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Year 2 Pharmacology > Anti-Microbials > Flashcards

Anti-Microbials Flashcards

1
Q

What does the term

BACTERICIDAL

mean?

A

It means to kill bacteria

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2
Q

What does the term

bacteriostatic

mean?

A

It means to inhibit/ arrest the growth of bacteria

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3
Q

Name the essential cellular structures and processes in bacteria

(hint organells)

A
  • Cell wall
  • Plasma membrane
  • Protein synthesis (ER)
  • DNA & RNA synthesis
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4
Q

True or false?

Bacteria species differ in Cell wall structure and composition…

A

TRUE

Gram staining reveals the differences. Gram POSITIVE have thick peptidoglycan chains. GRAM NEGATIVE have thin PG layers.

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5
Q

Which bacteria have a thick Peptidoglycan layer?

A

GRAM POSITIVE:

  • Stapylococci
  • Streptococci
  • Enterococci
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6
Q

Which bacteria have a thin Peptidoglycan layer?

A

GRAM NEGETIVE

  • E.Coli
  • Pseudomonas
  • Salmonella
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7
Q

What are Peptidoglycan layers made up of?

A

They’re made of chains built up of covalently linked sugars and then peptide chains linked to those sugars, which cross link via peptidyl bridges.

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8
Q

True or false….

Antibiotics that target Peptidoglycan biosynthesis are not as effective against Gram Negative bacteria.

A

TRUE

Because GRAM -VE have thinner PG layers so they’re not as effected by Antibiotics that break the PG wall as gram +ve antibiotics are.

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9
Q

What antibiotic categories target Peptidoglycan biosynthesis?

A

-Beta Lactams
(penicillins, cephalosporins, carbapenems)
-Vancomycin

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10
Q

Bacterial penicillinase (beta-lactamase) inactivates penicillin by cleaving its:

  • β-lactam ring
  • Hydroxyl group
  • Methyl group
  • Side chain
A

β-lactam ring

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11
Q

Gram+ve and Gram-ve bacteria differ in:

  • the structure of the cell wall
  • the presence of plasmids
  • the shape of the cells
  • their motility
A

the structure of the cell wall

They have different peptidoglycan layer thickness. Gram +ve have thick, gram -ve have thin PG layers.

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12
Q

Bacteria that are resistant to B-lactam antibiotics secret what enzyme which inactivates the antibiotic by breaking down their B-lactam ring.

A

Resistant bacterial species produce B-lactamase a secreted enzyme which inactivates antibiotics by breaking down their B-lactam ring

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13
Q

Are B-lactams bactericidal or bacteristatic

A

They’re Bactericidal

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14
Q

What’s the mechanism of B-lactam antibiotics?

A

They inhibit an enzyme that’s involved in the transpeptidase cross-linking reaction.
It interferes with linking the individual PG chains together.
It disrupts PG synthesis leading to autolysis (cell dealth)

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15
Q

Name some B-lactam antibiotics…

A
  • Penicillins (amoxicillin/ampicillin)
  • Cephalosporins (cefalexin, cefaclor, cefixime)
  • Carbapenems (Maropenem, Ertapenem, Imipenem)
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16
Q

Which B-lactam antibiotic has 4 generations which have different primary coverage?

A

CEPHLLOSPORINS
Different primary
coverage:
1st – Gram +ve

2nd – Anaerobes

3rd – Gram –ve

4th - Pseudomonas

17
Q

Which B-lactam antibiotic is broad spectrum and is generally effective against all but MRSA and VRE?

A

CERBAPENEMS

Only available in IV

18
Q

What antibiotic which inhibits cell wall synthesis is currently used to treat MRSA?

A

VANCOMYCIN
Given IV
Although new resistance is emerging for MRSA and VRE

19
Q

Which part of bacteria do these antibiotics effect:

  • Tetracycline
  • Aminoglycosides (Gentamycin, Streptomycin)
  • Macrolides (Erythromycin)
  • Chloramphenicol
A

They inhibit protein synthesis!

Most are bacteriostatic

Assosiciated with greater toxicity (sometimes human mitochondria ribsomes are inhibited too)

20
Q

Where do ‘FLUOROQUINOLONES’ act on bacteria cells?

