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MMMD 1 - QH > Other microbes + ANTIMICROBIAL DRUGS > Flashcards

Other microbes + ANTIMICROBIAL DRUGS Flashcards

1
Q

What is bactericidal?

ex:

A 
act on cell wall, cell membrane or DNA > kills
B-lactams
Vancomycin
Fluoroquinolones
Metronidazole
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2
Q

What is bacteriastic?

A

act on protein synthesis > halts growth
-some infection such as Group A strep > toxins benefit from inhibiting protein synthesis

Trimethoprim
Sulfamethoxazole
Aminoglycosides
macrolides
clindamycin
tetracyclines
oxazolidinones
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3
Q

Mechanisms for resistance? (3)

A
  • altered binding sites
  • drug inactivation
  • reduced drug accumulation
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4
Q

What is def of antibiotics?

A
  • substance made by one org to destroy another org

- old term - now for drugs we use antimicrobials

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5
Q

When were most drugs formed?

A

1940s-1960s

no major development since

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6
Q 
Naming:
-cillin
ceph or cef-
-penem
-floxacin
-thromycin
-micin or mycin
A 
Penicillins
Cephalosporins
Carbapenems
Fluoroquinolones
Macrolides
Aminoglycosides
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7
Q

What is ideal antimicrobial?

but there are none!

A
  • kill pathogens - 100% susceptible
  • safe, no sideeffects
  • ignores bystanders
  • does not induce resistance
  • cheap
    bonus: affects hosts’ bad effects (sepsis, ARDS)
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8
Q

What is NAM and NAG on bacteria?

A
  • sugars forming peptidoglycan on cell membrane
  • crosslinked by TRANSPEPTIDASE that connects d-ALA to D-ALA
  • N-actylglucosamide
  • N-acetylmuramic acid
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9
Q

B-lactams:

A
  • cidal
    ex: Penicillin, Cephalosporins, Carbapenems
  • have B-lactam ring with side chain = determine activity
  • bind TRANSPEPTIDASES > prevents D-ala-D-ala chain crosslingking > bad cell wall > cell death
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10
Q

Resistance to B-lactams?

A
  • drug inactivation
  • altered binding site
  • B-LACTAMASES from bacteria cleave ring >drug can’t bind
    ex: MRSA resistant to all
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11
Q

Overcome B-lactamases?

A
  • add bigger sidechains to penicllin > METHICILLIN
  • use drug with B-lactamases inhibitors > CLAVULANIC ACID, TAZOBACTAM
  • Ceph and -penems are resistant to B-lactamases
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12
Q

Penicillin?

A
  • b-lactam
  • still main drug for Group A strep and Strep pneumoniae

+B-lactamase inhibitor = broad spectrum

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13
Q

Amoxicillin and ampicllin?

A

A: oral form of penicillin
P: parenteral form

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14
Q

Piperacllin?

A
  • penicillin

- broad gram-ve

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15
Q

Cephalosporins?

A

B-lactam

  • Gen 1-4
  • cover gram+ and gram- (usually 1=+; 3=-ve but bad system)
  • not good for anerobes
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16
Q

Carbapenems?

A
  • B-lactam
  • broad
  • stable against extended spectrum b-lactamase
    ex: Doripenem, Ertapenem, Imipenem, Meropenem
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17
Q

What is a common problem with B-lactams?

A
  • Allergy!
  • reported vs actual
  • if true, 5% chance allergy to ceph-
  • most common: amox and ampi
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18
Q

Vancomycin?

A

-cidal
-glycopeptid with large tricylcic molecule
-binds directly to D-ala-D-ala to prevent crosslinking of peptidoglycan
-good for Gram+ve. too big for -ve
-weak - not as effective as B-lactams
»dosing issues. risk of renal failure

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19
Q

VISA and VRSA?

A

VISA: vanco-intermediatly susceptible Staph aureus: thickened cell wall to block drug access
*reducing drug accumulation
VRSA: vanco-resistant Staph aureus: alteration of peptidoglycan peptide terminus of D-ala-D-ala to have a D-lactate. Vanco can’t bind.
*altered binding site

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20
Q

Fluoroquinolones?

