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Pharm > Ch 26 > Flashcards

Ch 26 Flashcards

1
Q

antibacterial/antibiotics/antimicrobials drug MOA

A

bacteriostatic (inhibit bacteria growth) or batericidal (bacteria killing).

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2
Q

are bacterial antibiotics better than bacteriostatic agents?

A

• No evidence that bactericidal antibiotics are better than

bacteriostatic agents in most clinical situations

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3
Q

are bactericidal or bacteriostatic preferred in severe infections?

A

Bactericidal agents greatly preferred in severe infections

Endocarditis, meningitis, osteomyletis, neutropenia

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4
Q

classes of bacteriostatic antibiotics

A 
penicillins (PCN)
macrolides
linocosamides
tetracyclines
sulfonamides
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5
Q

classes of bactericidal antibiotics

A

cephalosporins
glycopeptides
aminoglycosides
fluoroquinolones

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6
Q

class of bacteria - gram pos

A

peptidoglycan cell wall composed of sugars & amino acids + phospholipid plasma layer; stain purple

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7
Q

class of bacteria - gram neg

A

have lipopolysaccharide outer membrain + peptidoglycan layer + plasma membrane. generally harder to treat, do not pick up stain.

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8
Q

bacterial morpholgies

A

coccus(round) - comes in clusters or chains
rods
spirochetes
misc - protozoans

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9
Q

common gram pos coci

A

Staphylococcus aureus
Streptococcus pneumoniae
Group B Streptococcus
Listeria

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10
Q

common gram pos rods

A

clostridium

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11
Q

common gram pos cocci and rods

A

acinetobacter - pleomorph

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12
Q

common gram neg cocci

A

Neisseria meningitides
Legionella
Bordetella

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13
Q

common gram neg rods

A 
Escherichia coli
Haemophilus influenzae
Klebsiella pneumoniae
Serratia
Shigella
Salmonella
Yersnia pestus
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14
Q

how to choose antibiotics

A

aerobe or anaerobic bacteria?

typical or atypical or other bacteria?

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15
Q

aerobe vs anaerobic bacteria

A

aerobe: oxygen required for growth
anaerobic: growth in absence of oxygen

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16
Q

typical vs atypical vs other bacteria

A

typical bacteria: everyday bacteria
atypical infections: protozoans, uncommon bacterial infections
other: fungi, viruses - do not respond to antibiotics

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17
Q

mechanisms of growth inhibition/destruction of microbes for antibiotics

A
  1. inhibition of bacterial cell wall synthesis > cell lysis (Ex Penicillin, Vancomycin, Cephalosporins)
  2. alteration of membrane permeability > cell lysis (Ex: Nystatin, Amphotericin B, Polymyxin)
  3. inhibition of protein synthesis (Ex: Aminoglycosides, Tetracyclines, Erythromycin)
  4. inhibition of synthesis of bacterial ribonucleic acid (RNA) and deoxyribonucleic acid (DNA) (Ex: Fluoroquinolones)
  5. interference w/metabolism within cell (Ex: Rifampin, Isoniazid, Trimethoprim, Sulfonamides)
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18
Q

pharmacokinetics of antibacterials

A
  1. BIND to and PENETRATE bacterial cell wall
  2. increased effect with longer time at binding site
  3. length of time at binding is controlled by distribution, half life, elimination of drug.
  4. antibacterials with a longer half life usually maintain greater concentration at binding site (require less frequent dosing)
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19
Q

PD of antibacterials

A

use safest, highest dose > low doses over long period promote microbial mutation/adaptation > resistance.

  • MIC
  • concentration/exposure of time to drug play role in bacterial eradication
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20
Q

MIC

A

minimum inhibitory concentration: lowest concentration of an antimicrobial that will inhibit visible growth of microorganism after overnight incubation; goal is 2-4 times MIC.

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21
Q

factors that impact antimicrobial treatment/efficacy

A

type of pathogen, site of infection, immunocompetence by host; age, nutritional status, immunoglobulins, WBCs, organ function and circulatory status
• Older adults/malnourished patients = less resistance to infection than younger, well-nourished population: immunoglobulins and WBCs needed to combat infection are depleted
• If circulation is impeded, antibiotics may not be distributed properly to the infected area of the body.&raquo_space; Consider patient co- morbidities.

