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Renal Too > UTI's > Flashcards

UTI's Flashcards

1
Q

Who get’s more UTI’s, women or men?

A

Women

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2
Q

What % of women have recurrent UTI’s at some point in their life?

A

20-30%

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3
Q

After what age do men experience UTI’s?

A

> 50

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4
Q

What is the route that bacteria normally take to cause a UTI?

A

from the urethra –> bladder

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5
Q

What is the main mechanism to cause nosocomial UTI’s?

A

catheters

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6
Q

What is the #1 cause of community and hospital acquired UTI’s?

A

E. coli

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7
Q

What % of community UTI’s are from E. coli?

A

80%

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8
Q

What % of community UTI’s are from coagulase-ned staph?

A

10%

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9
Q

What % of community UTI’s are from Proteus mirabilis?

A

5%

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10
Q

What % of nosocomial UTI’s are from E. coli?

A

40%

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11
Q

What % of nosocomial UTI’s are from other gram negatives?

A

25%

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12
Q

What % of nosocomial UTI’s are from other gram positives?

A

16%

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13
Q

What % of nosocomial UTI’s are from Proteus?

A

11%

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14
Q

What % of nosocomial UTI’s are from Cadida?

A

5%

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15
Q

What is the virulence factor for Proteus to cause urinary stones?

A

urease

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16
Q

Why are Cirobacter, Klebsiella, Enterobacter, Proteus, and Pseudomonas aeruginosa more frequently found in hospital-acquired UTI’s?

A

Because their resistance to antibiotics

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17
Q

Case: a young sexually active woman presents with a UTI. Which bug is common in these people?

A

Staphylococcus saprophyticus

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18
Q

So the other forms of coagulase-neg staph (epidermidis and enterococcus) are common in which patients?

A

Hospitalized pts

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19
Q

How do the human polyomaviruses (JC virus and BK virus) enter the body?

A

Respiratory tract

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20
Q

After entering the respiratory tract, where do the human polyomaviruses reside and become latent?

A

Kidneys

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21
Q

In which “situation” can human polyomaviruses reactivate asympatomatically and present as large amounts of viruses in the urine?

A

Pregnancy

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22
Q

Reactivation of human polyomaviruses in immunocompromised hosts may lead to what condition?

A

Hemorrhagic cystitis

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23
Q

In addition to human polyomaviruses, which other virus can cause hemorrhagic cystitis?

A

Adenovirus

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24
Q

Which parasite infectiosn result in cystitis and hematuria?

A

Schistosoma haematobium

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25
Q

What is the vector for Schistosoma haematobium?

A

Aquatic snails

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26
Q

How do the infected snail larvae enter the host?

A

By penetrating the skin

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27
Q

Where does Schistosoma haematobium mature in the body?

A

Liver

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28
Q

After maturing in the liver and entering the blood, how does Schistosoma haematobium enter the bladder to cause cystitis?

A

by penetrating the beins of the bladder wall

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29
Q

Schistosoma haematobium causes granulomatous reactions in the bladder, which leads to what change in the eggs?

A

calcification

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30
Q

Calcification of a Schistosoma haematobium egg in the bladder may obstruction of a ureter, leading to what pathology of the kidney?

A

Hydronephrosis

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31
Q

How can u screen for Schistosoma haematobium infections to make a Dx?

A

Look for eggs in urine

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32
Q

Where is the spine on the Schistosoma haematobium?

A

“T”erminal end

schistosoma haema”T”obium

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33
Q

Which form of Schistosoma has a spine on the lateral side?

A

Schistosoma mansoni

“M” for “M”iddle

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34
Q

What anatomical defect in females predisposes them to UTI’s?

A

Short urethra

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35
Q

What “activity” predisposes women to UTI’s?

A

Bumpin uglies

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36
Q

What leads to more instances of UTI’s in men, circumcised or uncircumcised?

A

Uncircumcised

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37
Q

How does pregnancy, BPH, renal calculi, tumors, and strictures predispose you to UTI’s?

A

Obstruction

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38
Q

How does loss of neurological control of the bladder and sphincters predispose you to UTI’s?

A

↑ residual volumes

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39
Q

This is the reflux of urine form the bladder cavity up the ureters, which can go to the renal pelvis or parenchyma.

A

Vesicoureteral reflux (VUR)

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40
Q

True or False: diabetes predisposes you to UTI’s.

A

True

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41
Q

This is the main E. coli strain to cause UTI’s.

A

Uropathogenic E. coli (UPEC)

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42
Q

What is the virulence factor on UPEC that allows these organisms to inhibit phagocytosis?

A

Capsular acid polysaccharide (K) antigens

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43
Q

What is the virulence factor on UPEC that allows it to colonize?

A

P. fimbriae (pyelonephritis-associated pili)

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44
Q

What is the virulence factor on UPEC that allows it to adhere to the bladder uroepithelial cells?

A

Mannose-sensitive fimbriae (FimH)

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45
Q

What is the virulence factor on UPEC that allows the organisms to cause damage to the kidney membranes?

A

Hemolysins

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46
Q

What is the virulence factor of Proteus that causes pyelonephritis and stones?

A

Urease

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47
Q

At what level of organisms/mL on urinalysis do you need to determine a UTI?

A

> 10^5 organisms/mL

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48
Q

During what part of the stream is urine collected?

A

Mid-stream

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49
Q

This is the term for collecting urine mid-stream and cleaning the external genetalia which allows you to contain the cleanest and purest result for a urinalysis.

A

Clean catch

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50
Q

How often do you collect routine specimens for M. tuberculosis?

A

3 early morning urine samples on consecutive days

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51
Q

How do you collect for a S. Haematobium infection?

A

the last few mL of a urine sample in the early afternoon after exercise

(get them eggs for brunch!)

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52
Q

What class of drugs is trimethoprim?

A

Antimetabolite/nucleic acid synthesis inhibitor

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53
Q

What is the increasing problem with trimethoprim?

A

incidence of resistant strains increasing

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54
Q

What class of drug is co-trimoxazole?

A

it’s a combo of trimethropim with sulphamethoxazole (also an antimetabolite nucleiuc acid synthesis inhbiitor)

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55
Q

What is the first line treatment for UTI’s?

A

co-trimoxazole

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56
Q

What is the class of drug for nitrofurantoin?

A

Urinary antiseptic

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57
Q

When do you use nitrofurantoin?

A

for uncomplicated UTI caused by E. coli and S. sapro

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58
Q

Why can’t you use nitrofurantoin for proteus?

A

It’s not active in alkaline pH

59
Q

What is the class of drug for cirpofloxacin-floxacin family?

60
Q

Though cipro is a pretty broad-spectrum agent, what bug does it not work against?

A

Enterococci

61
Q

What 3 parts of the kidney are affected by pyelonephritis?

A

Tubules, interstitum, and renal pelvis

62
Q

What is the main causitive agent for acute pyelonephritis?

A

bacterial infection

63
Q

In chronic pyelonephritis, bacterial infection plays a dominant role, but what other factors play a role?

A

VUR and obstruction

64
Q

What is the most common bacterial to cause pyelonephritis?

65
Q

Who is susceptible to pyelonephritis from polyomavirus, CMV, and adenovirus?

A

Immunocompromised

66
Q

What is the most common transmission for pyelonephritis?

A

From own fecal flora (endogenous infection)

67
Q

What are the 2 etiologies for the hematogenous cause of pyelonephritis?

A

Septicemia or infective endocarditis

68
Q

Where is the most common location where spread occurs from in pyelonephritis?

A

Lower urinary tract

69
Q

What is the first step in a UTI?

A

colonization of the distal urethra and introitus

70
Q

What virulence factors do bacteria use to adhere to the urethral epithelium?

A

Adhesions and pili

71
Q

After colonicaztion of the distal urethra, what is the 2nd step in ascending infections?

A

Spread from the urethra –> bladder

72
Q

What problems might exist to cause further ascending infection from the bladder?

A

Obstruction and subsequent stasis

73
Q

So if there’s an obstruction, the further ascending infection can continue of there’s what congenital problem?

74
Q

Once the VUR shoots bacteria up the ureter and into the renal pelvis, what can the kidney do to further spread bacteria to the papillae and into the renal parenchyma?

A

Intrarenal reflux

75
Q

What 2 locations in the kidney are most common for pyelonephritis?

A

Upper and lower poles

76
Q

This is an acute suppurative inflammation of the kidney caused by bacterial and sometimes viral infection, either from hematogenous or ascending spread.

A

Acute pyelonephritis

77
Q

What are the 3 hallmarks of acute pyelonephritis?

A

Patchy interstitial suppurative inflammation
Intratubular aggregates of neutrophils
Tubular necrosis

(PIT)

78
Q

Once bacteria spreads from the interstitial tissue –> tubules, what causes destruction of the tubules in acute pyelonephritis?

