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318 Cards in this Set
- Front
- Back
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Bugs with exotoxins
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"Some Say Cobra Venom Entering Buttocks Could Cause Complete Blindness So Suck"
[S aureus/pyogenes SuperAgs] [C. diptheria, V. Cholera, E. coli, B. pertusis----ADP ribosylation/A-B toxin] [C.perfringens, C. tetani, C. botulinum, B.antrhax, Shigela, S. pyogenes----other toxins] |
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some toxins encoded by lysogenic phages.
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ABCDE
-shigA-like toxin -Botulinum toxin -Cholera toxin -Diphtheria toxin -Erythrogenic toxin of -Streptococcus pyogenes |
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examples of Obligate anaerobes
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Anearobes know their ABC's
-Actinomyces -Bacterioides -Clostridium |
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Catalase
what it does and why it's bad |
Catalase degrades H2O2, an antimicrobial product of PMNs. H2O2 is a substrate for myeloperoxidase.
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what makes coagulase
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S. aureus makes coagulase,
whereas S. epidermidis and S. saprophyticus do not. |
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bacterial cAMP inducers
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cAMP
-Choerae -Anthrax -E.coli (imagine the heat (heat -labile) has caused the E to faint and as fallen over to make an M -Pertussis |
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Zoonotic bacteria
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Big Bad Bugs From Yer Pet
-Bartonella henselea -Borrelia burgdorferi -Brucella spp. -Francisella tularensis -Yersinia pestis -Pasteurella multocida |
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Cat scratch fever aka
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Bartonella henselae
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Bartonella henselae
disease states |
cat scratch fever
lymphadenopathy (swelling of the lymph nodes) and fever. and Peliosis Hepatis |
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Peliosis Hepatis
describe |
is an uncommon vascular condition characterised by randomly distributed multiple blood-filled cavities throughout liver.
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is an uncommon vascular condition characterised by randomly distributed multiple blood-filled cavities throughout liver.
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Peliosis Hepatis
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Peliosis Hepatis
causes |
HIV
bartonella malignancy drugs |
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treatment of choice for most
rickettsial infections. |
Tetracycline is the
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Rocky Mountain spotted fever
where in the country |
Endemic to East Coast (in spite of name).
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Classic cause of atypical “walking” pneumonia
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Mycoplasma pneumoniae
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Leptospira interrogans
appearance and where found |
Question marke shape spirochete bacteria in water contaminated with animal urine
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Question marke shape spirochete bacteria in water contaminated with animal urine
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Leptospira interrogans
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Leptospira interrogans
clinical findings |
fluelike with fever, headache, stomach pain and jaundace
also Weil's disease - severe form of jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia |
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Weil's disease
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aka icterohemorrhagic leptospirosis - severe form of jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia
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aka icterohemorrhagic leptospirosis - severe form of jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia
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Weil's disease
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VDRL mech
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VDRL detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, VDRL detects nonspecific antibody that reacts with beef cardiolipin. Used for diagnosis of syphilis, but many biologic false positives |
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detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, VDRL detects nonspecific antibody that reacts with beef cardiolipin. Used for diagnosis of syphilis, but many biologic false positives |
VDRL
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Systemic mycoses can mimic
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TB
(granuloma formation). |
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“Tricky T’s”
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-Typhoid fever=Salmonella typhi
-C.trachomatis=bacteria, STD. -Trichomonas vaginalis=protozoan, STD. -Trichinella spiralis=worm in pork. -Trypanosoma=Chagas’ disease or African ss. -Treponema=spirochete; causes syphilis (T. pallidum) or yaws (T. pertenue). |
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Rubella aka
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(German measles)
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German measles aka
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Rubella
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Hepatitis virus families
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HEP A-picornavirus
HEP B-Hepaddnavirus HEP C-flavivirus HEP D-deltavirus HEP E-Calicivirus/hepivirus |
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Rubella findings
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fever, lympadenopathy, arthralgias. mild in children, but serious congenital disease)
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congenital rubella findings
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# malformations of the heart (especially patent ductus arteriosus), eyes or brain
# deafness # eye defects (especially cataract and microphthalmia # thrombocytopenic purpura (presents as a characteristic "blueberry muffin" rash) |
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# malformations of the heart (especially patent ductus arteriosus), eyes or brain
# deafness # eye defects (especially cataract and microphthalmia # thrombocytopenic purpura (presents as a characteristic "blueberry muffin" rash) |
congenital rubella findings
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"lots of spots"
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rubella
rubeola varicella variola vaccina |
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TORCHES infection findings
Toxoplasma |
"clasic triad" of chorioretinitis, intracranial calcifications (ring enhanced lesions) and hydrocephalus
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TORCHES infection findings
rubella |
deafness, cataracts, PDA/pulmonary artery stenosis, retardation
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TORCHES infection findings
CMV |
petechial rash, intracranial calcifications, mental retardation, hepatosplenomgaly, jaundice. 90% are asymptomatic at birth
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TORCHES infection findings
HIV |
hepatosplenomgaly, neurologic problems, and frequent infections
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TORCHES infection findings
HSV2 |
encephalitis, conjunctivitis, vesicular skin lesions
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TORCHES infection findings
Syphilis |
cutaneous lesions, hepatosplenomgaly, jaundice, saddle nose, saber shins, hutchinson teeth, CNVIII deafness,
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hutchinson teeth
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teeth that are smaller and more widely spaced than normal and which have notches on their biting surfaces. a sign of congenital syphilis
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teeth that are smaller and more widely spaced than normal and which have notches on their biting surfaces.