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22
Q

what happens when bacteria are sensitive to a drug?

A

the pathogen is inhibited or destroyed

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23
Q

what happens when bacteria are resistant to a drug?

A

the pathogen will continue to grow»superinfection!

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24
Q

how do bacteria become resistant?

A

• A natural or inherent resistance without previous exposure to the antibiotic drug
• An acquired resistance caused by prior exposure to the antibiotic drug; more common
-resistance is major growing problem in healthcare.

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25
Q

what is antibiotic misuse?

A

frequent use, inappropriate use to treat viral infections, not completing entire antibiotic regimen
o 23-37.8% of patients in hospitals receive antibiotics; 50% of those patients are receiving them inappropriately, i.e. skipping doses or taking for viral infections when no bacteria is present

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26
Q

consumer education for viral infections

A
  • Antibiotics are ineffective for viruses!
  • Taking antibiotics promotes drug resistance to bacteria
  • Taking antibiotics may cause secondary or superinfection
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27
Q

how to avoid inappropriate dosing/antimicrobial choice

A

Culture and Sensitivity (C&S): used to detect the infective microorganism in a sample, and which drug can kill it
-local antibiogram?

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28
Q

culture

A

determines the organism causing infection

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29
Q

sensitivity

A

determines which antibiotics an organism is sensitive to

30
Q

local antibiogram?

A

?

31
Q

drug drug interactions affecting antibiotic efficacy

A

consider possibility of this.
o Ex: bacteriostatic tetracycline and bactericidal penicillin. When used together the desired effect may be greatly reduced: antagonistic effect

32
Q

what can bacteria do species to species leading to what?

A

Bacterial can transfer genetic instructions to another bacterial species, increasing antibiotic resistance, and creating more virulent, aggressive bacteria.
Ex: s. aureus

33
Q

example of bacteria mutating (S. aures)

A

• S. Aureus bacteria was once sensitive to penicillin G.
Repeated exposure > mutated, now resistant. Penicillinase, enzyme produced by mutated S. aureus,
metabolizes penicillin G. to be ineffective.
• Penicillinase-resistant penicillins effective against S. aureus have been developed and are now available: (Nafcillin, Oxacillin, Dicloxacillin).
• Methicillin-resistant S. aureus
Methicillin was first penicillinase-resistant penicillin>became resistant to not only methicillin but to all penicillins and cephalosporins
• This highly resistant strain became known as methicillin-resistant S. aureus (MRSA)
o Methicillin is now off the market and the treatment of choice for MRSA is vancomycin (there are other effective drugs to treat MRSA)
o A strain of MRSA has recently been reported to be resistant to vancomycin (VRSA); Vancomycin resistant enterococcus faecium (VREF)
o Resistance of bacterial enterococcus to vancomycin is increasing- treated with linezolid - effective against VREF and MRSA.

34
Q

clostridium lives in what form

A

spore form - proliferates in less other bacteria
diarrhea > dehydrate > sepsis
opportunistic

35
Q

the adverse rxns to antibacterials

A
  1. allergy (hypersensitivity, anaphylaxis) rxns
  2. superinfection
  3. organ toxicity
36
Q

adverse rxn: allergy + treatments

A
  • Mild allergic reaction - rash, pruritis, hives - tx with antihistamines
  • Severe allergic reaction: Anaphylaxis=life threatening! First symptom SOB, leading to swollen airway, bronchospasm, hypotension, cardiac arrest - Tx with epinephrine (subq), bronchodilators (Albuterol, Racemic Epinephrine), corticosteroids (IV), antihistamines (IV), and histamine blockers (IV) (famatodine/Pepcid).
37
Q

adverse rxn: superinfection

A
  • Secondary infection that occurs when the normal flora is disturbed during antibiotic therapy: profoundly difficult infection to treat.
  • Healthcare associated infections (HCAI) caused by drug-resistant bacteria – most at risk are hospitalized frequently or live in crowded conditions (jails, nursing homes). prolongs hospitalization/course of treatment.
38
Q

adverse rxn: organ toxicity

A

• Liver most commonly metabolizes antimicrobial therapy, kidneys excrete drug compound. antibacterials may result in damage to these organs.

