Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology for Anaesthetists > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What are the iatrogenic related factors that contribute toward the development of resistance to antimicrobial drugs

A
  1. Not indicated
  2. Wrong antibiotic (specific activity or effect site penetration)
  3. Inappropriate broad spectrum antibiotic
  4. Under dosing
  5. Too short or too long course of therapy
  6. Lack of knowledge of PK/PD optimal dosing strategy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Classify clinically common and relevant bacteria

A

NO WALL
- Myoplasma

FLEXIBLE THIN WALL

  • Treponema (Syphilis)
  • Borelia (Lyme)
  • Leptospira

RIGID THICK WALL
# Obligate intracellular
- Chlamydia
- Ricketsia

# Extracellular (Free-living)
1. Gram Positive 
----> Cocci (Strep and Staph)
----> Rods (BLANCC)
Bacillus (aerobic), Listeria, Actinomyces, Nocardia, Clostridium (anaerobic), Corynebacterium
  1. Gram Negative
    - —> Cocci (Neiserria)
    - —> Rods
    - ——-> Anaerobic (Bacteroides)
    - ——-> Aerobic (Pseudomonas)
    - ——-> Facultative
    - —————> Resp (Haemophilus, Bordatella, Legionella)
    - —————> Zoonotic (Yersinia (plague), Brucella)
    - —————> Enteric (CHEESSS VPK)
    - ——————————-> Campylobacter
    - ——————————-> Helicobacter
    - ——————————-> Escherichia
    - ——————————-> Enterobacter
    - ——————————-> Salmonella
    - ——————————-> Shigella
    - ——————————-> Serratia
    - ——————————-> Vibrio
    - ——————————-> Proteus
    - ——————————-> Klebsiella
  2. Acid Fast
    - -> Mycobacterium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define and list the beta lactam antibiotics

A

Definition: These are antibiotics with a B-lactam ring in their chemical structure

Penicillins (and derivatives: e.g. amoxicillin / pipericillin)
Cephalosporins
Monobactams (Aztreonam)
Carbapenems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the mechanism of action of beta lactam antibiotics. Which organisms are beta lactam antibiotics ineffective and why?

A

Bactericidal cell wall synthesis inhibitors

Penicillin binding proteins facilitate cross linking and structural integrity in the bacterial cell wall.

Bind to PGPs (penicillin binding proteins) preventing cross linking and weakening the peptidoglycan layer causing the cell to lyse due to osmotic pressure.

Ineffective against:

  1. M/O without cell wall –> mycoplasma
  2. Intracellular pathogens (Chlamydia, Brucella, Legionella)
  3. Impenetrable cell walls (mycobacterium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List 4 intracellular pathogens inaccessible to beta lactams

A
  1. Chlamydia (obligate intracellular organisms)
  2. Ricketsia (obligate intracellular organisms)
  3. Legionella (Gram - facultative resp. rod)
  4. Brucella (Gram - facultative zoonotic rod)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the natural penicillins and why were penicillin derivatives developed?

A

Benzylpenicillin / Penicillin G

Phenoxymethylpenicillin / Penicillin V

–> Narrow spectrum and resistance is common

Agents developed with broader spectrum, increased bioavailability and stability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Compare the spectrum of antimicrobial activity of the penicillins

A

Pen G and Pen V - Gram + only

Cloxaxillin - Gram + with beta lactamase resistance

Amoxicillin - Gram + and Some Gram - (Klebs and Proteus)

Pipericillin - Gram + and some Gram - and Pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe how the Gram + and Gram - coverage changes for cephalosporins with regard to the generation of the drug

A

With increasing generation there is increased Gram - cover and decreased Gram + cover

Except Generation 4 (Cefepime) which has good Gram + and Gram - coverage. No anaerobic coverage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Classify the drugs and spectrum of activity of the cephalosporins

A

Generation | Name | Activity

1st | Cefazolin | G + and little G - (PEcK)

2nd | Cefuroxime | G+ less and G - more (HEPEcK)

3rd | Ceftriaxone | G + less less and G - more including nosocomial. No anaerobic

4th | Cefepime | G + like 1st gen and G - good. Antipseudomonas. No anaerobic.