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hutchinson teeth-a sign of congenital syphilis
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"clasic triad" of chorioretinitis, intracranial calcifications (ring enhanced lesions) and hydrocephalus
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TORCHES infection findings
Toxoplasma |
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TORCHES infection findings
deafness, cataracts, PDA/pulmonary artery stenosis, retardation |
rubella
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TORCHES infection findings
petechial rash, intracranial calcifications, mental retardation, hepatosplenomgaly, jaundice. 90% are asymptomatic at birth |
CMV
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TORCHES infection findings
hepatosplenomgaly, neurologic problems, and frequent infections |
HIV
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TORCHES infection findings
encephalitis, conjunctivitis, vesicular skin lesions |
HSV2
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TORCHES infection findings
cutaneous lesions, hepatosplenomgaly, jaundice, saddle nose, saber shins, hutchinson teeth, CNVIII deafness, |
hutchinson teeth
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Top three causes of pneumonia in
Children (6 wks–18 yr) |
-Viruses (RSV)
-Mycoplasma -Chlamydia pneumoniae |
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Top three causes of pneumonia in
Adults (18–40 yr) |
-Mycoplasma
-C. pneumoniae -S. pneumoniae |
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Top three causes of pneumonia in
Adults (40–65 yr) |
-S. pneumoniae
-H. influenzae -Anaerobes |
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Top three causes of pneumonia in
Elderly >65 |
-S. pneumoniae
-Viruses -Anaerobes |
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What age group has this pneumonia pattern
-Viruses (RSV) -Mycoplasma -Chlamydia pneumoniae |
Children (6 wks–18 yr)
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What age group has this pneumonia pattern
-Mycoplasma -C. pneumoniae -S. pneumoniae |
Adults (18–40 yr)
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What age group has this pneumonia pattern
-S. pneumoniae -H. influenzae -Anaerobes |
Adults (40–65 yr)
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What age group has this pneumonia pattern
-S. pneumoniae -Viruses -Anaerobes |
Elderly >65
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Top three causes of meningitis in
Newborn (0–6 mos) |
-Group B streptococci
-E. coli -Listeria |
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Top three causes of meningitis in
Children (6 mos–6 yrs) |
-Streptococcus pneumoniae
-Neisseria meningitidis -Haemophilus influenzae type B |
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Top three causes of meningitis in
6–60 yrs |
-N. meningitidis
-Enteroviruses - S. pneumoniae |
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Top three causes of meningitis in
60 yrs + |
-S. pneumoniae
-Gram-negative rods -Listeria |
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What age group gets this pattern of meningitis
-Group B streptococci -E. coli -Listeria |
Newborn (0–6 mos)
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What age group gets this pattern of meningitis
-Streptococcus pneumoniae -Neisseria meningitidis -Haemophilus influenzae type B |
Children (6 mos–6 yrs)
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What age group gets this pattern of meningitis
-N. meningitidis -Enteroviruses - S. pneumoniae |
6–60 yrs
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What age group gets this pattern of meningitis
-S. pneumoniae -Gram-negative rods -Listeria |
60 yrs +
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UTI bugs
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SSEEK PP.
Serratia marcescens, staphylococcus saprophyticus E. coli, Enterobacter cloacae Klebsiella, Proteus mirabilis Pseudomonas aeruginosa |
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Name the Gram + Rods
Anaerobes |
Anaerobes
p Acne/ Clostridum/ fragilis (is gram but is in the mnemonic)/ a. Israeli / mobiluncus muleris |
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Name the Gram + Rods
Aerobes |
-Cornybacterium
-Listeria -Bacillus -Erysipelothrix |
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Name the Gram - Rods
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Yersinia / Haemophilus / vibrio / Helicobacter / Pseudomonas / Campylobacter / Bordatella / Bacteriodes fragilis (the only anaerobe) / Brucella / Legionella / Pasturella / Klebsiella / Shigella / E. coli / Salmonella / Francesella
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Name the Gram + Cocci
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Strep
Staph Enterococcus |
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Name the Gram - Cocci
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Nissera
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Name the Gram + Rods
Anaerobes |
Anaerobes
p Acne/ Clostridum/ fragilis (is gram but is in the mnemonic)/ a. Israeli / mobiluncus muleris |
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Name the Gram + Rods
Aerobes |
-Cornybacterium
-Listeria -Bacillus -Erysipelothrix |
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Name the Gram - Rods
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Yersinia / Haemophilus / vibrio / Helicobacter / Pseudomonas / Campylobacter / Bordatella / Bacteriodes fragilis (the only anaerobe) / Brucella / Legionella / Pasturella / Klebsiella / Shigella / E. coli / Salmonella / Francesella
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Name the Gram + Cocci
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Strep
Staph Enterococcus |
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Name the Gram - Cocci
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Nissera
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Penicillin
Clinical use |
-gram-positive cocci,
-gram-positive rods, -gram-negative cocci, and -spirochetes. |
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Penicillin
Toxicity |
Hypersensitivity reactions, hemolytic anemia.
