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257 Cards in this Set
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Conc. dependent antimicrobial killing
Definition |
amount of microbial killing depends on max concentration of drug above MIC
|
|
Conc. dependent antimicrobial killing
PK/PD parameters |
Peak/MIC
|
|
Conc. dependent antimicrobial killing
Examples |
Aminoglycosides
FQs Daptomycin Metronidazole |
|
Time dependent antimicrobial killing
Definition |
amount of microbial killing depends on time drug stays above MIC
|
|
Time dependent antimicrobial killing
PK/PD parameters |
T>MIC
|
|
Time dependent antimicrobial killing
Examples |
B-lactams (PCNs, cephalosporins, carbapenems)
Macrolides (Azithro, Clarithro, Erythro) Linezolid Vancomycin Clindamycin |
|
Post-antibiotic Effect (PAE)
|
continued suppression of bacterial growth after a short exposure to antimicrobial agents
|
|
Aminoglycosides PAE
|
Gram negative
Moderate to prolonged (>/- 2 hrs) |
|
Azithromycin PAE
|
Gram + and Gram -
Moderate to prolonged (>/- 2 hrs) |
|
Carbapenems PAE
|
Gram +
minimal (0.5-2 hrs) (PAE against some Gram -) |
|
Cephalosporins PAE
|
Gram + minimal (0.5-2 hr)
|
|
Clindamycin PAE
|
Gram + and Gram -
Moderate to prolonged (>/- 2 hrs) |
|
Daptomycin PAE
|
Gram + Moderate to prolonged (>/- 2 hrs)
|
|
FQs PAE
|
Gram + and Gram -
Moderate to prolonged (>/- 2 hrs) |
|
Linezolid PAE
|
Gram + minimal (0.5-2 hr)
|
|
PCNs PAE
|
Gram + minimal (0.5-2 hr)
|
|
Vancomycin PAE
|
Gram + minimal (0.5-2 hr)
|
|
Time-dependent and minimal PAE
Goal of therapy |
Maximize duration of exposure
|
|
Time-dependent and minimal PAE
PK/PD Parameter |
T>MIC
|
|
Time-dependent and minimal PAE
Antibiotics and activity spectrum |
Linezolid
PCNs Carbapenems Cephalosporins (All gram + activity) |
|
Time-dependent and minimal PAE
Vancomycin (Goal, PK/PD parameters, spectrum) |
Maximize amount of drug
24 hr AUC/MIC gram + |
|
Time-dependent and moderate to prolonged PAE
Goal of therapy |
Maximize amount of drug
|
|
Time-dependent and moderate to prolonged PAE
PK/PD parameter |
24-hr AUC/MIC
|
|
Time-dependent and moderate to prolonged PAE
Antibiotics and spectrum |
Clindamycin
Azithromycin (both have gram + and -) |
|
Conc.-dependent and prolonged PAE
Goal of therapy |
Maximize concentration
|
|
Conc.-dependent and prolonged PAE
PK/PD parameters |
Peak/MIC
|
|
Conc.-dependent and prolonged PAE
Antibiotics and spectrum |
Aminoglycosides (gram -)
Daptomycin (gram +) FQs (gram + and -) |
|
Examples of extended infusions
|
Pip/Tazo
cefepime carbapenems |
|
fT>MIC
|
amount of time the free or non-protein bound drug concentration exceeds the MIC
|
|
PK/PD parameter associated with extended infusions
|
fT>MIC
|
|
Near-maximal bactericidal effects when free drug conc. exceeds MIC for:
Cephalosporins |
60-70% of dosing interval
|
|
Near-maximal bactericidal effects when free drug conc. exceeds MIC for:
PCNs |
50% of dosing interval
|
|
Near-maximal bactericidal effects when free drug conc. exceeds MIC for:
Carbapenems |
40% of dosing interval
|
|
Advantages of extended infusions
|
superior pharmacodynamic profile (more fT>MIC)
allows for time between doses for admin. of drugs through same IV line cost savings |
|
Reasons to use antibiotic combos
|
1. broad-spectrum empiric therapy
2. polymicrobial infections 3. decrease resistance 4. decrease dose-related toxicity 5. increase inhibition or killing |
|
Synergism
|
significantly enhance inhibition or killing than either individually
|
|
Mechanisms for synergistic action
|
1. Blockade of sequential steps in a metabolic sequence
2. Inhibition of enzymatic inactivation 3. Enhancement of antibiotic uptake |
|
How is bactrim synergistic?
