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3rd Year Drugs > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

Name anaerobic antibiotics

A

Metronidazole

Orala or IV or Gel

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2
Q

Indications of using metronidazole

A

1) C.Diff (gram +ve) - this is 1st line
2) Oral infections - due to gram -ve in the mouth
3) Aspiration pneumonia
4) Surgical and gynae infections due to gram -ve anaerbobes from the colon
5) Protozoal infections e.g. trichomonal vaginosis, dysentry, giardasis

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3
Q

Mechanisms of metronidazole

A

Passively diffuses into anaerobic bacterial cells
Reduced to generate a nitroso free radical
Binds to DNA
Reduces syntheses causing widespread damage - DNA degradation and cell death

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4
Q

Why doesnt metronidazole work on aerobic bacteria

A

As they dont reduce it to a nitrosos free radical

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5
Q

Is there resistance to metronidazole

A

Generally low resistance

But can be resistanct due to decreased uptake and decreased generation of nitroso free radicals

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6
Q

ADverse effects of metronidazole

A

1) GI Upset
2) Hypersensitivity
3) Neuro effects –> if at high doses or prolonged courses e.g. peripheral and optic neuropathy, seizures and encephalopathy

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7
Q

Warnings of metronidazole

A

Metabolised by hepatic CP450 ensymes –> reduce dose in hepatic impairment

Inhibits acetalderhyde dehydrogenase enzye –> this clears intermediate alcohol metabolite –> hence if you drink a disulfram-like reaction occurs –> flushing, headach, nausea and vomiting

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8
Q

What cant you do whilst taking metronidazole

A

Drink alcohol

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9
Q

Interactions of metronidazole

A

1) inhibitory effect on CP450 en`ymes
2) Excitory effect on CP450 inducers
3) Increased risk of lithium toxicity

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10
Q

What do we measure if we treat longer than 10 days on metronidazole

A

Measure FBC and LFTs

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11
Q

Indications of nitrofurantoin

A

1) Uncomplicated lower UTI - 1st line

Reaches therapeutic concentration in the urine through renal excretion

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12
Q

Action of nitrofurantoin

A

Metabolised in bacterial cells by nitrofuran reuctase

Its active metabolite damages bacterial DNA causing cell death

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13
Q

what organisms is nitrofurantoin active against

A

Gram +ve (staph. saprophyticus) and gram -ve (E. Coli) that cause UTIs commonly

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14
Q

What bacteria are resistant to nitrofurantoin

A

Bacteria with reduced nitrofuran reductase activity

Also less common causes of UTIs e.g. Klebsiella, Proteus have intrinsic resistant

Relatively rare for E. Coli to develop resistance

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15
Q

Adverse effects of nitrofurantoin

A

1) GI upset
2) Hypersensitivity
3) Chronic pulmonary reactions - pneumonitis, fibrosis
4) Hepatitis and peripheral neuropathy
5) haemolytic aneamia in neonates –> as immature RBCs are unable to mop up nitrofurantoin stimulated superoxides which damages RBCs
6) can turn urine dark yellow or brown

Patiet whousl warn if any unexplained symtpoms e.g.breathlessness

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16
Q

Contrainidcatinos of nitrofurantoin

A

1) Pregnancy towards term
2) Under 3 months old
3) Renal impairment - as impaired excretion increases its toxicity and decreases its efficacy

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17
Q

Caution of using nitrofurantoin in who

A

Long term UTI prevention –> high risk of adverse effects

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18
Q

Interactions of nitrofurantoin

A

No significant interactions

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19
Q

How can we minimise GI upset in nitrofurantoin

A

Take with food or mulk

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20
Q

Why shouldn’t we prescribe nitrofurantoin for pyelonephritis

A

As tissue concentrations are low

Use co-amoxiclav or gentamicin instead

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21
Q

What does co-trimoxazole contain

A

Trimethoprim and sulfamethoxazole

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22
Q

Indications of trimethprim

A

1) UTI - 1st line for uncomplicated

2) Pneuocytis Pneumonia - use co-trimoxazole

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23
Q

Action of trimethoprim

A

Inhibits bacterial folate synthesis by inhibiting dihydrofolate reductase

Bacteria are unable to use external folate for DNA synthesis –> therefore inhibiting it is bacteriostatic