5th | Ceftobiprole | Antipseudomonas and Vancomycin Resistant Enterococci (VRE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Categorize and name common cephalosporings. USe parenthesis to demonstrate special characteristics for each drug

A

1st Gen
Cefazolin (G+)
Cefadroxil

2nd Gen
Cefuroxime (More G- and less G+ vs gen 1)
Cefoxitin (+ anaerobic cover)
Cefotetan (+ anaerobic cover)

3rd Gen
Ceftriaxone (Less G+. More G-. Nosocomial. Good CSF. No anaerobic. No pseudomonal.)

4th Gen
Cefepime (G+ good. G - good. Antipseudomonal. Resistant to B-lactamases. No anaerobic)

5th Gen
Ceftobiprole (Antipseudomonas and VRE)
Ceftaroline (MRSA but no VRE and no antipseudomonal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a monobactam. Give and example and state spectrum of coverage

A

Monobactam is a beta lactam antibiotic. Example: Aztreonam. Spectrum: G - only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What type of antibiotics are the carbapenems describe the important characteristics of these drugs

A

Beta lactam antibiotics with a broad spectrum of activity (reserved for nosocomial pathogens and MDR pathogens)

Particularly effective against G - (G + slightly lower)
Anaerobic activity present

Antipseudomonal EXCEPT ertapenem

No activity against atypical organisms (Chlamydia, Legionella, Mycoplasma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List and describe the ertapenems in common clinical use

A

Group 1 - Ertapenem:

  • Slightly reduced Gram - activity vs other carbapenems
  • No MRSA and No enterococcus
  • No atypical cover
  • Limited antipseudomonal
  • Half life 4 hours

Group 2 - Imipenem / Meropenem / Doripenem

  • Broad spectrum. Antipseudomonal.
  • No activity MRSA
  • No atypical cover
  • Half life 1 hour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do carbapenems rely on for transport into the bacterial cell wall

A

Porins (outer membrane proteins).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is cilastin and when is it used

A

Imipenem is deactivated in the kidneys by the enzyme dehydropeptidase 1 (DHP - 1).

To overcome this deactivation, it is administered with a DHP - 1 inhibitor –> cilastin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List the side-effects of Beta Lactams

A
  1. Neurotoxicity (seizures / spasms / hallucinations)

2. Hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Summarise ertapenem vs imipenem vs meropenem

A

Ertapenem - no antipseudomonal or enterococcus

Meropenem - more G - vs imipenem

Imipenem - more G + vs meropenem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Classify the cell wall synthesis antibacterial drugs

A

BETA LACTAMS

  1. Penicillins
  2. Cephalosporins
  3. Monobactams
  4. Carbapenems

GLYCOPEPTIDES
1. Glycopeptides (Vancomycin and Teicoplanin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the Glycopeptide antibioitcs. List them and describe the mechanism of action

A

Vancomycin and Teicoplanin are cell wall synthesis inhibitors that bind to PGP in the peptidoglycan layer of the bacterial cell wall to bring about loss of structural integrity and hydrolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the spectrum of the glycopeptides

A

G+ (poor G - )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe resistance to the glycopeptides

A

Vancomycin Resistant Enterococci (VRE)
Vancomycin Intermediate Staph Aureus (VISA)
Glycopeptide Intermediate Staph Aureus (GISA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the side effects of the Glycopeptides

A

Ototoxicity and Nephrotoxicity

Nephrotoxicity of Vancomycin has been blown out of proportion.
BUT –> Vancomycin accumulates in renal failure and drug level monitoring is indicated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens when vancomycin is infused rapidly

A

Histamine release –> ‘ red man syndrome’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Classify the antibiotics that inhibit protein synthesis

A

Aminoglycosides

  • Gentamicin
  • Amikacin
  • Streptomicin

Macrolides

  • Erythromycin
  • Azithromycin
  • Clarithromycin

Lincosamides
- Clindamycin

Tetracylcines
- Doxycycline

Oxazolidinones
- Linezolid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why are the aminoglycosides administered IV

A

Poorly absorbed from GIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Are aminoglycosides used for treatment of pneumonia? Why?

