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Pharmacology > Treatment Of Bacterial Infections (87,93) > Flashcards

Treatment Of Bacterial Infections (87,93) Flashcards

1
Q

Prokaryotes vs eukaryotes

A

Pro- cell with NO nuclei (bacteria)

Eu- cells with nuclei (fungi, Protozoa, helminths)

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2
Q

Prokaryotic cells

A

1-5 mm
-survive wide range of environments (extreme temp, anaerobic/aerobic)
-pathogenic or nonpathogenic

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3
Q

Infections

A

Invasion and multiplication of organisms
-foreign bacteria/normal flora

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4
Q

Colonization of body by normal flora

A

Not usually harmful, can help in controlling growth of potentially pathogenic organisms

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5
Q

Gram positive/gram negative

A

Wether or not wall stains with gram stain
-implications for action of antibacterial

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6
Q

Staphlococci vs streptococci

A

Staph- cocci in clumps
Strep- cocci in chains

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7
Q

Bacterial cell wall located

A

Outside plasma membrane
-non stretchable string bag encoding bacterium
-internal osmotic pressure for suppprt

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8
Q

Gram positive cell wall

A

Thick peptidoglycan layer
-gram strain (crustal violet) is trapped in peptidoglycan layer
-stains cells purple

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9
Q

Peptidoglycan

A

Polymer of amino acids and sugars, not found in eukaryotes

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10
Q

Gram negative cell wall

A

Contains a thin peptidoglycan layer
-outer membrane
-less gram stain is trapped
-LPS barrier to some antibacterial

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11
Q

Antibacterial drugs

A

Medications used to react bacterial infections
-exploit the differences between human cells and bacteria

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12
Q

Ideally one wants to identity what before initiating antibacterial therapy

A

Causative organism before beginning antibacterial therapy
-since there may be some antibacterial susceptibilities

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13
Q

Antibacterial can be effective against

A

-gram positive bacteria (staphylococcus aureus)
-gram negative bacteria (e.coli)

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14
Q

Narrow spectrum antibacterial

A

Are selective against one class of bacteria

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15
Q

Broad spectrum antibacterial

A

Are affective against both classes of bacteria (negative and positive)

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16
Q

Benefits of narrow spectrum antibacterial

A

Doesn’t harm your own bacteria, lowers risk of resistance

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17
Q

Bactericidal

A

Drugs are directly lethal to bacteria at clinically achievable concentrations

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18
Q

Bacteriostatic

A

Drugs can slow bacterial growth but do not cause cell death

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19
Q

Immune system is important for

A

Bacteriostatic antibiotics
-as it helps control and eleminate the infections

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20
Q

What is a superinfection?

A

New microbes take over when antibacterials kill normal flora

-this is normally a consequence of using antibiotics
-eg respiratory, genitourinary and GI tract

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21
Q

A microbe resistant to drug action equals being

A

Difficult to treat

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22
Q

What is an opportunistic infection?

A

Infections that would not normally harm an immunocompetent person

-but has occurred in an immunocompromised patient and will occur as fatal

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23
Q

opportunistic infections can be..

A

Viruses, fungi, bacteria or Protozoa

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24
Q

Globally __ ______ people die from antibacterial resistance

A

5 million

-but we still need antibiotics

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25
Q

Selection of mutant bacteria is enhanced by (things that increase drug resistant bacteria)

A

-improper choice/use of antibacterials
-dose of antibacterial is too low/continued too long
-prophylactic use of antibacterials

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26
Q

Examples of prophylactic use of antibacterials

A

In mass animal feed in order to improve meat (it barely does)

-an ongoing feed of antibiotics, where when needed it is okay to give animals drugs but when they don’t need them it creates drug resistance

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27
Q

Host factors for antibacterial therapy

A

Age, allergies, organ health, pregnancy, site of infection, general health

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28
Q

Allergic reactions are a

A

Immune response

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29
Q

Are GI upset’s a allergic reaction?