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penicillinase-resistant penicillins
names |
Methicillin, nafcillin, dicloxacillin
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Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)
Mechanism |
Same as penicillin
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Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)
Clinical use |
S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).
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Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)
Toxicity |
Hypersensitivity reactions; methicillin––interstitial nephritis.
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aminopenicillins
names |
Ampicillin, amoxicillin
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Ampicillin, amoxicillin (aminopenicillins)
Mechanism |
Same as penicillin. Wider spectrum; penicillinase
sensitive. Also combine with clavulanic acid |
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Ampicillin, amoxicillin (aminopenicillins)
Clinical use |
Extended-spectrum penicillin––certain gram-positive bacteria and gram-negative rods "HELPS" (Haemophilus influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, enterococci).
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Ampicillin, amoxicillin (aminopenicillins)
Toxicity |
Hypersensitivity reactions; ampicillin rash;
pseudomembranous colitis. |
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combine with clavulanic acid
(penicillinase inhibitor) to enhance spectrum. |
Ampicillin, amoxicillin (aminopenicillins)
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Ampicillin, amoxicillin (aminopenicillins)
wrt combinations |
combine with clavulanic acid
(penicillinase inhibitor) to enhance spectrum. |
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penicillin forms
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Penicillin G (IV form), penicillin V (oral)
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aminopenicillins
aka |
Ampicillin, amoxicillin
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Ampicillin, amoxicillin
aka |
aminopenicillins
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anti-pseudomonals
aka |
TCP: Takes Care of
Pseudomonas. Ticarcillin, carbenicillin, piperacillin |
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Ticarcillin, carbenicillin, piperacillin
aka |
TCP: Takes Care of
Pseudomonas. anti-pseudomonals |
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use with clavulanic acid.
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Ticarcillin, carbenicillin, piperacillin (anti-pseudomonals)
Ampicillin, amoxicillin (aminopenicillins) |
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Ticarcillin, carbenicillin, piperacillin (anti-pseudomonals)
use wit |
clavulanic acid (penicillinase inhibitor) to enhance spectrum.
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Ticarcillin, carbenicillin, piperacillin
Mechanism |
Same as penicillin. Extended spectrum.
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Ticarcillin, carbenicillin, piperacillin
Clinical use |
Pseudomonas spp. and gram-negative rods;
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Ticarcillin, carbenicillin, piperacillin
Toxicity |
Hypersensitivity reactions.
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β-lactam drugs that inhibit cell wall synthesis but are
less susceptible to penicillinases. Bactericidal. |
Cephalosporins
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Cephalosporins
Mechanism |
β-lactam drugs that inhibit cell wall synthesis but are
less susceptible to penicillinases. Bactericidal. |
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1st generation Cephalosporins
Clinical use |
PEcK.
gram-positive cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae. |
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2nd generation Cephalosporins
Clinical use |
HEN PEcKS.
gram-positive cocci, Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus, E. coli, Klebsiella , Serratia. |
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3rd generation Cephalosporins
Clinical use |
serious gram-negative infections resistant to other
β-lactams; meningitis (most penetrate the blood-brain barrier). Examples: ceftazidime for Pseudomonas; ceftriaxone for gonorrhea. |
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4th generation Cephalosporins
Clinical use |
↑ activity against Pseudomonas and gram-positive organisms.
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Cephalosporins
Toxicity |
Hypersensitivity reactions. Cross-hypersensitivity with
penicillins occurs in 5–10% of patients. nephrotoxicity of aminoglycosides; Disulfiram type reaction with ethanol |
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which Cephalosporins
Disulfiram type reaction with ethanol |
with a methylthiotetrazole group, e.g., cefamandole
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1st generation Cephalosporins
Names |
1st generation...All cephalosporin sounds like CEF except 1st generation in 1st generation there is PH rather CEF like..->CePHalothin ,CePHaprin, CePHradine, CePHalexin
dont be FAZed, this exception is out O' LINe ..CeFAZOLIN |
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2nd generation Cephalosporins
Names |
FOXes have FACe FUR
ceFOXitin, ceFAClor, ceFURoxime)– |
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3rd generation Cephalosporins
names |
TRI to TAX TAZ
cefTRIaxone, cefoTAXime, cefTAZidime |
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4th generation Cephalosporins
names |
Cefepime is the only one
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what generation Cephalosporin is
cephalexin |
1st generation
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what generation Cephalosporin is
cefazolin |
1st generation
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what generation Cephalosporin is
cefuroxime |
2nd generation
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what generation Cephalosporin is
cefaclor |
2nd generation
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what generation Cephalosporin is
cefoxitin |
2nd generation
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what generation Cephalosporin is
ceftriaxone |
3rd generation
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what generation Cephalosporin is
cefotaxime |
3rd generation
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what generation Cephalosporin is
ceftazidime |
3rd generation
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what generation Cephalosporin is
cefepime |
4th generation
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Aztreonam
Mechanism |
A monobactam resistant to β-lactamases. Inhibits cell wall synthesis (binds to PBP3). Synergistic with aminoglycosides. No cross-allergenicity with penicillins.