A

Neutrophils

79
Q

True or False: glomeruli are always destroyed in acute pyelonephritis.

80
Q

What are the 2 instances in which glomeruli are destroyed in acute pyelonephritis?

A

Only in severe large areas of necrosis and in fungal pyelonephritis (Candida)

81
Q

This is the complication of acute pyelonephritis in which there is coagulative necrosis of the renal papillae and is usually b/l.

A

Papillary necrosis

82
Q

What does SODA stand for in the causes of papillary necrosis?

A

Sickle Cell
Obstructive pyelonephritis
Diabetes
Analgesics

83
Q

This is a complication of acute pyelonephritis where total obstruction of the upper urinary tract causes suppurative exudates fill the renal pelvis, calyces, and ureter with pus.

A

Pyonephrosis

84
Q

This is a complciation of acute pyelonephritis where supporative inflammation bursts through the renal capsule and enters the perinephric tissue.

A

Perinephric abscess

85
Q

What are the acute Sx of acute pyelonephritis?

A

Flank pain, fever, malaise, and dysuria.

86
Q

What do you see in the urine in acute pyelonephritis?

A

sterile pyuria and WBC casts

87
Q

What do you see in the tubular epithelial cells in polymavirus pyelonephritis?

A

Intranuclear inclusions

88
Q

This is a disorder in which chronic tubulointerstitial inflammation and renal scarring leads to end stage renal disease.

A

Chronic pyelonephritis

89
Q

This si the more common form of chronic pyelonephritis where VUR and interarenal reflux causes renal damage.

A

Reflux nephropathy

90
Q

This is the other cause of chronic pyelonephritis where recurrent infections leads to bouts of renal inflammation and scarring.

A

Chronic obstructive pyelonephritis

91
Q

In chronic pyelonephritis, is renal involvement symmetrical or asymmetrical?

A

Asymmetrical

92
Q

What are the 3 hallmarks of chronic pyelonephritis?

A

Coarse, discrete corticomedullary scars
Blunted calyces
Flattened papilla

93
Q

This is the change in chronic pyelonephritis in which dilated tubules with flattened epithelium fill with colloid casts.

A

Thyroidization of the kidney

94
Q

What bug causes xanthogranulomatous pyelonephritis?

95
Q

What do you see on radiography for chronic pyelonephritis?

A

Asymmatrically contracted kidneys with coarse scars and blunted calyces

96
Q

What happens in the interstitum in chronic pyelonephritis?

A

Interstitial fibrosis?

97
Q

What happens to the tubules in chronic pyelonephritis?

A

Atrophy of tubules

98
Q

What structures confine an “Upper UTI”?

A

anything above the bladder: ureters, kidneys, and peri-renal tissues (pyelonephritis)

99
Q

What are the Sx to an upper UTI?

A

fever, n/v, flank pain, and CVA tenderness

100
Q

What are the Sx to a lower UTI (cystitis)?

A

dysuria, frequency, urgerncy, and viarable suprapubic tenderness

101
Q

What are the 3 first-line treatments to cystitis?

A

Nitrpfurantonin monohydrate or macryocrystals
TMP-SMZ
Fosformycin trometamol

102
Q

What is the 2nd line treatment for cystitis?

A

Flouroquinolones

103
Q

THis is the bactericidal agent (1st line for cystitis) that enters teh abcteria, gets reduced, and damages bacterial DNA.

A

Nitrofurantoin

104
Q

This is the drug that is a syndergistic combination of folate antagonists and blocks purine production and nucleic acid synthesis.

105
Q

This is the abctericidal that inhbiits baacterial cell wall biogenesis by inactivating the enzyme UDP-NAG-3-EPT (MurA).

A

Fosfomycin

106
Q

This is the antibiotic that inhibits nucleic acid synthesis by binding to the alpha subunit of DNA gyrase

A

Fluoroquinolones

107
Q

This is an extended spectrum penicillin that binds specifically to penicillin binding protein 2 (PBP2)

A

Pivmecillinam

108
Q

How long do you give nitrofurantoin, TMP-SMZ, Fosfomycin, and Fluoroquinolones for the treatment of cystitis?

109
Q

How long do u give Pevmecillinam and other B-lactams for the treatment of cystitis?

110
Q

Is the mechanism of resistant to nitrofurantoin known?

111
Q

What are the 3 mechanisms of resistance to TMP-SMZ?

A

Reduced cell permeability
Overproduction of dihydrofolate reductase
Production of altered reductase

112
Q

What is the mechanism of resistance to fluoroquinolones?

A

one or more point mutations in quinolone binding region of the target enzyme

113
Q

What is the mechanism of resistance for fosfomycin?

A

inadequate transport of drug into the cell

114
Q

What is the mechanism of resistance to pivmecillinam?

A

modification of target PBPs

115
Q

What is the first line treatment for pyelonephritis?

A

Fluroquinolones

116
Q

What is the 2nd line treatment for pyelonephritis?

117
Q

What is the treament for mild/moderate pyelonephritis?

A

Oral fluroquinolones + IV cephalosporin or aminoglycoside

118
Q

What are the drugs u give for severe pyelonephritis?

A

IV fluroquinolone, aminoglycoside, cephalosporin, PCN, or carapenam

119
Q

Are fluroquinolones bactericidal or bacteristatic?

A

Bactericidal

120
Q

Which enzymes does fluroquinolones bind to?

A

DNA gyrase (topoisomerase II) and topoisomerase IV

121
Q

What are the 2 main fluroquinolones used?

A

Cipro

Levofloxacin

122
Q

Are aminoglycosides bactericidal or bacteristatic?

A

Bactericidal

123
Q

Which subunit does aminoglcysides bind to?

124
Q

Which site of the subunit (EPA) does aminoglycosides bind to?

125
Q

What is the mechanism of aminoglycosides to kill bacteria?

A

Interferes with assembly of ribisomes

Causes misreading of RNA

126
Q

Are cephalosporins bactericidal or bacteristatic?

A

Bactercidal

127
Q

What class of drug are cephalosporins?

128
Q

What is the MOA of cephalosporins?

A

inhibit PBP crosslinking of the peptidoglycan wall –> cell lysis

129
Q

What are the 3 mechanisms of resistance to fluroquinolones?

A

chromosomal mutations in bacterial DNA gyrase
↓ porins
Efflux systems

130
Q

What are the 2 mechanisms of resistance to aminoglycosides?

A

Absence of O2-dependent transport system

Production of enzymes that modify and inactivate aminoglycosides

131
Q

What are the 3 mechanisms of resistance to cephalosporins?

A

B-lactamases
↓ permeability of the drug (or efflux pump)
Altered PBPs

132
Q

What is the 4th generation cephalosporin that may be used for the treatment of hospital-associated UTI?

133
Q

True or False: for the treament of asymptomatic bacteriuria, you can use amoxicillin, amoxicillin-clavulanate, cephalexin, fosfomycin, and nitrofurantoin

134
Q

Since nitrofurantoin can cause birth defects, what terms in pregnancy can you not use it?

A

1st and 3rd

135
Q

What are the 2 drug classes that are contraindicated in pregnancy?

A

Fluroquinolones (damage articular cartilage)

Tetracyclines (affect bone formation)

136
Q

What are the 4 drugs u can give for 3-7 days for complicated acute cystitis in pregnant women?

A

Amixicillin-clavulanate
Cefpodoxoime
Fosfomycin
Nitrofurantoin

137
Q

You can also use TMP-SMZ for complicated acute cysititis only during which term in pregnancy?

A

2nd

just like nitrofurantoin

138
Q

What is the class of drugs used for the treatment of acute pyelonephritis in pregnant women?

A

3rd generation B-lactams (ceftriaxone, carbapenams)

139
Q

Why are aminoglycosides avoided in the treatment of acute pyelonephritis in pregnant women?

A

Ototoxicity following prolonged fetal exposure

140
Q

This is the class of drugs that can cause adverse effects of the bone marrow, skin, and hair (leukopenia, megaloblastic anemia, stomatitis, GI ulderations, and alopecia).

A

Antifolates

141
Q

Which term should u not use antifolates because of the significant teratogenic risk?

142
Q

This is the drug that selectively inhibits bacterial dihydrofolate reductase (DHR) which is needed for the bacteria to make DNA.

A

Trimethoprim

143
Q

This is the sulfonamide drug that is a structural analong to PABA and inhibits dihydropteroate synthase (DHS) and folate synthesis.

A

Sulfamethoxazole

144
Q

Why are trimethoprim and sulfamethoxazole used together (TMP-SMZ)?

A

they provide syndergistic activity of sequential inhibition of folate synthesis

Renal Too (3 decks)

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