Antibacterial Drugs Flashcards
Invaders
-Prokaryotes
-Eukaryotes
-Viruses
Prokaryotes
-cell with no nuclei
-Bacteria- cause most infectious diseases
Eukaryotes
-Cells with nuclei
-Fungi
-Protozoa
-Helimiths
Viruses
-Live off human cells
Chemo therapy
-Drugs that are “selectively toxic”
-Minimal effect on host
Antibacterial attack
Bacteria
antifungals attack
-Fungus
-yeast
antivirals attack
viruses
antiparasitic attack
parasites
anthelmintics attack
helmiths
antiprotozoal attack
protozoa
antineoplastics attack
tumor cells
Bacterial infections (necrotizing fasciitis)
-flash eating disease
-caused by a variety of bacteria
Prokaryotic cells
-Average size (1-5 mcm)
-can survive a wide range of environments (hot or cold)
-pathogenic + non-pathogenic
Prokaryotic infections
-invasion and multiplication of organisms
-may be caused by bacteria of normal flora (immunocompromised)
prokaryotic colonization
-increase in bodies of normal flora colonies
-not usually harmful, can help control growth of potentially pathogenic organisms
Bacteria are described by
-Shape
-oxygenation
-Gram + and Gram -
Bacteria shapes
-cocci (circular) + bacilli (rod like)
-Staphylococci (cocci in clumps)
-Streptococci (Cocci in chains)
Bacteria oxygenation
-Aerobes (oxygenated)
-Anaerobes (deoxygenated)
Bacterial cell wall
-Gram + or Gram -
-Does wall stain or not
-fundamental differences in wall structure
-implications for actions with antibacterial
What does the bacterial cell wall do
-outside plasma membrane
-structural support
-protection
Gram positive
-thick peptidoglycan (up to 40 layers)
-Gram stain (crystal violet) trapped in peptidoglycan layer
Gram Negative
-thin peptidoglycan
-outer membrane
-less gram stain is trapped
-LPS layer to some antibacterial
Peptidoglycan
-polymer of amino acids and sugars
-not in eukaryotes
Antibacterial is interchangeable with
antibiotics
Antibacterial are
Meds used to treat bacterial infections
-exploit the differences between human and bacterial cell
antibacterial must
legally identify causative organisms before antibacterial therapy
-potential susceptibility
Antibacterial can be effective against
-gram neg
-gram pos
Narrow spectrum
selective against one class of bacteria
-better
Broad spectrum
effective against both classes of bacteria
how do antibacterial effect bacteria (2 ways)
Antibacterial either kill or slow bacteria growth so immune system can attack
-bactericidal
-bacteriostatic
Bactericidal
lethal to bacteria at clinically achievable concentrations
Bacteriostatic
slows bacteria growth so immune system can attack
the immune system
is critical to help the body control + eliminate infections
What else is important other than antibacterials
host defenses/immune system
Superinfection
new microbes take over when antibiotics kill normal flora
-microbes resistant to drug action = difficult to treat
Opportunistic infection
infections that wouldn’t normally happen in an immunocompetent person
-immunocompromised
-existing colonization becomes infection
What can become opportunistic infections
-virus
-fungi
-protozoa
How many people die due to drug resistance
-globally 5 million
-even against last resort drugs
-little resistance to new drugs
Why does resistance occure
select mutant bacteria are enhanced due to
-improper choice of antibacterial
-too dose
-dose not continued long enough
-improper treatment
-prophylactic use of antibacterial (animal food)
Host factors to antibacterial therapies
-age
-allergies
-organ health
-site of infection
