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2015 Spring 307 Midterm > Basic Principles > Flashcards

Basic Principles Flashcards

1
Q

What meds increases risk of kernicterus?

A

Sulfonamides and Ceftriaxone

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2
Q

Grey baby sydrrome was caused by?

A

Chlorimphenicol

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3
Q

Gasping syndrome is caused by?

A

Benxyl Alcohol (in some IV solutions)

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4
Q

Pharmocokinetics is what?

A

What the BODY does with the DRUG

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5
Q

ADME stands for what?

A

Absorption, Distribution, Metabolism and Elimination

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6
Q

Absorption =

A

bioavailability

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7
Q

Distribution =

A

Volume of Distribution

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8
Q

Elimination =

A

Clearance, half-life and rate constant

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9
Q

What are some routes of ABSORPTION?

A

IV, PO, PT, PR, IM, PERCUTANEOUS, IO, INHALED

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10
Q

Drug absorption = Bioavailability = (F)

A

Bioavailability is how much drug enters the systemic circulation

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11
Q

For IV meds (F) = 100%

A

consider F for other routes (PO, PR, SC, etc)

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12
Q

Rate of absorption is not the same as F

A

oral liquids, not tabs, compounded meds

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13
Q

What factors will affect drug absorption?

A

formulation of the medication, pH of stomach, lipid solubility

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14
Q

Patient factors that affect drug absorption;

A

1st pass, co-administration with food, gastric contents/emptying time, pH, surface area, size of bile salt pool (biliary atresia), bacterial colonization, and underlying diseases (short gut, etc)

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15
Q

1st pass mechanism

A

gut metabolism + liver metabolism; absorbed thru the gut then the portal vein then the liver; decreased in infants (hepatic immaturity)

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16
Q

Frequent feedings interfere with absorption because:

A

always something in the stomach; frequent Q 3 hour feeds; there is a constant buffer

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17
Q

Gastric emptying:

A

erratic in infants, slower vs adults (adult values at 6-8 months), contributes to reflux, affects time the drug reaches the Small intestine, caloric density of feeds

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18
Q

Gastric pH

A

less acid prduction (increased pH vs adults), term is 6-8 but drops to 1-3 within 24 hrs, but takes longer to normalize in preemies (~3wks), acid production does not correlate with PCA, but instead PNA

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19
Q

Why does pH matter?

A

affects stability ad ionization of a drug

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20
Q

PO phenobarb and phenytoin are weak acids, so absorption is:

A

decreased

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21
Q

PO PCN G, AMP, NAFF are acid-labile, so absorption is:

A

increased

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22
Q

GIT Surface area

A

more surface=more absorption; tight junctions are not as tight (higher molecular weighted meds sneak thru) which causes an increased permeability in infants vs children/adults

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23
Q

pancreatic function

A

if decreased (CF), decreased rate of synthesis, pool size and intestinal transport

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24
Q

immature gut flora in infants

A

affected by: age, delivery method, feeding type (EBM), drug therapy (acid suppression)

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25
Q

What medication is dependent upon gut bacteria?

A

Digoxin (10% is dependent on gut bacteria)

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26
Q

Decreased GI Absoption:

A

Reflux, short bowel syndrome, cardiac defects (shunting), hypo/hyperthyroidism (increases or decreases gut transit time)

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27
Q

RECTAL absorption ADVANTAGES:

A

less 1st pass, absorbed into the hemorrhoidal veins and if in the lower rectum, absorbed directly into system, upper rectum undergoes 1st pass

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28
Q

RECTAL absorption DISadvantages

A

Erratic PR absorption, infant forms not commercially available, dutting is not accurate, PO/IV suspensions and is often expelled before absorbed

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29
Q

IM absorption determined by:

A

blood flow at the site of injection, muscle mass, muscle activity

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30
Q

IM absorption is altered in preemies because:

A

less muscle mass, poor perfusion, peripheral vasomotor instability, insufficient muscle contractions

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31
Q

Which route is preferred in neonates?

