequate

wont use unless life threatening

wit k is slow release

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13
Q

Transdermal Drug Absorption

A

Directly related to:
Degree of skin hydration
Relative absorptive area

Inversely related to:
Thickness of stratum corneum

Substantially increased percutaneous absorption:
Underdeveloped epidermal barrier
Compromised skin integrity
Increased skin hydration
Ratio of BSA to total body weight highest in youngest
Relative systemic exposure higher

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14
Q

Rectal Drug Absorption

A 
May be important alternative site when oral agents cannot be used:
Nausea
Vomiting
Seizure activity
Preparation for surgery

Erratic absorption depending on formulation and retention time

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15
Q

Body Weight (%) Composed of Water

A

Premature Newborn
85%

Term Newborn
70-80%

One Year
60-65%

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16
Q

Extracellular Water

A

Similar decline from 40-45% (newborn) to 20-25% (1 year)

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17
Q

GentamicinVolume of Distribution

A

Premature Neonate
0.5-0.7 L/kg

One Year
0.4 L/kg

Adulthood
0.2-0.3 L/kg

have to give more drug to fill the space

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18
Q

Body Fat

A

Total body water varies inversely with fat tissue

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19
Q

Protein Binding IS DECREASED

A

Due to: reduced levels of albumin and α1-acid glycoprotein (+ decreased affinity)

Bilirubin non-covalently bound to albumin with lower affinity in newborn than

so increase free drug to act at receptors

bilirubin displaces drugs and vis versa causing kernictures (3rd gen cephalosporin)

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20
Q

Drug Metabolism

Phase I

A

Oxidation, reduction, hydroxylation, hydrolysis
Develop at varying rates during childhood
CYP3A develop early in life
CYP2D6 similar to adult values within 2 weeks of life
CYP2C9 and 2C19 develop throughout childhood
CYP2E1 similar to adult values at 3 months
CYP1A2 negligible in newborn not exposed to caffeine
Alcohol dehydrogenase only reaches adults levels at 5 years

21
Q

CYP3A develop early in life

A

erythromycin, alprazolam, simvastatin)

22
Q

CYP2D6 similar to adult values within 2 weeks of life

A

codeine

23
Q

CYP2C9 and 2C19 develop throughout childhood

A

(warfarin, phenytoin)

24
Q

CYP2E1 similar to adult values at 3 months

A

acetaminophen)

25
Q

CYP1A2 negligible in newborn not exposed to caffeine

A

(caffeine)

26
Q

Alcohol dehydrogenase only reaches adults levels at 5 years

A

chloramphenicol

27
Q

drug metabolism

phase II

A

Glucuronidation undeveloped

Sulfation well-developed

Acetylation

see more sulfides instead of glucuronides

28
Q

Drug Elimination

A 
Glomerular Filtration
Ability to filter, excrete, reabsorb not maximized until 1 year
Rapid rise in GFR:
     Increased renal blood flow
     Increased function of nephrons
     Appearance of additional nephrons

Tubular Secretion
Reduced immediately after birth, increases over 1styear

Closely monitor renal function
Urine output often used diaper weights

29
Q

MEDICATION DOSINGIN CHILDREN

A

Pediatric Drug References:
Lexicomp, Pediatric & Neonatal Dosage Handbook
NeoFax
UpToDate

Weight chosen as best estimate of growth

References provide doses in units per weight:
mg/kg/day
mcg/kg/dose
Exception: chemotherapeutic agents (BSA)

Doses outside of reference ranges should always be questioned

Older children/adolescents transition to adult dosing when calculated weight-based dose exceeds adult doses

30
Q

PREVENTING MEDICATION ERRORS

A

Weight-based dosing may lead to mathematical errors

Caution: unit conversions and decimal point errors
Ten-fold overdose of narrow therapeutic window drug can be fatal(clonidine, digoxin, morphine, fentanyl)

Methods to Reduce Potential Medication Errors:
Standard concentrations
Smart pump technology
Barcoding
Electronic prescribing

Outpatient Setting:
Patient specific information on Rx
Appropriate medication measurement tools

31
Q

NEONATAL SEPSIS overview

A

Incidence inversely proportional to birth weight and GA

Mortality 30-50% (highest observed in neonates

32
Q

NEONATAL SEPSIS

risk factors

A 
Preterm birth
Maternal GBS colonization
Rupture of membranes > 18 hours
Maternal signs/symptoms of intra-amniotic infection
Ethnicity
Male sex
Low Apgar scores
33
Q