A

No. Very poor tissue and lung penetration - so not good for pneumonia. However, nebulized aminoglycosides (in addition to targeted intravenous therapy ) is finding favour due to extremely high concentrations in the alveolar fluids that this delivery mode yields.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the spectrum cover for aminoglycosides

A

Good Activity

  1. Gram -
  2. Staphylococci

No activity

  1. Streptococci
  2. Anaerobes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the important side effects of aminoglycosides

A

Nephro and ototoxicity

Narrow therapeutic window (monitor peaks and troughs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the mechanism of resistance to aminoglycoside antibioitcs

A

Aminoglycoside-modifying enzymes (AME) –> inactive the drug by modifying the structure of the aminoglycoside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the Macrolides and what is their mechanism of action

A

Bacteriostatic

Protein synthesis inhibitors - bind 50S ribosomal subunit –> cessation of bacterial protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Make a table of the common bacteristatic and bacteriocidal antibiotics

A

Bactericidal

  1. Beta - Lactams
  2. Aminoglycosides
  3. Glycopeptides
  4. Fluoroquinolones
  5. Nitroimidazoles (Metronidazole)

Bacteriostatic

  1. Macrolides
  2. Clindamycin
  3. Sulphamethaxazole/trimethoprim
  4. Linezolid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the special use with regard to each Macrolide

A

Erythromycin

  • Prokinetic (ICU enteral feeding)
  • Prokinetic dose 250 mg 6 hourly (vs. 500 mg 6 hourly)
  • Gram + action in penicillin allergic patients

Azithromycin and Clarithromycin
- Excellent activity against atypical organisms: Chlamydia, Legionella, Ricketsia, Brucella and have important role in the treatment of severe community acquired pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the mechanism of action of Clindamycin and to what group of drugs does this belong

A

Clindamycin is a lincosamide antibiotic which acts as a protein synthesis inhibitor inhibiting the 50S ribosomal subunit of bacterial RNA inhibiting protein synthesis

Similar spectrum of activity as erythromycin with better anaerobic cover.

Excellent penetration into bone and soft tissue (received bad press as it was the first antimicrobial to cause pseudomembranous colitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What type of antibiotic is Linezolid and what is its mechanism of action

A

It is an Oxazolidinone and a protein synthesis inhibitor. Bacteriostatic.

Good activity vs. MRSA and Enterococcus faecium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

List the antibiotics that inhibit bacterial nucleic acid synthesis

A
  1. Quinolones
    - -> Ciprofloxacin, Moxifloxicin, Levofloxacin, Nalidixic acid
  2. Rifamycins
    - -> Rifampicin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the mechanism of action of the Quinolones

A

Inhibit bacterial DNA replication by inhibiting DNA topoisomerase and GNA gyrase

37
Q

Describe the spectrum of activity of the Quinolones

A

Gram +
Gram -
Some Anaerobes
Antipseudomonas

38
Q

What are the side effects of quinolones

A
  1. Photosensitivity
  2. Neurotoxicity
  3. Tendinitis and tendon rupture (esp. elderly, pts with renal impairment, on corticosteroids)
  4. Possibly increased risk of aortic dissection in patients with AAA.
  5. Adverse effect on cartilage development
39
Q

Why are quinolones not recommended in pregnancy or in children

A

They have an adverse effect on cartilage development

40
Q

What is the mechanism of action of Rifampicin

A

Blocks synthesis of bacterial mRNA

Rx TB

41
Q

What are the side effects of Rifampicin

A

Hepatic dysfunction

Skin Rashes

42
Q

What is the mechanism of action of Sulfamethoxazole

What is the mechanism of action of Trimethoprim

What organisms does this combination drugs treat effectively

A

Both affect tetrahydrofolic acid metabolism and impair the synthesis of purines and pyrimidines