39
Q

therapeutic index with some antibacterials

A
  • Some drugs have a narrow therapeutic index requiring peak and trough to determine if the drug is within therapeutic range
  • If peak is too high, drug toxicity
  • If trough is too low, antimicrobial therapy is sub therapeutic: bacterial resistance
  • Drawn at lowest trough level, before next antibiotic dose is given
  • Ex – vancomycin, gentamycin (given intravenously)
40
Q

antibiotics are classed as?

A

narrow spectrum or broad spectrum

41
Q

narrow spectrum antibiotics

A
  • Selective. Primarily effective against one type of organism
  • Ex: penicillin and erythromycin are used to treat infections caused by gram-positive bacteria
42
Q

broad spectrum antibiotics

A
  • Effective against gram-positive and gram-negative organisms
  • Ex: tetracycline and cephalosporins
  • tx infections when an infective microorganism has not been identified by C&S
  • More likely to cause superinfection: C. dificile and antibiotic related diarrhea
43
Q

Pt ed for all antimicrobial therapy

A
  1. Drug-drug interactions – inform provider of other drugs ur taking or sudden new symptoms.
  2. Inform your provider if done another round of antibiotics recently
  3. Know s/s of allergic reaction
  4. Do not take with any antacid, dairy, mineral compound (Calcium, iron, magnesium supplement): they bind the med, render the antibiotic ineffective.
    Do not take with acidic juices > can impact efficacy of drug.
  5. Complete your dose always (don’t stop when symp stop)
  6. If taking warfarin or aspirin – monitor for sx of bleeding
  7. If taking contraceptives – use a back up method
  8. Can consider taking probiotic rich foods or supplement at least 2 hours separate from antibiotic therapy.
44
Q

rules of practice prior to antibiotic administration

A

A. Draw C&S PRIOR to antibiotic administration
B. Always check for allergies – the patient most likely to experience an adverse reaction is someone who has never had that antibiotic before.
C. Anaphylaxis most likely to occur within first 20 mins of infusion or infection – stay with your patient
D. Use narrowest spectrum antibiotic possible that is still effective to treat the infection
E. Always monitor for sx of opportunistic infections or superinfections– ie C. difficile

45
Q

penicillins

A

Penicillin

Beta-Lactamase Inhibitors

46
Q

Penicillin

A

(Beta-lactam antibacterial)
• Has beta-lactam ring structure that inhibits bacterial cell wall synthesis > cell lysis.
• First antibiotic synthesized from mold. Not as effective as it once(bacterial resistance and mutations over time)
• Some bacteria are able to render structure of PCN ineffective by secreting beta-lactamase enzyme (Ex: H. influenza).

47
Q

Beta-Lactamase Inhibitors

A

Broad-spectrum antibiotics combined with beta-lactamase enzyme inhibitors: obstruct action of bacterial beta-lactamases > promotes antibiotic effectiveness against gram pos/gram neg bacteria.
Ex: clavulanic acid, tazobactam
These are not given alone: combine with beta-lactamase sensitive penicillins such as amoxicillin, ampicillin, piperacillin
Ex: amoxicillin paired with clavulanic acid (Augmentin) allows for proper treatment against persisting Otitis Media or sinusitis.

48
Q

beta-lactamases

A

enzymes produced by bacteria that provide resistance to antibiotics such as penicillins and cephalosporins.

49
Q

amoxicillin

A

Aminopenicillin
tx HEENT dx (upper resp infection, otitis media, sinusitis, tonsilitis) by inhibiting enzyme in cell wall synthesis.
CI: PCN allergy. prominent GI SE
Serious SE: hemolytic anemia, blood dyscrasias
common SE: GI distress (may also cause crystalluria + rash)
NI: pt with lower GFR-consider renal dosing: work w/pharmacist/doc to reduce dose to preserve kidneys. do coagulation panel PT&INR

50
Q

cephalosporins

A

“cousin” to PCN – also fungus based – also has a beta lactam structure.
A. ~10% of persons allergic to penicillin are also allergic to cephalosporins (similar molecular structures)
-Higher generations of cephalosporins: significantly less likelihood of having cross sensitivity allergic reactions to penicillins.
5 generations of cephalosporins:
each generation is effective. a broader spectrum of bacteria has increased resistance to beta lactamase, and increased ability to cross the blood brain barrier.

51
Q

if drugs can become renal toxic, they can also become ototoxic

A

hint

even if pt is deaf, ototoxic drugs can be concern: affect balance

52
Q

5 generations of cephalosporins

A

1-cefazolin(Ancef): covers gram pos exept MRSA
2-Cefotetan: covers anaerobes (gram post and neg except pseudomonas)
3-Ceftriaxone(Rocephin): covers gram neg except pseudomonas + gram pos
4-Cefepime: covers gram pos, gram neg, PSEUDOMONAS, except MRSA
5-Ceftaroline: covers MRSA

53
Q

ceftriaxone(Rocephin)

A

3rd gen cephalosporin.
Bactericidal (inhibits cell wall synthesis)
Tx broad range of infections, but ESP gram neg infections ie K. pneumonia and E.coli
CI: colitis/hepatic/renal
serious se: angioedema, blood dyscrasias, renal failure, stevens-johnson
drug-drug: increased nephrotox (monitor renal fx) w/loop diuretics/aminoglycosides/vancomycin
also monitor liver fx. watch their pee!

54
Q

macrolides

A

i. Broad-spectrum antibiotics: Azithromycin, clarithromycin, erythromycin
ii. Low-mod doses have bacteriostatic effect
iii. High doses have a bactericidal effect
iv. administered PO/IV but NOT IM
v. Gastric acid destroys erythromycin in the stomach: acid-resistant salts must be added
vi. Active against most gram-pos, moderately active against some gram-neg
vii. tx mild-mod infections of resp tract, sinuses, GI tract, skin, soft tissue, diphtheria, impetigo, STI

55
Q

azithromycin(Zithromax)

A

Macrolide
inhibits bacterial synthesis.
good alternative for pt allergic to PCN. works well for atypical infection (URI, STD, PID, skin infection).
SE: tinnitus, abd cramps, electrolyte derangements (hypokalemia, hpomagnesemia)
SERIOUS: superinfection, hearing loss, angioedema, SJ
drg-drg: anticoagulant bleeding, statin rhabdo, potentiates heart slowers
monitor for ototox
better on empty stomach (2hrs) but take w/food if GI upset

56
Q

ketolides

A

Structurally related to macrolides

ii. Used in adults 18 and over to treat mild to moderate community-acquired pneumonia

57
Q

telithromycin(Ketek)

A

tx mild-mod community acquired pneumonia by inhibiting protein synth in microorganisms by binding to bacterial ribosomal RNA > cell death

ci: MG - potentiates muscle weakness.
se: altered taste, visual disturbs, liver failure.

58
Q

tetracyclines

A

i. Effective against gram-neg and gram-pos: inhibit bacterial protein synthesis
ii. Cannot be given to children <8 y/o: irreversible discoloration of permanent teeth.
iii. no pregnant: teratogenic effect.
iv. damage to vestibular part of inner ear > difficulties with balance
v. ↑↑↑photosensitivity, ↑ likelihood of sunburn – pt must wear sunblock, long sleeves, sunglasses, minimize prolonged sun exposure.

59
Q

doxycycline

A

tetracycline.
tx wide variety of conditions by inhibiting protein synthesis.
CI: Preg D: teratogenic. caution for breastfeeding. not for <8yo.
SE: GI distress - C. diff
tooth discoloring. photosensitivity. LIFE THREAT: colitis, SJ
drg drg: the usual + dec eff of antiseizure drugs, rifampin, ciprofloxacin, PCN. alters lithium levels.
Ed: sun protection. back up birth control + no pregnant. Check exp date of med

60
Q

glycopeptides

A

used to tx drug resistance S. aureus: MRSA

61
Q

vancomycin

A

Glycopeptide reserved for srs infections.
for several gram pos micros, drug resistant infections: MRSA, C DIFF
SE: nephrotoxic, ototoxic, red man syndrome (toxic effect), blood dyscrasias, SJ, cardiac arrest.
drgdrg: nephro/ototox w/other drugs w/similar side effects
narrow therapeutic index: peak/trough every 24h (esp renal pt) draw trough 90mins before next dose

