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Week 3--even more Flashcards

1
Q

define SIDS

A

the sudden death of an infant under one year of age which remains unexplained after thorough case investigation, including the performance of a complete autopsy, examination of the death scene and review of the clinical history

generally agreed that takes places during sleep

multifactorial disorder arising from a combination of genetic, metabolic, and environmental factors

overlap in risk factors for suffocation/entrapment

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2
Q

describe a model for SIDS risk

A

the triple-risk model

vulnerable infant + critical development period (0-12 post natal months) + exogenous stressor

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3
Q

intrinsic risk factors for SIDS

A

male gender (65%)

prematurity (30%)

genetic polymorphisms (35%)

prenatal exposures to cigarettes and/or alcohol (54% prenatal exposure to smoke–the more the mother smokes, the higher the risk of SIDS)

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4
Q

extrinsic risk factors for SIDS

A

prone or side sleep position

bed sharing

over bundling

soft bedding

face covered

**majority of deaths associated with a new sleeping arrangement

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5
Q

where does SIDS rank in the causes of infant death

A

third top cause

top is perinatal conditions, then congenital abnormalities

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6
Q

when is the peak of SIDS death (infant age wise)

A

peaks between 2-4 months–fewer SIDS deaths occur after 6 mo

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7
Q

where is the safest place for an infant to sleep

A

a crib, cradle or bassinet that meets current Canadian regulations

avoid loose bedding, pillows, toys and bumper pads

avoid caregiving, especially if caregiver smokes, is under the influence of drugs/alcohol or is over tired, or if the infant is under 4 mo

baby should sleep supine

*infants who share a room with a parent or caregiver (but not the same bed–crib next to adults bed) have a lower risk of SIDS

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8
Q

how are breastfeeding and SIDS related

A

breastfeeding is protective

exclusive breastfeeding may decrease the risk of SIDS by as much as 50%

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9
Q

how do you diagnose diabetes mellitus

A
  1. symptoms of hyperglycemia AND random plasma glucose above 11.1 mmol/L
  2. fasting plasma glucose above 7 mmol/L
  3. plasma glucose above 11.1 mmol/L 2 hours post 75g oral glucose load (GTT)
  4. HbA1c above 6.5%
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10
Q

what investigations should be done when working up DM

A 
CBC
BUN
ACR
Cr
lipids 
UA
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11
Q

how to manage DM in new diagnosis

A
  1. lifestyle modifications
  2. patient education–> wider health problems, like smoking, elevated cholesterol, obesity, HTN (may accelerate bad effects of DM)
  3. medications
  4. vaccinate for pneumococcus and influenza
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12
Q

name the 6 types of anti-hyperglycemics used in DM

A
  1. sulfonylureas
  2. meglitinides
  3. thiazolidinediones
  4. alpha-glucosidase inhibitor
  5. peptide analogues
  6. biguianides
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13
Q

name two sulfonylureas

A

glyburide

diamicron

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14
Q

how do sulfonylureas like glyburide and diamicron work

A

are insulin secretagogues which trigger insulin release (can cause hypoglycemia)

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15
Q

name one meglitinide

A

replaglinide

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16
Q

how do meglitinides like replaglinide work

A

are short acting insulin secretagogues

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17
Q

name one biguanide

A

metformin

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18
Q

how do biguanides like metformin work

A

insulin sensitizer–reduces hepatic glucose output and increases glucose uptake by cells

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19
Q

name two thiazolidinediones

A

rosiglitazone, pioglitazone

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20
Q

how do thiazolidinediones like rosiglitazone, pioglitazone work

A

insulin sensitizers

bind PPARy leading to better glucose use by the cell

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21
Q

how do thiazolidinediones like rosiglitazone, pioglitazone work

A

insulin sensitizers

bind PPARy leading to better glucose use by the cell

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22
Q

name one alpha-glucosidase inhibitor

A

acarbose

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23
Q

how do alpha-glucosidase inhibitors like acarbose work

A

slow digestion of starch in the small intestine so that glucose from the meal enters the blood stream more slowly and can be matched more effectively by impaired insulin response or sensitivity

