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Pharmacology > Module 16 > Flashcards

Module 16 Flashcards

1
Q

Bacteria

A

Single celled organisms shaped as rods, spheres, spirals

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2
Q

Bacteria + the body

A
  • most rendered harmless by immune system
  • some are beneficial
  • some are pathogenic + cause disease
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3
Q

Bacterial Pathogenicity - virulence factors

A
  • Fimbriae and pilli
  • flagella
  • secretion of toxins and enzymes
  • invasion
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4
Q

Fimbriae and Pilli - what

A

Hair-like structures that project from the surface of bacteria cells

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5
Q

Fimbriae and Pilli - function

A

allow bacteria to attach to certain sites in our body so they are not washed away

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6
Q

Fimbriae and Pilli - example of bacterium

A

E. Coli (use fimbriae that attach to urogenital tract –> bladder infection)

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7
Q

Flagella - what, function

A
  • projection of bacteria

- allows bacteria to “swim” through aqueous environment –> get to sites where they may survive

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8
Q

Toxin symptoms (bacteria) (7)

A
  • nausea, vomiting, diarrhea, cramps, pain, fever, paralysis
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9
Q

Toxin function (bacteria)

A
  • (some cases) bacterial toxins produced outside of our body can mediate toxic reactions if the gain entry to our body
  • ex poisoning
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10
Q

Enzymes (bacteria)

A
  • can degrade tissue or breakdown antibodies (our defense against infection)
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11
Q

Invasion (what, Example x2)

A

some bacteria can invade our cells

  • EX salmonella invade cells of intestine –>diarrhea
  • EX2 tuburculosis causing bacteria enter body in the lungs and can “hide” inside cells making it impossible for immune system to act on the
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12
Q

Gram staining of Bacteria

A
  • classify bacteria as gram positive or gram negative

- gram stain –> tells us about cell wall structure of bacteria (amount of peptidoglycan) which impacts antibiotic use

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13
Q

Characteristics of Gram positive stain (6)

A
  • thick peptidoglycan wall (Cell wall)
  • stains purple
  • Techoic acids (rigid cell wall)
  • no LPS
  • no outer membrane
  • Do not have porins
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14
Q

Characteristics of Gram negative bacteria (6)

A
  • thin peptidoglycan layer (cell wall)
  • no techoic acids
  • LPS (lipopolysaccharides) are component of outer membrane
  • outer membrane (protect bacteria from bile salt + detergents)
  • stain pink during staining
  • porins (allow sugar, ions, amino acids to enter)
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15
Q

Signs of Infection

A
  • fever, malaise, local redness, swelling
  • increased respiratory rate, tachycardia
  • other specific symptoms (ex UTI = frequency of urination)
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16
Q

Selective toxicity (bacteria)

A

Therapy that destroys bacteria without harming the host

- target differences between cellular chemistry of bacteria and humans

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17
Q

Antibiotic therapy produces selective toxicity by (3)

A
  • disrupting bacterial cell wall (human cells do not have cell wall)
  • targeting enzymes unique to bacteria
  • disrupting bacterial protein synthesis (bacterial and human ribosomes are different)
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18
Q

4 questions for selection of an antibiotic

A

1) has the infectious bacteria been identified
2) bacterial sensitivity to the antibiotic?
3) can antibiotic access site of infection?
4) is the patient able to battle the infection?

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19
Q

Identification of the Bacteria (2)

A
  • ideally done before selection of treatment
  • gram stain (rapid, provides info on structural features of bacteria)
  • culturing = best basis for selection of the therapy
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20
Q

Identification of Bacteria - barriers (2)

A
  • cant take culture from child ear infection

- lower respiratory infections may have several species of bacteria)

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21
Q

Bacterial Sensitivity to Antibiotic - 2 categories

A
  • bacteriostatic

- bactericidal

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22
Q

Bacteriostatic

A
  • stops growth and replication of bacteria (stops spread of infection)
  • body’s immune system can then attack and remove bacteria
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23
Q

Bactericidal

A

drugs kill the bacteria

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24
Q

MIC

A

MIC = minimum inhibitory concentration

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25
Q

MBC

A

minimum bactericidal concentration

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26
Q

Penetration to the site of action - which infections require careful selection of antibiotics?