A

IV

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32
Q

PERCUTANEOUS Absorption:

A

Enhanced in NN and infants due to thinner statum corneum, increased blood flow to the skin, increased total body surface area, can see systemic exposure to topically applied meds, WHAT ELSE IN IN THE CREAM

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33
Q

Aquaphor has been shown to

A

increase skin integrity and decrease losses

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34
Q

IO absorption

A

alternative; transport setting; marrow very vascular, up until 5 yrs

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35
Q

INTRApulmonary absorption

A

Goal is for local effects, but systemic absorption can occur, (tobi, dex), developmental changes and altered capacity of lungs alters the pattern of drug absorption

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36
Q

DISTRIBUTION

A

determined by: binding affinity of drugs for proteins, hydrophilic vs lipophilic, body composition (% of ECF and TBW), molecular weight, degree of ionization at body pH, hemodynamic factors (cardiac output)

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37
Q

Distribution and classical examples of difficult to treat infections in NICU include:

A

osteomyelitis, meningitis, endocarditis and MUST CONSIER DISTRIBUTION OF PARTICULAR MEDICATION WHILE CHOOSING DRUG THERAPY AND TARGET CONCENTRATIONS

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38
Q

VOLUME of distribution

A

The volume in which the amount of drug would need to be uniformly distributed to produce the observed blood concentrations

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39
Q

What explains the measured concentration to total amount of drug in the body?

A

Volume of Distribution

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40
Q

Protein Binding

A

binding of drugs to protein is decreased in infants: decreased amounts of plasma proteins, lower binding capacity, decreased affinity of proteins, competition for binding sites (bilirubin and kernicterus)

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41
Q

NICU patients have lowered albumins?

A

True

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42
Q

There is less Protein binding = more “free” drug

A

unbound drug is free to distribute out of plasma into the tissues and increases the volume of the distribution for total drug (Total = BOUND + UNBOUND; the BOUND is what IS NOT WORKING); you will have more than you want

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43
Q

Body Composition

A

Total body water (big bag of water, not fat), higher proportion of ECF and TBW, ECF (plasma and interstitial fluid), premature is % ECF; Aminoglycosides tales “MORE” to fill up the bucket of water (large Vd)

44
Q

Aminoglycosides

A

increased mg/kg dosing needed
NICU:- 4-5 mg/kg
Older child 2-5 mg/kg
Adult 1mg/kg

45
Q

premature babies have less body fat so

A

drugs that are lipophilic will have a smaller vd

46
Q

METABOLISM = CLEARANCE

A

CL is dependent on: initial hepatic metabolism, followed my excretion of a parent drug/metabolites by liver or kidney

47
Q

Most drugs are Metabolized by the LIVER

A

(Other routes are kidneys, intestines, lungs, skin)

48
Q

Hepatic Metabolism:

A

various hepatic pathways for drug metabolism mature at different times; Ingants have a delayed maturation of drug-metabolizing enzymes (phase I&II)

49
Q

Phase I Hepatic Metabolism (CYP enzymes)

A

(delayed) Oxidation, hydrololysis, hydroxilation, reduction

50
Q

Phase II Hepatic Metabolism (Synthetic metabolism)

A

(polar cmpd) conjugation, glucuronilation, Sulfation

51
Q

Hepatic Metabolism

A

Non-Polar is LIpid soluable; Polar is water soluable
active metabolites
inactive parents drug (prodrug) to active drug

52
Q

Phase I of Hepatic Metabolism (CYP450)

A

absolute mass of enzymes is decreased, measured by absolute weight as a percent of liver weigh; different enzymes mature at different times

53
Q

Phase 1 Hepatic Metabolism

A

Diazepam: there is a hydroxilation deficient in preemie and term infants, so there is along half life

54
Q

Phase 2 Hepatic Metabolsim

A

Methylation is present in infants, but NOT adults
Infants can methylate theophylline into caffeine; at 4-6 months oxidative pathways mature and this shortens the half-life

55
Q

Theophylline Metabolism

A

CYP1A2 in adults = metabolite

N-Methylation in infacts = caffeine=excreted renally which is prolonged in infants and can accumulate

56
Q

Phase II of Hepatic Metabolism

A

Sulfation mutures to adult levels at birth: ACETOMINOPHIN: infants are less susceptable to toxity from overdose, infants conjugate with sulfate and adults conjugate with glucuronic acid (harmful metabolite)