A

No a GI upset is not an allergic reaction

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30
Q

Four common mechanisms of action

A

-disruption of critical metabolic reactions
-interference with cell wall synthesis
-interference with protein synthesis
-interference with DNA replication

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31
Q

Cell wall synthesis

A

PVC
-penicillins
-vancomycin
-cephalosporins

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32
Q

Protein synthesis

A

ATM
-aminoglycosides
-tetracyclines
-macrolides

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33
Q

Transcription mechanisms

A

F
-fluroquinolones

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34
Q

Metabolic pathways

A

S/T
-sulfamethoxazole/trimethoprim

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35
Q

Sulfonamides

A

-broad spectrum
-sulfa drug

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36
Q

Sulfonamides prevent

A

Synthesis of folic acid

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37
Q

Sulfonamides combined with trimethoprim (importance/drug names/treat)

A

Extremely good at their job as they both target two aspects of the bacterial folic acid cycle = greater chance of success
-Bactrim or Septra
-uti and middle ear infections

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38
Q

Sulfonamides: contraindicated (when will they never be given/used) conditions

A

-known allergies (sulfa allergy)
-pregnant women
-not advised during breast feeding
-infants less than 2 months of age

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39
Q

Sulfonamides treat

A

Urinary tract infections and upper respiratory tract infections

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40
Q

Sulfa allergies and sulfonamides

A

Make taking sulfonamides very dangerous depending on extent of allergy
-there are several derivatives of sulfa like drugs that can also put the person at risk

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41
Q

What does sulfonamides do during pregnancy

A

-linked to birth defects (first trimester)

-close to end of pregnancy may increase fetal bilirubin (which may lead to brain damage)

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42
Q

Adverse effects of sulfonamides

A

-integumentary allergies
-blood (by bone marrow depression)
-nausea and vomiting

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43
Q

What are the adverse effects of sulfonamides in integumentary allergies

A

-stevens johnson syndrome (toxic epidermal necrosis) **most severe
-photosensitivity

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44
Q

What are the adverse effects of sulfonamides in blood by bone marrow depression

A

-agranulocytosis (severely low neutrophil levels)

-thrombocytopenia (bone marrow doesn’t make enough platelets)

-aplastic anemia (bone marrow is damaged and you can’t make enough blood cells)

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45
Q

Sulfamethoxazole

A

Sulfonamide antibiotic
-bacteriostatic, disrupts folic acid
-for urinary tract and middle ear infections

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46
Q

B-Lactam Antibacterials were discovered by

A

Sir Alexander Fleming
-1928

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47
Q

Staph aureus was destroyed by
-but now..

A

The mold penicilium form fungus
-but now 95% of S. aureus now resistant to penicillin

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48
Q

B-Lactam Antibacterials function

A

Inhibit cell wall enzyme responsible for peptidoglycan synthesis
-causing lysis and cell death
-bactericidal

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49
Q

Four groups of B-Lactam Antibacterials

A

-penicillins
-cephalosporins
-monobactams
-carbapenems

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50
Q

B-Lactam Antibacterials are characterized by

A

The common B-Lactam ring in their structures

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51
Q

Which of the B-Lactam Antibacterials are commonly used in Canada?

A

-penicillins
-cephalosporins
-carbapenems

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52
Q

What are the two major types of penicillins? Explain them

A

Naturally occuring penicillin —> hasn’t been changed in any way, these are sensitive to b-lactamase

Sem synthetic penicillin —> has been modified in the lab to be useful but different, more broad spectrum

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53
Q

Narrow spectrum penicillins

A

Naturally occuring penicillin that is extremely narrow
-cannot target gram negative
-Penicillin G and penicillin V

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54
Q

Aminopenicillins (broader spectrum) +two examples

A

Semi synthetic penicillins, with a much greater range
-Amoxicillin (more acid stable so can be taken PO)
-ampicillin (IV/IM)

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55
Q

Antipseudomonal penicillins (extended spectrum)

