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IPCS > ID exam 2 > Flashcards

ID exam 2 Flashcards

1
Q

____________ describes the presence of bacteria in the bloodstream and is quantified by blood cultures

A

bacteremia

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2
Q

Introduction of _____________ commonly occurs due to a focal source (primary)

A

bacteria

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3
Q

Risk factors for bacteremia

A

age
liver disease, ESRD
functional or anatomic asplenia
immunosuppression
intravenous drug use
corticosteroid use
recent surgical procedures
trauma
urinary retention

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4
Q

bacteremia common gram positive pathogens

A

staphylococcus aureus
stretococcus pneumoniae
enterococcus spp

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5
Q

bacteremia common gram negative pathogens

A

e. coli
klebsiella spp
pseudomonas aeruginosa
salmonella spp

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6
Q

Sepsis is categorized by what while septic shock is categorized by what

A

sepsis: multi-system organ failure
septic shock: sepsis that is refractory to initial resuscitative interventions

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7
Q

pathophysiology of sepsis shock

A

hypovolemic
obstructive
distributive
cardiogenic

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8
Q

Decreased cardiac output causes what

A

decreased venous return
decreased preload

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9
Q

Hypotension causes what

A

decreased organ perfusion
increased anaerobic metabolism

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10
Q

Multi-organ failure categorization

A

progressive
additive

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11
Q

Etiology of distributive shock

A

systemic inflammatory response syndrome (SIRS)
SEPSIS
anaphylaxis
drug/toxin reactions

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12
Q

Distributive shock clinical presentation

A

dyspnea
chills
fatigue
malaise
tachypnea
tachycardia

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13
Q

What is SIRS (systemic inflammatory response syndrome)

A

-bacteremia or systemic infection may be present
-must correlate to PE and lab findings
-does not indicate sepsis w/out meeting 2 or more criteria with presence of confirmed or suspected infection

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14
Q

Criteria for SIRS

A

HR: >90bpm
Temp: <36 C or >38 C
WBC <4,000 or >12,000 cells/mm3 or >10% bands
RR >20 breaths per minute or PaO2 mmHg

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15
Q

SOFA score (sequential organ failure score)

A

not diagnostic or prognostic
multifaceted quantification
-max SOFA score
-mean SOFA score
-delta SOFA score

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16
Q

What is max SOFA score

A

sum of highest score per individuals during entire ICU stay
>15 = predicted mortality of 90%

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17
Q

What is mean SOFA score

A

average of all score for ICU stay
high averages = higher rate of mortality

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18
Q

What is delta SOFA score

A

objective marker for trending progress

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19
Q

qSOFA score (quick sequential organ failure assessment)

A

predictor of outcomes
-not diagnostic or prognostic
- >/= 2 indicates approximately 10% mortality

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20
Q

End Organ Damage

A

lactate >2 mmol/L (lead to acidosis)
systolic BP <90 mmHg (or decrease from >40)
mean arterial pressure <65 mmHg
kidney dysfunction
-creatinine >2 mg/dL
-platelets <100,000 cells/mm3
Liver dysfunction
-INR >1.5

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21
Q

The primary treatment of bacteremia, sepsis, and septic shock relies upon what

A

the eradication of the infection
-Crystalloid fluids
-Vasopressors
-Corticosteroids, +/- thiamine and ascorbic acid – highly controversial

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22
Q

Fluid Resuscitation

A

30 mL/kg of crystalloid fluid
Administered prior to other treatments
May consider colloidal fluids if initial crystalloid resuscitation fails
-Albumin

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23
Q

Fluid Selection

A

0.9% sodium chloride is historic fluid of choice

Concerns about:
-Hyperchloremic acidosis
-Sodium content
-Tonicity

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24
Q

Other fluid selections rather than 0.9% nacl

A

Recent evaluations considering buffered crystalloid solutions:
-Lactated Ringer’s solution
-Plasma-Lyte

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25
Q

Peripheral Line sites

A

hand
foot
AC fossa

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26
Q

Peripheral Line safe for what

A

most medications
fluids
blood products

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27
Q

Central Line: Provides venous access directly to the what

A

superior/inferior vena cava

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28
Q

What are the central line sites and what its safe for

A

subclavian
femoral
AC fossa

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29
Q

What are central lines safe for

A

Medications – necessary for some
Fluids
TPN
Blood products

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30
Q

What is mean arterial pressure

A

average pressure w/in artery
MAP = [(2 x DBP) + SBP] / 3
normal range 70-90 mmHg

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31
Q

What is cardiac output

A

Calculation of blood ejected from ventricle per minute
CO = SV x HR
Males = 5.6 L/min
Females = 4.9 L/min

