ID exam 2 Flashcards

1
Q

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

A

bacteremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

bacteremia common gram positive pathogens

A

staphylococcus aureus
stretococcus pneumoniae
enterococcus spp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

bacteremia common gram negative pathogens

A

e. coli
klebsiella spp
pseudomonas aeruginosa
salmonella spp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

pathophysiology of sepsis shock

A

hypovolemic
obstructive
distributive
cardiogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Decreased cardiac output causes what

A

decreased venous return
decreased preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hypotension causes what

A

decreased organ perfusion
increased anaerobic metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Multi-organ failure categorization

A

progressive
additive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Etiology of distributive shock

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Distributive shock clinical presentation

A

dyspnea
chills
fatigue
malaise
tachypnea
tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SOFA score (sequential organ failure score)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is max SOFA score

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is mean SOFA score

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is delta SOFA score

A

objective marker for trending progress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

qSOFA score (quick sequential organ failure assessment)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Fluid Selection

A

0.9% sodium chloride is historic fluid of choice

Concerns about:
-Hyperchloremic acidosis
-Sodium content
-Tonicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Other fluid selections rather than 0.9% nacl

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Peripheral Line sites
hand foot AC fossa
26
Peripheral Line safe for what
most medications fluids blood products
27
Central Line: Provides venous access directly to the what
superior/inferior vena cava
28
What are the central line sites and what its safe for
subclavian femoral AC fossa
29
What are central lines safe for
Medications – necessary for some Fluids TPN Blood products
30
What is mean arterial pressure
average pressure w/in artery MAP = [(2 x DBP) + SBP] / 3 normal range 70-90 mmHg
31
What is cardiac output
Calculation of blood ejected from ventricle per minute CO = SV x HR Males = 5.6 L/min Females = 4.9 L/min
32
Vasopressors
indicated in profound hypotension after failure of fluid resuscitation -MAP is target, titrate to >65 mmHg
33
What are the criteria for qSOFA
Hypotension <100 AMS: GCS <13 Tachypnea: RR >22
34
What drug is the first line agent in septic shock
NE -influences BP (increase HR) -potent agonist of adrenergic receptors
35
What drug is the first line agent in anaphylaxis
Epi -additive agent in sepsis and cardiogenic -agonist of adrenergic receptors
36
What must you monitor for phenylephrine
peripheral venous return
37
What drug is generally preferred in cardiogenic shock
dobutamine -beta agonism -increases stroke volume milrinone -non adrenergic MOA -increased cardiac output
38
Adverse effects of vasopressors can be reversed by what
central line preferred for continuous administration extravasation is serious risk reversed by: -phentolamine -terbutaline -nitroglycerin ointment
39
Main adverse effect of vasopressors
digital necrosis
40
Initial therapy in shock management
hypovolemia: NE, Epi sepsis: NE cardiogenic: dobutamine, milrinone
41
What agents to use if pseudomonas is a concern in bacteremia
cefepime piperacillin/tazobactam ceftazidime antipseudomonal carbapenem
42
What agents to use if pseudomonas is a concern in bacteremia and patients are immunodeficient and local rate of resistance is >10-20%
antipseudomonal beta lactam + aminoglycoside fluoroquinolone
43
What agents to use if MRSA is a concern in bacteremia
vanco dapto
44
What agents to use if MSSA is a concern in bacteremia
nafcillin cefazolin
45
Duration of therapy in bacteremia
7-14 days with antibiotics
46
What are the adjunctive therapies in bactermia
corticosteroids (septic shock) Vitamin Supplementation Ascorbic Acid Thiamine
47
MOA of Vancomycin
bind D-alanyl-D-alanine preventing amino acids from being incorporated into peptidoglycan synthetase preventing cross-linking
48
Vancomycin ADME
poor oral, IV amin 55% protein bound glomerular filtration dose adjust for renal patients
49
Vancomycin effects of age
exhibit increased tissue binding, increase Vd and half-life decrease clearance and increase half life
50
ADE of vancomycin
rash erythema hypotension ototoxicity nephrotoxicity
51
MOA of Daptomycin
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
52
Daptomycin ADME
IV 92% protein bound
53
ADE of daptomycin
GI metabolic hematological: anemia musculoskeletal: myalgia nervous system respiratory CV
54
DDI in daptomycin
increase risk of statin-induced myalgias
55
Oxazolidinones are totally ___________ and bear no structural relationship to microbial biochemicals
synthetic
56
Linezolid MOA
bind to 50s ribosomal subunit 23s rRNA interfere with A site assembly in initiation stage of protein synthesis and distorts P site
57
Linezolid ADME
100% bioavailability low protein binding non-enzymatic kidney excretion
58
Linezolid ADE
N/V/D hematologic effects inhibition of MAO
59
Rifampin MOA
inhibit bacterial DNA dependent RNA polymerase by binding to polymerase subunit deep w/in DNA/RNA channel, causing blockage of elongating RNA
60
Rifampin ADME
80% protein bound metabolized in liver to active metabolite
61
Rifampin ADE
N/V/D discolor excreted liquids (yellow, orange, red, brown) stain teeth and contact lens liver disease C. diff thrush
62
Rifampin precautions
allergies alcohol induce liver disease decrease bacterial vaccine efficacy not for pregnancy
63
Rifampin DDI
speed up removal of many drugs decrease effectiveness of birth control
64
Pathophysiology of infective endocarditis
endothelial damage platelet-fibrin deposition and form lesion bacteremia allows bacterial colonization form vegetation structural abnormality in a valve
65
Pathological criterial for endocarditis
microorganisms by culture or histological exam of vegetation, embolized, intracardiac abscess specimen pathological lesions vegetation or intracardiac abscess conformed showing active endocarditis
66
Clinical criteria for IE
2 major 1 major, 3 minor 5 minor
67
Major criteria for endocarditis
positive blood cultures evidence of endocardial involvement echocardiogram positive (TEE)
68
Minor criteria for endocarditis
predisposition or IVDA temp >38 C vascular hemorrgaging or emboli glomerularnephritis, osler nodes, roth spots, rheumatoid factor microbio evidence present
69
Native Valve: PCN sensitive staph and strep drugs
pen G ceftriaxone pen G plus gentamicin ceftriaxone plus gentamicin vancomycin (if can not take -cillins)
70
Native Valve: PCN resistant staph and strep drugs
Naficillin/Oxacillin Cefazolin Vancomycin Daptomycon
71
Native Valve: methicillin resistant staph and strep drugs
Vancomycin Daptomycin
72
Enterococci Infections: Sensitive strains drugs
Ampicillin plus gentamicin pen G plus gentamicin ampicillin plus cefrtiaxone vancomycin plus gentamicin
73
Enterococci Infections: Penicillin Resistant strains drugs
ampicillin-sulbactam plus genta vanco plus genta
74
Enterococci Infections: Enterococcus Faecium Resistant strains drugs
Linezolid Dapto (use this)
75
Gram negative infection drugs endocarditis
ceftriaxone ampicillin or amp-sulbactam cipro
76
Prosthetic valve: strep and staph spp penicillin susceptible drugs
pen G ceftriaxone
77
Prosthetic valve: strep and staph spp oxacillin susceptible drugs
nafcillin or oxacillin -plus rifampin or genta vanco -plus rifampin or genta
78
Prosthetic valve: strep and staph spp oxacillin resistant drugs
Vanco -plus rifampin or genta
79
Culture-negative endocarditis native valve drugs
vanco plus cefepime vanco plus ampicillin-sulbactam
80
Culture-negative endocarditis, early (<1 year) prosthetic valve drugs
vanco plus cefepime plus rifampin plus genta
81
Culture-negative endocarditis, late (>1 year) prosthetic valve drugs
vanco plus ceftriaxone
82
Fluoroquinolone side effects
tendon reputure photosensitivity
83
Can you use moxifloxacin in children
no
84
Moxifloxacin ADME
well protein bound M: glucuronide, sulfate conjugation E: feces/urine
85
Clindamycin formulations
liquid, parenteral, topical
86
Side effect of clindamycin
C. diff
87
Clindamycin therapeutic uses
osteomyelitis or joint infections pelvic inflammatory disease
88
Clindamycin MOA
bind to 50S ribosomal unit of bacteria early chain elongation
89
Clindamycin ADME
F: 90% D: penetrates bone E: urine, bile (extended half-life for hepatic failure)
90
Clindamycin DDI
CYP3A4 inhibitors neuromuscular-blocking agents macrolides chloramphenicol
91
Metronidazole MOA
anaerobic organisms processing nitroreductase activity destabilize the imidazole ring nitroso free radical -metabolites are lethal to anaerobes (cidal action)
92
Metronidazole ADME
GIT complete crosses placenta hepatic metabolism kidney, feces
93
ADE of Metronidazole
disulfram-like alcohol intolerance deep red-brown color urine
94
DDI Metronidazole
antidepressants albuterol cancer meds BP meds antipsychotics malaria, HIV blood thinners
95
Purulent SSTI (skin and soft tissue infections)
furuncles (hair folicule), carbuncles, cutaneous abcesses, impetigo -has drainage
96
Non-Purulent SSTI (skin and soft tissue infections)
erysipeals, cellulitis, necrotizing fasciitis
97
Pathophysiology of SSTI
disruption in skin barrier, inadequate blood/nutrient supply, inflammation occurs
98
Risk factors for SSTI
disruption or break in skin barrier*** vascular insufficiency obesity uncontrolled DM IV drug abuse poor hygiene
99
Pathogens for SSTI
Strep spp S. aureus Candida spp MRSA
100
Severity of SSTI
mild - w/out systemic signs moderate - systemic signs of infection severe - temp >38C, HR >90, RR >24, WBC (>12 or <4), immunocompromised patient
101
What are purulent SSTIs caused by
S. aureus -present with pain, erythema, edema, warmth, drainage
102
Treatment duration for purulent SSTI
5-14 days (mainly 5-7 days)
103
Treatment for mild purulent SSTI
I and D alone
104
Treatment for moderate purulent SSTI
I and D w/ culture and susceptibilities TMP/SMX or Doxycycline de-escalate to cephalexin
105
Treatment for severe purulent SSTI
I and D w/ culture and susceptibilities Vanco, Dapto, Linezolid de-escalate to cefazolin
106
What are non-purulent SSTIs caused by
strep pyogens strep spp -present with pain, erythema, edema, warmth (NO drainage)
107
non-purulent SSTIs treatment duration
5-14 days -may need extension if surgical debridement is required
108
non-purulent SSTIs mild treatment
(PO therapy) Pen VK Amox Cephalexin
109
non-purulent SSTIs moderate treatment
(IV therapy) Cefazolin Ceftriaxone Ampicillin Pen G
110
non-purulent SSTIs severe treatment
(surgical debridement) pip-taz, cefepime, meropenem AND vanco or dapto clindamycin (plus 2 above) linezolid (plus 1 above in place of vanco/dapto)
111
Clinical presentation of non-purulent SSTIs necrotizing fasciitis
erythma, warmth, edema, pain, fever, tachycardia, -involves extremities, perineum, head/neck region -crepitus or cracking on PE (gas in tissues)
112
non-purulent SSTIs necrotizing fasciitis treatment
surgical debridement to prevent injury empiric therapy should be broad and de-esculated on results
113
non-purulent SSTIs necrotizing fasciitis pathogens
strep pyogenes staphyococcus aureus
114
diabetic foot infections (DFI)
common cause of hospitalizations neuropathy, uncontrolled DM, skin trauma, anatomic abnormalities
115
Not all DFU are _______: its important to not overtreat due to concerns for adverse effect and antimicrobial resistance
DFI
116
Mild clinical manifestation of DFI
at least 2 -swelling or induration erythema >0.5 cm to < 2 cm ulcer tenderness/pain warmth purulent discharge
117
Moderate clinical manifestation of DFI
local infection with > 2 cm form wound margin OR deeper infection (abcess, osteomyelitis, fasciitis) AND w/out systemic sign of infection
118
Severe clinical manifestation of DFI
local infection with SIRS (2: temp >38C or <36C, HR >90, RR >20, WBC >12k ot <4K)
119
mild pathogens and agents in antimicrobial treatment for DFI
MSSA, strep spp, MRSA Cephalexin, Augmentin, Doxycyline, Bactrim
120
Pathogens in moderate and severe DFI
MSSA strep spp MRSA enterobacterales +/- anaerobes
121
DFI treatment in moderate to severe infection with no complicating features
augmentin amp-sulb cefuroxime ceftriaxone cefazolin +/- metronidazole
122
DFI treatment in moderate to severe infection with recent antibiotics (within last 30 days)
Ceftriaxone and Vanco +/- metronidazole
123
DFI treatment in moderate to severe infection with macerated ulcer
pip-taz OR cefepime + vanco +/- metronidazole
124
DFI treatment in moderate to severe infection with ischemic limb/necrosis/gas forming
ceftriaxone + vanco + metronidazole/clindamycin
125
Duration of treatment for mild, moderate/severe, and bone/joint DFI
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
Osteomyeltits common organisms
MSSA MRSA -present with edema, pain
127
Infection of bone occurs in 3 ways what are they
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
What are the 4 imagine ways of osteomyelitis
X-ray (first) MRI (gold standard) CT (not bone marrow edema) Ultrasound (evaluation of soft tissue)
129
osteomyelitis cultures and biomarkers
Erythocyte sedimentation rate (ESR) c-reactive protein (CRP)
130
Osteomyelitis aerobic gram-positive cocci and aerobic gram-negative bacilli treatment
ceftriazone + vanco
131
Osteomyelitis MRSA treatment
MRSA colonization pior positive cultures for MRSA
132
Osteomyelitis pseudomonas treatment
prior positive culture for psedomonas, gangrenous wounds, surgical procedure in prior 3 months
133
Osteomyelitis treatment: hematogenous, contiguous, DFI with osteo, retained implant
hematogenous: max 6 weeks contiguous: max 6 weeks DFI with osteo: 3-4 weeks retained implant: 6-12 weeks
134
Septic arthritis common organisms
mainly s. streptococci and gram negative bacilli
135
Septic arthritis pathophysiology
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
Septic arthritis clinical presentation
fever, rigor, acute onset of warm/swollen/painful joint with limited range of motion
137
Septic arthritis diagnosis
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
Septic arthritis treatment
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
Common pathogens in meningitis
s. pneumonia*** n. meningitidis (A, B, C, W135, Y pathogenic, gram -) h. influenzae tybe b (children, infants)
140
Pathophysiology of meningitis
meninges (direct or indirect inoculation) inflammation in CSF, spine, ventricles) decreased blood and CSF flow headache, fever, nuchal rigidity, AMS
141
Symptoms of meningitis
headaches altered mental status high fever stiff neck phonophobia
142
Lab tests of meningitis
CSF culture -absence does not rule out (factor timeline) -presence does not confirm (identify differential diagnosis)
143
Considerations in lumbar puncture for meningitis
measure opening pressure -oncotic gradient (foreign materials increase pressure) traumatic puncture -presence of erythrocytes in culture -must adjust WBC count in CSF
144
Protein and Glucose in bacterial CSF
protein: elevated (>50) glucose: low (<45)
145
<1 month therapy for meningitis
ampicillin + cefotaxime OR ampicillin + aminoglycoside
146
<1 month common bacterial pathogens for meningitis
strep agalactiae e. coli listeria monocytogenes klebsiella species
147