62
Q

aminoglycosides

A

i. Typically end in –cin/mycin/micin
ex - gentamicin, neomycin, streptomycin, tobramycin, amikacin
ii. Cannot be absorbed into the GI tract, do not cross BBB in adults (does in children)

63
Q

gentamycin

A

Aminoglycoside. reserved for srs infection
for Gram neg serious inf.
ci: renal dx, colitis, preg D
serious SE: renal, ototoxic, hepatotoxic, blood dyscrasias, superinf, oliguria, neuromuscular block
narrow therapeutic: check trough every 24h (esp in renal), draw trough 90 mins before nxt dose
Increase fluid intake

64
Q

fluoroquinolones (quinolones)

A

i. include ciprofloxacin and levofloxacin
ii. Interferes with enzyme DNA gyrase, which is needed to synthesize bacterial deoxyribonucleic acid (DNA)
iii. Spectrum includes gram-positive and gram-negative organisms

65
Q

levofloxacin(Levaquin)

A

fluoroquinolone
tx mod-severe lower resp tract, renal, skin, bone, joint infection, anthrax by interfering with enzyme DNA gyrase, which is needed for bacterial DNA synthesis
• Bactericidal effect
Ci: renal, MG, preg/breastfeeding
prec: children <14, theophyllines, seizure,dehydration
adv: tendon rupture. lfie threat: SJ, encephalopathy, pseudo colitis, SI
food: inc caffeine. do liver labs. 2hrs bfore/after antacids or iron for absorption. risk of inc eff of oral hypoglycemic in DMs
photosensitivity: sun protection.
QT prolongation.
dysrhythm. tendonitis.

66
Q

lipopeptides

A

i. bind to bacterial membrane. cause rapid depolarization of its membrane potential, inhibit DNA, RNA, protein synthesis
ii. Indicated for complicated skin infections, infective endocarditis
iii. Works against gram pos – especially S. aureus/MRSA

67
Q

daptomycin

A

lipopeptide
tx Complicated skin infections due to gram-positive microorganism, Septicemia due to S. aureus, Infective endocarditis from MRSA
by binding to cell membrane.
adv: HTN, hypotn, burning on urination, pallor, chest pain, kalemias, glycemias, rhado, pleural effusion

68
Q

sulfonamides

A

A. First group of drugs used against bacteria
B. Not an antibiotic: they are not obtained from biologic substances
i. Synthetically derived for treatment of gram neg/gram-pos infections
C. Bacteriostatic: inhibition of bacterial synthesis of folic acid, which is essential for bacterial growth
i. Humans acquire folic acid through their diet
ii. Folic acid is required by cells for synthesis of RNA, DNA and proteins
iii. selectively inhibit bacterial growth without affecting normal cells
D. tx urinary tract and ear infections, may be used as alternative for patients with allergy to penicillin
E. Also used for treatment of meningococcal meningitis, Chlamydia, and Toxoplasma gondii
F. 90% effective against E. coli: preferred treatment for UTI
G. Not effective against fungi or viruses
H. often used in combination with other antibiotics because of synergistic or potentiative effect (ex: Trimethoprim and Sulfamethoxazole (TMP-SMZ) (brand name Bactrim)

69
Q

trimethoprim-sulfamethoxazole (Bactrim)

A

sulfonamide
tx UTI, resp tract inf, otitis media, MRSA by inhibiting folic acid synth/protein synth of nucleic acids (bactericidal).
prec: malnutrition, hypothyroid
severe rxn: erythema multiforme
life threat: blood dyscrasias, anemias, crystalluria, pseudo colitis, SJ, renal failure
SE: photosens, tinnitus, arthralgia
dfl: inc hypoglycemic eff of other drugs. increase potassium, digoxin, phenytoin, methotrexate tox.
do BUN and ASTS. monitor urine. drink with full glass of water (prevent crystals/kidney stones).
check platelet +WBCs
avoid taking during last 3 mos of preg.
do not take w antacids (dec absorption rate)
1 hr before or 2 hr after meal.
sun protection

70
Q

antibiotic drug drug interactions

A

statins > rhabdo (renal failure, coffee urine)
anticoagulants > bleeding
Drugs affecting heart rate (slowing it) > potentiated therapeutic effect

Pharm (20 decks)

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