Antibiotics Flashcards

1
Q

What do antimicrobials target

A

An infectious disease

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2
Q

Describe how beta lactam antibiotics work

A

Act by inhibiting penicilin binding protein (PBP). PBP causes crosslinking of the peptidoglycan in the cell wall, therefore inhibiting this action weakens the cell wall

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3
Q

What are examples of beta lactam antibiotics

A

Penicillins and cephalosporins

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4
Q

Which bacteria can’t be targeted by synthesis inhibitors

A

Bacteria that don’t have a cell wall e.g. mycoplasma and urea plasma

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5
Q

Describe gram +ve bacteria

A

Bacteria that only have one plasma membrane surrounded by a thick cell wall which is made up of peptidoglycan which acts as a sort of exo-skeleton

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6
Q

Describe gram -ve bacteria

A

Have two cell membranes: the inner membrane and the outer membrane. Between the inner and outer membrane is a much thinner cell wall made of peptidoglycan

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7
Q

What are the 5 targets for antimicrobials

A

Cell wall synthesis, protein synthesis, nucleic acid synthesis, folate metabolism, cell membrane

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8
Q

Describe cell wall synthesis inhibitors

A

They inhibit synthesis of the cell wall. Beta lactam antibiotics characterised by the beta lactam ring and all inhibit transpeptidase by binding to the PBP

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9
Q

Why is nucleic acid synthesis a target for antibitoics

A

Bacteria divide every 20 minutes which means that they have to unwind their DNA, unwound DNA is a target for antibiotics

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10
Q

How do fluroquinolones (target nucleic acid synthesis) work

A

Inhibits topooisomerase II resulting in the strand breaking

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11
Q

How do fluroquinolones enter the cell

A

Through pores working synergistically with beta-lactams

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12
Q

What are side effects of fluroquinolones

A

Cartilage erosion and tenditis (therefore avoided in pregnancy and children).

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13
Q

What are examples of antimicrobials that target nucleic acid synthesis and how do they work

A

Nitrofurantoin directly damages DNA, Methronidazole interferes with DNA and protein interaction (anaerobic bacteria and amoebes), Rifampicin is an alternative fluoroquinolone which can be used if people suffer ADRs with the other types of fluoroquinolones. Rifampicin inhibits mRNA synthesis.

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14
Q

Why are there so many different antibiotics

A

Bacteria don’t react the same way to antibiotics in a test tube as they do in the human body. ADRs in patients. Superinfection. Bacteria can be resistant to antibiotics

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15
Q

What are examples of cell wall synthesis inhibitors

A

Benzylpenicillin, penicillin V, amoxicillin, flucloxacillin, co-amoxiclav, cefotaxime, vancomycin

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16
Q

What are examples of protein synthesis inhibitors

A

Clarithromycin, gentamicin, oxytetracyline

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17
Q

What are examples of DNA/ RNA synthesis inhibitors

A

Ciprofoxacin, nitrofuratoin, metronidazole

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18
Q

What are examples of metabolism inhibitors

A

Trimethoprim

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19
Q

Describe how antibiotics possess a degree of selective toxicity

A

They can have effects on bacteria without major effects on host mammalian cells, related to differences in structure (e.g. cell wall) and metabolic function of the two types of cell

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20
Q

What are the two things you have to consider when selecting an antibiotic

A

Infectious agent e.g. what it it and is it susceptible to the antimicrobial/ antibiotic. Patient- site of infection, patient factors, safety of agent, costs (pharmacokinetics/ pharmacodynamics, from uptake, everything that happens in between and secretion

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21
Q

How is identification of an infectious agent done

A

Taking a sample fro the patient, culture grown then studied by microscopic visualisation for the detection of microbial antigens. DNA/ RNA detection, antibody detection or mass spectrometry.

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22
Q

How do you chose the right antimicrobial

A

Suseptibility, antibiotic resistance, minimal inhibitory concentration- minimal drug concentration where no bacterial growth is detected

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23
Q

What can be used to assess is a respiratory infection is caused by bacteria or a virus

A

The biomarker C-reactive protein (CRP)

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24
Q

What are the key aspects to consider in differential diagnosis/ empiric therapy

A

Clinical symptoms, site of infection, patient’s history, where acquired, known association in clinical setting, antibiotic resistance

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25
Q

What is the most important cause for toxicity in children

A

Impaired hepatic function, especially in neonates

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26
Q

What can tetracyclines interfere with in children

A

Bone and teeth staining

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27
Q

What can fluorosquinolones interfere with

A

Cartilage

28
Q

What is the most important factor in elderly

A

Reduced renal function- gentamycin contraindicated.