1-23 month therapy for meningitis
vanco + 3rd gen cephalosporin
148
1-23 month common bacterial pathogens for meningitis
strep pneumoniae neisseria meningitidis s. agalactiae h. influenzae e. coli
149
2-50 year therapy for meningitis
vanco + 3rd gen cephalosporin
150
2-50 year month common bacterial pathogens for meningitis
n. meningitidis s. pneumoniae
151
>50 year therapy for meningitis
vanco + 3rd gen cephalosporin + ampicillin
152
>50 year common bacterial pathogens for meningitis
s. pneumoniae n. meningitidis l. monocytogenes aerobic gram negative bacilli
153
strep pneumoniae therapy
vanco + 3rd gen cephalosporin
154
neisseria meningitidis therapy
3rd gen cephalosporin
155
listeria monocytogenes and strep agalactiae therapy
ampicillin or pen G
156
haemophilus influenzae and e. coli therapy
3rd gen cephalosporin
157
Duration of therapy for meningitis
10-14 days must make sure antimicrobials cross BBB
158
What does inflammation caused by meningitis do
increase cerebral edema/intracranial pressure neurologic tissue damage increase permeability of BBB
159
How to dose dexamethasone
give with or before antibiotics 0.15 mg/kg IV q6h -max 10 mg/day over 4 days
160
Oral vanco MOA
bind D-alanyl-D-alanine preventing peptidoglycan synthetase
161
Oral vanco ADME
poor absorbed (good for c. diff) feces excretion
162
ADE of vanco
dysgeusia (distorted taste) neurotoxicity
163
MOA fidaxomicin
inhibition of RNA synthesis as mediated by RNA polymerase -PAE for c. diff
164
ADME fidaxomicin
little absorption active metabolites feces excretion
165
Rifaximin MOA
inhibition of bacterial RNA synthesis by binding to beta subunit of RNA polymerase
166
ADME Rifaximin
poor oral intestinal tract accumulation feces excretion
167
ADE of Rifaximin
flatulence rectal tenesumus defecation urgency
168
What is the cornerstone of treating diarrhea
fluid and electrolyte replacement
169
What is the clinical presentation of watery diarrhea
<10 stools per day reduced absorption metabolically etiology of v. cholerae, ETEC, rotavirus, noroviruses
170
What is the clinical presentation of inflammatory diarrhea
bloody stool >10 stools per day mucosal invasion mechanism etiology of shigella spp, salmonella spp, campulobacter spp, EHEC, C. diff
171
What are the 3 oral replacement therapies in diarrhea
pedialyte infalyte oralyte
172
Watery: Causative agent of vibrio cholerae how to get it, clinical presentation, and treatment
sewage or drinking water lose up to 1 L every hour Doxycycline x1 300 mg dose Azithromycin 500 mg PO qd x 3d
173
Watery: Causative agent of e. coli how to get it, clinical presentation, and treatment
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
Inflammatory: Causative agent of salmonellosis enterica how to get it, clinical presentation, and treatment
gram negative bacilli contaminated food, w/in 72 h, N/V, diarrhea after 72 h Cipro 750 mg po qd x5-7d
175
Inflammatory: Causative agent of campylobacter jejuni how to get it, clinical presentation, and treatment
flagellated curved, gram negative bacilli pain, fever, diarrhea, frequent stool NO ANTIMOTILITY agent s
176
When does travelers diarrhea usually occur
w/in 10 days of traveling
177
Treatment for travelers diahhrea
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
Antibiotic treatment options for travelers diarrhea
Cipro 750 mg po x1 azithromycin (first line for women and pregnant) rifaxamin
179
Risk factors for C. diff
elderly cancer patients pt with ng tube PPIs exposure to antimicrobial agents
180
Risk factors for recurrent infection of c. diff
recurrent CDI infection w/in 6 months >65 yo immunocompromised severe infection on presentation
181
How to prevent spread of c. diff
gloving and gowning soap and water separate room with dedicated toilet
182
What is the diagnostic criteria for c. diff
new onset >3 unformed stools in 24 h -nucleic acid amplification test (PCR/NAAT) -toxin A/B
183
When is c. diff considered HO CDI
3 days in hospital to 28 days after discharge
184
When is c. diff considered Co-HCFA CDI
28 days after discharge to <12 weeks
185
When is c. diff considered CA CDI
<12 weeks
186
Non-severe vs severe c. diff classification
non-severe: WBC <150,000 AND SCr <1.5 severe: WBC >150,000 OR SCr >1.5
187
FIdaomicin is a macrolide that is bactericidal against _____________, inhibiting RNA synthesis by RNA polymerase
c. diff (>18 yo approved)
188
When to use bezoltoxumab in c. diff
bind toxin B (BBW for CHF) use in high risk of recurrence
189
C. diff mainstays of treatment
fidaxomicin vanco metronidazole bezlotoxuman hydration discontinue anti-peristaltic meds
190
What to use in initial CDI episode
Fidaxomicin OR vanco
191
What to use in first CDI episode
Fidaxomicin OR vanco OR bezlotoxumab (tapered vanco)
192
What to use in second or subsequent CDI recurrence
Fidaxomicin OR vanco tapered OR vanco x10d fecal microbiota transplant recommended to treat w/ 3 courses of antibiotics
193
What to use in fulminant CDI
vanco OR NG tube if ileus ADD rectal instillation vanco IV metronidazole added to vanco in ileus
194
Amphotericin B MOA
binds to sterol moiety (ergosterol) in membrane of sensitive fungi polyenes form pores or channels that increase permeability of the membrane
195
Amphotericin B ADME
GI negligible does not penetrate anything half life of 2 weeks urine negligible
196
Amphotericin B ADE
infusion site rxn dose-limiting
197
What are the azoles
ketoconazole itraaconazole fluconazole voriconazole
198
Azole MOA
inhibition of 14-alpha-sterol demethylase impair biosynthesis of ergosterol increase membrane permeability
199
Ketoconazole and Itraconazole ADME
oral route has been replaced (for keto) liver metabolism high rate of ADRs (for keto)
200
Is ketoconazole a CYP450 isozyme inhibitor
yes
201
Fluconazole ADME
oral, IV only azole to get into CNS eliminated by kidneys*** low side effects: hepatotoxicity, rash
202
Itraconazole ADR
hepatotoxicity BBW heart failure because it has a negative ionotrope
203
Vorriconazole ADME
high oral bioavailability (also given IV) metabolized by CYP2C19
204
Vorriconazole ADR
not for pregnancy hepatotoxicity auditory hallucinations
205
Posaconazole ADME
cherry suspension take with food high protein bound eliminated in feces
206
Posaconazole DDI and ADRs
CYP3A4 increase AUC of cyclosporine and midazolam N/V/D, hepatotoxicity
207
What are the echinocandins
caspofungin anidulafungin micafungin
208
echinocandins ADME
lack oral protein bound not for pregnancy
209
caspofungin ADME
catabolized by hydrolysis and N-acetylation excreted in urine and feces
210
caspofungin DDIs and ADRs
cyclosporine, increase tacrolimus levels, CYP3A4 phlebitis at injection site, histamine like rxns
211
micafungin ADME and DDIs
linear pharmacokinetics eliminated in feces immunosuppressant: sirolimus, CYP3A4
212
micafungin ADRs
histamine release elevated blood levels of immunosuppressant drugs, cyclosporine and sirolimus
213
anidulafungin ADME
cleared by slow chemical degradation diluent for IV infusion is ethanol
214
Griseofulvin MOA
inhibit microtubule function disrupting assembly of mitotic spindle
215
Griseofulvin ADME
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
Griseofulvin ADRs and DDIs
photosensitivity hepatic CYPs disulfiram like reaction with ethanol
217
Terbinafine MOA
inhibition of fungal squalene epoxidase, blocking ergosterol biosynthesis
218
Terbinafine ADME
extensive first pass metabolism highly protein bound not for pregnancy
219
Terbinafine DDIs
rifampin decrease plasma cimetidine increase plasma
220
Nystatin MOA
same as amphotericin B -co admin w/ antibacterial agents or corticosteroids
221
Clotrimazole MOA
alter permeability of fungal cell wall and inhibits activity of enzymes w/in fungal cell
222
Clotrimazole DDIs
CYP450 oxidase
223
Miconazole ADRs
vaginal: burning, itching, irritation cutaneous: irritation, burning, maceration USE during pregnancy
224
Risk factors for fungal skin and nail infections
skin trauma immune suppression (diabetes, HIV) climate occlusive clothing poor nutrition/hygiene poor circulation
225
Tinea capitis (head)
infection begins in hair follicles inflammatory: pustules and kerions non-inflam: yellow scaling
226
Tinea corporis (body, ringworm)
oval patch with inflamed border common in children
227
Tinea cruris (groin, jock itch)
more in males inflammed legions, pustules, bilateral, spares genitals
228
Tinea pedis (foot, athletes foot)
toes or soles of feet, wet garments white scaly patches red inflamed areas
229
Tinea unguium (nails, oncymycosis)
nail and nail bed yellow, thick, brittle
230
Treatment duration for tinea capitis and tinea unguium
rx treatment
231
Treatment duration for tinea corporis, tinea cruris, and tinea pedis
corporis: 4 wk cruris: 2 wk pedis: >4 wk
232
Tinea pedis treatment: small, vesicles, scaling, no inflammation
topical antifungal agent (4 wks)
233
Tinea pedis treatment: inflammatory lesions
aluminum acetate soln (up to 1 wk) topical antifungal agent (4 wks)
234
Tinea pedis treatment: wet, soggy
aluminum chloride 20-30% (up to 1 wk) topical antifungal agent (4 wks)
235
Tinea pedis treatment: wet, soggy, fissures
aluminum chloride 10% (1 wk) aluminum chloride 20-30% (up to 1 wk) topical antifungal agent (4 wks)
236
What are the topical OTC antifungal agents
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
When to use aluminum salts
astringent: wet, soggy tinea pedis infection decrease inflammation
238
Tea tree oil has antifungal activity against what
c. albicans -nail fungal infection -athletes foot: 2bidx4wk 10%
239
Cure rate for honey mixture in antifungal use
for tinea corporis and tinea cruris
240
Alternative medicines OTC for antifungal
Vick Vapor: 48 wk (not cure) Mustard Oil: microsporum spp, trichophyton spp Lavender Oil: trichophton spp, c. albicans
241
What topicals to use in <2 years
avoid terbinafine
242
What topicals to use in 2-12 years
clotrimazole, miconazole, tolnaftate
243
What topicals to use in >12 years
clotrimazole, miconazole, tolnaftate, terbinafine, butenafine
244
Risk factors for fungal infections
immunosuppression: active chemo AIDS high dose steroids Clinical marker: ANC <500 (active neutrophil count)
245
What is ketoconazole used for
fungal skin infections seborrhea dermatitis (dandruff)
246
What is fluconazole used for
candidiasis cryptococcus (renal dose adjustment for po dose)
247
Itraconazole BBW and counseling
PPIs decrease F take with empty stomach ventricular dysfunction and heart failure due to QT prolongation
248
Voriconazole counseling points
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
Posaconazole counseling points
LFT, electrolytes take with full meals
250
Isavucinazonium counseling points
short QT SJS/TEN monitor LFT, electrolytes
251
What are echinocandins used for
candidal infections ADE: hepato, electrolyte, hyperglycemia monitor: LFT, electro, glucose
252
Flucytosine MOA
penetrate fungal cell membrane then converted to fluorouracil renal impairment myelosuppression NEVER monotherapy
253
What are the premedications preferred to prevent ADE in amphotericin B
NS bolus APAP Diphenhydramine morphine/meperidine
254
What is the most common candida infection
c. albicans (c. krusei is increasing)
255
Candida infection risk factors
stem or solid organ transplant, HIV, GI surgery, IV catheters, broad antibiotics
256
Initial therapy fo candida infections
echinocandin > ampho B, azole
257
What are histoplasmosis
histoplasma capsulatum -soil, chicken feces, bat feces treatment: ampho B (1-2 wk) then itraconazole 1-2 yr
258
What are blastomycosis
blastomyces spp treat: ampho B (2-6 wk) then itraconazole 1-2 yr
259
What are coccidioidomycosis
coccidioides spp (valley fever) mild mod: fluconazole severe: ampho B > conventional
260
What is aspergillus
mold mostly pulmonary infections treatment: voriconazole then ampho B if vor is untolerated