A

Really broad spectrum
-even against pseudomonas aeruginoas (opportunistic infections)

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56
Q

Pseudomonas aeruginoas

A

Opportunist infection
-respiratory, ears, eyes, CNS, UTI, endocarditis

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57
Q

Penicillins mechanism of action

A

Enters the bacteria, where it binds to penicillin binding proteins disrupting normal cell wall synthesis
-bacteria cell ruptures

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58
Q

Penicillins do not

A

Kill other cells in the body

59
Q

Penicillin targets…

A

Active against most gram positive bacteria, as well as some gram negative (depends on the penicillin)
-bactericidal

60
Q

Penicillin is bactericidal (true or false)

A

TRUE!!!

61
Q

Drug resistance to penicillins

A

Some bacteria produce enzymes capable of destroying penicillins called B-lactamases which destroy the B-lactam ring

62
Q

B-lactamase inhibitors

A

Given in the tablet of penicillins in order to allow them to work
-clavulanic acid, used with amoxicillin

63
Q

Which of the B-lactam antibacterials are resistant to B-lactamase

A

Monobactam and carbapenem

64
Q

Broad and extended penicillins types kill..

A

Gram negative

65
Q

Administration of penicillin

A

PO, IM, IV
-depends on the type of penicillin

66
Q

Penicillins adverse effects

A

Generally well tolderated
-GI problems, disturbing normal gut flora
-allergic reactions: subcutaneous edema or rashes
-could be fatal

67
Q

What are Cephalosporins?

A

Semisynthetic derivatives from a cephalosporins fungus

68
Q

Cephalosporins are structurally and pharmacologically related to

A

Penicillins

69
Q

Do cephalosporins have bactericidal action?

A

Yes they do

70
Q

As the five generations progress of cephalosporins what increases

A

-better gram negative coverage
-better b lactamase resistance

71
Q

Cephalosporins are divided based off

A

Into groups based according to their introduction to clinical use

Such as:
-inc permeability to gram negative cell
-increased stability against B-lactamase

72
Q

Cephalosporins first generation: use for

A

Surgical prophylaxis, URIs, otitis media

73
Q

Cephalosporins second generation: coverage

A

-good for gram positive
-better gram positive than first gen

74
Q

Cephalosporins third generation

A

Broader spectrum
-better again gram negative than previous

75
Q

Cephalosporins fourth generation: coverage

A

Broader spectrum of antibacterial activity than third Gen
-especially against gram positive bacteria

76
Q

Cephalosporins fifth generation: drug

A

Ceftaroline
-MRSA infections

77
Q

Adverse effects of cephalosporins

A

Similar to penicillins
-history of allergies (cross hypersensitivity, but does not exclude its use)

78
Q

Carbapenems coverage

A

Broad spectrum antibacterial action
-gram negative, positive and anaerobic

79
Q

Carbapenems are effective for…. And not for..

A

Effective for mixed infections, but not MRSA

80
Q

How are carbapenems given?

A

Parentally given, not PO

81
Q

Carbapenems are used for

A

reserved* for severe complicated body vanity and connective tissue infections

-last resort
-something that cannot be treated by a narrower drug

82
Q

Imipenem-cilastatin

A

Carbapenems
-combination drug
-the cilastatin inhibits breakdown of imepenem in the kidney

83
Q

Carbapenems drug resistance

A

-carbapenem resistant enterobasteriaceae (CRE)
-KPC (klebsiella pneumonias carbapenemase) and NDM (new delhi metallic-beta-lactamase)
-most antibacterial drugs
-opportunistic infections

84
Q

Three Macrolides

A

-erythromycin
-azithromycin
-clarithromycin

85
Q

Macrolides mechanism of action

A

Inhibits protein synthesis by binding to ribosomes

86
Q

Macrolides coverage

A

Broad spectrum
-most gram positive, some gram negative
-bacteriostatic

87
Q

Are macrolides bacteriostatic or bactericidal?

A

BOTH!!!!
-depends on concentration and bacterial suspectibilty

88
Q

Macrolides are given to patients who are..

A

-allergic to b-lactamase antibacterials
-penicillin resistant infections (as they look nothing like penicillin)

Good alternative!!

89
Q

Macrolides: azithromycin and clarithromycin example

A

Used in combination for people with HIV/AIDS for opportunistic infections

90
Q

Macrolides are used primarily for

A

Infections of respiratory, skin, soft tissue

91
Q

Adverse effects of macrolides

A

-nausea, vomiting, diarrhea
-provoke cardiac dysthymia (long Q-T)

92
Q

Macrolides: azithromycin and clarithryomycin

A

-fewer drug drug interactions
-little to no inhibition of CYP enzymes

Azithromycin: does not affect liver enzymes, which is very important if people are taking multiple drugs to take the strain off of liver enzymes (advantage)

93
Q

Tetracyclines coverage

A

Broad spectrum
-gram negative and positive
-bacteriostatic

94
Q

Tetracyclines mechanism of action

A

Inhibit protein synthesis

95
Q

Tetracyclines are

A

Bacteriostatic

96
Q

Major tetracycline

A

Tetracycline

97
Q

Tetracyclines bind to

A

Metal ions
-calcium, magnesium, iron, aluminum
-things like milk products, supplements, laxatives, antacids
-will form insoluble complexes

98
Q

You cannot take tetracyclines with..

A

Dairy products, antacids and iron salts
-reduced absorption of tetracyclines

99
Q

Never take tetracyclines

A

-if pregnant/breast feeding
-children less than 8 years old

100
Q

Averse effects of tetracyclines

A

-strong affinity for calcium
-GI disturbance
-alteration in intestinal fora
-photosensivity
-antagonist to bactericidal antibacterials

101
Q

Averse effects of tetracyclines: strong affinity for calcium

A

-discolouration of permanent teeth and tooth enamel in fetuses and children
-may retard fetal skeletal development during pregnancy

102
Q

Averse effects of tetracyclines: Gi disturbances

A

-direct irritation
-gut flora disturbance

103
Q

Averse effects of tetracyclines: the alteration in intestinal flora may result in

A

Is a broad spectrum drug so it will affect many bacteria including the good ones found in the GI tract
-leave risk for opportunistic infections (CDIFF)

Superinfections

104
Q

Averse effects of tetracyclines: antagonistic to bactericidal antibacterials….

A

So must be timed for use usually at least an hour apart

105
Q

Aminoglycosides

A

Natural and semisynthetic
-produced from streptomyces

106
Q

Aminoglycosides were the first antibacterial effective against

A

Gram negative bacteria

107
Q

Aminoglycosides mechanism of action

A

Bactericidal
-preventing abnormal protein synthesis

108
Q

Aminoglycosides coverage

A

Mostly gram negative and some gram positive

109
Q

Aminoglycosides (5)

A

-gentamicin
-neomycin
-streptomycin
-to army in
-amikacin

110
Q

Aminoglycosides are active against

A

Gram negative bacteria

111
Q

Aminoglycosides are often used in combination with

A

Other antibacterials for synergistic effect

112
Q

How are Aminoglycosides administered

A

Given parenterally IV or IM
-as they are poorly absorbed

113
Q

Then why would aminoglycosides used orally?

A

They are given orally to decontaminate the GI tract before surgical procedures
-or if the infection is in GI lumen

114
Q

Unfortunately aminoglycosides have…

A

Serious toxic effects
-ototoxicity
-nephrotoxicity

115
Q

Ototoxicity of aminoglycosides

A

-auditory impairment (ringing, tinnitus, deafness)
-vestibular (balance problems, dizziness, vertigo)

116
Q

Ototoxicity is made worse if

A

Other ototoxic drugs are given
-loop diuretics

117
Q

Nephrotoxicity from aminoglycosides

A

Extreme in neonates and pre existing renal conditions
-must monitor plasma drug levels to prevent toxicities

118
Q

Is nephrotoxicity reversible?