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32
Q

Vasopressors

A

indicated in profound hypotension after failure of fluid resuscitation
-MAP is target, titrate to >65 mmHg

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33
Q

What are the criteria for qSOFA

A

Hypotension <100
AMS: GCS <13
Tachypnea: RR >22

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34
Q

What drug is the first line agent in septic shock

A

NE
-influences BP (increase HR)
-potent agonist of adrenergic receptors

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35
Q

What drug is the first line agent in anaphylaxis

A

Epi
-additive agent in sepsis and cardiogenic
-agonist of adrenergic receptors

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36
Q

What must you monitor for phenylephrine

A

peripheral venous return

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37
Q

What drug is generally preferred in cardiogenic shock

A

dobutamine
-beta agonism
-increases stroke volume

milrinone
-non adrenergic MOA
-increased cardiac output

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38
Q

Adverse effects of vasopressors can be reversed by what

A

central line preferred for continuous administration
extravasation is serious risk
reversed by:
-phentolamine
-terbutaline
-nitroglycerin ointment

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39
Q

Main adverse effect of vasopressors

A

digital necrosis

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40
Q

Initial therapy in shock management

A

hypovolemia: NE, Epi
sepsis: NE
cardiogenic: dobutamine, milrinone

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41
Q

What agents to use if pseudomonas is a concern in bacteremia

A

cefepime
piperacillin/tazobactam
ceftazidime
antipseudomonal carbapenem

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42
Q

What agents to use if pseudomonas is a concern in bacteremia and patients are immunodeficient and local rate of resistance is >10-20%

A

antipseudomonal beta lactam +
aminoglycoside
fluoroquinolone

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43
Q

What agents to use if MRSA is a concern in bacteremia

A

vanco
dapto

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44
Q

What agents to use if MSSA is a concern in bacteremia

A

nafcillin
cefazolin

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45
Q

Duration of therapy in bacteremia

A

7-14 days with antibiotics

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46
Q

What are the adjunctive therapies in bactermia

A

corticosteroids (septic shock)
Vitamin Supplementation
Ascorbic Acid
Thiamine

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47
Q

MOA of Vancomycin

A

bind D-alanyl-D-alanine preventing amino acids from being incorporated into peptidoglycan synthetase preventing cross-linking

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48
Q

Vancomycin ADME

A

poor oral, IV amin
55% protein bound
glomerular filtration dose adjust for renal patients

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49
Q

Vancomycin effects of age

A

exhibit increased tissue binding, increase Vd and half-life
decrease clearance and increase half life

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50
Q

ADE of vancomycin

A

rash
erythema
hypotension
ototoxicity
nephrotoxicity

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51
Q

MOA of Daptomycin

A

interfere with integrity of cell membrane in gram-positive bacteria. Lipopeptides bind to bacterial membranes and cause rapid depolarization of membrane potential leading to cell death

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52
Q

Daptomycin ADME

A

IV
92% protein bound

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53
Q

ADE of daptomycin

A

GI
metabolic
hematological: anemia
musculoskeletal: myalgia
nervous system
respiratory
CV

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54
Q

DDI in daptomycin

A

increase risk of statin-induced myalgias

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55
Q

Oxazolidinones are totally ___________ and bear no structural relationship to microbial biochemicals

A

synthetic

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56
Q

Linezolid MOA

A

bind to 50s ribosomal subunit
23s rRNA
interfere with A site assembly in initiation stage of protein synthesis and distorts P site

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57
Q

Linezolid ADME

A

100% bioavailability
low protein binding
non-enzymatic
kidney excretion

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58
Q

Linezolid ADE

A

N/V/D
hematologic effects
inhibition of MAO

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59
Q

Rifampin MOA

A

inhibit bacterial DNA dependent RNA polymerase by binding to polymerase subunit deep w/in DNA/RNA channel, causing blockage of elongating RNA

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60
Q

Rifampin ADME

A

80% protein bound
metabolized in liver to active metabolite

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61
Q

Rifampin ADE

A

N/V/D
discolor excreted liquids (yellow, orange, red, brown)
stain teeth and contact lens
liver disease
C. diff
thrush

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62
Q

Rifampin precautions

A

allergies
alcohol induce liver disease
decrease bacterial vaccine efficacy
not for pregnancy

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63
Q

Rifampin DDI

A

speed up removal of many drugs
decrease effectiveness of birth control

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64
Q

Pathophysiology of infective endocarditis

A

endothelial damage
platelet-fibrin deposition and form lesion
bacteremia allows bacterial colonization
form vegetation
structural abnormality in a valve

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65
Q

Pathological criterial for endocarditis

A

microorganisms by culture or histological exam of vegetation, embolized, intracardiac abscess specimen
pathological lesions
vegetation or intracardiac abscess conformed showing active endocarditis