|
blocks sequential steps in metabolic sequence
|
|
How is augmentin synergistic?
|
Inhibition of enzymatic inactivation
|
|
How is gentamycin/PCN synergistic?
|
Enhancement of antibiotic uptake
|
|
Antagonism
|
Decreased inhibition or killing than either individually
|
|
Mechanisms of antagonistic action
|
1. Inhibition of cidal activity by static agents
2. Induction of enzymatic inactivations |
|
How is linezolid given with vancomycin antagonistic?
|
Inhibition of cidal activity (vanc) by static agents (linezolid)
|
|
How is imipenem given with cefoxitin antagonistic?
|
Induction of enzymatic inactivations
|
|
Synergistic or antagonistic?
trimeth + sulfa |
synergistic
|
|
Synergistic or antagonistic?
Amoxicillin + clavulanate |
synergistic
|
|
Synergistic or antagonistic?
gentamycin + penicillin |
synergistic
|
|
Synergistic or antagonistic?
linezolid + vancomycin |
antagonistic
|
|
Synergistic or antagonistic?
imipenem + cefoxitin |
antagonistic
|
|
Aminoglycoside coverage
|
Gram -
Pseudomonas |
|
Aminoglycoside toxicities
|
renal toxicity
ototoxicity |
|
Aminoglycoside resistance
|
gentamycin > vancomycin > amikacin
|
|
Gent/tobra desired peak serum conc.:
uncomplicated lower UTI |
2-4 mcg/mL
|
|
Gent/tobra desired peak serum conc.:
gram + endocarditis (synergistic with PCN) |
4-5 mcg/mL
|
|
Gent/tobra desired peak serum conc.:
gram - infections (sepsis) |
6-8 mcg/mL
|
|
Gent/tobra desired peak serum conc.:
gram - pneumonia |
8-10 mcg/mL
|
|
Gent/tobra desired peak serum conc.:
gram - pneumonia with cystic fibrosis |
10-12 mcg/mL
|
|
Gent/tobra desired trough serum conc.:
|
< 1-2 mcg/mL
|
|
High trough levels with aminoglycosides lead to...
|
nephrotoxicity
|
|
Low aminoglycoside trough levels
|
Ok because drug with continue killing after dose is gone (PAE)
|
|
Amikacin desired peak serum conc:
gram - infections (sepsis) |
20-30 mcg/mL
|
|
Amikacin desired peak serum conc:
gram - pneumonia |
25-35 mcg/mL
|
|
Amikacin desired trough serum conc
|
< 5-10 mcg/mL
|
|
When should you sample for aminoglycoside peak concentrations?
|
0.5-1 hr after 30 minute infusion
If 1 hr infusion, draw within 15 minutes after end of infusion |
|
Why can you not sample for peak serum concentrations immediately?
|
must allow for adequate distribution
|
|
When should you sample for aminoglycoside trough concentrations?
|
</= 30 minutes before next dose
|
|
When should you sample for aminoglycoside random concentrations when drawing after the first dose?
|
Drawing after >/= one half life from peak concentration
|
|
When should you sample for aminoglycoside random concentrations when drawing after dialysis?
|
Wait 2 hours for redistribution
|
|
Aminoglycoside ADEs/Toxicities
|
1. Nephrotoxicity
2. Neurotoxicity 3. Ototoxicity |
|
When does nephrotoxicity occur with aminoglycosides?
|
Can occur within 4-5 days
Usually takes 5-10 days Highest risk with use > 10 days |
|
When is nephrotoxicity risk with aminoglycoside use highest?
|
Use > 10 days
|
|
Urine output effects with aminoglycoside nephrotoxicity
|
nonoliguric (normal urine production)
|
|
Is aminoglycoside nephrotoxicity reversible?
|
Mostly
|
|
Which aminoglycoside is most likely to cause nephrotoxicity?
|
Similar risk with all
|
|
Average incidence of aminoglycoside nephrotoxicity
|
~20%
|
|
Risk factors for aminoglycoside nephrotoxicity
|
age
other disease states other nephrotoxic drugs |
|
Symptoms of aminoglycoside neurotoxicity
|
muscle twitching
numbness seizures tingling |
|
How does ototoxicity occur?
|
damage to CN VIII
|
|
Is aminoglycoside ototoxicity uni- or bi- lateral?
|
Either
|
|
When does aminoglycoside ototoxicity occur?
|
Onset variable
|
|
Incidence of aminoglycoside ototoxicity
|
0.5-3%
|
|
Types of ototoxicity
|
Cochlear (hearing) or vestibular loss
|
|
Symptoms of cochlear loss ototoxicity
|
loss of hearing
tinnitus feeling of ear fullness |
|
Is cochlear loss ototoxicity caused by aminoglycosides reversible?
|
Usually
|
|
Symptoms of vestibular loss ototoxicity
|
vertigo
ataxia (lack muscle coordination) nystagmus (involuntary eye movement) dizziness N/V unsteadiness |
|
Is vestibular loss ototoxicity caused by aminoglycosides reversible?
|
Usually
|
|
Aminoglycoside Drug-Drug Interactions
|
amphotericin B
cisplatin cyclosporine furosemide skeletal muscle relaxants **due to possible additive nephrotoxicity |
|
Aminoglycosides and Cyp450 interactions
|
All AGs are renally excreted so don't have to worry about Cyp450 interactions
|
|
Ascites/Pancreatitis and aminoglycosides
|
Increase Vd >/= 25%
|
|
Burns and aminoglycosides
|
Increase clearance
Decrease half-life |
|
Cancer and aminoglycosides
|
Increase Vd
|
|
Critically ill patients with sepsis and aminoglycosides
|
Increase/decrease Vd and clearance
|
|
Cystic fibrosis and aminoglycosides
|
Increase Vd or clearance
Decrease half-life |
|
Fever and aminoglycosides
|
Increase clearance
|
|
Hemodialysis/Peritoneal Dialysis and aminoglycosides
|
Increase clearance
Decrease half-life |
|
ICU and aminoglycosides
|
Increase Vd 25-50%
|
|
Post-op/ventilated patient and aminoglycosides
|
Increase Vd
|
|
Postpartum and aminoglycosides
|
Increase Vd
|
|
Surgery and aminoglycosides
|
Increase Vd
|
|
Speed of aminoglycoside distribution
|
rapid
related to ICF |
|
Aminoglycoside distribution in relation to protein binding
|
low protein binding
|
|
Aminoglycoside CSF penetration
|
poor
|
|
Aminoglycoside concentration in kidney, liver, lung
|
high
|
|
T/F. Aminoglycosides accumulate over time in the body.
|
True
|
|
What factors influence aminoglycoside distribution?
|
Age
Weight Disease/conditions |
|
% of aminoglycoside excreted by kidney
|
95%
|
|
Are aminoglycosides mostly excreted via kidney or liver?
|
kidney
|
|
Are aminoglycosides dialyzable?
|
Yes
Need extra doses after dialysis because drug removed |
|
Is aminoglycoside clearance affected by renal function?
|
Yes
Can estimate GFR/CrCl by aminoglycoside clearance |
|
What factors influence aminoglycoside clearance?
|
Age
Disease/conditions |
|
Usual PK population parameters used for dosing
|
Clearance: based on age group average renal function
Vd Half-life and time to steady state |
|
Factors that overestimate CrCl
|
cachexia (physical wasting)
elderly liver disease CrCl < 20 mL/min |
|
T/F. Unstable SCr can cause inaccurate CrCl results.
|
True
|
|
Factors that influence CrCl
|
malnourishment/cachexia (physical wasting)
liver disease paralysis myasthenia gravis muscular dystrophy MS |
|
What should be considered if blood concentration is extremely high?
|
Question if concentration was drawn from infusion line
|
|
What should be considered if blood concentrations are drawn sooner than 0.5 hr after the end of a 0.5 hr infusion?
|
Drug may not be totally distributed
Ke and Cpeak will be overestimated Vd will be overestimated |
|
When might Ke and Cpeak be overestimated?
|
if blood concentrations are drawn sooner than 0.5 hr after the end of a 0.5 hr infusion
|
|
When might Vd be overestimated?
|
if blood concentrations are drawn sooner than 0.5 hr after the end of a 0.5 hr infusion
|
|
What PK parameter may be inaccurate if blood concentrations not drawn at least one half-life apart?
|
Ke
|
|
Discrepancies in blood concentrations due to:
|
CrCl estimation
patient variability from population Conc. not drawn at specified time Doses not charted/missed Doses not infused at time intended Doses inaccurately prepared |
|
Gent/Tobra extended interval dosing based on IBW/ABW
|
7 mg/kg
|
|
Amikacin extended interval dosing based on IBW/ABW
|
15 mg/kg
|
|
What body weight should be used for calculations if patient is obese?
|
Adjusted BW
|
|
What body weight should be used for calculations if patient is underweight?
|
Actual BW
|
|
Aminoglycoside extended interval dosing with CrCl >/= 60
|
q24h
|
|
Aminoglycoside extended interval dosing with CrCl 40-59
|
q36h
|
|
Aminoglycoside extended interval dosing with CrCl < 40
|
Do not use extended interval dosing method
|
|
Steps to determining extended interval AG dosing
|
1. Calculate dose based on weight
2. Calculate CrCl 3. Determine dosing interval based on CrCl |
|
When should random serum concentrations be drawn with extended interval AG dosing?
|
6-14 hours after end of infusion (1 hr infusion)
|
|
How is extended interval AG dosing frequency adjusted?
|
Use Hartford nomogram
(graphs given on exam) |
|
What should you do for extended AG dosing interval if point appears on line using Hartford nomogram?
|
Choose longer interval
|
|
What should you do for extended AG dosing interval if point appears off graph using Hartford nomogram?
|
Stop next dose and follow levels to determine appropriate time of next dose
|
|
Patient exclusions for extended interval AG dosing
|
Peds
burns ascites dialysis cystic fibrosis ICU patients elderly UTI treatment endocarditis osteomyelitis |
|
Rationale for extended interval AG dosing
|
1. conc-dependent bactericidal activity
2. relationship b/w peak/MIC ratio and patient outcome 3. PAE 4. traditional dosing often leads to low efficacy and significant toxicity 5. less frequent dosing and monitoring 6. less accumulation |
|
T/F.
More AG accumulation occurs with extended interval AG dosing/ |
False
|
|
T/F.
Less monitoring is necessary with extended interval AG dosing. |
True
|
|
Oral vancomycin absorption
|
Insignificant with capsules/oral solution (except with colitis)
|
|
When is oral vancomycin appropriate? Why?
|
with colitis (PC)
PC-> inflammation/destruction of mucosal integrity -> increase systemic absorption |
|
Vancomycin distribution into body
|
distributes widely into body tissues
|
|
Where all does vancomycin distribute?
|
pericardial, pleural, ascitic, synovial, bile, lung, lymph, feces
|
|
Vancomycin distribution with inflamed meninges
|
15% serum conc.
|
|
Vancomycin distribution with un-inflamed meninges
|
minimal penetration
|
|
PK model used for vancomycin dosing
|
One-compartment model
(although 2-comp. more realistic) |
|
Vancomycin half life first distribution vs. second distribution
|
first distribution: 0.1-0.4 hr
second distribution: 0.5-3.6 hr |
|
Vancomycin elimination half life
|
4-8 hrs in adults with normal renal function
|
|
Vancomycin Vd calculation based on what body weight?
|
TBW (ABW if obese)
|
|
Does vancomycin Vd increase or decrease in obese patients?
|
decrease
|
|
Vancomycin bound to albumin
|
50-60%
|
|
vancomycin metabolism
|
minimal
|
|
How does hepatic disease affect vancomycin metabolism/kinetics?
|
Does not really affect
|
|
How much vancomycin is recovered in urine?
|
80-100% IV dose in 24 hrs in normal adults
|
|
Can you use vancomycin excretion to estimate CrCl?
|
No
clearance is proportional (some reabsorption/secretion) |
|
What is the basis for vancomycin dosing nomograms?
|
CrCl
|
|
How much vancomycin is removed by HD/CAPD?
|
minimal removal
|
|
Vancomycin concentrations after dialysis
|
Large rebound effect to original conc. pre-dialysis anticipated in hours after dialysis
|
|
How long might anuric (no urine) patients have elimination half life?
|
Up to 7 days
|
|
Who may have increase vancomycin clearance?
|
obese
peds burn pts |
|
Vancomycin PK parameters in elderly
|
Increase half life
Increase Vd Decrease clearance (not correlated to CrCl) |
|
Vancomycin ADEs/toxicities
|
1. Nephrotoxicity
2. Ototoxicity 3. Red Man Syndrome 4. Thrombophlebitis |
|
What is vancomycin nephrotoxicity most likely due to?
|
impure formulation
being combined with AGs (additive nephrotoxic effects) |
|
What was vancomycin nephrotoxicity originally attributed to?
|
high troughs (>10-20 mcg/mL)
|
|
Vancomycin ototoxicity incidence
|
unclear/rare
|
|
What is vancomycin ototoxicity associated with?
|
high peaks > 50-80 mcg/mL
|
|
What may cause red man syndrome?
|
fast vancomycin infusion
|
|
What type of reaction is red man syndrome?
|
histamine-mediated response
|
|
Symptoms of red man syndrome
|
redness
pruritis of upper torso, arms, neck |
|
What can be given/done to help prevent red man syndrome?
|
diphenhydramine 30 min. before infusion
slow infusion rate |
|
Vancomycin thrombophlebitis incidence
|
rare
|
|
T/F.
Vancomycin thrombophlebitis is related to serum conc. |
False
|
|
Renal dysfunction effects on vancomycin
|
Decrease clearance
|
|
Burns effects on vancomycin
|
Increase GFR
Increase clearance Decrease half life |
|
Obesity (>30% over IBW) effects on vancomycin
|
Increase clearance
Decrease half life |
|
What serum concentrations are usually drawn with vancomycin?
|
mostly only see troughs drawn
|
|
When should peak and troughs be drawn with vancomycin?
|
At time of steady state
|
|
How long before you should draw vancomycin peaks?
|
>/= 1-2 hrs after end of infusion
|
|
Why wait to check vancomycin peak?
|
Avoid distributive phase which may result in erroneous calculations
|
|
How long before you should draw vancomycin troughs?
|
< 1hr before next dose
|
|
How long before you should draw vancomycin random levels?
|
>/= one half life from previous levels
(ensures accuracy when calculating Ke) |
|
Vancomycin dosing by weight for normal adults
|
15 mg/kg q12h
|
|
Vancomycin dosing by weight for renal patients
|
20 mg/kg LD + 15 mg/kg dose based on CrCl
|
|
Vancomycin dosing interval with CrCl >70
|
q12h
|
|
Vancomycin dosing interval with CrCl 40-70
|
q24h
|
|
Vancomycin dosing interval with CrCl 30-40
|
q48h
|
|
Vancomycin dosing interval with CrCl 20-30
|
q72h
|
|
Vancomycin dosing interval with CrCl <10
|
q5-7days
|
|
How long should you wait between vancomycin LD and MD?