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Aztreonam
Clinical use |
Gram-negative rods––Klebsiella spp., Pseudomonas spp., Serratia spp. No activity against
gram-positives or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides. |
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Aztreonam
Toxicity |
Usually nontoxic; occasional GI upset.
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Synergistic with aminoglycosides. No cross-allergenicity with penicillins.
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Aztreonam
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Gram-negative rods––Klebsiella spp., Pseudomonas spp., Serratia spp. No activity against
gram-positives or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides. |
Aztreonam
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Imipenem/cilastatin, meropenem
Mechanism |
Imipenem is a broad-spectrum, β-lactamase-resistant
carbapenem. |
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Imipenem/cilastatin, meropenem
Clinical use |
Gram-positive cocci, gram-negative rods, and
anaerobes. Drug of choice for Enterobacter (esp UTI) |
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Imipenem/cilastatin, meropenem
Toxicity |
GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.
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Always administered with cilastatin
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Imipenem
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Imipenem Always administered with what and why
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Always administered with cilastatin (inhibitor of renal dihydropeptidase I) to ↓
inactivation in renal tubules. With imipenem, “the kill is LASTIN’ with ciLASTATIN.” |
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Drug of choice for Enterobacter.
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Imipenem/cilastatin, meropenem
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Vancomycin
Mechanism and resistance |
Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Resistance occurs with amino acid change of D-ala D-ala to
D-ala D-lac. |
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Vancomycin
Clinical use |
Used for serious, gram-positive multidrug-resistant organisms, including S. aureus and Clostridium difficile (pseudomembranous colitis).
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Vancomycin
Toxicity |
Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing––“red man syndrome”
(can largely prevent by pretreatment with antihistamines and slow infusion rate). Well tolerated in general––does NOT have many problems. |
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Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing
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“red man syndrome” Vancomycin
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Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Resistance occurs with amino acid change of D-ala D-ala to
D-ala D-lac. |
Vancomycin
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30S inhibitors:
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A = Aminoglycosides [bactericidal]
T = Tetracyclines [bacteriostatic] |
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50S inhibitors:
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C = Chloramphenicol, Clindamycin
E = Erythromycin [bacteriostatic] L = Lincomycin [bacteriostatic] L = Linezolid [bacteriostatic] |
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Aminoglycosides
names |
Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin.
“Mean” GNATS canNOT kill anaerobes. |
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Aminoglycosides
Mechanism and resistance |
Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Require O2 for
uptake; therefore ineffective against anaerobes. |
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Aminoglycosides
Clinical use |
Severe gram-negative rod infections. Synergistic with
β-lactam antibiotics. Neomycin for bowel surgery. |
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Aminoglycosides
Toxicity |
Nephrotoxicity (especially when used with cephalosporins ,Ototoxicity (especially when
used with loop diuretics). Teratogen. -“Mean” GNATS canNOT kill anaerobes. |
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Severe gram-negative rod infections. Synergistic with
β-lactam antibiotics. |
Aminoglycosides
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Bactericidal; inhibit formation of initiation complex
and cause misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes. |
Aminoglycosides
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Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin.
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Aminoglycosides
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Tetracyclines
names |
-CYCLINE
TetracCYCLINE, doxyCYCLINE, demecloCYCLINE, minoCYCLINE. |
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Tetracyclines
Mechanism |
bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
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Tetracyclines
Clinical use |
VACUUM THe BedRoom.
Vibrio cholerae, Acne, Chlamydia, Ureaplasma Urealyticum, Mycoplasma pneumoniae, Tularemia, H. pylori, Borrelia burgdorferi (Lyme disease), Rickettsia. |
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Tetracyclines
Toxicity |
GI distress, discoloration of teeth and inhibition of
bone growth in children, photosensitivity. |
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bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
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Tetracyclines
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Tetracyclines
contraindications |
-Doxycycline is fecally eliminated and can be used
in patients with renal failure. -Contraindicated in pregnancy. |
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Must NOT take with milk, antacids, or iron-containing
preparations because divalent cations inhibit its absorption in the gut. |
Tetracyclines
|
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GI distress, discoloration of teeth and inhibition of
bone growth in children, photosensitivity. |
Tetracyclines
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Macrolides
names |
Erythromycin, azithromycin, clarithromycin.
|
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Macrolides
Mechanism |
Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S
|
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Macrolides
Clinical use |
URIs, pneumonias, STDs––gram-positive cocci (streptococcal infections in patients
allergic to penicillin), Mycoplasma, Legionella, Chlamydia, Neisseria. |
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Macrolides
Toxicity |
GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis,
eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral anticoagulants. |
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eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral
anticoagulants. |
Macrolides
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Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S
|
Macrolides
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Clindamycin
Mechanism |
Blocks peptide bond formation at 50S ribosomal subunit.
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Clindamycin
Clinical use |
Treats anaerobes above the
diaphragm. (e.g., Bacteroides fragilis, Clostridium perfringens). |
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Clindamycin
Toxicity |
Pseudomembranous colitis (C. difficile overgrowth),
fever, diarrhea. |
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Sulfonamides
names |
Sulfamethoxazole (SMX), sulfisoxazole, triple sulfas, sulfadiazine.
|
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Sulfonamides
Mechanism |
PABA antimetabolites inhibit dihydropteroate synthase.