A
  • meningitis
  • urinary tract infections
  • osteomyelitis
  • abscesses
  • otitis Media
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27
Q

Meningitis (what)

A
  • infection of the meninges (membranes covering brain and spinal cord)
  • bacterial meningitis (rare, more life threataning)
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28
Q

Meningitis - treatment

A
  • antibiotic that penetrates the meninges
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29
Q

Urinary Tract Infections (UTIs) = what?

A
  • when bacteria enteres any part of urinary system

- most often = infection of bladder (cathaterization)

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30
Q

UTI treatment

A

antibiotic that enters urinary system

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31
Q

Osteomyelitis (what)

A
  • infection of the bone
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32
Q

Osteomyelitis - treatment

A
  • very few antibiotics enter bone = limited treatment

- usually treat with antibiotics for 4-6 weeks

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33
Q

Abscesses (what)

A
  • pus or other infected material collect under skin
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34
Q

Abscesses - treatment

A
  • difficult to treat with antibiotics (poorly perfused with blood)
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35
Q

Otitis Media (what)

A
  • infection of the middle ear (ear infection)

- much more common in children

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36
Q

Otis Media - treatment

A
  • many antibiotics do not penetrate inner ear = not effective to treat otitis media
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37
Q

Ability of the patient to battle infection - selection of antibiotic

A
  • immunological state
    • bactericidal antibiotics KILL bacteria –> can be used in
      immunocompromised patients
      - bacteriostatic antibiotics require actions of immune function = less
      used in immunocomprimised patients
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38
Q

Complications of antibiotic therapy (6)

A
  • resistance
  • allergy
  • serum sickness
  • superinfection
  • destruction of normal bacterial flora
  • bone marrow toxicity
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39
Q

Antibiotic resistance

A
  • a bacteria that did respond to an antibiotic and has lost sensitivity over time
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40
Q

Antibiotic resistance (3 major mechanisms)

A
  • Reduction of the drug at the site of target
  • increased drug inactivation
  • alteration of the bacterial target
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41
Q

Antibiotic resistance - reduction of the drug at the site of the target

A
  • bacteria decreases uptake of antibiotics
  • bacteria increases expression of efflux pumps (extrude antibiotics)
  • COMBo - drug that is less able to access its bacterial target
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42
Q

Antibiotic resistance - increased drug inaction (+ example)

A
  • bacteria that evolved to produce increased enzymes that inactivate antibiotics
  • EX enzyme beta lactamase will degrade antibiotics with beta lactam ring (penicillin, cephalosporins)
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43
Q

Alteration of bacterial target (Antibiotic resistance)

A
  • bacteria may evolve mutations in the target htat make antibiotic ineffective
  • EX a mutation in bacterial ribosomes renders some antibiotics ineffective
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44
Q

Preventing resistance (4)

A

1) prevent infection (vaccinate, get catheters out if possible)
2) diagnose and treat effectively (patients with cold / a virus want antibiotics despite that it will not be effective)
3) use antibiotics wisely (only when necessary)
4) prevent transmission (isolate pathogen and prevent its spread, wash hands)

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45
Q

Allergy - most common antibiotic

A

penicillin

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46
Q

Signs of allergy (antibiotics) (5)

A
  • urticaria (hives)
  • anxiety
  • swelling of hands, feet, throat
  • difficulty breathing
  • hypotension
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47
Q

time of onset (fatal allergy to antibiotic)

A

20 minutes of dosing

48
Q

What to do if patient is experiencing an allergic reaction?

A
  • stop antibiotic
  • monitor vitals
  • diphenhydramine (antihistamine)
  • epipen (epinephrine, vasoconstrictor)
49
Q

Serum sickness (time of onset)

A
  • similar to allergy but deveops 7-21 days after antibiotic exposure
50
Q

What is serum sickness

A
  • body’s immune system improperly identifies drug or drug protein complex as harmful
  • body then produces immune reaction (inflammation)
51
Q

Serum sickness symptoms (7)

A
  • fever
  • hives
  • rash
  • joint pain
  • itching
  • angioedema
  • enlarged lymph nodes
52
Q

Serum Sickness - treatment (4)

A
  • antihistamine (for itching)
  • analgesics (for pain)
  • corticosteroids (for inflammation)
  • stop antibiotic???
53
Q