A

They Inhibit DNA biosynthesis.

‘emagine if the FLU acted on our DNA’

21
Q

Give examples of antibiotics that inhibit DNA biosynthesis.

Hint: emagine if FLU inhibited our DNA!

A

Fluroquinolones

  • ciproflaxicin
  • norfloxacin
  • levofloxacin
  • moxifloxacin
22
Q

Which Antibiotic works by inhibiting bacteria RNA synthesis

Hint R for Rna

A

RIFAMPICIN

Used to treat TB and inhibits bacteria but not human RNA polymers so non toxic for us!

23
Q

Which antibiotic is used predominantly for treating TB!!!

hintTB/RNA targetting

A

RIFAMPICIN the antibiotic which targets RNA (R for Rna)

24
Q

Why is it effective to target the Biosynthesis of Nucleic acids when treating bacterial infections?

A

Because Nucleic acid (nucleitides) require folic acid which is synthesized by the bacteria. But humans can’t make folic acid so by targeting folic acid it doesn’t affect us but it affects the bacteria.

25
Q

Name some antibiotics that target nucleac acid biosynthesis ….
(folic acid)

A

Trimethoprim
Co-trimethoprim
Sulfonides

(remember: Folic acid is given to pregnant women + women are more likely to get utis= trimethoprim)!!!

26
Q

True or false:

Fungal pathogens are Prokaryotic…

A

FALSE

They are Eukaryotes - which has implications for drug targets and therapy

They belong to the categoty of opportunistic infections

27
Q

Name some of the most common opportunistic fungal pathogens…

A
  • Candida Albicans (commensal)
  • Aspergillus Fumigatus (environmental)
  • Cryptococcus neoformans (environmental)
28
Q

Name the targets of anti-fungal treatments

A
  • Call wall
  • Plasma Membrane
  • Nucleus (DNA & RNA synthesis)
29
Q

Why is the cell wall a good target for anti-fungals?

A

Because there is no equivalent in humans so it wouldn’t cause damage to us treating it.

30
Q

What are the components of the fungal cell wall?

Hint 2 parts

A

-Skeletal components
(glucagon + chitin)

-Matrix (Mannan) components
(complex of mannoproteins/ glycosylated proteins) 35-50% of cell wall

31
Q

Anti-fungals such as Echinocandins (caspofungin and micafundin) target which part of fungi?

A

The Cell Wall

Remember: if your walking down lots of WALLs… it can ECHO - Echinocandins

32
Q

Where do most of the currently used anti-fungals target?

A

The plasma membrane

33
Q

What is the difference between human plasma membranes and that of fungi?

A

Humans PM contain Cholesterol whereas fungi contain Ergosterol (therefore a possible target for anti-fungals)

34
Q

Mycoses are diseases caused by:

  • Fungi
  • Parasites
  • Viruses
  • Bacteria
A

FUNGI

35
Q

What are the 2 categories of anti-fungals that target the Plasma membrane (ergosterol)

A
  • Anti-fungals that bind to ergosterol (Polyene antifungals, Mystatin, Amphotericinb)
  • Anti-fungals that inhibit ergosterol (AZOLES, Allylamines)
36
Q

Where does the anti-fungal drug MYSTATIN act?

A

It acts on the lipid fungi cell membrane. by binding to ergosterol.

(hint: Mystatin like a statin- targets lipids)

37
Q

Where do AZOLES act?

NOTE: There are 2 types of Azoles:

  • Imidazoles
  • Triazoles
A

They are anti-fungals that inhibit ergosterol in the fungi cell membrane)

(hint: AZOLES are sometimes cream which you put on skin MEMBRANE)

38
Q

In fungi, flucytosine inhibits the biosynthesis of:

  • DNA and RNA
  • Cell wall chitin
  • Carbohydrates
  • Ergosterol
A

DNA and RNA

Hint: Imagine if having the FLU affected our DNA!!

39
Q

What is a BIOFILM?

A

It’s a formation/growth of fungi on plastic surfaces which aids in the resistance to anti-fungals.

Year 2 Pharmacology (11 decks)

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