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Sulfonamides
Clinical use |
Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.
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Sulfonamides
Toxicity |
Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (TIN), kernicterus in infants, displace other drugs from albumin (e.g., warfarin).
|
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Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (TIN), kernicterus in infants, displace other drugs from albumin (e.g., warfarin).
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Sulfonamides
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Trimethoprim
Mechanism |
Inhibits bacterial dihydrofolate reductase.
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Trimethoprim
Clinical use |
Combination TMP-SMX used for recurrent UTIs, Shigella,Salmonella, Pneumocystis carinii pneumonia.
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Trimethoprim
Toxicity |
Trimethoprim = TMP:
“Treats Marrow Poorly.” Megaloblastic anemia, leukopenia, granulocytopenia. (May alleviate with supplemental folinic acid.) |
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Why TMP with SMX
|
synergy
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Trimethoprim
Toxicity Tx |
Megaloblastic anemia, leukopenia, granulocytopenia.
(May alleviate with supplemental folinic acid.) |
|
|
Fluoroquinolones
names |
-Floxacin (fluoroquinolones)
and nalidixic acid (a quinolone). |
|
|
Fluoroquinolones
Mechanism |
Inhibit DNA gyrase (topoisomerase II)
|
|
|
Fluoroquinolones
Clinical use |
Gram-negative rods of urinary and GI tracts (including Pseudomonas), Neisseria,
|
|
|
Fluoroquinolones
Toxicity |
GI upset, superinfections, skin rashes, headache,
dizziness. Contraindicated in pregnant women and in children damage to cartilage. Tendonitis and tendon rupture in adults; leg cramps and myalgias in kids. FluoroquinoLONES hurt attachments to your BONES. |
|
|
GI upset, superinfections, skin rashes, headache,
dizziness. Contraindicated in pregnant women and in children damage to cartilage. Tendonitis and tendon rupture in adults; leg cramps and myalgias in kids. |
Fluoroquinolones
|
|
|
Inhibit DNA gyrase (topoisomerase II)
|
Fluoroquinolones
|
|
|
Metronidazole
Mechanism |
Forms toxic metabolites in the bacterial cell.
|
|
|
Metronidazole
Clinical use |
GET GAP on the Metro!
Anaerobic infection below the diaphragm. Antiprotozoal. Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, anaerobes (Bacteroides, Clostridium). Used with bismuth and amoxicillin (or tetracycline) for “triple therapy” against H. Pylori. |
|
|
Metronidazole
Toxicity |
Disulfiram-like reaction with alcohol; headache, metallic taste.
|
|
|
Disulfiram-like reaction with alcohol; headache, metallic taste.
|
Metronidazole
|
|
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Polymyxins
names |
Polymyxin B, polymyxin E.
|
|
|
Polymyxins
Mechanism |
’MYXins MIX up membranes.
Bind to cell membranes of bacteria and disrupt their osmotic properties. Polymyxins are cationic, basic proteins that act like detergents. |
|
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Polymyxins
Clinical use |
Resistant gram-negative infections.
|
|
|
Polymyxins
Toxicity |
Neurotoxicity, acute renal tubular necrosis.
|
|
|
Anti-TB drugs
names and complications |
INH-SPiRE (inspire). 2C
-Isoniazid (INH), -Streptomycin, -Pyrazinamide, -Rifampin, -Ethambutol. -Cycloserine (2nd-line therapy). All are hepatotoxic. |
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Isoniazid aka
|
INH
|
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|
INH aka
|
Isoniazid
|
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|
Isoniazid (INH)
Mechanism |
↓ synthesis of mycolic acids.
|
|
|
Isoniazid (INH)
Clinical use |
Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB.
|
|
|
Isoniazid (INH)
Toxicity |
"INH Injures Neurons and
Hepatocytes" Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicity, SLE-like syndrome. Pyridoxine (vitamin B6) can prevent neurotoxicity. |
|
|
Isoniazid (INH)
half-life |
Different INH half-lives in fast
vs. slow acetylators. |
|
|
Rifampin
Mechanism |
Inhibits DNA-dependent RNA polymerase.
|
|
|
Rifampin
Clinical use |
Mycobacterium tuberculosis; delays resistance to
dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenzae type B. |
|
|
Rifampin
Toxicity |
Minor hepatotoxicity and drug interactions (↑ P-450).
orange body fluids |
|
|
Inhibits DNA-dependent RNA polymerase.
|
Rifampin
|
|
|
↓ synthesis of mycolic acids.
|
Isoniazid (INH)
|
|
|
Minor hepatotoxicity and drug interactions (↑ P-450).
