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Crrab2 > UTI Micro > Flashcards

UTI Micro Flashcards

1
Q

What are the major defenses of the Urinary tract?

A
  1. Chemistry
  2. Flow
  3. IgA (adaptive immune)
  4. Different surface proteins of epithelial than GI tract
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2
Q

What are the chemistry defenses of the urinary tract?

A
  1. pH
  2. Lysozyme- breaks down peptidoglycan
  3. Lactoferrin– sequesters iron from bacteria
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3
Q

What are the major threats to the urinary system?

A
  1. Microorganisms
  2. Blocked/decreased flow
  3. Hematoganous threat from another anatomical location
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4
Q

What is the cause of cloudy urine in a UTI?

A

WBC’s

Bacteria

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5
Q

What are the Sings and sx’s of cystitis?

A 
Sudden onset pain
Dysuria 
Frequency/urgency 
Cloudy urine
Orange or red urine
Fever/n
Back pain
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6
Q

What is an uncomplicated UTI?

A

Structurally or Neurological normal urinary tract

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7
Q

What are some examples of complicated UTI?

A
  • Persistent infections
  • Foreign bodies like calculi and catheters
  • Obstruction
  • Immunosuppression
  • Renal failure
  • Renal transplant
  • Urinary retention from neuro dz
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8
Q

What are the bacterial causes of UTI’s?

A
  1. E. Coli 80%
  2. Staph saprophyticus 10%
    - The rest are 10%:
    3a. Enterococcus spp
    3b. Klebsiella
    3c. Citrobacter spp
    3d. Proteus mirabilis
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9
Q

Is the E. Coli that causes Bloody diarrhea and watery diarrhea cause UTI’s?

A

no

  • Those are EHEC and ETEC
  • UPEC is what causes UTI’s
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10
Q

What does UPEC stand for?

A

Uropathogenic E. Coli

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11
Q

What percent of women who get UTI’s have them reoccur?

A

25-30%

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12
Q

What is the most common nosocomial infection?

A

Catheter related UTI’s

accounts for 40%

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13
Q

Who is at less risk for UTI?

A

Children and men

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14
Q

Why would a child get a UTI?

A

Sexual assault

Atomic or functional abnormalities

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15
Q

Why would a man get a UTI?

A

Usually UT abnormality
Obstruction
Enlarged prostate

Can lead to prostitis or epidydimitis

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16
Q

What the sx’s of pyelonephritis?

A 
Flank pain
Fever
Nausea
Dysuria
Vomiting 
Malaise

1/4 mil cases/year

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17
Q

Which patients have risk factors for papillary necrosis (complication of pyelonephritis)?

A

in DM pts
Obstruction
Sickle cell
Analgesic abuse (can happen without infection)

Necrotic tissue can slough off and block downstream

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18
Q

What are some gross anomalies with pyelonephritis?

A
  • Enlarged
  • Discrete yellowish raised abscesses
  • Histo- Suppurative necrosis
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19
Q

How does one diff between chronic glomerulonephritis and chronic pyelonephritis?

A

In Chronic pyelonephritis the kidneys are not scared evenly bilaterally.

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20
Q

What is periglomerular fibrosis?

A

Concentric fibrosis about the parietal layer of the Bowman’s capsule

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21
Q

What are some characteristics of pyelonephritis?

A
  • Colloid casts
  • Periglomerular fibrosis
  • Dilated tubules
  • Atrophy of endothelial lining
  • Parenchymal with interstitial fibrosis and inflammatory infiltrates
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22
Q

Can one see necrotic papilla on a plain film?

A

Yes

Radiopague

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23
Q

What is common sight of abscesses for pts with Staph Aureus endocarditis?

A

Kidneys
Via Hematogenous spread

Gram - rarely spreads this way

24
Q

What do O K and H stand for in serotyping of bacteria?

A

O- Polysaccharide sugars
K- Capsule ag
H- Flagellar ag

25
Q

Are the serotypes of E Coli that cause cystitis vs pyelonephritis the same?

A

Nope

Genetically distinct

26
Q

What are some virulence factors for E coli?

A 
Adherence
Resistance
K ag
Siderophore receptor
Toxins and factors
27
Q

What is main virulence factor for E coli?

A

P Fimbriae

  • Binds to globoseries glycophingolipid found on uroepithelial cells
  • Resists neutrophil destruction
28
Q

What does Type 1 fimbriae bind to?