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24
Q

name two peptide analogues used int he treatment of DM

A

GLP-1

GIP

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25
Q

how do peptide analogs like GLP-1 and GIP work

A

insulin secretagogues that inhibit glucagon release and may also decrease gastric motility

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26
Q

who should receive a yearly mammogram

A

women between ages 40-79 of normal risk

under or over that by special request

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27
Q

generalized menopause sx

A

hot flashes

mood

cognitive changes

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28
Q

focal menopause sx

A

dyspareunia

pruritis

urethritis

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29
Q

when is HRT indicated for menopause

A

for osteoporosis and hot flashes

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30
Q

when is HRT contraindicated for menopause

A

pregnancy

hepatic disease

clots

postmenopausal bleeding

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31
Q

what are the risks of HRT treatment for menopause

A

increase breast ca risk if over 5 years of use

increased risk VTE if over 5 years use (less with transdermal vs oral route)

CVD risk if started when over 70 or if more than 10 years since menopause onset

controversial stroke risk

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32
Q

what two cancers are decreased in risk with HRT for menopause

A

colon and ovarian

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33
Q

in addition to HRT, what other meds can be used to help with menopause sx

A

SSRI

SNRI

clonidine

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34
Q

what % fractures in women over 50 are fragility fractures

A

80%

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35
Q

what history suggests possible colon ca

A

change in bowel habits

blood in stool or rectum

thin stools

weight loss

fever

night sweats

general stomach discomfort

frequent gas pains

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36
Q

risk factors for colon ca

A

family history

IBD

polyps

post radiation therapy

obesity

age above 50

family history of inherited cancers

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37
Q

when should you start screening for colon ca

A

men over 50

FOB q2years (low sens and spec)

can use colonoscopy for screening q10 years after 50 years old

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38
Q

when do you start paps

A

within 3 years of first sexual contact (includes touching and intercourse)

yearly until 3 normal tests in a row then every 2 years

stop at age 69 if 3 or more normal results in a row in last 10 years and no history of moderately or severely abnormal paps

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39
Q

what does “mild atypia” represent on a pap result

A

low risk lesion

repeat pap in 6 months then follow for 2 years

may resolve spontaneously

if still present at 2 years, follow with colposcopy and biopsy

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40
Q

how do you manage moderate or severe atypica on pap result

A

refer for colposcopy and biopsy

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41
Q

who should get PSA testing

A

recommend for asymptomatic men who are well informed about the risks of over diagnosis and over treatment but still wish to pursue the benefits of early diagnosis of prostate cancer

evidence from RCTs suggest that mortality decreases with PSA screening for early detection but that significant number of men will need to be treated (with all those risk) who would otherwise not have had a problem

decision should be individualized

offer to asymptomatic men over 50

abnormal–refer to uro

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42
Q

what factors influence abx selection

A
  1. agent factors
    - type of bacteria suspected
    - suspected resistance patterns
  2. host factors
    - site of infection
    - abx aimed at certain site
    - pregnancy
    - renal failure
    - allergy
    - immunocompromised
  3. enviro factors
    - nosocomial vs community
    - travel
    - exposures
    - IVDU
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43
Q

what is the abx target usually when u are treating gram + bugs

A

the cells wall is it is large

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44
Q

what is the target of abx in most gram - bugs

A

inner and outer membrane

can also target intrecellularly

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45
Q

name 4 classes of abx that are cell wall synthesis inhibitors

A

penicillins

cephalosporins

carbapenems

glycopeptides

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46
Q

name 5 classes/drugs of abx that are protein synthesis inhibitors

A

aminoglycosides

tetracyclines

macrolides

clindamycin

linezolid

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47
Q

name 3 meds/classes of abx that are DNA gyrase inhibitors

A

quinolones

flagyl

rifampin

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48
Q

name one abx that is an antimetabolite

A

sulphonamides

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49
Q

what is the general structure of the B lactam/cell wall agent abx

A

all contain a B-lactam nucleus in molecular structure

work by inhibiting cell wall synthesis

there is cross reactivity between classes

engage in TIME DEPENDENT killing of bugs (need frequent dosing to keep around for a sustained time)