-pregnancy
-persons general health
Allergic reactions
-immune response
-GI upset isn’t an allergic reaction
Antibacterial mechanism of action
-Disruption of critical metabolic reaction
-interference with cell wall synthesis
-interference with protein synthesis
-interference with DNA replication
Antibiotics that affect cell wall synthesis
-penicillins
-vancomycin
-cephalosporins
Antibiotics that impact transcription mechanisms
floroquinulones
Antibiotics that affect protein synthesis
-macrolides
-tetracyclines
-aminoglycosides
Antibiotics that affect metabolic pathways
-sulfamethoxazole
-trimethoprim
Sulfonamides: Metabolic inhibitors
-broad spectrum
-sulfa-drug
-bacteriostatic
Sulfonamides: drugs
-sulfamethoxazole
-sulfadiazine (prevent synthesis of folic acid)
Sulfonamides: indications
-combined with trimethoprim (co-trimoxazole)
-reaches effective concentrations in urinary tract
-Bactrim or septra for URI and otitis media
Sulfonamides: other clinical uses
-upper respiratory tract infections
-malaria
-chlamydia
Sulfonamides: contraindications
-known allergy: applies to other derivatives of sulfa drugs (antidiabetic agents, thiazide and loop diuretics)
-Pregnant women
-not advised for breast feeding
-not for infants less than 2 months
Sulfonamides: what happens when its given during pregnancy
-1st trimester = birth defects
-end of pregnancy increases bilirubin = jaundice
-end of pregnancy kemicterus (brain damage)
Sulfonamides: Adverse effects
-integumentary system (allergies/hypersensitivity)
-blood (bone marrow depression = agranulocytosis, thrombopenia, aplastic anemia)
-GI (nausea + vomiting)
B-lactam Antibiotics:
-sir alexander flemming (1928)
-bacterium staphylococcus aures destroyed by the mold penicillium notatu
-inhibit cell wall enzyme responsible for peptidoglycan synthesis
What effect do B-lactam Antibiotics have
Bactericidal
B-lactam Antibiotics: 4 groups
-penicillin
-cephalosporins
-carbapenems
-monobactams
B-lactam Antibiotics: characterized by
B-lactam ring structure
Penicillin: two types
-naturally occurring
-semi-synthetic
Penicillin: natural
sensitive to B-lactamase
Penicillin: Semi-synthetic
-B-lactamase resistant
-broad spectrum (aminopenicillins)
-extended spectrum (anti-pseudomonal penicillin’s)
Penicillin: narrow spectrum
-Penicillin G (penicillin/benzylpenicillin)
-penicillin V
Penicillin: B-lactamase resistant and penicillinase resistant
Cloxacillin
Penicillin: broader spectrum
-Amoxicillin (acid stable)
-ampicillin
Penicillin: Anti-pseudomonal
-Extended spectrum
-Ticarcillin
-Piperacillin
-works against pseudomonas aeruginosa infections
Penicillin: Pseudomonas aeruginosa infections
-in immunocompromised, cystic fibrosis
-Respiratory tract
-ears
- UTIs
-eyes
-CNS
-endocarditis
Penicillin: Mechanism of Action
-enter bacteria
-in cell bind to penicillin building protein
-normal cell wall synthesis disrupted
-bacteria cell ruptures
-don’t kill other body cells
Penicillin: attack method
bactericidal
-affects most gram pos and some gram neg
Penicillin: Drug Resistance
-some bacteria produce penicillin killing enzymes
-Bacteria make B-lactamases
Penicillin: beta-lactamases
split Beta-lactam rings
Penicillin: Beta-lactam inhibitors
-used with penicillin’s to combat beta-lactamases
-Clavanic acid
-tazobactam
Penicillin: indications
-Gram pos bacteria
-broad/extended types kill gram neg
Penicillin: Administration
-PO
-IM
-IV
Penicillin: G is administered
IV
Penicillin: V is administered
PO
Penicillin: Adverse Effects