orange body fluids |
Rifampin
|
|
|
Rifampin mnemonic
|
Rifampin’s 4 R’s:
RNA polymerase inhibitor Revs up microsomal P-450 Red/orange body fluids Rapid resistance if used alone |
|
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Resistance mechanisms for various antibiotics
Penicillins/ cephalosporins |
β-lactamase cleavage of β-lactam ring
|
|
|
Resistance mechanisms for various antibiotics
β-lactamase cleavage of β-lactam ring |
Penicillins/
cephalosporins |
|
|
Resistance mechanisms for various antibiotics
Aminoglycosides |
Modification via acetylation, adenylation, or phosphorylation
|
|
|
Resistance mechanisms for various antibiotics
Modification via acetylation, adenylation, or phosphorylation |
Aminoglycosides
and Chloramphenicol (acetylation only) |
|
|
Resistance mechanisms for various antibiotics
Vancomycin |
Terminal D-ala of cell wall component replaced with D-lac; ↓ affinity.
|
|
|
Resistance mechanisms for various antibiotics
Terminal D-ala of cell wall component replaced with D-lac; ↓ affinity. |
Vancomycin
|
|
|
Resistance mechanisms for various antibiotics
Chloramphenicol |
Modification via acetylation
|
|
|
Resistance mechanisms for various antibiotics
Macrolides |
Methylation of rRNA near erythromycin’s ribosome-binding site
|
|
|
Resistance mechanisms for various antibiotics
Methylation of rRNA near erythromycin’s ribosome-binding site |
Macrolides
|
|
|
Resistance mechanisms for various antibiotics
↓ uptake or ↑ transport out of cell |
Tetracycline
|
|
|
Resistance mechanisms for various antibiotics
Tetracycline |
↓ uptake or ↑ transport out of cell
|
|
|
Resistance mechanisms for various antibiotics
Sulfonamides |
Altered enzyme (bacterial dihydropteroate synthetase), ↓ uptake, or ↑ PABA synthesis
|
|
|
Resistance mechanisms for various antibiotics
Altered enzyme (bacterial dihydropteroate synthetase), ↓ uptake, or ↑ PABA synthesis |
Sulfonamides
|
|
|
Nonsurgical antimicrobial prophylaxis
Meningococcal infection |
Rifampin (drug of choice), minocycline.
|
|
|
Nonsurgical antimicrobial prophylaxis
Rifampin (drug of choice), minocycline. |
Meningococcal infection
|
|
|
Nonsurgical antimicrobial prophylaxis
Gonorrhea |
Ceftriaxone.
|
|
|
Nonsurgical antimicrobial prophylaxis
Ceftriaxone. |
Gonorrhea
|
|
|
Nonsurgical antimicrobial prophylaxis
penicillin. |
Syphilis (Benzathine penicillin G)
Endocarditis with surgical or dental procedures (penicillin) |
|
|
Nonsurgical antimicrobial prophylaxis
Syphilis |
Benzathine penicillin G.
|
|
|
Nonsurgical antimicrobial prophylaxis
TMP-SMX. |
-History of recurrent UTIs
Pneumocystis jiroveci pneumonia |
|
|
Nonsurgical antimicrobial prophylaxis
-History of recurrent UTIs |
TMP-SMX.
|
|
|
Nonsurgical antimicrobial prophylaxis
|
TMP-SMX (DOC) , aerosolized pentamidine.
|
|
|
Nonsurgical antimicrobial prophylaxis
Endocarditis with surgical or dental procedures |
Penicillins.
|
|
|
Amphotericin B
Mechanism |
Amphotericin “tears” holes in
the fungal membrane by forming pores. Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes and disrupt homeostasis. |
|
|
Amphotericin B
Clinical use |
Used for wide spectrum of systemic mycoses.
Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier. |
|
|
Amphotericin B
Toxicity |
Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis
(“amphoterrible”). Hydration reduces nephrotoxicity. |
|
|
Nystatin
mechanism |
Binds to ergosterol, disrupting fungal membranes
|
|
|
Nystatin
Clinical use |
Too toxic for systemic use.
“Swish and swallow” for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis. |
|
|
Binds to ergosterol, disrupting fungal membranes. Too toxic for systemic use.
|
Nystatin
|
|
|
-AZOLES
Mechanism |
Inhibit fungal steroid (ergosterol) synthesis. by blocking the final step from Lanosterol to ergosterol
|
|
|
-AZOLES
Clinical use and which ones |
Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal
infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, Coccidioides, Histoplasma, Candida albicans; hypercortisolism. |
|
|
-AZOLES
Toxicity |
Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome
P-450), fever, chills. |
|
|
Inhibit fungal steroid (ergosterol) synthesis. by blocking the final step from Lanosterol to ergosterol
|
-AZOLES
|
|
|
Flucytosine
Mechanism |
Inhibits DNA synthesis by conversion to fluorouracil, which competes with uracil.
|
|
|
Flucytosine
Clinical use |
Used in systemic fungal infections (e.g., Candida, Cryptococcus).
|
|
|
Flucytosine
Toxicity |
Nausea, vomiting, diarrhea, bone marrow suppression.
|
|
|
Terbinafine
Mechanism |
Inhibits the fungal enzyme squalene epoxidase. by blocking the initial step from squaline to Lanosterol (in ergesterol synthesis)
|
|
|
Terbinafine
Clinical use |
Used to treat dermatophytoses (especially onychomycosis).
|
|
|
Inhibits the fungal enzyme squalene epoxidase. by blocking the initial step from squaline to Lanosterol (in ergesterol synthesis)
|
Terbinafine
|
|
|
Caspofungin
Mechanism |
Inhibits cell wall synthesis.