Sulfamethoxazole

  • Bacteriostatic
  • Competes para-aminobenzoic acid (PABA) and enzyme involved in the catalysis of tetrahydrofolic acid (THFA) –> required for the synthesis of purines and pyramidines
  • May cause Steven-Johnson Syndrome

Trimethopim
- Prevents synthesis of THFA later in the pathway than sulfamethoxazole

Organisms

  1. Pneumocystis jerovecii
  2. Nocardia
43
Q

What type of antibiotic is Daptomycin. What is its mechanism of action and specific clinical use

A

Group: Antibiotics which depolarise the cell membrane
–> Daptomycin is a lipopeptide

MOA: Lipophilic tail of the molecule inserts into the bacterial cell membrane, causing rapid depolarisation and efflux of potassium ions. DNA, RNA and protein synthesis are arrested and the bacteria dies.

Rx: MRSA, GISA, VRE and coagulase negative Staph

44
Q

What is the penetration of Daptomycin

A

Excellent skin and soft tissue

Does not penetrate BBB

45
Q

What is MEtronidazole

A

Nitroimidazole
Bacteriocidal
Destroys bacterial DNA
Also acts against parasites

MOA: Must enter bacterial cell wall –> requires reduction by bacteria. Only possible in anaerobic bacteria. No aerobic cover

46
Q

Classify antibiotic resistance

A

Intrinsic
- Innate resistance despite dose given e.g. Vanco ineffective G- cell envelope

Acquired (induced)

  • Developed resistance
  • -> Chromosomal mutations
  • -> Introduce new genetic material into bacterium

Adaptive
- Induced by env. stressor e,g, sub-inhibitory levels antibiotics.

47
Q

Summarise the mechanisms of antibiotic resistance

A
  1. Altered TARGET SITE e.g. altered cell wall in MRSA
  2. Altered ACCESS to target site e.g. Gram -‘ve altered porins or efflux pumps e.g. Gram -‘ve lipopolysaccharide outer membrane permits AB access through pores only. If the pores change –> no access
  3. DISABLING ENZYMES produced to antibiotic e.g. beta-lactamases and Aminoglycoside Modifying Enzymes (AME)
48
Q

How do Beta-lactamases disable beta-lactam antibioitcs

A

The open the Beta-lactam ring –> unable to bind PBPs

49
Q

List the beta-lactamase inhibitors and their mechanism

A

Clavulanate
Tazobactam
Sulbactam
Avibactam

“suicide inhibitors” –> nil antimicrobial activity but beta lactam ring present depleting beta lactamase so reduced available to disable active agent.

50
Q

What are inducible B-lactamases

A

Essentially = cephalosporinases.

In IBL-producing organisms beta-lactamases are suppressed until the presence of cephalosporins when rapid emergence of resistance to multiple beta lactams occurs.

51
Q

What are extended spectrum beta lactamases, what organisms produce them and what antibioitcs should be used to treat these infections

A

Produced by enterobacteriacae –> confering resistance to all beta lactams except carbapenems.

Carbapenems to treat
OR
2nd Gen cephamycins (cefotetan and cefoxitin) are resistant to ESBLs

52
Q

What are carbapenemases and what drug should be used to treat these infections

A

Resistant to all beta lactams including carbapenems.
Carbapenem Resistant Enterobacteriales (CREs)
Rx: Ceftazidine-avibactam

53
Q

What are the effects of the secretion of a biofilm by a bacterial colony

A
  1. Prevents detection by host’s immune system
  2. Thick/Sticky consistency retards antimicrobial penetration
  3. Slower bacterial growth rate retarding bacteriostatic agents
54
Q

What factors does choice of antibiotic depend

A
  1. Organism susceptibility
  2. Effect site concentration
  3. Collateral and side effects
  4. PK and PD profiles
55
Q

Define minimum alveolar concentration

A

MIC - Lowest concentration of antibiotic (ug/mL) required that inhibits growth of a strain of bacteria

56
Q

Can the MIC of one antibioitc be compared the MIC from another antibiotic?