NEONATAL SEPSIS

pathogenesis

A

Organisms ascend birth canal

Organisms can also enter amniotic fluid via occult tears

Chorioamnionitis: intra-amniotic infection
Clinical diagnosis –maternal fever (≥ 38 ˚C; 100.4 ˚ F)
Other criteria used in clinical trials (2 of the following):
Maternal leukocytosis > 15,000 cells/mm3
Maternal tachycardia > 100 bpm
 Fetal tachycardia > 160 bpm
 Uterine tenderness
Foul odor of amniotic fluid

34
Q

NEONATAL SEPSIS

pathogetns early onset

A 
Early Onset (within 5-7 days)
GBS (50%)
E. coli (20%)
Others:
     Listeria monocytogenes
     Enterococcus
     Gram-negative bacilli
35
Q

NEONATAL SEPSIS

pathogens late onset

A 
Late Onset (after 5-7 days’ PNA)
CONS (68%)
S. aureus
Pseudomonas
Anaerobes
Candida
36
Q

NEONATAL SEPSIS

antimicrobial agents

A

Ampicillin (covers gram pos)

Gentamicin (gram neg)

Third generation cephalosporin (dftraxone dont use bc it displaces bilirubin andyou get kernicterus)

Acyclovir (not routinely used) (if viral seizures are indicative)

37
Q

NEONATAL SEPSIS

treatment

A

Ampicillin
MOA: inhibits bacterial cell wallsynthesis

Gentamicin
MOA: inhibits bacterial proteinsynthesis

Third Generation Cephalosporin
Cefotaxime vs. ceftriaxone
MOA: inhibits bacterial cell wallsynthesis

Acyclovir
MOA: inhibits viral DNA synthesisand viral replication

38
Q

drug resistant gram pos use

A

vanco for late onset

39
Q

Viral myocarditis overview

A

Incidence –1:100,000

Implicated in up to 12% of sudden cardiac deaths in adolescents and young adults

40
Q

viral myocarditis pathophysiology

A

Acute phase: inflammatory cell invasion of myocardium and myocardial necrosis and apoptosis

T-cell invasion: most destructive 7-14 days after inoculation

Healing phase: myocardial fibrosis; continued inflammation and persistent viremia may lead to left ventricular dysfunction and dilation
;
for lvh: use inotropes for

afterload reduction

ecmo to let heart heal

41
Q

viral myocarditis treatment

A 
Acute phase
Inotropes
Afterload reduction
Mechanical ventilation
Extracorporeal membrane oxygenation (ECMO)
Immune therapy
     Intravenous immunoglobulin (IVIG) (used in myocarditis bc high rate of mortality)
     Immunosuppressive agents
42
Q

INTRAVENOUS IMMUNOGLOBULIN

A

Sterile solution of human immune globulin
> 98% gamma globulin(IGG), trace IgA and IgM

MOA: protects recipient against infection and suppresses inflammatory and immune mediated processes
Replacement for 1˚ and 2˚immunodeficienciesand IgG antibodies against bacteria, viral, parasitic antigens
Interferes with Fc receptors for autoimmune cytopeniasand ITP
Provides passive immunity by increasing antibody titer and antigen-antibody reaction potential

43
Q

IVIG PK

A

Provides immediate antibody levels

Immune effect: 3-4 weeks

44
Q

IVIG AE

A

Chills, fever, flushing, myalgia, malaise, headache

Tachycardia, chest tightness, dyspnea, sense of doom

Thrombotic complications

Acute kidney injury

45
Q

EXTRACORPOREAL MEMBRANE OXYGENATION(ECMO)

A 
Prolonged cardio-pulmonary bypass (3-10 days)

upports patients with life-threatening respiratory or cardiac failure

Neonatal indications:
Primary pulmonary hypertension
Meconium aspiration syndrome
Respiratory distress syndrome
Group B Streptococcal sepsis
Asphyxia
Congenital diaphragmatic hernia
46
Q

ECMO CIRCUIT

A

Blood siphoned, driven by right arterial pressure

oller pump draws blood into bladder and pushes it through oxygenators and heat exchanger

47
Q

ECMO COMPLICATIONS

A 
Clots in circuit (19%)
Oxygenator failure
Seizures
Intracranial bleeding
Hemolysis and coagulopathy
Arrhythmias
Oliguria (within 24-48 hours)
Metabolic acidosis
48
Q

MEDICATION USE IN ECMO

A

Site of drug delivery
Directly into patient?
Proximal, distal, or directly into venous reservoir? (give proximal)

Hemodilution
Circulating blood volume will double (blood mixing with priming solution) affecting drugs with small volumes of distribution and those that are highly protein bound

Drug binding interactions with the circuit
Adsorption and sequestration onto plastic cannula and/or silicone oxygenator

Altered renal, hepatic, and cerebral blood flow
Non-pulsatile blood flow

CV Exam III (17 decks)

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