|
|
|
Caspofungin
Clinical use |
Invasive aspergillosis.
|
|
|
Caspofungin
Toxicity |
GI upset, flushing.
|
|
|
Tx for Invasive aspergillosis.
|
Caspofungin
|
|
|
Griseofulvin
Mechanism |
Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing
tissues (e.g., nails). |
|
|
Griseofulvin
Clinical use |
Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea,
ringworm). |
|
|
Griseofulvin
Toxicity |
Teratogenic, carcinogenic, confusion, headaches, ↑ P-450 and warfarin metabolism.
|
|
|
antifunfal that is Teratogenic, carcinogenic, confusion, headaches, ↑ P-450 and warfarin metabolism.
|
Griseofulvin
|
|
|
Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea,
ringworm). |
Griseofulvin
|
|
|
Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues
|
Griseofulvin
|
|
|
Amantadine
Mechanism |
“A man to dine” takes off his
coat. Blocks viral penetration/uncoating (M2 protein); may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals. |
|
|
Amantadine
Clinical use |
Prophylaxis and treatment for influenza A and rubellA; Parkinson’s disease.
|
|
|
Amantadine
Toxicity |
Ataxia, dizziness, slurred speech.
|
|
|
Amantadine
Mechanism of resistance |
Mutated M2 protein. In 2006, 90% of influenza A were resistant to amantadine.
|
|
|
Amantadine
mnemonic |
Amantadine blocks influenza
A and rubellA and causes problems with the cerebellA. |
|
|
Rimantidine
|
a derivative of Amantadine with fewer CNS side effects. Does not cross the BBB.
|
|
|
a derivative of Amantadine with fewer CNS side effects. Does not cross the BBB.
|
Rimantidine
|
|
|
Zanamivir, oseltamivir
Mechanism |
Inhibit influenza neuraminidase. So release of progeny virus is decreased.
|
|
|
Zanamivir, oseltamivir
Clinical use |
Both influenza A and B.
|
|
|
Blocks viral penetration and uncoating (M2 protein);
|
Amantadine
|
|
|
Inhibit influenza neuraminidase
|
Zanamivir, oseltamivir
|
|
|
Ribavirin
Mechanism |
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
|
|
|
Ribavirin
Clinical use |
RSV, chronic hepatitis C.
|
|
|
Ribavirin
Toxicity |
Hemolytic anemia. Severe teratogen.
|
|
|
drug for
RSV, chronic hepatitis C. |
Ribavirin
|
|
|
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
|
Ribavirin
|
|
|
Acyclovir
Mechanism |
Preferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine
kinase. |
|
|
Acyclovir
Clinical use |
HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in
immunocompromised patients. |
|
|
Acyclovir
Toxicity |
Delirium, tremor, nephrotoxicity.
|
|
|
Acyclovir
Mechanism of resistance |
Lack of thymidine kinase.
|
|
|
drug for
Prophylaxis and treatment for influenza A; Parkinson’s disease. |
Amantadine
|
|
|
drug for
Both influenza A and B. |
Zanamivir, oseltamivir
|
|
|
drug for
CMV, especially in immunocompromised patients. |
Ganciclovir
|
|
|
Ganciclovir
Mechanism |
Phosphorylation by viral kinase; preferentially inhibits CMV DNA polymerase.
|
|
|
Ganciclovir
Clinical use |
CMV, especially in immunocompromised patients.
|
|
|
Ganciclovir
Toxicity |
Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes
than acyclovir. |
|
|
Ganciclovir
Mechanism of resistance |
Mutated CMV DNA polymerase or lack of thymidine kinase.
|
|
|
Preferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.
|
Acyclovir
|
|
|
Phosphorylation by viral kinase; preferentially inhibits CMV DNA polymerase.
|
Ganciclovir
|
|
|
Foscarnet
Mechanism |
FOScarnet = pyroFOSphate
analog. Viral DNA polymerase inhibitor that binds to the pyrophosphate binding site of the enzyme. Does not require activation by viral kinase. |
|
|
Foscarnet
Clinical use |
CMV retinitis in immunocompromised patients
when ganciclovir fails; acyclovir-resistant HSV. |
|
|
Foscarnet
Toxicity |
Nephrotoxicity.
|
|
|
Foscarnet
Mechanism of resistance |
Mutated DNA polymerase.
|
|
|
drug for
CMV retinitis in immunocompromised patients when ganciclovir fails; |
Foscarnet
|
|
|
drug for
acyclovir-resistant HSV. |
Foscarnet
|
|
|
HIV therapy
Protease inhibitors names |
SaquiNAVIR, ritoNAVIR, indiNAVIR, nelfiNAVIR, ampreNAVIR.
