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semester 2 (1st year) > Wk 25 > Flashcards

Wk 25 Flashcards

1
Q

The bladder receives afferent (sensory) and efferent (motor) innervation via what 2 nerves?

A

Hypogastric and pelvic splanchnic nerves

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2
Q

Changes in ____ nerves in the bladder wall, structural changes in the _____ or ____ _____ muscles can lead to incontinence

A

Sensory

Sphincters or pelvic floor

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3
Q

What is the bladder wall mostly made up of?

A

Smooth muscle

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4
Q

What do the sympathetic neurons do to the bladder?

A
  • Relaxation of detrusor

- Contraction of internal sphincter

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5
Q

Neurotransmitters that control bladder smooth muscle…

What receptors does Acetylcholine act on?

What receptors does Noradrenalin act on?

The external sphincter is closed by ___ acting on what receptors?

A

Ach= excitatory muscarinic

NA= excitatory alpha or inhibitory beta adrenoceptors

External sphincter closed by Ach acting on nicotinic receptors

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6
Q

When the bladder fills, there is an increase in sensory impulses to what part of the brain?

A

Pontine micturition centre (Barrington’s nucleus)

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7
Q

What stops adults urinating when their bladder is full?

What allows adults to urinate?

A

Sympathetic control (tells detrusor muscle to relax and tells internal sphincter to stay closed)

Parasymp (tells detrusor muscle to contract and internal sphincter to open)
- And then somatic control allows adults to open/ close external sphincter when they are ready

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8
Q

Which has a thicker wall, Gram + bacteria or Gram - bacteria?

What colour does gram + stain and what colour does gram - stain?

A

Gram + have the thick peptidoglycan wall

Gram + stains purple and gram - stains pink (because they have thin cell wall)

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9
Q

What is penicillin binding protein (PBP) involved in?

A

It is a transpeptidase which cross links peptide chains to build the peptidoglycan cell wall

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10
Q

What does transpeptidase do in bacteria?

What does glycosyltransferase do in bacteria?

A

Links amino acids for peptidoglycan wall
(B-Lactams block it)

Links sugars for peptidoglycan wall
(Vancomycin)

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11
Q

B-Lactams…

What do they do?

Are they bactericidal or bacteristatic?

A

Block bacterial cell wall synthesis by blocking transpeptidase

Bactericidal

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12
Q

What are the 4 classes of B-lactams?

A

Penicillins

Cephalosporins

Monobactams

Carbapenems

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13
Q

What bond do B-Lactams form with PBP and what effect does this have?

A

Covalent bonds

Inhibiting PBP transpeptidase = weakens cell wall
= bacterial cell lysis and death

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14
Q

Spectrum of action for B-Lactams…

Out of hydrophilic penicillins and hydrophobic penicillins, which is broad spectrum (and why) and which is narrow spectrum?

A

Hydrophilic is broad spectrum because it can get through the cell wall and cell membrane (gram -) better

Hydrophobic is narrow

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15
Q

What is another inhibitor of cell wall synthesis (that isn’t B-Lactam)

How does it work?

A

Vancomycin (glycopeptide)

Inhibits release of AA/ sugar building blocks of peptidoglycan cell wall by glycosyltransferase

Reduced number of building blocks= reduced cell wall synth

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16
Q

Does Vancomycin mainly affect Gram pos or Gram neg bacteria?

A

Gram pos (because gram pos has big cell wall)

17
Q

How do sulfonamides work?

Are they bactericidal or static?

Are they wide spectrum or narrow?

A

Inhibit folate synthesis so no DNA replication

They are bacteristatic (then host immune system kills it)

Wide spectrum against gram pos and gram neg

18
Q

What do enzyme topoisomerases do?

What are the 2 topoisomerases Quinolones block and what do they do?

What is the effect of this?

A

They uncoil and separate DNA strands

Topoisomerase II (DNA gyrase) 
- Uncoil DNA strands

Topoisomerase IV
- Separate the strands

Stops DNA transcription and replication

19
Q

Are Quinolones bactericidal or static?