-most common drug allergy
~skin rashes
~subcutaneous edema- lips
~can be fatal
-generally well tolerated
-GI problems (nausea, vomiting, diarrhea, abnormal pain)
Cephalosporins
-semi-synthetic derivatives from cephalosporium fungus
-structurally + pharmacologically related to penicillin’s
Cephalosporins: attack method
bactericidal
Cephalosporins: are ___ antibiotics
Beta-lactam
Cephalosporins: are organized into___ ranging from
Divided into groups generations, ranging from better gram negative coverage to better Beta-lactamase resistance
Cephalosporins: Generation 1 vs. 5
-1: best gram neg coverage, worst beta-lactam resistance
- Middle generations gradually change
-5: worse gram neg coverage, best beta-lactam resistance
Cephalosporins: first gen
-Cefazolin (IV)
-Cephalexin (PO)
-Cefadroxil
-Surgical prophylaxis, UTIs, Otitis media
Cephalosporins: Second gen
-good gram pos coverage
-better gram neg coverage then gen 1
-Cefuroxime (PO) -surgical prophylaxis
-Cefoxitin (IV + IM)
Cephalosporins: Third gen
-Broader spectrum (better gram neg)
-Cefotaxime (IV + IM) -easily passes meninges into CSF
-Cefixime (PO) -best oral cephalosporin against gram neg
Cephalosporins: Third gen is best for
Treating meningitis
Cephalosporins: fourth gen
-broader spectrum of antibacterial activity (especially against gram neg)
-Cefepime
Cephalosporins: fifth gen
-Broadest spectrum (kills gram neg well)
-Ceftaroline (MRSA infections)
Cephalosporins: Adverse Effects
-generally well tolerated
-GI problems (nausea, vomiting, diarrhea, abnormal pain)
-Allergies
Carbapenems: action is
Broad spectrum
Carbapenems: Broad spectrum attacks
-gram pos
-gram neg
-anerobic
-effective for mixed infections
Carbapenems: Don’t affect what infections
MRSA infections
Carbapenems: must be given __ not __
must be given IV not PO
Carbapenems: drugs, are used in
-imipenem
-meropenem
- used in combination therapy
Carbapenems: reserved for
severe complicated body cavity and connective tissue infections
Carbapenems: are classified as __ for infections ___
last resort antibacterial for infections that can’t be treated by narrow drugs
Carbapenems: Drug resistance
-Carbapenem-resistant entero-bacteriaceae (CRE)
-Klebsiella pneumonia carbapenemases (KPC) and New-dehli metallo-beta lactamase (NDM)- enzymes that break down Carbapenems
Carbapenems: opportunistic infections
are veery hard to treat
Carbapenems: treat bacteria that are
resistant to most antibacterial
Macrolides: size and drugs
-Very large
-Erythromycin
-Azithromycin
-Clarithromycin
Macrolides: Mechanism of action
-Inhibit protein synthesis
-Broad spectrum
-Bacteriostatic and Bactericidal (depending on concentration)
Macrolides: Given to people with what allergies/resistances
-allergies to Beta-lactam antibacterial
-Penicillin resistances
Macrolides: Azithromycin
and Clarithromycin are used
in combination therapy for those with HIV/AIDs to stop opportunistic infections
Macrolides: Treat infections of
-Respiratory, skin, soft tissues
-Strep
-Streptococcus pyogenes (group A beta-hemolytic streptococci)
-Mild to moderate upper respiratory tract infections
-Hemophilus influenzae
-Spirochetal infections
-Syphilis + Lyme disease
-Gonorrhea
-Chlamydia
- Mycoplasma
Macrolides: Adverse Effects
-GI Disturbances (Nausea, Vomiting, diarrhea)
-Provoke cardiac dysrhythmias (long Q-T)
Macrolides: Azithromycin
and Clarithromycin adverse efects
-Fewer drug-drug interactions (Theophylline, warfarin, cyclosporin)
-little to no inhibition of CYP enzymes