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24
Q

What organisms is trimethoprim effective against

A

Broad spectrum against gram -ve and gram +ve - Particularly E. Coli

BUT widespread bacterial resistance

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25
How do sulfonamide antibiotics work
Inhibits bacterial folate syntheisis - but inhibits dihydropteroate syhnthetase as structual analoge of PABA
26
Why do we combine trimethoprim and sulfomethoxazole?
As both are bacteriostatic and in combination they cause more inhibition making it bacteriacidial
27
Adverse effects of trimethoprim
1) GI upset - common 2) Skin rash - 3-7% 3) Severe hypersensitivity reactions 4) Haematological disorders --> as a folate anatgonists can cause megaloblastic aneamia, leucopenia and thrombocytopenia 5) Hyperkaelamia and eleation of plasma creatinine
28
Why can trimethoprim cause megaloblastic anaemia, leucopenia and thromboyctopenia
As it is a dihydrofolate reductase inhibitor hence this means that it reduces the amount of folate available
29
Contraindications of using trimethoprim
1) 1st trimester --> increased risk of foetal abnormalities
30
Caution in which patients when using trimethoprim
1) Folate deficiency - more susceptible to haematological effects 2) Renal impairment ---> may need dose reduction as exreted mostly unchanged by the kidneys 3) Neonates, elderly, HIV infection --> more susceptible to adverse effects
31
Interactions of trimethoprim
1) Potassium raising drugs --> predisposes to hyperkaleamia 2) Folate antagonists (e.g. methotrexate) and drugs that increase folate metabolism (e.g. phenytoin) --> increase the risk of adverse effects 3) Enhances warfarin --> as it kills the gut flora that synthesise vitamin K
32
What would use as prophylaxis for UTIs
Low dose trimethoprim
33
What do we need to monitor if we give long term trimethoprim
FBC monitoring | For the early detection of haematological disorders
34
What is the relationship between trimethoprim and creatnine
Trimethoprim competitively inhibits creatinine secretion in the renal tubules This causes a small reversible increase in creatining without reducing GFR Hence this means trimethoprim is less effective in those with renal impairment as it is outcompeted by creatinine for secretion into the urinary tract
35
Name a glycopeptide
Vancomycin
36
Indications for vancomycin
1) Gram +ve infections --> if severe infection and penicillines cant be used 2) Antibiotic associated colitis due to C. Diff - 2nd line to metronidazole
37
Action of glycopeptides
Inhibit frowth and cross-linking of peptidoglycan chains --> hence inhibiting the synthesis of the cell wall of gram +ve bacteria
38
Why are glycopeptides inactive against gram -ve bacteria
Due to a different cell walll structure
39
Adverse effects of glycopeptides
1) Thrombophlebitis --> common at infusion site 2) Red Man Syndrome --> general erythema, hypotension and bronchospasm Anaphylactoid reactions are NOT antigen-mediated hence they are not true allergies They are due to the non-specific degranulation of mast cells 3) Nephrotoxicity --> when IV 4) Ototoxicity --> report any changes in hearing 5) Blood disorders: Neutropenia and thrombocytopenia
40
Warnings of using glycopeptides
Caution and dose reduction in elderly and renal impairment
41
Interactions of glycopeptides
1) Aminoglycosides, loop diuretics and ciclorpin Increased risk of ototoxicity/nephrotoxicity if used together!!
42
What is vancomycin good for C. Diff reatment
As it is a large hydrophilic molecule so is poorly absorbed across lipid membranes
43
Indications for tetracyclines
1) Acne vulgaris 2) LRTI --> including COPD exacerbations and atypical pneumonia 3) Chlamydia 4) Typhoid, anthrax, malaria and Lyme Disease
44
Action of tetracyclines
Bind to 30S ribosome --> inhibits bacterial protein synthesis Relatively broad spectrum but widspread resistance due to a pump that allows bacteria to pump out tetracyclines
45
Adverse effects of tetracylcines
1) GI upset - take with food to reduce risk 2) Hypersesntivity 3) Oesophageal irritation, ulceration and dysphagia 4) Photosensitivity 5) Discououration and/or hypoplasia of tooth enamel in chilren 6) Intracreanial hypertesnin --> headaches and visual disturbatnces