A

Yes!!!!!!!!!!

119
Q

aminoglycosides has increased risk for nephrotoxicity if used with

A

-vancomycin
-cyclosporine
-amphotericin B

120
Q

Quinolones mechanism of action

A

Alters DNA of bacteria
-prevents proper super coiling
-does not affect human DNA

-bactericidal

121
Q

Ciprofloxacin

A

Very effective and most common quinolones used
-PO

122
Q

Quinolones coverage

A

Gram negative organisms and some gram positive organisms
-broad spectrum

123
Q

Quinolones are used for

A

-urinary tract infections
-anthrax
-lower resp infections
-bone, joint infections
-diarrhea
-skin infections
-STD

124
Q

Adverse effects of quinolones

A

-nausea, vomiting, diarrhea
-skin rashes
-CNS (headache, dizziness)

125
Q

Interactions of quinolones

A

drug to drug —> very good at CYP inhibition
-if other drugs are metabolized by CYP then there is a problem…

126
Q

Quinolones oral absorption is reduced by

A

-antacids
-iron, zinc, calcium containing preparations (so drugs need to be given 1-2 hours before)

127
Q

Vancomycin mechanisms of actions

A

Inhibits cell wall synthesis
-bactericidal
-a different protein target to B-lactams

128
Q

Vancomycin is administered by

A

IV
-given orally for pseudomembranous colitis/ C diff
-because it is such a large molecule!!!

129
Q

Vancomycin is the treatment of choice for

A

MRSA and other gram positive infections

130
Q

Adverse effects of vancomycin

A

-flushing syndrome (need to infuse over 1 hour)
-fever chills and phlebitis
-ototoxicity
-nephrotoxicity

131
Q

Flushing syndrome

A

Subjective sensation of warmth accompanied by visible skin erythema
-face mostly

132
Q

Antimircrobials covers what categories of drugs?

A

-antiboiodics
-antifungals
-antivirals

133
Q

What is the rising worry with last resort drugs?

A

That they too are becoming at risk for drug resistance

-bad because the whole idea of last resort is using these drug less so that they have less chances of becoming resistant

134
Q

How do bacteria resist drugs?

A

They mutant and are able to gain selective advantages
-such as a pump that gets rid of the antibiotics, or enzymes that break down antibiotics and render them useless

-essentially survival of the fittest

135
Q

What is a common adverse effect of antibacterials?

A

GI upset
-almost every antibacterial has risk of GI upset of some sort

136
Q

What was the first drug group to be discovered

A

Sulfonamides

137
Q

How were B-lactam antibiotics discovered

A

Alexander Fleming left the petriy disc out by a window and both fungus and bacteria were colonized, but around the fungus there was a circle of space with no bacteria formed which lead to him hypothesizing the poitential for fungus to create something that kills bacteria -> penicillin

138
Q

Which two B-lactam antibacterials are very similar?

A

Penicillins and cephalosporins

139
Q

How do sulfonamides destroy folic acid?

A

They are very similar in structure to PABA (precursor to folic acid) and are able to bind with the enzyme that PABA normally does which reduces the amount of folic acid made = less DNA/RNA in a bacteria

140
Q

Penicillin G is given…

A

IV or IM

141
Q

Penicillin V is given…

A

PO

142
Q

Patients with a history of allergy to penicillin may indicate an allergy towards what types of drug?

A

Cephalosporins
-since they are so similar

143
Q

How are the toxic effects of aminoglycosides monitored

A

Since these are given IV after a dump of drugs is administered patients are given a blood test to monitor the level of toxins in blood and give a break to hold off more severe symptoms as a result of the drug

144
Q

Is ototoxicity reversible?

A

No because it is killing the hair cells in the ear which do not grow back
-this is why when you age your hearing can get worse

Pharmacology (37 decks)

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