A

mannose containing host epithelial receptors

  • Uroplankin 1 and 2
  • however mannose sensitive because they bind so strongly to mannose that bacteria doesn’t infect us with excess mannose in urine
29
Q

What is needed in order for E coli to cause cystitis?

A

Type 1 Fimbriae

30
Q

What is the MOA of Linezolid?

A

Binds to 23S subunit of the 50S subunit and inhibits protein synthesis

31
Q

What are the 50S inhibitors?

A 
CCEL= Sell 
C= Chloramphenicol and clindamycin
E= Erythromycin (macrolides)
L= Linezolid

All static but linezolid can be cidal

32
Q

What are the 30 S inhibitors ?

A

AT
A=Aminoglycosides (cidal)
T= Tetracyclines (static)

33
Q

What is the mnemonic for 30s and 50s inhibitors?

A

buy AT 30, CCEL (sell) at 50

34
Q

What are the common nosocomial infections pathogens? Treatment?

A
  1. E. Coli
  2. K. pneumoniaie (Carbapenum resistant enterobacteriaceae (CRE)
  3. VRE- vancomucin resistent enterococci

Linezolid

35
Q

What is needed for bacteriuria?

A

> 10^5 colony forming units per ml

36
Q

What is pyruia?

A

10 or more neutrophils per high power field of unspun, voided midstream urine

37
Q

How does one diff between staph and enterococcus?

A

Catalase test

Staph is positive

38
Q

How does one diff between staph a and staph saprophyticus?

A

Coagulase test

SS is negative

39
Q

What is a positive catalase test?

A

Oxygen bubble production

  • Some bacteria protein H202 and O2- and thus need enzymes to break this down and protect themselves.
  • Catalase converts these reactive species to H20 and O2.
40
Q

What is coagulase?

A

Free and bound

- causes bacteria to clump together with fibrinogen which results in a precipitation

41
Q

How does one diff between staph epi and staph saprophyticus?

A

Novobiocin test

Epi is sensitive
Sapro is resistant

42
Q

What does novobiocin do?

A

Inhibits bacterial DNA gyrase in susceptible organisms

43
Q

What is unique about E coli in terms of Indole, citrate, MR and VP tests?

A

only enteric organisms that is both always Positive for indole and negative for citrate

44
Q

What are the first line treatments for UTIs? Contraindicated?

A
  1. Nitrofurantoin–> with suspected pyelonephritis as it has poor affect there
  2. TMP-SMX–> >20% local resistance and used in last 3 months
45
Q

What are the alternative treatments for UTIs?

A
  1. Fluoroquinolones

2. Amoxicillin/clavulanate (augmentin)

46
Q

What is first line treatment for staph saprophyticus?

A

Augmentin

47
Q

What is the MOA of Nitrofurantoin?

A

Inhibits bacterial acetyle-coenzyme A

  • interferes with organisms carb metabolism
  • disrupt cell wall formation too
48
Q

How does nitrofurantoin get activated?

A

By bacteria flavoprotein
Thus its a prodrug
30-40% excreted in urine unchanged

49
Q

Can pregnant people take nitrofurantoin? Renal pts?

A

no

  • it crosses the placenta and distributed through breast milk
  • accumulates and can be toxic in renal pts
50
Q

What do sulfonamides inhibit?

A

pteridine synthetase

- Inhibits Pteridine + PABA from forming into dihydropteroic acid

51
Q

What does trimethoprim inhibit?

A

Dihydrofolate reductase

- inhibits production of tetrahydrofolic acid from dihydrofolic acid

52
Q

What else can Bactrim be used for?

A
  • Acute bronchitis
  • Otitis media
  • Pneumocystis jirovecii pneumonia
  • Traveler’s diarrhea
  • Shigellosis
  • UTI
53
Q

What does Bactrim interact with that could be fatally bad?

A

CYP450 and CYP2C9

54
Q

What is the MOA of Quinolones?

A

Inhibits DNA gyranse and topo IV

  • contraindicated while using antiacids
  • contraindicated in people taking iron supplements
55
Q

What is potent enough quinolone to fight again P aeruginosa?

A

Levofloxacin

56
Q

What are the current uses of quinolones?

A

most active against aerobic gram-negative bacilli, particularly members of the family Enterobacteriaceae and Haemophilus spp., and against gram-negative cocci, such as Neisseria spp. and Moraxella (Branhamella) catarrhalis. Relative to nalidixic acid, the fluoroquinolones also have additional activity against gram-negative bacilli, such as P. aeruginosa and against staphylococci.

Crrab2 (14 decks)

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