29
Q

Who are commonly affected by poor circulation and what does this mean

A

Common in diabetics, may need to use a topical application and change of dose and dosage

30
Q

What is the most common cause of antimicrobial allergies

A

Beta lactam antibiotics

31
Q

Why is compliance important regarding antibiotics

A

Important to finish the course, otherwise the infection may come back, it creates antibiotic resistance

32
Q

Why is a properly working immune system still very important even when taking antibiotics

A

Helps the antibiotics in clearing the infection, and also takes care of removing dead bacteria and initiate and accomplish an adaptive immune response

33
Q

What are several factors that can affect the immune system

A

Primary (neutropenia, C-deficiencies) and secondary deficiencies (T-cell depletion in HIV) and other conditions like alcoholism and malnutrition, age (optimal at 20y), immunosuppressive drugs after e.g. transplantation, or viral infection

34
Q

What do drugs that show bacteriostatic characteristics do

A

Stops growth. Host immune system will help eradicate microorganism: neutrophils, macrophages, complement system

35
Q

What do drugs that show bactericidal characteristics do

A

Kills

36
Q

What type of drug do you use in immunecompressed or immuneprivileged areas

A

Bactericidal

37
Q

What are the different routes of antimicrobial administration

A

Oral, topical, intravenous (quick), intramuscular, intrathecal (not preferred as results on fits)

38
Q

How long does it take antibiotics to reach maximal plasma levels after oral administration and what effect does food have

A

Takes 1-2 hours for antibiotics to reach maximal plasma levels after oral administration. Further delayed when ingested with food

39
Q

What route of administration should you use if someone is critically ill

A

Not oral, quicker administration needed therefore IV antibiotics required

40
Q

How can drugs be used to treat GI infections

A

Some drugs now come in a special coating meaning that the drug is only released after the stomach

41
Q

Describe chemical properties that effect distribution of the drug

A

Lipid-soluble, polar, protein binding

42
Q

How does being lipid soluble effect distribution of the drug

A

Well absorbed, general wide distribution (including cells, fat, CSF) as they can go through cell membranes

43
Q

How does being polar effect distribution of the drug

A

Extracellular, low volume of distrubution, pKa/ pH dependent. Usually just distributed in the plasma bu when pH changes occur uptake is sometimes possible

44
Q

How does protein binding effect distribution of the drug

A

Limits distribution, displaces other drugs. Best known carrier is albumin, this can cause displacement of other drugs or metabolic products

45
Q

What are difficult drug targets in the body

A

Blood brain barrier, prostate, eye, intracellular bacteria. Poor circulation in diabetes can also be an issue.

46
Q

What is one of the few antibiotics that can penetrate the blood brain barrier and enter the CSF under normal conditions

A

Chloramphenicol (only used in serious cases due to toxicity)

47
Q

Describe how penicillins and cephalosporins are effective in treating bacterial meningitis

A

Normally cannot penetrate, But during this type of infection the meninges are inflammed and the blood brain barrier is broken down (tight junctions aren’t so tight) so these antibiotics can enter the CSF and reach therapeutic levels

48
Q

What does the fact that some microorganisms can survive intracellularly mean

A

Can only use agents that penetrate the cell of the infected cells

49
Q

Why is the fact that some antibiotics are metabolised important

A

You have to consider hepatic function

50
Q

What occurs in liver disease

A

Drugs contraindicated- erythromycin and tetracyline that are concentrated or eliminated by the liver.

51
Q

What effect does competition for the same pathway of metabolism have on the liver

A

Shortage of enzymes, slower metabolism, longer half life

52
Q

What effect does inhibition of metabolism have on the liver

A

Caused by several antibiotics. Longer half-life e.g. warfarin- bleeding

53
Q

What effect does enhancement of metabolism have on the liver

A

Caused by drugs e.g. rifampicin. Shorter half life of other drugs e.g. warfarin, oral contraceptives

54
Q

What impact do drugs that cause gut disturbances have on the efficacy of the oral contraceptive

A

Less uptake

55
Q

Describe elimination of antibiotics

A

Nearly all antibiotics eliminated via the kidneys (renally impaired, course of treatments for UTIs)

56
Q

Why are combinations of antibiotics used

A

TB- only one antibiotic used= quick resistance. Serious infection- need less of each individual, less toxicity, more effiacy. Infection more than one microorganism- differences in sensitivites/ resistance. Unknown microorganism- use broad spectrum. Enhance effiacy

57
Q

Describe when synergism is most favourable

A

Cell wall synthesis inhibitors weaken cell wall and so facilitate the entry of aminoglycosides and fluoroquinolones that normally cannot penetrate the cell wall. Each on their own would not be able to kill bacteria, combination does

58
Q

Example of agent that has no antibiotic activity itself

A

Clavulanic acid, but mimics the structure of b-lactam antibiotics and so fools the b-lactamase: not synergism but a very useful combination: co-amoxyclav: combination of amoxicillin and clavulanic acid. The use of cell wall weakening antibiotics facilitates other antibiotics resulting in effective killing.

59
Q

How do inhibitors of folate synthesis work

A

Bacteria cannot take up folate from the environment so have to make it themselves. Folate is important building block for the synthesis of amino acids and nucleotides

60
Q

Describe how sulfonamides and trimethroprim work synergistically

A

Sulfonamides inhibit folate synthesis. Trimethoprim acts on the next metabolic step= act synergistically

61
Q

What is the advantage of using two drugs in the way sulfonamides and trimethroprim work

A

You get an enhanced effect but you used the drugs at a lower dose and thus have less chance of toxicity

62
Q

Describe a type A ADR

A

Toxicity- predictable, concentration dependent

63
Q

Describe a type B ADR

A

Allergy- unpredictable, dose dependent

64
Q

Describe a superinfection

A

Interference with commensal bacterial flora

65
Q

What do you do in the case of resistance

A

Stop treatment, change treatment, treat side effect