A

No. The antibiotic breakpoint is used for this.

The breakpoint is a previously agreed upon concentration of antibiotic which defines whether a species of bacteria is susceptible or resistant to the antibiotic i.e. where bacteria start to show resistance.

If MIC < breakpoint then the bacterial isolate is reported as being susceptible/sensitive to the antibiotic

The closer the MIC is to the breakpoint, the less susceptible the organism

Breakpoints are updated and published annually

57
Q

What does the term ‘resistant’ and ‘intermediate’ mean with regard to an organisms susceptibility to an agent?

A

‘Resistant’ implies that normally achievable serum drug levels are inadequate to inhibit bacterial growth.

‘Intermediate’ implies that organisms are likely to be inhibited only if maximally recommended doses are used to achieve serum concentrations.

High enough concentrations (such as significant concentrations of gentamicin in the urine might be sufficient to treat LUTS deemed gentamicin resistant

58
Q

Define Mutant Prevention Concentrations MPC

A

MPC is defined as the concentration of antibiotic the prevents the development of single step mutations. This means that above MPC microbes need to mutate more than once to develop resistance.

dosing in the concentration window between MIC and MPC encourages mutations and selects for resistant organisms

59
Q

What dosing range selects for resistant organisms and encourages mutations

A

Dosing between MIC and MPC = Mutant Selection Window MSW

60
Q

Where does Augmentin penetrate poorly

A

CSF

61
Q

Where does ceftriazone penetrate poorly

A

Penetrates well everywhere

CSF requires high dose for good penetration

62
Q

Where do aminoglycosides penetrate poorly

A

CSF
Lung
Soft tissue

63
Q

Where does cotrimoxazole penetrate poorly

A

Penetrates well everywhere

64
Q

Where does ertapenem pentrate poorly

A

CSF

65
Q

Where does MEropenem penetrate poorly

A

CSF requires high doses for good penetration

66
Q

Where does imipenem penetrate poorly

A

Penetrates everywhere well

67
Q

Where does vancomycin penetrate poorly

A

CSF, Lung and soft tissue

68
Q

List the drugs with Good CSF penetration

A

Ceftriaxone (high dose)
Meropenem (high dose)
Imipenem
Co-trimoxazole

69
Q

List the drugs that penetrate the lung poorly

A

Aminoglycosides

Vancomycin

70
Q

List the drugs that penetrate the soft tissue poorly

A

Aminoglycosides

Vancomycin

71
Q

Define Therapeutic Drug monitoring

A

Measurement of specific drugs at designated drug intervals to optimise individual dosing regimens and achieve required PK/PD targets.

Most TDM measures plasma concentration and does not measure conc. at effect site

72
Q

What is collateral damage with regard to antibiotic prescribing

A

Unintended adverse effects on the ecology due to antibiotic use which causes the development of colonization with MDR pathogens

Quinolones –> MRSA + Pseudomonas resistance

Gen 3 ceph –> C. difficile infections / VREs / ESBL Klebs pneumoniae

Also avoid nephrotoxic agents in renal failure etc

73
Q

What are the three categories of antibiotics in terms of their pharmacokinetic - pharmacodynamic PKPD intractions

A
  1. Time-dependent killing ( t > MIC)
  2. Concentration dependent killing ( Cmax/MIC)
  3. Combination of 1 and 2 expressed as AUC 0 -24 hr / MIC
74
Q

Which antibiotics have time dependent based efficacy with regard to PKPD (t > MIC) and what does this mean

A

With these antibiotics we should aim to maximise the DURATION of EXPOSURE

Exert their effects by the length of time that the plasma conc. is above MIC. TIME ABOVE MIC ! Dosing interval should lead to 100% of the time Conc > MIC

  1. Penicilins
  2. Cephalosporins
  3. Carbapenems
    (Linezolid)
75
Q

Which antibiotics have concentration dependent based efficacy with regard to PKPD (Cmax/MIC) and what does this mean