|
Wait length of dosing interval
|
|
Vancomycin Intrathecal dosing
|
10-20 mg/24hr
|
|
Vancomycin Intrathecal dosing in children
|
10 mg/24hr
|
|
Vancomycin intraventricular dosing
|
5 mg/24 hr
Up to 20 mg q24h if fail to eradicate |
|
Vancomycin intraventricular dosing in infants
|
5-10 mg/24hr
|
|
Vancomycin dosing in children (<12 yo)
|
15 mg/kg q8h
|
|
Vancomycin dosing in neonates
|
Varies based on post-conceptual age
|
|
Goal vancomycin peak
|
20-35 mcg/mL
|
|
Goal vancomycin trough
|
10-20 mcg/mL
|
|
Vancomycin peak recommendations
|
Keep peak conc. ~8x MIC
|
|
Vancomycin trough recommendations
|
Keep trough conc. 2-3x MIC for duration of interval
|
|
What is dialysis?
|
Process where substances move by concentration gradient across semi-permeable membrane
|
|
What substance pass into dialysis fluid?
|
Substances small enough to pass through semi-permeable membrane pores can pass out of blood into dialysis fluid
|
|
What happens once substances are in dialysis fluid?
|
Waste products/other compounds can be removed from the body
|
|
Why might dialysis be used to remove drugs from circulation?
|
drug overdose
experiencing severe ADEs |
|
T/F.
Drugs are removed primarily in dialysis. |
False
drugs mostly removed from body coincidental to removal of toxic waste |
|
When is supplemental dosing post-dialysis necessary?
|
When there is significant dialysis clearance of the drug
|
|
What are the 2 processes involved with dialysis?
|
Diffusion and ultrafiltration
|
|
What is diffusion?
|
Concentration gradient
substance goes from high to low conc. |
|
What is ultrafiltration?
|
water being pulled off
|
|
What leads to higher filter efficiency is dialysis? What does this correlate with?
|
increased surface area -> higher filter efficiency (flow rate of dialysate)
|
|
What drug characteristics affect dialysis removal?
|
Molecular weight
Water solubility/Lipid solubility Plasma protein binding Vd Inherent clearance (rate and route) |
|
What about molecular weight influences dialysis clearance?
|
Molecular size vs. semipermeable membrance pore size
|
|
Small drug molecules (<500 daltons) and dialysis
Examples? |
readily eliminated by dialysis
Ex. lidocaine, procainamide, theophylline |
|
Moderate drug molecules (500-1000 daltons) and dialysis
Examples? |
Decreased ability to pass
Many of these drugs still require post-dialysis replacement doses Ex. aminoglycosides, digoxin |
|
Large molecules (>1000 daltons) and dialysis
Examples? |
not significantly removed
can be removed in high-flux filters Ex. vancomycin |
|
In regards to molecular weight, what size is vancomycin?
|
Large molecule (>1000 daltons)
|
|
In regards to molecular weight, what size are aminoglycosides?
|
Moderate (500-1000 daltons)
|
|
In regards to molecular weight, what size is digoxin?
|
Moderate (500-1000 daltons)
|
|
In regards to molecular weight, what size is lidocaine?
|
Small (<500 daltons)
|
|
In regards to molecular weight, what size is procainamide?
|
Small (<500 daltons)
|
|
In regards to molecular weight, what size is theophylline?
|
Small (<500 daltons)
|
|
High water soluble drugs and dialysis
|
Partition into water based dialysis fluid
|
|
High lipid soluble drugs and dialysis
|
Remain in blood
|
|
Unbound drugs and dialysis
|
Unbound drug able to pass through membrane pores
|
|
What types of protein bound drugs are most likely to have a better dialysis clearance?