Superinfection

A
  • type of resistance
  • when a new type of infection develops during the course of antibiotic therapy
  • broad spectrum antibiotics kill both pathogenic bacteria and normal flora
  • -> allowing new bacteria to flourish
  • superinfection caused by drug-resistant bacteria
54
Q

Superinfection - treatment

A

hard to treat (drug resistant bacteria has grown)

55
Q

Destruction of normal bacterial flora - 3 effects

A

1) impair intestinal bacterial synthesis of vitamin K. (danger = anticoagulant Warfarin requires vitamin K –> increased risk of bleeding)
2) impair Intestinal bacteria metabolize + first pass effect (danger = increased blood drug levels = toxicity
3) Enterohepatic recycling of drugs (danger = drug therapy, contraceptive failure with birth control pills)

56
Q

Bone marrow toxicity (what, signs, symptoms)

A
  • rare but serious complication
  • SIGNS = aplastic anemia, thrombocytopenia, agranulocytosis, leukopenia
  • symptoms = sore throat, bruising, fatigue
57
Q

Autolysins

A
  • bacterial enzymes that degrade peptigdoglycan cell wall
58
Q

Transpeptidases

A
  • enzymes that function to form cross bridges between peptidoglycan strands therefore making cell wall strong
59
Q

Penicillin Binding Proteins (PBPs)

A
  • transpeptidases

- autolysis

60
Q

Penicillins - mechanism of action

A
  • inhibid transpeptidases (disrupt synthesis of cell wall)
  • activate autolysins (promote cell wall destruction)
  • net result = cells take up excess water and die (lyse)
61
Q

Penicillin - target bacteria

A

more effective against gram positive bacteria (since they do not have outer membrane)

62
Q

Penecillin - class of antibiotic

A
  • bactericidal

- only effective against bacteria that are actively growing and dividing

63
Q

Penicillin resistance (3 types)

A
  • inability to reach target
  • inactivation
  • mutation in PBPs (low affinity for penicillins IE MRSA)
  • PREDOMINANT = beta lactamase inhibiting
    • treat with beta lactamase inhibitors
64
Q

Classes of penicillins

A
  • narrow spectrum penicillins
  • narrow spectrum penicillinase resistant penicillins
  • broad spectrum penicillins
  • extended spectrum penicilins
65
Q

Narrow Spectrum Penicillins - target bacteria

A
  • gram positive bacteria
66
Q

Narrow Spectrum Penicillins - route of administration

A
  • IV or IM (destroyed by gastric acid)
67
Q

Narrow Spectrum Penicillins - target types infections

A
  • pneumonia and meningitis
68
Q

Narrow Spectrum Penicillins - adverse effects

A

allerguy

69
Q

Narrow Spectrum Penicillinase Resistant Penicillins - what

A
  • altered side chain that makes them not susceptible to inactivation by beta lactamase enzymes
70
Q

Narrow Spectrum Penicillinase Resistant Penicillins - target bacteria

A
  • effective in treating penicillinase producing staphylococci
71
Q

Narrow Spectrum Penicillinase Resistant Penicillins - not effective (bacteria, and condition)

A
  • bacteria - non-penicillinase producing bacteria

- not effective in treating absecess or penetrating into bone

72
Q

Narrow Spectrum Penicillinase Resistant Penicillins - resistance?

A

some are (ex MRSA)

73
Q

Broad Spectrum Penicillins - target bacteria

A
  • gram positive and gram negative bacteria (bc it can penetrate outer wall)
74
Q

Broad Spectrum Penicillins - resitance

A

easily inactivated by beta lactamases

75
Q

Extended Spectrum Penicillins - target bacteria (2)

A
  • gram positive and gram negative bacteria +

- Pseudomonas aeruginosa (is resistant to all other penicillins)

76
Q

Extended Spectrum Penicillins - resistance

A

degradation by beta lactamase enzymes

77
Q

Cephalosporins - mechanism of action

A
  • same mechanism of action as penicillin

- inhibit transpeptidases, activate autolysins

78
Q

Cephalosporins - classification

A

bactericidal, 4 generations

1st generation
2nd generation
3rd generation
4th generation

79
Q

Cephalosporins - difference between generations (3)

A

moving from 1 to 4, drugs will

  • increase in activity against gram negative bacteria
  • increase in resistance to destruction by beta lactamases
  • increase in ability to penetrate cerebrospinal fluid
80
Q