57
Q

Phase II Hepatic Metabolism

A

Glucuronidation does not mature until 3 years of age (slower Cl so use smaller doses)
Chloramphenicol: grey baby because doses not adjusted for decresed glucuronidation

58
Q

Phase II Hepatic Metabolism

A

Alcohol dehydgogenase does not mature until 5 yrs of age: gasping syndrome
Also seen with chloryl hydrate

59
Q

Elimination=Clearance

A

Clearance measures the drugs elimination; volume of blood/plasma from which drug is completely removed per unit of time

60
Q

Kidney and liver is responsible for what?

A

most of the drug elemination

61
Q

First-Order Elemination

A

CL is constant over the range of concentrations; linear; increase in dose = proportional increase in drug concentration EXAMPLE=Gentamicin

62
Q

Zero-order elimination

A

Cl is not independent of drug concentration; non-linear or “Michaelis-Minton”; capacity-limited/ satruable drug elimination; small increase in dose = large increase in concentration:
EXAMPLE: Phenytoin

63
Q

Hepatic Clearance is the primary site of drug metabolism and is responsible for the ulitmatedrug cl

A

Hepatic CL is influenced by: drugs affinity for certain enzymes, hepatic blood flow, protein binding, liver disease, cardiac function

64
Q

ELIMINATION RENAL

A

GFR+tubular secretion - tubular reabsorption

65
Q

Renal elimination

A

GFR, Secretion (active transport), reabsorption (lipid-soluble or non-ionized able thru membrane), Water-soluble meds are excreted with no changes int he urine

66
Q

Renal Elimination = GFR =

A

dependent on blood flow and protein binding, physiologically decreased in the newborn, premature infants have 2-4 fold decrease in GFR vs term, increases rapidly within the first year of life; increases in cardiac output + changes in vascular resistence leads to increased renal blood flow

67
Q

Indomethacin/Ibuprofen for PDA does what

A

Decreases PGE=decrease vasodilitation=decreased renal blood flow

68
Q

What affects GFR?

A

GA, PNA (accelerated increase can be seen in ELBW); calls for dose change during first 4 weeks of life
Example: Cefepime increase at DOL

69
Q

GFR example med for elimination is Gentamicin

A

NICU is 4-5 mg/kg/dose Q 24-48 hours

Older kids: 2.5 mg/kg/dose every 8-12 hours

70
Q

Assessment of GFR

A

Creatinine CrCl is is Gold Standard; 100% filtered at the glomerulus, only lightly secreted by tubular cells, not reabsorbed by the tubule, CrCl will not factor in secretion or reabsorption of drugs; a high SCr is common in ELBW (PDA)

71
Q

Estimating GFR in infants/NN

A

age specific equations, but not as precise (transplacental Scr/low Scr), Schwartz equation

72
Q

Tubular secretion lags behind glomerular maturation

A

active process ( goes against the concentration gradient by using transporter proteins

73
Q

Fursemide

A

potential blunted diuretic effect due to immaturity of secretion into intraluminal space (cant get to the site of action)

74
Q

Renal-Tubular secretion

A

drug-rug interactions can occur if both are eliminated thru the same tubular secretion protein=decreased excretion, increased drug levels, increaed side-effects
Example is probenecide combined with PCN for secretion resulting in increased PCN

75
Q

Amphotericin B

A

can cause renal tubular toxicity and alter tubular secretion of other meds

76
Q

PDA and GFR

A

PD can increase VD, decreaed BF to kidneys; NSAIDS -closely monitor renally eleminated meds

77
Q

Dopamine and GFR

A

Used freq for hypotension and oliguria, can result in increase renal blood flow, thus increasing GFR (thus causing subtherapeutic levels (gent and vanc)

78
Q

Furosemide and GFR

A

loop diuretic; must be secreted into the luminal side of the renal tubule in order to inhibit chloride reabsorption: effectiveness is dependent on renal funcion;
increases renal blood flow thru PGE activation (casodilitation); PGE effects my blunt response to PDA treatment with endomethacin

79
Q

Half-Life

A

Time needed for drug concentration to decrease by 1/2

80
Q

Half-life

A

elimination rate constant (K) can be used to predict concentration at any time

81
Q

Accumulation

A

After 11 half-life, drug concentration is 50% of steady state, after 2 half-lifes at 75% and after 3.3-5 half-lifes are the same dose concentration is at 90-97% of final steady-state concentration

82
Q

Steady State is

A

when it is a good time to check a level

83
Q

Pharmacodynamics is

A

What the drug does to the body; not as much known for neonates;

84
Q

Therapeutic Drug monitoring

A

drug actions directly related to the drug concentration at the site of action n(example concentration of cefotaxime to treat meningitis) and concentration of vanc in the blood to treat CONS bacteremia

85
Q

Why monitor therapeutic levels?

A

Toxicity (narrow therapeutic ranges (dig, theophylline), known toxicity at certain toxicity thresholds (getamicin)

86
Q

Therapeutic levels and efficacy

A

Time above the MIC-time dependent on medications (Vanc)

87
Q

Therapeutic levels imprtant

A

preemie vs term infants, inadequate responses, drug-drug interactions, organ dysfunction, MIC information (Mean inhibitory concentration)

88
Q

Therapeutic Range

A

range of concentrations where there is a high efficacy and low risk of toxicity in the maority of patients; may need to individualize ; like vanc doses therapeutic for blood infections, not osteo

89
Q

Distribution phase

A

30 minute infusion time allows for distribution within the tissue compartment as rapidly as the dose is administered resulting in decreased side-effects and toxicity

90
Q

when to draw gent peaks?

A

30 minutes after the end of the 30 minute infusion time to allow for distribution; before changing a regimen-consider the timing and draw levels at correct times

91
Q

Aminoglycosides (Gent, tobramycin, amikacin)

A

Why do NICU babies need a higher dose and an extended interval of 24-48 hrs? increased Vd, decreased CL, decreased glomelular filtration (AG excreted unchanged in kidneys) and a longer 1/2 life;
can use the trough to estimate overall renal fx

92
Q

Side-effects of aminoglycosides

A

ototoxicity and nephrotoxicity

93
Q

Concentration killing effect in AG

A

optimal effect of certain conentrations; goal in nicu is to achieve appropriate peak concentration with 4-5 mk/kg/dose , then allowing the concentraion to fall throughout the 24-48 hr dosing interval

94
Q

AED’s

A

Phenobarb (predictable)-for each 1mg.kg-level increases by 1ml/L; Phenytoin is squirly with a non-linear PK and is highly protein bound (need to check levels)

95
Q

Total Drug Concentration

A

Protein bound + Unbound “free”; protein bound is non-active, unbound is what is active

96
Q

Alpha and beta Receptors

A

SNS: Flight or fight: Neurotransmitters are norepinephrine, epinephrine and Dopamine
Stimulate different adrenergic receptors

97
Q

Receptor Physiology

A

Adrenergic: Alpha 1, Beta 1, Alpha 2, Beta 2

98
Q

Alpha 1

A

present in vascular beds and in skeletal muscle
Vasoconstriction of arteries and veins
increases cardiac contractility; increases b/p

99
Q

Alpha 2

A

presynaptic nerve endings; inhibits presynaptic release of norepinephrine thru feedback mechanisms; decreases sympathetic outflow; lowers b/p

100
Q

Beta 1

A

in cardiac muscle; increases heart rate and cardiac contractility

101
Q

Beta 2

A

in bronchial muscle and peripheral vasculature; bronchiodolitation of lungs; vasodilitation pf peripheral vasculature; decreases b/p

102
Q

Alpha=PNS

A

Beta=SNS

103
Q

other receptors

A

dopaminergic (kidneys and viscera); dilates arterioles in renal and splanchnic circulation

104
Q

Vasopressin I

A

causes vasoconstriction in smooth muscle, liver and other tissues

105
Q

Vasopressin 2

A

in kidneys; increases water permeability and reabsorption in the collecting tubules; H2O reabsorbed; increases oncotic pressure; diabetes insipidus

2015 Spring 307 Midterm (7 decks)

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