NAVIR (navir) tease a pro— pro-tease inhibitors. |
|
|
HIV therapy
Protease inhibitors Mechanism |
Inhibit assembly of new virus by blocking protease
in progeny virions. |
|
|
HIV therapy
Protease inhibitors Toxicity |
GI intolerance (nausea, diarrhea), hyperglycemia,
lipodystrophy, thrombocytopenia (indinavir). |
|
|
HIV therapy
Reverse transcriptase inhibitors Nucleosides names |
DINE , SINE, and BINE
Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC), stavudine (d4T), lamivudine (3TC), |
|
|
Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC),
stavudine (d4T), lamivudine (3TC), |
HIV therapy
Reverse transcriptase inhibitors Nucleosides |
|
|
SaquiNAVIR, ritoNAVIR, indiNAVIR, nelfiNAVIR, ampreNAVIR.
|
HIV therapy
Protease inhibitors NAVIR (navir) tease a pro— pro-tease inhibitors. |
|
|
HIV therapy
Reverse transcriptase inhibitors Non-nucleosides names |
Nevirapine, efavirenz, delavirdine.
Never Ever Deliver nucleosides. |
|
|
Nevirapine, efavirenz, delavirdine.
|
HIV therapy
Reverse transcriptase inhibitors Non-nucleosides Never Ever Deliver nucleosides. |
|
|
HIV therapy
Reverse transcriptase inhibitors Mechanism |
Preferentially inhibit reverse transcriptase of HIV;
prevent incorporation of viral genome into host DNA. |
|
|
HIV therapy
Reverse transcriptase inhibitors Toxicity |
Bone marrow suppression (neutropenia, anemia),
peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT). |
|
|
HIV therapy
Reverse transcriptase inhibitors Clinical use |
Highly active antiretroviral therapy (HAART) generally entails combination therapy with protease inhibitors and reverse transcriptase.
AZT is used during pregnancy to reduce risk of fetal transmission. |
|
|
HAART
when initiated |
protease inhibitors and reverse transcriptase
inhibitors. Initiated when patients have low CD4 counts (< 500 cells/mm3) or high viral load. |
|
|
HIV therapy
what is used during pregnancy to reduce risk of fetal transmission. |
AZT
|
|
|
Interferons
Mechanism |
Glycoproteins from human leukocytes that block various stages of viral RNA and DNA
synthesis. Induce ribonuclease that degrades viral mRNA. |
|
|
Interferons
Clinical use |
IFN-α––chronic hepatitis B and C, Kaposi’s sarcoma.
IFN-β––MS. IFN-γ––NADPH oxidase deficiency. |
|
|
Interferons
Toxicity |
Neutropenia.
|
|
|
Antibiotics to avoid in pregnancy
just names |
SAFE Moms Take Really Good Care.
Sulfonamides, Aminoglycosides, Fluoroquinolones, Erythromycin, Metronidazole, Tetracyclines, Ribavirin, Griseofulvin, Chloramphenicol |
|
|
Antibiotics to avoid in pregnancy problem/cause
Sulfonamides |
kernicterus
|
|
|
Antibiotics to avoid in pregnancy problem/cause
kernicterus |
Sulfonamides
|
|
|
Antibiotics to avoid in pregnancy problem/cause
Aminoglycosides |
ototoxicity
|
|
|
Antibiotics to avoid in pregnancy problem/cause
ototoxicity |
Aminoglycosides
|
|
|
Antibiotics to avoid in pregnancy problem/cause
Fluoroquinolones |
cartilage damage.
|
|
|
Antibiotics to avoid in pregnancy problem/cause
cartilage damage. |
Fluoroquinolones
|
|
|
Antibiotics to avoid in pregnancy problem/cause
Erythromycin |
acute cholestatic hepatitis in mom
|
|
|
Antibiotics to avoid in pregnancy problem/cause
acute cholestatic hepatitis in mom |
Erythromycin
|
|
|
Antibiotics to avoid in pregnancy problem/cause
Metronidazole |
mutagenesis.
|
|
|
Antibiotics to avoid in pregnancy problem/cause
mutagenesis. |
Metronidazole
|
|
|
Antibiotics to avoid in pregnancy problem/cause
teratogenic. |
Ribavirin
Griseofulvin |
|
|
Antibiotics to avoid in pregnancy problem/cause
Tetracyclines |
discolored teeth, inhibition of bone growth.
|
|
|
Antibiotics to avoid in pregnancy problem/cause
discolored teeth, inhibition of bone growth. |
Tetracyclines
|
|
|
Antibiotics to avoid in pregnancy problem/cause
Ribavirin |
teratogenic.
|
|
|
Antibiotics to avoid in pregnancy problem/cause
Griseofulvin |
teratogenic.
|
|
|
Antibiotics to avoid in pregnancy problem/cause
“gray baby.” |
Chloramphenicol
|
|
|
Antibiotics to avoid in pregnancy problem/cause
Chloramphenicol |
“gray baby.”
|
|
|
uses of Antiparasitic drugs
Ivermectin |
Onchocerciasis (rIVER blindness treated with IVERmectin).
|
|
|
uses of Antiparasitic drugs
Praziquantel |
Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis)
cysticercosis (tania solium) Diphilobotorum latum |
|
|
uses of Antiparasitic drugs
Primaquine |
Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P. ovale).
|
|
|
uses of Antiparasitic drugs
Nifurtimox |
Chagas’ disease, American trypanosomiasis (Trypanosoma cruzi ).
|
|
|
uses of Antiparasitic drugs
Suramin |
African trypanosomiasis (sleeping sickness).
|