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66
Q

Clinical criteria for IE

A

2 major
1 major, 3 minor
5 minor

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67
Q

Major criteria for endocarditis

A

positive blood cultures
evidence of endocardial involvement
echocardiogram positive (TEE)

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68
Q

Minor criteria for endocarditis

A

predisposition or IVDA
temp >38 C
vascular hemorrgaging or emboli
glomerularnephritis, osler nodes, roth spots, rheumatoid factor
microbio evidence present

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69
Q

Native Valve: PCN sensitive staph and strep drugs

A

pen G
ceftriaxone
pen G plus gentamicin
ceftriaxone plus gentamicin
vancomycin (if can not take -cillins)

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70
Q

Native Valve: PCN resistant staph and strep drugs

A

Naficillin/Oxacillin
Cefazolin
Vancomycin
Daptomycon

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71
Q

Native Valve: methicillin resistant staph and strep drugs

A

Vancomycin
Daptomycin

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72
Q

Enterococci Infections: Sensitive strains drugs

A

Ampicillin plus gentamicin
pen G plus gentamicin
ampicillin plus cefrtiaxone
vancomycin plus gentamicin

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73
Q

Enterococci Infections: Penicillin Resistant strains drugs

A

ampicillin-sulbactam plus genta
vanco plus genta

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74
Q

Enterococci Infections: Enterococcus Faecium Resistant strains drugs

A

Linezolid
Dapto (use this)

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75
Q

Gram negative infection drugs endocarditis

A

ceftriaxone
ampicillin or amp-sulbactam
cipro

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76
Q

Prosthetic valve: strep and staph spp penicillin susceptible drugs

A

pen G
ceftriaxone

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77
Q

Prosthetic valve: strep and staph spp oxacillin susceptible drugs

A

nafcillin or oxacillin
-plus rifampin or genta
vanco
-plus rifampin or genta

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78
Q

Prosthetic valve: strep and staph spp oxacillin resistant drugs

A

Vanco
-plus rifampin or genta

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79
Q

Culture-negative endocarditis native valve drugs

A

vanco plus cefepime
vanco plus ampicillin-sulbactam

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80
Q

Culture-negative endocarditis, early (<1 year) prosthetic valve drugs

A

vanco plus cefepime plus rifampin plus genta

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81
Q

Culture-negative endocarditis, late (>1 year) prosthetic valve drugs

A

vanco plus ceftriaxone

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82
Q

Fluoroquinolone side effects

A

tendon reputure
photosensitivity

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83
Q

Can you use moxifloxacin in children

A

no

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84
Q

Moxifloxacin ADME

A

well protein bound
M: glucuronide, sulfate conjugation
E: feces/urine

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85
Q

Clindamycin formulations

A

liquid, parenteral, topical

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86
Q

Side effect of clindamycin

A

C. diff

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87
Q

Clindamycin therapeutic uses

A

osteomyelitis or joint infections
pelvic inflammatory disease

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88
Q

Clindamycin MOA

A

bind to 50S ribosomal unit of bacteria
early chain elongation

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89
Q

Clindamycin ADME

A

F: 90%
D: penetrates bone
E: urine, bile
(extended half-life for hepatic failure)

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90
Q

Clindamycin DDI

A

CYP3A4 inhibitors
neuromuscular-blocking agents
macrolides
chloramphenicol

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91
Q

Metronidazole MOA

A

anaerobic organisms processing nitroreductase activity destabilize the imidazole ring
nitroso free radical
-metabolites are lethal to anaerobes (cidal action)

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92
Q

Metronidazole ADME

A

GIT complete
crosses placenta
hepatic metabolism
kidney, feces

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93
Q

ADE of Metronidazole

A

disulfram-like alcohol intolerance
deep red-brown color urine

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94
Q

DDI Metronidazole

A

antidepressants
albuterol
cancer meds
BP meds
antipsychotics
malaria, HIV
blood thinners

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95
Q

Purulent SSTI (skin and soft tissue infections)

A

furuncles (hair folicule), carbuncles, cutaneous abcesses, impetigo
-has drainage

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96
Q

Non-Purulent SSTI (skin and soft tissue infections)

A

erysipeals, cellulitis, necrotizing fasciitis

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97
Q

Pathophysiology of SSTI

A

disruption in skin barrier, inadequate blood/nutrient supply, inflammation occurs

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98
Q

Risk factors for SSTI

A

disruption or break in skin barrier***
vascular insufficiency
obesity
uncontrolled DM
IV drug abuse
poor hygiene