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50
Q

how do penicillins work

A

stop cell wall cross linking

results in loss of cell wall integrity in the bug

leads to osmotic lysis

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51
Q

what bugs do penicillins target

A

mainly gram + –> streptococcus species (GAS, strep. viridans) and syphilis (IM, or IV if neurosyphilis)

resistance is common

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52
Q

what are the anti-staphylococcal penicillins

A

cloxacillin and methicillin

IV and PO

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53
Q

what is the drug of choice for a serious S. aureus infection

A

cloxacillin or methicillin

*these drugs have a very narrow spectrum, not for use if dont know whether staph or strep

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54
Q

name the animo penicillins

A

ampicilling

amoxicillin

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55
Q

what do we use the aminopenicillins (ampicillin, amoxicillin) for

A

gram + –> strep, enterococcus, listeria

has an extended spectrum–> covers some gram - rods–> E coli, H influenzae, proteus

can combine with clavulin to get a broad spectrum oral abx that covers G+, G- and ANAEROBES

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56
Q

what diseases are often well treated by amox clav

A

sinus infections
otitis media
URTI

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57
Q

name the ureidopenicillin

A

piperacillin

58
Q

what does piperacillin cover

A

broad spectrum–> G+, G- (including PSEUDOMONAS), and ANAEROBES

combine it with tazobactam for extended spectrum coverage

59
Q

what is the empiric treatment for polymicrobial/suspected resistant /unknown source of infection

A

pip-tazo

60
Q

how does coverage change for cephalosporins across the generations

A

as go from 1st to 3rd–> decrease gram + and increase gram -

61
Q

name two 1st gen cephalosporins

A

cefazolin (ancef)–> IV

cephalexin (keflex)–> PO

62
Q

what do the first gen cephalosporings (ancef, keflex) cover

A

G+

some Gram - (proteus, klebsiella, e coli)

63
Q

what diseases are well treated by 1st gen cephalosporins (ancef, keflex)

A

cellulitis
pre-operative coverage
UTI

64
Q

name one 2nd gen cephalosporin

A

cefuroxime–> PO/IV

65
Q

what does cefuroxime cover

A

some gram + but less than 1st gen (good for s. pneumo)

increased gram - (proteus, klebsiella, e coli, h influenzae, enterobacter, neisseria)

66
Q

what diseases are well treated by second gen cephalosporins (cefuroxime)

A

resp infections

67
Q

name 3 3rd . gen cephalosporins

A

ceftriaxone

cefotaxime

cefixime

68
Q

what do the 3rd gen cephalosporins cover

A

much more gram -, less gram +

69
Q

what is important about the 3rd gen cephalosporins (ceftriaxone, cefotaxime, cefixime) in terms of disease coverage/treatment

A

cross the BBB–> used as empiric coverage for Neisseria in meningitis

has long half life, do once daily dosing

*also used for CAP, pyelonephritis

70
Q

what covers pseudomonas

A

ceftazidime

71
Q

name one 4th gen cephalosporin

A

cefepime

72
Q

what does cefepime cover

A

powerful, broad spectrum

less anaerobic than pip-taz

73
Q

name two carbapenems

A

imipenem

meropenem

74
Q

what do the carbapenems cover

A

broad spectrum gram + and -

includes pseudomonas, ESBL and anaerobes coverage

75
Q

when do you use the carbapenems

A

reserved for serious sepsis, nosocomial infections where resistance likely

76
Q

name a glycopeptide abx

A

NOT a beta lactam

vancomycin

77
Q

how does vancomycin (a glycopeptide abx) work

A

bacteriocidal

78
Q

what does vanco cover

A

G+–> MRSA, coagulase - staph, enterococci

oral use for C diff

79
Q

adverse effects of vanco

A

redman syndrome

nephrotoxic

rare ototoxicity with long term exposure

*measure levels at trough

80
Q

name the cell membrane agent abx

A

lipopeptides–> DAPTOMYCIN

*covers cell membrane of gram + only

81
Q

what do we use daptomycin for

A

VRE

MRSA

82
Q

what are the 5 types of protein synthesis inhibitor abx

A
  1. aminoglycosides
  2. tetracyclines
  3. macrolides
  4. lincosamides
  5. oxazolidinones
83
Q