Tetracyclines: Mechanism of action
-Broad spectrum
-Inhibit protein synthesis
-Bacteriostatic
Tetracyclines: Drugs
-Tetracycline
-Doxycycline
-Minocycline
-Demeclocycline
Tetracyclines: Indications
-Gram neg and gram pos
-Bind to metal ions
Tetracyclines: Bind to what metal ions
-Bind to Ca2+, Mg2+, Iron, and aluminum
Tetracyclines: Don’t take at the same time as what products
-Don’t take at the same time as any metal ion products
-Milk, supplements, laxatives, antacids
Tetracyclines: why can’t you take these with metal ions
-form insoluble complexes (Chelation)
-Which passes out of the body reducing absorption
Tetracyclines: Adverse effects
-Strong affinity for calcium
-GI disturbances
-Gut flora disturbances (Candida, Colitis/C-diff)
-Photosensitivity
-Antagonistic to bactericidal antibiotics (Time 1h apart)
Tetracyclines: Do NOT give to, why
-Pregnant people
-Breastfeeding moms
-Children younger then 8 years
-Due to calcium binding (Tooth discoloration, bone deformities)
Aminoglycosides:
-Amino Sugars
-Natural and synthetic (produced from streptomyces)
-First effective bacteria against gram neg
Aminoglycosides: mechanisms of action
-Bactericidal
-Prevents abnormal protein synthesis
-Attack mostly gram neg and some gram pos
Aminoglycosides: Drug types
-Gentamicin
-Neomycin
-Streptomycin
-Tobramycin
-Amikacin
Aminoglycosides: Indicators
-Acts against gram neg
-used best in combination
Aminoglycosides: are given, because
-Parenterally due to poorly absorbed through GI given parenterally (IM or IV)
-Given orally or as enema to decontaminate prior to surgery
Aminoglycosides: Adverse effects
Serious toxicities
-Ototoxicity
-Nephrotoxicity
Aminoglycosides: Ototoxicity
Hearing or balancing loss
-Irreversible
-Ringing (tinnitus)
-Deafness
-Vestibular (balance)
Aminoglycosides: What makes ototoxicity worse
-Made worse if other ototoxic drugs are given
Aminoglycosides: Nephrotoxicity
-Reversable
-Extreme neonates + existing renal conditions
-Measure protein, urea, serum creatine levels, BUN
Aminoglycosides: Nephrotoxicity steps to limit
-Time each dose and test blood to limit effects
-Monitor drug plasma levels
Aminoglycosides: What increases nephrotoxicity risk
-Vancomycin (antibacterial)
-Cyclosporine (Immunosuppressant)
-Amphotericin B (Antifungal)
Quinolone’s or Fluroquinolones: Drug types
-Ciprofloxacin (Effective and most common)
-Norfloxacin
-Gemifloxacin
-Levofloxacin
-Gemifloxacin
Quinolone’s or Fluroquinolones: Mechanism of Action
-Bactericidal
-Gram neg and some gram pos
-Alters DNA of bacteria
Quinolone’s or Fluroquinolones: Indications
-UTI
-Lower respiratory tract infection
-Bone and Joint infections
-Infectious diarrhea
-Skin infections
-STD
-Anthrax
Quinolone’s or Fluroquinolones: Adverse Effects
-GI (Nausea, Vomiting, Diarrhea)
-Skin (Rashes)
-CNS (Headaches, dizziness)
Quinolone’s or Fluroquinolones: Interactions
-Drug-Drug (CYP inhibition)-Theophylline (asthma), Warfarin
-Oral absorption reduced by (antacids, iron, zinc, calcium containing preparations)- give 1-2h prior to drugs
Vancomycin: methods of action
-Inhibits cell wall synthesis
-Bactericidal
-Only protein target to Beta-lactams
Vancomycin: Administration
-IV
Vancomycin: Indications
-MRSA and other gram pos infections
-Oral for Pseudomembranous colitis
Vancomycin: Adverse Effects
-Resistance increasing
-Infusion rate-related (infuse over 1h)
-Fever, chills, phlebitis
-Ototoxicity
-Nephrotoxicity
Vancomycin: What do you do to reduce adverse effects
Blood drug monitoring