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99
Q

Pathogens for SSTI

A

Strep spp
S. aureus
Candida spp
MRSA

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100
Q

Severity of SSTI

A

mild - w/out systemic signs
moderate - systemic signs of infection
severe - temp >38C, HR >90, RR >24, WBC (>12 or <4), immunocompromised patient

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101
Q

What are purulent SSTIs caused by

A

S. aureus
-present with pain, erythema, edema, warmth, drainage

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102
Q

Treatment duration for purulent SSTI

A

5-14 days (mainly 5-7 days)

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103
Q

Treatment for mild purulent SSTI

A

I and D alone

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104
Q

Treatment for moderate purulent SSTI

A

I and D w/ culture and susceptibilities
TMP/SMX or Doxycycline
de-escalate to cephalexin

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105
Q

Treatment for severe purulent SSTI

A

I and D w/ culture and susceptibilities
Vanco, Dapto, Linezolid
de-escalate to cefazolin

106
Q

What are non-purulent SSTIs caused by

A

strep pyogens
strep spp
-present with pain, erythema, edema, warmth
(NO drainage)

107
Q

non-purulent SSTIs treatment duration

A

5-14 days
-may need extension if surgical debridement is required

108
Q

non-purulent SSTIs mild treatment

A

(PO therapy)
Pen VK
Amox
Cephalexin

109
Q

non-purulent SSTIs moderate treatment

A

(IV therapy)
Cefazolin
Ceftriaxone
Ampicillin
Pen G

110
Q

non-purulent SSTIs severe treatment

A

(surgical debridement)
pip-taz, cefepime, meropenem
AND
vanco or dapto

clindamycin (plus 2 above)
linezolid (plus 1 above in place of vanco/dapto)

111
Q

Clinical presentation of non-purulent SSTIs necrotizing fasciitis

A

erythma, warmth, edema, pain, fever, tachycardia,
-involves extremities, perineum, head/neck region
-crepitus or cracking on PE (gas in tissues)

112
Q

non-purulent SSTIs necrotizing fasciitis treatment

A

surgical debridement to prevent injury
empiric therapy should be broad and de-esculated on results

113
Q

non-purulent SSTIs necrotizing fasciitis pathogens

A

strep pyogenes
staphyococcus aureus

114
Q

diabetic foot infections (DFI)

A

common cause of hospitalizations
neuropathy, uncontrolled DM, skin trauma, anatomic abnormalities

115
Q

Not all DFU are _______: its important to not overtreat due to concerns for adverse effect and antimicrobial resistance

A

DFI

116
Q

Mild clinical manifestation of DFI

A

at least 2
-swelling or induration
erythema >0.5 cm to < 2 cm
ulcer
tenderness/pain
warmth
purulent discharge

117
Q

Moderate clinical manifestation of DFI

A

local infection with > 2 cm form wound margin
OR
deeper infection (abcess, osteomyelitis, fasciitis)
AND
w/out systemic sign of infection

118
Q

Severe clinical manifestation of DFI

A

local infection with SIRS
(2: temp >38C or <36C, HR >90, RR >20, WBC >12k ot <4K)

119
Q

mild pathogens and agents in antimicrobial treatment for DFI

A

MSSA, strep spp, MRSA
Cephalexin, Augmentin, Doxycyline, Bactrim

120
Q

Pathogens in moderate and severe DFI

A

MSSA
strep spp
MRSA
enterobacterales
+/- anaerobes

121
Q

DFI treatment in moderate to severe infection with no complicating features

A

augmentin
amp-sulb
cefuroxime
ceftriaxone
cefazolin
+/- metronidazole

122
Q

DFI treatment in moderate to severe infection with recent antibiotics (within last 30 days)

A

Ceftriaxone and Vanco +/- metronidazole

123
Q

DFI treatment in moderate to severe infection with macerated ulcer

A

pip-taz
OR
cefepime + vanco +/- metronidazole

124
Q

DFI treatment in moderate to severe infection with ischemic limb/necrosis/gas forming

A

ceftriaxone + vanco + metronidazole/clindamycin

125
Q

Duration of treatment for mild, moderate/severe, and bone/joint DFI

A

mild: 1-2 weeks or 10 days following surgery
moderate/severe: 2-4 weeks
bone/joint:
-resected 1-2 weeks
-debrided 1-2 weeks
-positive culture of bone margins AFTER resection: 3 wks
-no surgery/dead bone: 6 wks

126
Q

Osteomyeltits common organisms

A

MSSA
MRSA
-present with edema, pain

127
Q

Infection of bone occurs in 3 ways what are they

A

contiguous spread: erosion into bone or bony structures from adjacent tissue (most common)
hematogenous spread: direct inoculation from bacteria within the bloodstream
traumatic or surgical contamination