what ribosome do the aminoglycosides act on

A

30s

84
Q

name 3 aminoglycosides

A

gentamycin

tobramycin

amikacin

85
Q

how do the aminoglycosides work

A

protein synthesis inhibitors vs 30 s ribosome

work against gram - (good for gram - sepsis)

synergy against gram + enterococcal endocarditis with ampicillin

*concentration dependent killing–need peak and trough levels

86
Q

adverse events of aminoglycosides (gentamycin, tobramycin, amikacin)

A

nephrotoxic

ototoxic

vestibulotoxic

87
Q

what must you do if you plan to prescribe aminoglycosides for more than 4 days

A

CONSENT PATIENT for the nephro/oto/vestibulotoxic possible adverse effects

88
Q

what ribosome do tetracyclines work against

A

30s

89
Q

name 2 tetracyclines

A

doxycycline

tetracycline

90
Q

spectrum of tetracyclines

A

fairly broad –> atypical cell walls or intracellular

good for mycoplasma, chlamydia, spirochetes, Rickettsia

91
Q

who should NOT use tetracyclines

A

children or pregnant women

92
Q

what ribosome do the macrolides work against

A

50s

93
Q

what abx should you use in the case of a penicillin allergy

A

erythromycin

94
Q

name 3 macrolides

A

erythromycin
clarithromycin
azithromycin

95
Q

what diseases are well treated by clarithromycin

A

CAP
sinusitis
H. pylori
legionella

96
Q

what diseases are well treated by azithromycin

A 
resp tract infections
atypicals
moraxella
h influenza
legionella
97
Q

what ribosome does the lincosamides work against

A

50s

98
Q

name one lincosamide

A

clindamycin–> PO and IV, great bioavailability

99
Q

how do the lincosamides (clindamycin) work

A

bacteriostatic–> decreased toxin production

100
Q

spectrum of lincosamides (clindamycin)

A

G+ and anaerobes

101
Q

what diseases are well treated by lincosamides (clindamycin)

A

cellulitis
abscess
some diabetic foot infections

102
Q

what is the risk with lincosamides (clindamycin)

A

c diff

103
Q

what ribosome do the oxazolidinones work against

A

50s

104
Q

name one oxazolidinone

A

linezolid

good PO avail

105
Q

adverse effects of oxazolidinones (linezolid)

A

cytopenias

drug reactions with SSRIs

possibly neurotoxic

106
Q

spectrum of oxazolidinones (linezolid)

A

Staph–> MRSA, coag - staph aureus

enterococcus–> VRE

107
Q

name 3 quinolones

A

cipro

levofloxacin

moxifloxacin

108
Q

what are the quinolones often used to treat

A

good for RESP infections

treat intracellular pathogens–> legionella, mycoplasma and gram - bacteria

109
Q

what does flagyl (metronidazole) treat

A

anaerobes and PARASITES

110
Q

what does rifampin treat

A

mycobacteria (TB)

MRSA (with fusidic acid)

listeria

neisseria

h influenza

legionella

111
Q

which antibiotics work against pseudomonas

A
  1. gentamycin, tobramycin, amikacin (aminoglycosides)
  2. cipro, levo, moxi (quinolones)
  3. cephalosporins
  4. anti-pseudomonal penicillins–> piperacillin, ticarcillin
  5. carbapenems–> mero and imi
    * all given my injection except tobramycin and quinolones
112
Q

what is the clinical role of daptomycin

A

usually reserved for those with vancomycin intolerance

*does NOT work for pulmonary infection !!!!