46
Contraindication of tetracyclines
1) Pregnancy 2) Breastfeeding 3) Under 12 As tetracylicnes bind to teeth and bones during development
47
When should we also avoid tetracyclines
Renal impairment | Their anti-anabolic effect can raise plasma urea and reduced excretion increase the risk of adverse effects
48
Interactiosn of tetracyclines
Bind to divalent cations --> seperate 2 horus from calcium, antacids or Iron Wargarin --> exacerbates antcoagulant efffects as kills normal gut flora
49
How should you take a tetracycilne tablet
Swallow whole with plenty of water to avoid oesophageal irritation
50
Name macrolides
Clarithromycin erythryomycin Azithromycin
51
Indicatinos of macrolides
1) Respiratory and soft tissue infections (penicillin alternative) 2) Severe pneumonia --> add to penicilin to cover atypical 3) H. Pylori eradicated --> incombo with either PPI and amoxicillin or metronidazole
52
Action of macrolides
Inhibits bacterial protein synthesis --> binds to the 50S ribsosome and blocks translocation. This prevents elondation of polypeptide It is bacteriostatic so the immune system can then kill it and remove it from the body
53
What organisms does each type of macrolide have on?
``` Eryhtormucin --> broad spectrum against +ve and -ve Synthetic molecules (clarithromycin + azithromycin) hace increaesd activity against gram -ve (particularly H. Infunenzae) ```
54
Adverse efecs of macrolides
Most ommon and sever 1) Macrolides are irritant --> nause, ovmitng, thrombophlebiti 20 Antibitoics associated colitis 2) Liver abnormlaities 4) Prolongation of the QT interval 5 Ototoxicity
55
Contrainidication ofsing macrolides
1) Macrolide hypersensitivity
56
Caution of using macrolides
Severe hepatic and renal impairment
57
Interactino of macrolides
1) the drugs are metablised by the P450 enzymes (ecept emma) | 2) Drugs that prolong the QT intervatl e.g. amiodarone, antipsychoics and quinin , SSRI
58
Do macrolides cover penicillin resistant organsimis
Yes they cover things such as legionella that cause pneumonia but not other organisms that cause LRTI
59
Name quinolones
Ciprofloxacin Moxifloxacin Levofloxacin
60
Indicitatios for use of quinolones
Generally reserved for 2nd or 3rd line treatment due to potential for rapid resistance and C. Diff 1) UTI 2) Severe GI infection e.g. Shigella or campulobacter --> ciprofloxacin 3) LRTI - use moxi or levo 4) Pseudomonas aureginos
61
What antibitoic should we treat pseudomonas with
Ciprofloxacin - this is the only oral antibiotic with action against it
62
Action of quinonones
Inhibit DNA synthesis - particularly active against anaerbovin gram -ve hence useful in UTI and GI infections Moxi and levo hace enhaved activity against gram _ve hence can be used to treat LRTIs that are caused by gram_ve and -ve
63
How does rapid resistance arise to quinolones
Prevent intracellular accumumlation be reducing permeablility/increasing efflux Mutations in target enzymes
64
Adverse effects of quinonlones
1) GI Upset 2) Hypersesnitivty 3) Neuro adverse effects --> lower the seizure thresholod 4) INflammation and rupture of muscle tendons 5) Prolong the QT interval --> Arrhythmias risk --> particularly moxi 6) Promote C. Diff
65
Warnings of using quinolones
At risk of seizures Growing - increased risk of arthropaty Risk factosr for QT prolongation e.g. electroloye disturbances or cardiac diseases
66
Interactions of quinolones
1) Drugs containing divalent cations --> e.g. calcium and atacids --> these decrease its absorption and efficacy 2) Cipro inhibits certain CP450 enzymes 3) Co-prescription with NSAIDS --> high risk of seizures 4) Co-prescription with prednisolone increaess risk of tendon rupture 5) Caution with other drugs that prolong the QT interval or cause arrhytmias e.g. amiodarone, antipsychotic, SSRIs, macrolides, quinine
67
What happens if co-prescription of quinolones and prednisolone
Increased chance of tendon rupture

3rd Year Drugs (10 decks)

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