128
Q

What are the 4 imagine ways of osteomyelitis

A

X-ray (first)
MRI (gold standard)
CT (not bone marrow edema)
Ultrasound (evaluation of soft tissue)

129
Q

osteomyelitis cultures and biomarkers

A

Erythocyte sedimentation rate (ESR)
c-reactive protein (CRP)

130
Q

Osteomyelitis aerobic gram-positive cocci and aerobic gram-negative bacilli treatment

A

ceftriazone + vanco

131
Q

Osteomyelitis MRSA treatment

A

MRSA colonization pior positive cultures for MRSA

132
Q

Osteomyelitis pseudomonas treatment

A

prior positive culture for psedomonas, gangrenous wounds, surgical procedure in prior 3 months

133
Q

Osteomyelitis treatment: hematogenous, contiguous, DFI with osteo, retained implant

A

hematogenous: max 6 weeks
contiguous: max 6 weeks
DFI with osteo: 3-4 weeks
retained implant: 6-12 weeks

134
Q

Septic arthritis common organisms

A

mainly s.
streptococci and gram negative bacilli

135
Q

Septic arthritis pathophysiology

A

bacteria reach joint space, adhere to synovium causing inflammation and tissue ischemia
direct injury to cartilage tissue and purulent exudate increase joint space pressure and cause symptoms

136
Q

Septic arthritis clinical presentation

A

fever, rigor, acute onset of warm/swollen/painful joint with limited range of motion

137
Q

Septic arthritis diagnosis

A

ESR, CRP, WBC elevation
CT or MRI to reveal inflammation or effusion
WBC >50 in synovial fluid***
Antimicrobial therapy should be withheld if patient stable until arthrocentesis can be performed

138
Q

Septic arthritis treatment

A

vanco, dapto, linezolid
gram negative coverage: cefepime or pip=taz (critical ill, immuno, IV drugs)
TMP/SMX, minocycline, linezolid, doxycycline, clindamycin (oral agents for stable pt)

3 weeks treatment

139
Q

Common pathogens in meningitis

A

s. pneumonia***
n. meningitidis (A, B, C, W135, Y pathogenic, gram -)
h. influenzae tybe b (children, infants)

140
Q

Pathophysiology of meningitis

A

meninges (direct or indirect inoculation)
inflammation in CSF, spine, ventricles)
decreased blood and CSF flow
headache, fever, nuchal rigidity, AMS

141
Q

Symptoms of meningitis

A

headaches
altered mental status
high fever
stiff neck
phonophobia

142
Q

Lab tests of meningitis

A

CSF culture
-absence does not rule out (factor timeline)
-presence does not confirm (identify differential diagnosis)

143
Q

Considerations in lumbar puncture for meningitis

A

measure opening pressure
-oncotic gradient (foreign materials increase pressure)
traumatic puncture
-presence of erythrocytes in culture
-must adjust WBC count in CSF

144
Q

Protein and Glucose in bacterial CSF

A

protein: elevated (>50)
glucose: low (<45)

145
Q

<1 month therapy for meningitis

A

ampicillin + cefotaxime
OR
ampicillin + aminoglycoside

146
Q

<1 month common bacterial pathogens for meningitis

A

strep agalactiae
e. coli
listeria monocytogenes
klebsiella species

147
Q

1-23 month therapy for meningitis

A

vanco + 3rd gen cephalosporin

148
Q

1-23 month common bacterial pathogens for meningitis

A

strep pneumoniae
neisseria meningitidis
s. agalactiae
h. influenzae
e. coli

149
Q

2-50 year therapy for meningitis

A

vanco + 3rd gen cephalosporin

150
Q

2-50 year month common bacterial pathogens for meningitis

A

n. meningitidis
s. pneumoniae

151
Q

> 50 year therapy for meningitis

A

vanco + 3rd gen cephalosporin + ampicillin

152
Q

> 50 year common bacterial pathogens for meningitis

A

s. pneumoniae
n. meningitidis
l. monocytogenes
aerobic gram negative bacilli

153
Q

strep pneumoniae therapy

A

vanco + 3rd gen cephalosporin

154
Q

neisseria meningitidis therapy

A

3rd gen cephalosporin

155
Q

listeria monocytogenes and strep agalactiae therapy

A

ampicillin or pen G

156
Q

haemophilus influenzae and e. coli therapy

A

3rd gen cephalosporin

157
Q

Duration of therapy for meningitis

A

10-14 days
must make sure antimicrobials cross BBB

158
Q

What does inflammation caused by meningitis do

A

increase cerebral edema/intracranial pressure
neurologic tissue damage
increase permeability of BBB

159
Q

How to dose dexamethasone

A

give with or before antibiotics
0.15 mg/kg IV q6h
-max 10 mg/day over 4 days

160
Q

Oral vanco MOA

A

bind D-alanyl-D-alanine preventing peptidoglycan synthetase

161
Q

Oral vanco ADME

A

poor absorbed (good for c. diff)
feces excretion

162
Q

ADE of vanco

A

dysgeusia (distorted taste)
neurotoxicity

163
Q

MOA fidaxomicin

A

inhibition of RNA synthesis as mediated by RNA polymerase
-PAE for c. diff

164
Q

ADME fidaxomicin

A

little absorption
active metabolites
feces excretion

165
Q

Rifaximin MOA

A

inhibition of bacterial RNA synthesis by binding to beta subunit of RNA polymerase

166
Q

ADME Rifaximin

A

poor oral
intestinal tract accumulation
feces excretion

167
Q

ADE of Rifaximin

A

flatulence
rectal tenesumus
defecation urgency

168
Q

What is the cornerstone of treating diarrhea

A

fluid and electrolyte replacement

169
Q

What is the clinical presentation of watery diarrhea

A

<10 stools per day
reduced absorption metabolically
etiology of v. cholerae, ETEC, rotavirus, noroviruses

170
Q

What is the clinical presentation of inflammatory diarrhea

A

bloody stool
>10 stools per day
mucosal invasion mechanism
etiology of shigella spp, salmonella spp, campulobacter spp, EHEC, C. diff

171
Q

What are the 3 oral replacement therapies in diarrhea

A

pedialyte
infalyte
oralyte

172
Q

Watery: Causative agent of vibrio cholerae how to get it, clinical presentation, and treatment

A

sewage or drinking water
lose up to 1 L every hour
Doxycycline x1 300 mg dose
Azithromycin 500 mg PO qd x 3d

173
Q

Watery: Causative agent of e. coli how to get it, clinical presentation, and treatment

A

travelers diarrhea, food poisoning
nausea, ab cramp
Loperamide and bismuth subsalicylate
Cipro 750 mg po qd x1-3d
Azithromycin 500 mg po qd x3d

174
Q

Inflammatory: Causative agent of salmonellosis enterica how to get it, clinical presentation, and treatment

A

gram negative bacilli
contaminated food, w/in 72 h, N/V, diarrhea after 72 h
Cipro 750 mg po qd x5-7d

175
Q

Inflammatory: Causative agent of campylobacter jejuni how to get it, clinical presentation, and treatment

A

flagellated curved, gram negative bacilli
pain, fever, diarrhea, frequent stool
NO ANTIMOTILITY agent s

176
Q

When does travelers diarrhea usually occur

A

w/in 10 days of traveling

177
Q

Treatment for travelers diahhrea

A

rehydration therapy
bismuth subsalicylate 525 mg po q30 min up to 8 doses
loperamide 4 mg stat, 2 mg w/ each stool max 16mg/d

178
Q

Antibiotic treatment options for travelers diarrhea

A

Cipro 750 mg po x1
azithromycin (first line for women and pregnant)
rifaxamin

179
Q

Risk factors for C. diff

A

elderly
cancer patients
pt with ng tube
PPIs
exposure to antimicrobial agents

180
Q

Risk factors for recurrent infection of c. diff

A

recurrent CDI infection w/in 6 months
>65 yo
immunocompromised
severe infection on presentation

181
Q

How to prevent spread of c. diff

A

gloving and gowning
soap and water
separate room with dedicated toilet

182
Q

What is the diagnostic criteria for c. diff

A

new onset >3 unformed stools in 24 h
-nucleic acid amplification test (PCR/NAAT)
-toxin A/B

183
Q

When is c. diff considered HO CDI

A

3 days in hospital to 28 days after discharge

184
Q

When is c. diff considered Co-HCFA CDI

A

28 days after discharge to <12 weeks

185
Q

When is c. diff considered CA CDI

A

<12 weeks

186
Q

Non-severe vs severe c. diff classification

A

non-severe: WBC <150,000 AND SCr <1.5
severe: WBC >150,000 OR SCr >1.5

187
Q

FIdaomicin is a macrolide that is bactericidal against _____________, inhibiting RNA synthesis by RNA polymerase

A

c. diff
(>18 yo approved)

188
Q

When to use bezoltoxumab in c. diff

A

bind toxin B
(BBW for CHF)
use in high risk of recurrence

189
Q

C. diff mainstays of treatment

A

fidaxomicin
vanco
metronidazole
bezlotoxuman
hydration
discontinue anti-peristaltic meds

190
Q

What to use in initial CDI episode

A

Fidaxomicin
OR
vanco

191
Q

What to use in first CDI episode

A

Fidaxomicin OR vanco OR bezlotoxumab
(tapered vanco)

192
Q

What to use in second or subsequent CDI recurrence

A

Fidaxomicin OR vanco tapered OR vanco x10d
fecal microbiota transplant
recommended to treat w/ 3 courses of antibiotics

193
Q

What to use in fulminant CDI

A

vanco OR NG tube
if ileus ADD rectal instillation vanco
IV metronidazole added to vanco in ileus

194
Q

Amphotericin B MOA

A

binds to sterol moiety (ergosterol) in membrane of sensitive fungi
polyenes form pores or channels that increase permeability of the membrane

195
Q

Amphotericin B ADME

A

GI negligible
does not penetrate anything
half life of 2 weeks
urine negligible

196
Q

Amphotericin B ADE

A

infusion site rxn
dose-limiting

197
Q

What are the azoles

A

ketoconazole
itraaconazole
fluconazole
voriconazole

198
Q

Azole MOA

A

inhibition of 14-alpha-sterol demethylase
impair biosynthesis of ergosterol
increase membrane permeability

199
Q

Ketoconazole and Itraconazole ADME

A

oral route has been replaced (for keto)
liver metabolism
high rate of ADRs (for keto)

200
Q

Is ketoconazole a CYP450 isozyme inhibitor

A

yes

201
Q

Fluconazole ADME

A

oral, IV
only azole to get into CNS
eliminated by kidneys***
low side effects: hepatotoxicity, rash

202
Q

Itraconazole ADR

A

hepatotoxicity
BBW heart failure because it has a negative ionotrope

203
Q

Vorriconazole ADME

A

high oral bioavailability (also given IV)
metabolized by CYP2C19

204
Q

Vorriconazole ADR

A

not for pregnancy
hepatotoxicity
auditory hallucinations

205
Q

Posaconazole ADME

A

cherry suspension
take with food
high protein bound
eliminated in feces

206
Q

Posaconazole DDI and ADRs

A

CYP3A4
increase AUC of cyclosporine and midazolam
N/V/D, hepatotoxicity

207
Q

What are the echinocandins

A

caspofungin
anidulafungin
micafungin

208
Q

echinocandins ADME

A

lack oral
protein bound
not for pregnancy

209
Q

caspofungin ADME

A

catabolized by hydrolysis and N-acetylation
excreted in urine and feces

210
Q

caspofungin DDIs and ADRs

A

cyclosporine, increase tacrolimus levels, CYP3A4
phlebitis at injection site, histamine like rxns

211
Q

micafungin ADME and DDIs

A

linear pharmacokinetics
eliminated in feces
immunosuppressant: sirolimus, CYP3A4

212
Q

micafungin ADRs

A

histamine release
elevated blood levels of immunosuppressant drugs, cyclosporine and sirolimus

213
Q

anidulafungin ADME

A

cleared by slow chemical degradation
diluent for IV infusion is ethanol

214
Q

Griseofulvin MOA

A

inhibit microtubule function disrupting assembly of mitotic spindle

215
Q

Griseofulvin ADME

A

take with fatty meal
M: liver
E: bile
barbiturates decrease absorption
deposited in keratin precursor cells (new hair or nail growth first to free disease)

216
Q

Griseofulvin ADRs and DDIs

A

photosensitivity
hepatic CYPs
disulfiram like reaction with ethanol

217
Q

Terbinafine MOA

A

inhibition of fungal squalene epoxidase, blocking ergosterol biosynthesis

218
Q

Terbinafine ADME

A

extensive first pass metabolism
highly protein bound
not for pregnancy

219
Q

Terbinafine DDIs

A

rifampin decrease plasma
cimetidine increase plasma

220
Q

Nystatin MOA

A

same as amphotericin B
-co admin w/ antibacterial agents or corticosteroids

221
Q

Clotrimazole MOA

A

alter permeability of fungal cell wall and inhibits activity of enzymes w/in fungal cell

222
Q

Clotrimazole DDIs

A

CYP450 oxidase

223
Q

Miconazole ADRs

A

vaginal: burning, itching, irritation
cutaneous: irritation, burning, maceration
USE during pregnancy

224
Q

Risk factors for fungal skin and nail infections

A

skin trauma
immune suppression (diabetes, HIV)
climate
occlusive clothing
poor nutrition/hygiene
poor circulation

225
Q

Tinea capitis (head)

A

infection begins in hair follicles
inflammatory: pustules and kerions
non-inflam: yellow scaling

226
Q

Tinea corporis (body, ringworm)

A

oval patch with inflamed border
common in children

227
Q

Tinea cruris (groin, jock itch)

A

more in males
inflammed legions, pustules, bilateral, spares genitals

228
Q

Tinea pedis (foot, athletes foot)