SSTI and MSSA/MRSA bacteremia and endocarditis are all appropriate indications

113
Q

what are polymixins and name one

A

cell membrane abx

colistin is one

114
Q

what are polymixins like colistin used to treat

A

MDR gram - infections like CPO klebsiella

binds to outer cell membrane then acts on the cell wall and inner membrane

IV or inhaled

115
Q

why cant quinolones be used in kids

A

affects cartilage

116
Q

what is a possible side effect of quinolones like cipro in adults

A

QT issues

achilles tendon rupture in older adults

117
Q

what is nitrofurantoin used for

A

UTI agent

good against e coli, enterococcus

less good for klebsiella and other GNB .
proteus usually resistant

118
Q

what should you use to treat:

SSTI due to Group A, C or G strep

A

PO cephalexin

119
Q

what should you use to treat:

invasive group A, C, G strep disease

A

IV Pen G

120
Q

what should you use to treat:

Group A, C, G pharyngitis

A

PO penicillin

121
Q

what should you use to treat:

group B strep

A

PO amoxicillin

IV Pen G/ampicillin for invasive disease

122
Q

what should you use to treat:

strep pneumo

A

PO amox or amox-clav (uncomplicated disease)

IV ceftriaxone (CAP, bacteremia)

IV vanco (empiric for ?meningitis)

123
Q

what should you use to treat:

enterococcus species

A

PO amoxicillin

PO nitrofurantoin if UTI

IV ampicillin for invasive disease

IV ampicillin + gentamicin for endocarditis

124
Q

what should you use to treat:

MSSA

A

PO cephalexin, clindamycin if skin

IV cloxacillin for invasive

125
Q

what should you use to treat:

MRSA

A

IV vanco or dapto

PO linezolid

126
Q

what should you use to treat:

community acquired MRSA

A

doxycycline or TMP-SMX

127
Q

what should you use to treat:

gram - agents like E coli, Klebsiella, proteus

A

ceftriaxone (or other 3rd gen cephalosporins)

gentamicin

cipro

TMP-SMX

128
Q

what should you use to treat:

pseudomonas

A

pip-tazo

ceftazidime

cefepime

imipenem

tobramycin

cipro

129
Q

what should you use to treat:

anaerobes

A

pip tazo

imipenem

clinda

metronidazole

130
Q

what are the likely organisms in cellulitis, impetigo and in wound infections

A

MSSA/GAS
MRSA

(sometimes gram - in open wounds)

treat for 7-10 days

131
Q

what should you consider covering for in purulent cellulitis

A

MRSA empiric coverage

132
Q

what are the likely organisms in CAP

A

atypicals (chlamydia, mycoplasma), strep pneumo, h influenza, moraxella

133
Q

what should you use to treat CAP

A

macrolide (azithro or clarithro) or doxycycline

134
Q

likely organisms for inpatient CAP

A 
s pneumo
klebsiella
h influenza
gram -
atypicals
135
Q

what should you use to treat inpatient CAP

A

ceftriazone + macrolide or doxy

136
Q

what should you use to treat inpatient HAP

A

pip tazo, consider adding vanco

137
Q

what are the likely organisms for inpatient HAP

A

SPACE gram -
pseudomonas
anaerobes
maybe MRSA

138
Q

how long should you treat CAP for

A

minimum 5 days

AND
afebrile 48-72 hours
no clinical signs of instability

139
Q

how long should you treat VAP for

A

IF demonstrated improvement at 72 hours, treat for 8 days

if pseudomonas or s. aureus, treat for 14 days

if complicated infection, treat 4-8 weeks

140
Q

likely organisms in UTIs

A

e coli
klebsiella
proteus
enterococcus

141
Q

what should you use to treat UTI

A

nitrofurantoin 5-7 days
Septra 3 days
cipro 3 days UTI, 7 days outpatient pyelo

142
Q

if a women requires hospitalization for pyelo, how long should you treat for, and with what?

A

10-14 days of beta lactam or aminoglycoside or quinolone

IV initially then step down to PO

PMP (9 decks)

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