Are they broad or narrow spectrum? How?

A

Bactericidal

Broad because topoisomerase IV for gram pos and topoisomerase II for gram neg

20
Q

Classes of antibiotics…

Inhibitors of cell wall synthesis=

Inhibitors of DNA synth/ replication=

Inhibitors of transcription and translation=

A

B-Lactams and Vancomycin

Sulfonamides and Quinolones

RATMLC

  • Rifamycin
  • Aminoglycosides
  • Tetracyclins
  • Macrolides
  • Lincosamides
  • Chloramphenicol
21
Q

How does Rifamycin work?

Is it bacteriocidal or static?

What disease does it treat?

A

Inhibits RNA polymerase so inhibits transcription

Bactericidal

TB

22
Q

How do aminoglycosides work?

Gram pos or neg?

Static or cidal?

A

30s ribosome inhibitor

Gram neg

Bacteriocidal

23
Q

How do Tetracyclines work?

Gram pos or neg>

Static or cidal?

A

30S ribosome inhibitor

Both! (broad spectrum)

Bacteriostatic

24
Q

How do Macrolides work?

Gram pos or neg

Static or cidal

A

50S ribosome inhibitor

Gram pos

Bacteriostatic

25
Q

How do lincosamides work?

Gram pos or neg?

Static or cidal?

A

50S ribosome inhibitor

Gram pos

Bacteriostatic

26
Q

How does chloramphenicol work?

A

50S ribosome inhibitor

Both (broad spectrum)

Bacteriostatic

27
Q

What are bacterial plasmids?

What are R plasmids

A

Short, circular double stranded DNA that self replicate (involved in antibiotic resistance)

R plasmids carry genes for resistance to antibiotics (R genes)

28
Q

What are the 3 genetic changes bacteria undergoes to become more resistant to antibiotics?

A

Chromosomal mutations

Gene duplication and amplification (for antibiotic destroying enzymes and efflux pumps, etc)

Plasmids

29
Q

How do bacteria share resistance genes?

A

The cells come into contact by conjugation and the plasmids move from one to another, taking the resistance gene and making the new cell resistant too

30
Q

What are transposons?

+ in relation to resistance genes

A

DNA sequence that can change position in the genome so resistance genes can move around genome

31
Q

How do gram neg bacteria reduce the entry of antibiotics?

A

Mutate or lose the porin channel

32
Q

How do certain bacterias become resistant to tetracyclines, B-lactams and macrolides?

A

They have efflux pumps so antibiotics can’t stay in cell for long enough to have an effect

33
Q

Some bacteria release microbial enzymes that inactivate/ destroy which antibiotics?

A

Macrolides and B-lactams (by B-Lactamases)

34
Q

How do B-Lactamases work?

What stops that process?

A

they cleave the B-lactam ring of the B-lactams

clavulanic acid stops this process so penicillin is often administered with clavulanic acid

35
Q

How to bacteria change their protein targets (such as PBP)?

A

Single point or multiple point mutations

36
Q

What does a mutation in the aminoglycoside binding site on 30s ribosome give resistance to?

What does a point mutation in DNA gyrase give resistance to?

What does a chromosomal mutation in RNA polymerase give a resistance to?

A

Aminoglycosides

Quinolones

Rifampicin

37
Q

General considerations when chosing empiric antibiotic treatment: 3 qs to ask

A

1) what is the most likely organism
2) what is the resistance pattern for that organism
3) What are the potential consequences for this patient if we chose an antibiotic with too narrow spectrum?

38
Q

What is the antibiotic creed?

What is the acronym?

A

Restraint in the use of antimicrobials is the best way to ensure their efficacy

M- Microbiology guides therapy
I-Indications should be evidence based
N- Narrowest spectrum
D- Dosage appropriate to site and type of infection

M- Minimise duration of therapy
E- Ensure monotherapy in most situations

semester 2 (1st year) (13 decks)

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