Cephalosporins - adverse effect

A
  • allergy

- cross sensitivity with allergy to penicillin is rare

81
Q

Vancomycin - when used

A
  • potentially toxic drug

- only treats serious infection (ex caused by MRSA)

82
Q

Vancomycin - target infections

A

MRSA infecting osteomyelitis, meningitis, pneumonia, septicemia

83
Q

Vancomysin - mechanism of action

A
  • inhibits cell wall synthesis by binding to precursors of cell wall synthesis to block the transglycosylation step in cross bridge synthesis
84
Q

Vancomysin - adverse events

A
  • ototoxicity

- Red person syndrome = flushing, rash, itching, hypotension

85
Q

Tetracylines - mechanism of action

A
  • bind to 30S ribosomal subuint of bacteria and prevent amino acid addition to peptide chain
86
Q

tetracyclines - class

A
  • Bacteriostatic
87
Q

tetracyclines - target infections

A
  • typhys fever, clamydia, cholera
88
Q

tetracyclines - adverse effects

A
  • GI upset
  • photosensitivity (avoid UV and wear sun block)
  • susceptibility to superinfection
89
Q

Macrolide Antibiotics - mechanism of action

A
  • block 50S ribosomal subunit of bacteria –> block addition of amino acids to peptide chain
90
Q

Macrolide Antibiotics - classification

A
  • bacteriostatic
91
Q

Macrolide Antibiotics - adverse effects (2)

A
  • GI upset’

- QT interval prolongation

92
Q

Tetracyclines - target bacteria

A

Broad spectrum (gram + and -)

93
Q

Macrolide Antibiotics - target bacteria

A
  • broad spectrum (gram + and - )
94
Q

Oxazolidinones - classification

A

bacteriostatic

95
Q

Oxazolidinones - target bacteria

A
  • narrow spectrum

- gram positive bacteria

96
Q

Oxazolidinones - mechanism of action

A
  • bind to specific region of 50S ribosomal subunit to inhibit protein synthesis
97
Q

Oxazolidinones - target bacteria species

A

treat MRSA and vancomycin resistant enterococci (VRE)

98
Q

Oxazolidinones - adverse events

A
  • reversible myelosupression
99
Q

Aminoglycosides - class

A
  • bacteriocidal
100
Q

Aminoglycosides - target bacteria

A

narrow spectrum (gram negative)

101
Q

Aminoglycosides - mechanism of action

A
  • protein synthesis inhibitors

- bind to 30S ribosomal subunit to prevent protein synthesis

102
Q

Aminoglycosides - mechanism of action

A
  • rapidly lethal to bacteria

- mechanism unknown

103
Q

Aminoglycosides - adverse effects (2)

A
  • irreversible ototoxicity

- reversible nephrotoxicity

104
Q

Sulfonamides and trimethoprim - mechanism of action

A
  • bacteria depend on synthesis of folic acid to incorporate into DNA
  • Sulfoamides and trimethoprim act on different stages to block synthesis of folic acid
105
Q

Sulfonamides and trimethoprim - class

A
  • bactericidal
106
Q

Sulfonamides and trimethoprim - target infection

A
  • UTIS
107
Q

Sulfonamides and trimethoprim - adverse effect

A
  • hypersensitivity reactions (fever, photosensitivity)

- small risk of severe hypersensitivity reaction called Stephens-JOHNSON SYNDROME

108
Q

Fluroquinoones - mechanism of action

A
  • inhibit DNA replication

- inhibit 2 enzymes, DNA gyrase and topoisomerase IV

109
Q

Fluroquinoones - class

A
  • bacgtericidal
110
Q

Fluroquinoones - target bacteria

A

broad spectrum (gram + and -

111
Q

Fluroquinoones - target infection

A
  • UTI, osteomyelitis, soft tissue infections
112
Q

Fluroquinoones - adverse effects

A

GI symptoms (nausea, vomitting, diarrhea)

113
Q

Isoniazid - target infection

A

tuburculosis

114
Q

Isoniazid - mechanism of action

A

inhibiting synthesis of mycolic acid, component unique to cell wall of tuburculosis causing bacteria

115
Q

Isoniazid - adverse effects (2)

A

peripheral neuropathy and hepatotoxicity

Pharmacology (6 decks)

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