A

toes or soles of feet, wet garments
white scaly patches
red inflamed areas

229
Q

Tinea unguium (nails, oncymycosis)

A

nail and nail bed
yellow, thick, brittle

230
Q

Treatment duration for tinea capitis and tinea unguium

A

rx treatment

231
Q

Treatment duration for tinea corporis, tinea cruris, and tinea pedis

A

corporis: 4 wk
cruris: 2 wk
pedis: >4 wk

232
Q

Tinea pedis treatment: small, vesicles, scaling, no inflammation

A

topical antifungal agent (4 wks)

233
Q

Tinea pedis treatment: inflammatory lesions

A

aluminum acetate soln (up to 1 wk)
topical antifungal agent (4 wks)

234
Q

Tinea pedis treatment: wet, soggy

A

aluminum chloride 20-30% (up to 1 wk)
topical antifungal agent (4 wks)

235
Q

Tinea pedis treatment: wet, soggy, fissures

A

aluminum chloride 10% (1 wk)
aluminum chloride 20-30% (up to 1 wk)
topical antifungal agent (4 wks)

236
Q

What are the topical OTC antifungal agents

A

lotrimin ultra cream - butenafine 1%
lotrimin AF cream - clotrimazole 1%
lotrimin AF powder - miconazole nitrate 2%
cruex - miconazole 2%
lamisil AT gel - terbinafine 1%
tinactin cream - tolnaftate 1%

237
Q

When to use aluminum salts

A

astringent: wet, soggy tinea pedis infection decrease inflammation

238
Q

Tea tree oil has antifungal activity against what

A

c. albicans
-nail fungal infection
-athletes foot: 2bidx4wk 10%

239
Q

Cure rate for honey mixture in antifungal use

A

for tinea corporis and tinea cruris

240
Q

Alternative medicines OTC for antifungal

A

Vick Vapor: 48 wk (not cure)
Mustard Oil: microsporum spp, trichophyton spp
Lavender Oil: trichophton spp, c. albicans

241
Q

What topicals to use in <2 years

A

avoid terbinafine

242
Q

What topicals to use in 2-12 years

A

clotrimazole, miconazole, tolnaftate

243
Q

What topicals to use in >12 years

A

clotrimazole, miconazole, tolnaftate, terbinafine, butenafine

244
Q

Risk factors for fungal infections

A

immunosuppression:
active chemo
AIDS
high dose steroids
Clinical marker:
ANC <500 (active neutrophil count)

245
Q

What is ketoconazole used for

A

fungal skin infections
seborrhea dermatitis (dandruff)

246
Q

What is fluconazole used for

A

candidiasis
cryptococcus
(renal dose adjustment for po dose)

247
Q

Itraconazole BBW and counseling

A

PPIs decrease F
take with empty stomach
ventricular dysfunction and heart failure due to QT prolongation

248
Q

Voriconazole counseling points

A

3A4 and 2C9 inhibitor
monitor LFT, SCr, vision, serum
take on empty stomaach 1 hour ac/pc, caution when driving at night, avoid sunlight

249
Q

Posaconazole counseling points

A

LFT, electrolytes
take with full meals

250
Q

Isavucinazonium counseling points

A

short QT
SJS/TEN
monitor LFT, electrolytes

251
Q

What are echinocandins used for

A

candidal infections
ADE: hepato, electrolyte, hyperglycemia
monitor: LFT, electro, glucose

252
Q

Flucytosine MOA

A

penetrate fungal cell membrane then converted to fluorouracil
renal impairment
myelosuppression
NEVER monotherapy

253
Q

What are the premedications preferred to prevent ADE in amphotericin B

A

NS bolus
APAP
Diphenhydramine
morphine/meperidine

254
Q

What is the most common candida infection

A

c. albicans
(c. krusei is increasing)

255
Q

Candida infection risk factors

A

stem or solid organ transplant, HIV, GI surgery, IV catheters, broad antibiotics

256
Q

Initial therapy fo candida infections

A

echinocandin > ampho B, azole

257
Q

What are histoplasmosis

A

histoplasma capsulatum
-soil, chicken feces, bat feces
treatment: ampho B (1-2 wk) then itraconazole 1-2 yr

258
Q

What are blastomycosis

A

blastomyces spp
treat: ampho B (2-6 wk) then itraconazole 1-2 yr

259
Q

What are coccidioidomycosis

A

coccidioides spp (valley fever)
mild mod: fluconazole
severe: ampho B > conventional

260
Q

What is aspergillus

A

mold
mostly pulmonary infections
treatment: voriconazole then ampho B if vor is untolerated

IPCS (9 decks)

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