A

With these antibiotics we should aim to maximise the concentration of antibiotic

  1. Aminoglycosides
  2. Metronidazole
    (Fluoroquinolones)
76
Q

Which antibiotics have concentration and time dependent based efficacy with regard to PKPD (Cmax/MIC) and what does this mean

A

With these antibiotics we should aim to maximise the amount of drug exposure

These drugs exhibit a POST ANTIBIOTIC EFFECT (PAE) and are taken up into the organism so continue to be effective despite plasma conc falling below MIC

  1. Vancomycin
  2. Colistin
  3. Azithromycin
    (Fluoroquinolones)
    (Linezolid)
77
Q

When should peak level aminoglycosides be taken

A

30 minutes after the FIRST dose (underdosing is extremely common).

78
Q

How doe concentration dependent antibiotics continue to exert their effect despite falling below MIC

A

Post Antibiotic Effect (PAE) –> antibiotic is taken up into the organism and continues to exert its effects from within, even though the serum concentration has fallen.

79
Q

When should trough levels be taken for aminoglycosides and why

A

On day 3. Immediately before the dose is administered and relate to the toxicity of aminoglycosides (ototoxicity and nephrotoxicity) since the uptake of aminoglycosides in the ear and nephron is most pronounced with sustained levels.

80
Q

How are trough levels minimized

A

By extended the dosing intervals –> usually once daily dose

81
Q

How is a combination of concentration and time dependent killing expressed mathematically

A

AUC 0 - 24 hr / MIC

82
Q

Why is subtherapeutic dosing bad

A
  1. Ineffective killing
  2. Worse clinical outcome
  3. Non-lethal selection pressure
    - -> Proliferation of Multi-drug resistant strains
    - -> Selection of hypermutatable strains
    - -> Increased movement mobile genetic elements like plasmids
83
Q

Which antimicrobials are hydrophilic and which are lipophilic> why is this relevant?

A

Hydrophilic (most)

  • Beta lactams / aminoglycosides / glycopeptides
  • Critically ill patients have increased Vd and renal clearance. Increased Vd and renal clearance (e.g. hyperdynamic CVS in sepsis) of hydrophilic agents results in subtherapeutic concentrations of the hydrophilic antibiotics. Reduced PB in critical illness helps initially but more free drug means more renal clearance in the long term.

Lipophilic

  • Fluoroquinolones and macrolides
  • Fast intracellular accumulation and hepatic clearance SO only need maintenance dose adjusted in severe hepatic failure.
84
Q

What is Augmented Renal Clearance and what PKPD interaction toes it predominantly affect and why

A

AUC –> urinary creatinine clearance exceeds 130 mL/min/1.73m^2 (Normal 88 - 125)

Mechanism: Related to Inflammation / increased CO and RBF / ANP / Fluid resuscitation.

AUC associated with subtherapeutic hydrophilic antimicrobials with time-dependent PKPD efficacy

(does not affect conc. dependent)

85
Q

What is the appropriate dosing for amikacin and gentamicin in the critically ill versus non-critically ill patient

A

Amikacin
- 25 - 30 mg/kg (NOT 15 mg/kg)

Gentamicin
- 7 - 9 mg/kg (NOT 5 mg/kg)

86
Q

What is a good principle with regard to dosing of antibiotics in AKI in the first 24 to 72 hours

A

Dose as normal (Vd increased) After 72 hours the dose reduction can be considered to prevent accumulation and toxicity

87
Q

Which are the only antibiotics need dose adjustments for Child Pugh C

A

Metronidazole

Tigecycline

88
Q

By what % must hepatic function reduce before drug clearance is affected

A

90%

Hepatic flow often elevated in critical illness which may compensate for the reduction in liver enzyme activity in drugs which have a high extraction ratio.

89
Q

When should IV antibiotics be preferred to PO

A
  1. Meningitis
  2. Osteomyelitis
  3. Endocarditis
  4. Septicaemia (Blood)

Patients unable to swallow / absorb
Haemodynamic unstable
Initial therapy in severe infections
If no PO forms available

Pharmacology for Anaesthetists (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions