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Clin Sci IMS, Respiratory, Renal, Cardiovascular, Nutrition & Energy > Week 6 - Infection, Antibiotics & Resistance > Flashcards

Week 6 - Infection, Antibiotics & Resistance Flashcards

1
Q

Describe the sepsis 6

A
  • High O2 flow
  • Blood Cultures
  • IV Antibiotics
  • IV Fluid resuscitation
  • Measure Lactate
  • Measure Urine output + Strict fluid balance
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2
Q

Describe hospital acquired infections

A

Nosocomial Infections
Mostly due to bacteria, since antibiotics are used frequently in hospitals, types of bacteria and their resistance is different to bacteria outside of the hospital.

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3
Q

What is a nosocomial infection?

A

An infection not present or incubating prior to hospital admittance but generally occurring 24 hours after admittance

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4
Q

What are the risk factors for nosocomial infections?

A
  • Duration of hospital stay
  • Inwelling Catheters
  • Mechanical ventilation
  • Use of total parenteral nutrition
  • Antibiotic usage
  • Use of histamines receptor blockers owing to relative bacterial overgrowth
  • Age - more common in neonates, infants and elderly
  • Immune deficiency
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5
Q

Describe Hospital acquired pneumonia (HAP)

A
  • Nosocomial pneumonia - pneumonia acquired from the hospital 48-72 hours after admittance
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6
Q

Describe community acquire pneumonia (CAP)

A

Caused by bacterial infection rather than a virus

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7
Q

What are 5 bacterias contributing to pneumonia development?

A
  1. Pseudomionas aeruginosa
  2. staphylococcus Aureus
  3. klebsiella Pneumoniae
  4. Escherichia Coli - E.Coli
  5. Non enterobacteriaceae
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8
Q

Describe urinary tract infections

A
  • involves urinary system, urethre, bladder, ureter and kidney
  • most common heath care associated infection
  • 75% associated with a urinary catheter
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9
Q

Describe bacteria associated with UTI’s

A
  • Enteric pathogens
  • Pseudomonas species
  • Enterococcus species
  • Staphylococcus aureus
  • Coagulase
  • Enterobacter species + yeast
  • Candida
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10
Q

Describe sepsis

A
  • Body’s response to infection injures its own tissue and organs
  • life threatening when body’s abnormal immune system response to infection causes organs to fail
  • Triggered by any infection, most common = bacteria in lungs, uti and abdominal organs
  • Cause multi organ failure
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11
Q 
Describe sepsis associations with 
GI Tract 
GU Tract 
Pelvis
Lower respiratory tract 
Vascular system 
Heart + cardiac vasculature
A

GI Tract - liver disease, gallbladder, colon abscess, intestinal obstruction + instrumentation
GU Tract - pyelonephritis, intra or peri-nephric abscess, renal calculi, urinary tract obstruction, acute prostatitis or abscess, renal insufficiency, + GU instrumentation
Pelvis - Peritonitis + pelvic abscess
Lower respiratory tract - community acquired anaemia, empyema + lung abscess
Vascular System - infected IV Line or prosthetic device
heart and cardia vasculature - acute bacterial endocarditis and myocardial/ perivalvular ring abscess

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12
Q

Describe the pathophysiology of sepsis

A

Infection
Excessive cytosine release
Amplification - capillary dilation and increased permeability, oedema of tissues
Hypotension - tachycardia, reduced urine output, reduced cardiac output, multiple organ failure
Anaerobic respiration increases blood lactate
Death or significant morbidity

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13
Q

What are the symptoms of sepsis?

A
  • Shivering, fever, cold
  • Extreme pain
  • Pale discoloured skin
  • Sleepy/ difficult to rouse
  • ’ I feel like I might die’
  • Short of breath
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14
Q

Describe NEWS for sepsis

A

National Early Warning Score

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15
Q

Describe methicillin resistant staphylococcus aureus

A
  • Gram positive
  • different to other staph aureus strains
  • resistant to many antibiotics
    Treatment
  • vancomycin
  • teicoplenin
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16
Q

Describe clostridium difficile

A
  • Spore forming anaerobic gram positive bacillus bacteria
  • Spores facilitate survival in adverse conditions - resistant to heat, stomach acid, alcohol and alcohol gel
  • Produces exotoxins A + B when growing
  • Human habitat = large intestine
  • Found in soil
  • Faeco- oral transmission
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17
Q

Describe the clinical presentation of diahorrea caused by clostridium difficile

A
  • Toxins cause inflammation of intestinal wall resulting in spectrum of disease
    1. antibiotic associated diahorrea
    2. antibiotic associated colitis
    3. Pseudomembranous colitis
    4. Fulminant colitis
    Signoidoscopy and biopsy required to assess extent and severity of clostridium difficile
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18
Q

What are the risk factors for clostridium difficile?

A
  • Current/ recent antibiotic treatment
  • Any antibiotic can induce
  • Antibiotics alter gut flora allowing clostridium difficile to flourish
  • can occur within two months of antibiotic treatment
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19
Q

What are the risks of antibiotics treating clostridium difficile - categorise the antibiotics

A 
High risk 
- Cefalosporins 
- Ciprofloxacin 
- Clindamycin 
- IV, multiple/ prologued courses
Intermediate 
- Penicillins
- Co- amoxiclav 
- macrolides 
Low 
- Trimothoprim 
- Nitrofurantoin 
- Metrondazole
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20
Q

What is the treatment for clostridium difficile ?

A

Conservative treatment
Stop antibiotics and allow reestablishment of normal microflora
- rehydrate and observations for sepsis

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21
Q

Describe glycopeptide resistant enterococci

A

Enterococcus species found in normal healthy individuals
Can cause a range of illnesses e.g
- UTI
- Bacterianaemia
- Wound Infections
Resistant to glycopeptide antibiotics - Vancomycin and teicoplanin

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22
Q

What are the two main species of glycopeptide resistant enterococci and their antibiotics?

A

E. Taccalis - amoxicillin

E. Faecium - Linezoid or daptomycin

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23
Q

Describe the extended spectrum beta lactamases (ESBLs)

A
  • Enzymes produced by bacteria resistant to cefalosporins
  • New cases of ESBLs - CTX-M enzymes have emerged and detected across E.Coli bacteria
  • ESBLs producing E.coli are resistant to penicillins and cefalosporins found in UTI’s
24
Q

What are the treatment antibiotics for ESBL’s and AMC?

A 
Aminoglycoside 
Carbapenem 
Ciprofloxacin 
Trimethoprim
Nitrofurantoin 
Tigecycline
Temocillin
25
Q

What is start smart?

A

Prompt action of antibiotics within an hour
Review and decision making within 24 hours
Help reduce antibiotic resistance

26
Q

What is the antimicrobial stewardship?

A

Organised or healthcare system with approach to promoting and maintaining judicious use of antimicrobials to preserve their future effectiveness

27
Q

Describe bacteria growth optimum conditions

A
  • temperature
  • pH
    Atmospheric conditions - anaerobic, aerobic, facultative - can use )2 but also anaerobic
28
Q

Describe the classification of bacteria

A
  • Gram positive
  • Gram Negative
  • Acid fast bacilli
  • Atypicals
29
Q

What are sone preventative methods of the body to reduce bacteria invasion?

A
  • Skin
  • Respiratory tract
  • GI tract
  • Urogenital system
  • Conjunctiva - eyes
30
Q

What is an antibiotic?

A

Substance produced by microorganisms of synthetically produced that selectively destroys or inhibits growth of microorganisms

31
Q

What is bactericidal?

A

Antibiotics that kill bacteria

32
Q

What is bacteriostatic?

A

Suppress growth/ reproduction of bacteria

33
Q

What are the bactericidal antibiotic classes?

A
  • Beta lactams
  • Aminoglycosides
  • Glycopeptides
  • Ansamycins
  • Quinolones
  • Streptogramins
  • Lipopeptides
34
Q

What are the bacteriostatic antibiotic classes?

A
  • Sulfanomides
  • Tetraglycyclines
  • Chloramphericol
  • Macrolides
  • Oxazolidinones
35
Q

How do antibiotics work against bacteria?

A
  • Cell wall synthesis
  • Cell wall integrity
  • DNA synthesis
  • RNA synthesis
  • Cytoplasmic membrane
  • Translocation
  • Protein synthesis
36
Q

What are two cell wall synthesis inhibitory antibiotic classes ?

A
  • Beta lactams

- Glycopeptides

37
Q

What are beta lactams?

A

Structural analogues of cell wall precursors, inhibiting cell wall synthesis

38
Q

What antibiotic classes have an effect on protein synthesis?

A
  • Aminoglycosides
  • Chloramphenicol
  • Sodium Fusidate
    Macrolides
    Tetracyclines
39
Q

What antibiotic classes inhibit folate synthesis?

A
  • Sulphonamides
  • trimethoprim
    Inhibit dihydrofolate reductase enzyme involved in folic acid
40
Q

What antibacterial classes inhibit transcription of bacterial RNA?

A

Ritampicin

Binds to bacterial DNA dependent RNA polymerase

41
Q

What antibiotic classes inhibit DNA gyrase and topoisomerase?

A

Quinolones

Modulate replication/ expression of DNA

42
Q

Describe Beta lactams

A

Intefere with cross links of peptidoglycan
- Bactericidal
- Penicillins, cephalosporins, carbapens, clavans, monobactams, glycopeptides
- Prevent joining of N-acetylglucosamine and N-acetylmuramic acid dimers
- Molecules too large to penetrate Gram negative outer membrane
Spectrum of activity largely gram positive organisms
Used mainly for staphylococci and streptococci

43
Q

Describe tetracyclins with regard to ribosomal effect

A

Bind to 30s ribosomal subunit and block attachment of transfer RNA and addition of amino acids to protein chain.
Inhibits binding of amino acyl tRNA to the mRNA ribosome complex

44
Q

Describe aminoglycosides with regard to ribosomal effect

A

Interfere with mRNA attachment to ribosome

45
Q

Describe Chloramphenicol with regard to ribosomal effect

A

Binds 50s ribosomal subunit and interferes with binding of amino acids to the growing chain

46
Q

Describe macrolides and lincosomides with regard to ribosomal effect

A

attach to the 50s ribosomal subunit causing termination of growing protein chain

47
Q

Describe linezoids with regard to ribosomal effect

A

binds to 23s ribosomal RNA for 50s subunit and prevents binding of functional 70s initiation complex, necessary for protein synthesis

48
Q

Describe Quinolones ie ciprofloxacin in relating to its affect on nucleic acid synthesis

A

Selective inhibition of DNA gyrase and typeztopoisomerase type 4 topoisomerase necessary to separate bacterial DNA therefore inhibiting cell division

49
Q

Describe Ritampicin relating to its affect on nucleic acid synthesis

A

Inhibits DNA dependent RNA polymerase activity by forming state complex with enzymes with enzyme therefore reduce initiation of RNA synthesis

50
Q

Describe metronidazole relating to its affect on nucleic acid synthesis

A

Binds to bacterial DNA leading to strand breakage

51
Q

Describe how trimethoprim interferes with the metabolic pathway

A

Inhibits dihydrofolate reductase a key stage in nucleic acid development
- exerts antimicrobial activity by blocking the reduction of dihydrofolate to tetrahydrofolate the active form of folic acid

52
Q

Describe antibiotic resistance

A

Antibiotics are losing their effectiveness at an increasing rate
- Bacteria adapt and find new ways to survive therefore longer use of antibiotic increases resistance

53
Q

Describe intrinsic antibiotic resistance

A
  • Entire species resistant before any antibiotics introduced through
  • Lack of penetration via cell wall
  • lack of suitable cell wall target sites
  • susceptibility of antibiotic to naturally produced enzymes
54
Q

Describe how antibiotic use encourages resistance

A
  • Acquired resistance is absent from antedating the antibiotic era
  • Introduction of a new antibiotic is repeatedly followed by resistance
  • Resistance develops in the normal bacteria flora of individuals
  • One dose of antibiotic can change gut flora
  • Resistance is increased in areas of increased use
55
Q

Describe gene transmission in bacteria for antibiotic resistance

A

Conjugation - plasmids moves from one bacteria to an other
Transduction - bacteriophages move between bacteria carrying genes
Transformation - take up DNA from solution

56
Q

Describe antibiotic inactivation

A

Bacteria acquired genes encoding enzymes that inactivate antibiotics

57
Q

What are the 5 resistance mechanisms?

A
  • Inactivation ion enzymes
  • Alteration of antibiotics target site
  • Modification of bacteria cell wall
  • Activation of drug efflux pump
  • Transfer of DNA between bacteria

Inactivation, impermeability, efflux, altered target, bypass, hyper production

Clin Sci IMS, Respiratory, Renal, Cardiovascular, Nutrition & Energy (17 decks)

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