|
Drugs not highly protein bound have a high free fraction of drug in blood prone to better dialysis clearance
|
|
High Vd (>2L/kg) and dialysis
Why? |
Less likely to be removed by dialysis
mostly located at tissue binding sites and not in blood |
|
Low Vd (<1 L/kg) and dialysis
|
more likely to be removed by dialysis
|
|
Renal elimination of drug and dialysis
|
If kidney is primary rout of elimination, increased likelihood drug will be removed by dialysis
|
|
HD
|
Hemodialysis
|
|
CAPD
|
continuous ambulatory peritoneal dialysis
|
|
CVVH
|
continuous venovenous hemofiltration
|
|
CCPD
|
continuous cyclic peritoneal dialysis
|
|
CAVH
|
continuous arteriovenous hemofiltration
|
|
CAVHD
|
CAVH (continuous arteriovenous hemofiltration) with dialysis
|
|
What dialysis technique(s) are most common?
|
HD
CAPD CVVH |
|
Differences in dialysis techniques
|
indication and clinical condition
delivery system filter flow rate (blood and dialysis) duration |
|
How is peritoneal dialysis performed?
|
catheter surgically inserted into lower abdomen into peritoneal cavity
|
|
How much dialysis fluid is given with peritoneal dialysis?
|
1-3L
|
|
What happens when dialysis fluid is given with peritoneal dialysis?
|
Given via catheter, waste products move from blood vessels of peritoneal membrane (semipermeable) into dialysis fluid via concentration gradient
|
|
Is dialysis fluid continuously or periodically removed with peritoneal dialysis?
|
periodically
|
|
Which more effectively removes drug from body: peritoneal dialysis or HD?
|
HD
|
|
T/F.
Drugs can be added to peritoneal dialysis fluid. |
True
|
|
What happens if drug added to dialysis fluid is absorbed into the body?
|
systemic effects may occur
|
|
What infection is common with peritoneal dialysis?
|
peritonitis
|
|
How are antibiotics given to treat peritonitis with peritoneal dialysis?
|
Antibiotics administered intraperitoneally for local treatment of infection using dialysis fluid as delivery vehicle
|
|
What is used for the delivery vehicle of antibiotics for use during peritoneal dialysis?
|
dialysis fluid
|
|
GFR with peritoneal dialysis (CAPD)
|
10-20 mL/min
|
|
Is removal of fluids and solutes continuous or periodical with cont. renal replacement dialysis (CAVH, CVVH)?
|
continuous
|
|
Which dialysis methods remove larger molecules?
|
CAVH, CVVH (cont. renal replacement dialysis)
|
|
T/F.
Both bound and unbound drug portion is removed with CAVH and CVVH. |
False.
Only unbound drug portion is removed |
|
GFR with CAVH/CVVH
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~30 mL/min (depending on filter)
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Rate at which blood is pumped out during HD
How is it pumped out? |
blood pumped out of patient at 300-400 mL/min through one side of semi-permeable membrane of articifical kidney by HD machine
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What happens to cleansed blood during HD?
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pumped back into vascular system
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Is HD fluid electrolyte and/or osmotically balanced?
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Both
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How does ultrafiltration occur during HD?
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by adding solutes to increase osmolarity of dialysis fluid relative to blood, it's possible to remove fluid from body by osmotic pressure across semi-permeable membrane of artificial kidney
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HD: high or low flux filters
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low
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How often is HD performed?
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3-4 hrs three times a week
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Pre-distribution
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If drug given too close/during HD, expect larger removal of dose
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If drug given too close/during HD, expect larger or smaller removal of dose?
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larger
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Post-distribution
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rebound in serum concentration can occur after end of HD
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Why does post-distribution occur?
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Due to differences in rate of transfer of drug between tissue and vascular compartments
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