A
  • most overused
  • bind DNA during supercoiling process > error > repair process > damage the DNA > cell death
  • Gram+: depends on activity of DNA gyrase A - causes -ve supercoiling during replication
  • Gram -ve: depends on Topoisomerase IV parC
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21
Q

Resistance to fluoroquinolones?

A
  1. altered binding site: MUTATIONS in DNA topoisomerases

2. altered activity and reduce accumulation: EFFLUX PUMPS and ALTERED PORINS > drug doesn’t get in cell

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22
Q

Trimethoprim and Sulfamethoxazole?

A
  • cidal when used together. static separately?
  • block 2 steps of folic acid metabolism > affect DNA production > preventing cell synthesis
  • used together = broad spectrum
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23
Q

Aminoglycosides?

A

-static + cidal
ex: GENTAMICIN, TOBRAMYCIN, AMIKACIN
side effects: nephro and ototoxicities!
-bind 30s ribsomal subunit > inhibit protein synthesis
-also bind membrane > cell leaky = bactericidal
*can’t penetrate gram+ve cell wall

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24
Q

Resistance to aminoglycosides?

A
  • change drug activity: modify drug > can’t enter, can’t bind
  • increase efflux
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25
Q

Macrolides?

A
  • static
    ex: ERYTHROMYCIN, CLARITHROMYCIN, AZITHROMYCIN
  • bind 50S subunit > prevent protein synthesis
    sideeffect: GI intolerance, QT intervals > sudden death
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26
Q

Clindamycin?

A
  • in lincosamide class
  • static
  • similar activity to macrolides
  • bind 50S subunit > prevent protein synthesis
    sideeffect: GI intolerance
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27
Q

Resistance to macrolides and clindamycin?

A
  • modification of 23S RNA > change conformation> drug can’t bind the 50S
  • altered binding site
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28
Q

Tetraclyclines?

A
  • static
    ex: TERTRACLYINE, DOXYCYCLINE, MINOCYCLINE, TIGECLYCINE
  • bind 30S subunit
  • broad gram+ and -ve
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29
Q

Linezolid?

A
  • static
  • in Oxazolidinone class (pretty new)
  • bind 50S
  • good for gram +ve
  • $, no gram-ve
    side: neutropenia and neuropathy
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30
Q

Metronidazole

A
  • cidal: aneorobes and some parasites!
  • overused (no resistance yet)
  • small, diffuses into cell > takes e > radicals
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31
Q

What are the main antifungals?

A
  • Polyenes
  • azoles
  • echinocandins
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32
Q

Polyenes?

how to avoid toxicities?

A

-antifungals
ex: AMPHOTERICIN B
-bind ergosterol in fungal wall > holes > leaky > death
-broad spec
side: amphoterrible!
-attack host cells because sterols similar > inflammation
-cytokines > symptoms: fever, chills
-nephrotoxic
To avoid toxicity: use slow infusion or bind to liposomes < $

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33
Q

Azoles?

A
  • most used antifungals
    ex: CLOTRIMAZOLE, FLUCONAZOLE, ITRACONAZOLE, KETOCONAZOLE, POSACONAZOLE, VORICONAZOLE
  • inhibit lanosterol 14aplah-demethylase (p450 ensyme)> prevent conversion of lanosterol > ergosterol > cell membrane perm changes > growth issues and exposed toxic sterols
  • static
  • drug interactions
  • resistance
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34
Q

Echinocandins?

A
  • new antifungals
  • inhibit 1,3,beta glucan synthase > inhibit cell wall production
    ex: ANIDULAFUNGIN, CASPOFUNGIN, MICAFUNGIN
  • $, safe
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35
Q

what is antimicrobial stewardship?

A
  • pt get right drug only when they need
  • refers to coordinated interventions designed to improve and measure appropriate use of antimicrobials by promoting seletion of optimal antimicrobial drug regimen, dose, duration, route
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36
Q

How toward stewardship?

A
  • many things we don’t know - length, use.. = research!
  • restricted formulaary
  • pre-authorization to some drugs
  • audit and feedback of prescribers
  • education
  • guideliines
  • de-escalation - use narrow spectrums
  • use more oral drugs to save cost

-in UK: prescribers should be competent in
infection preve and control, resistance, prescribing, stewardship, monitoring, ongoing learning

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37
Q

What are mycobacteria

ex

A
  • mycolic acid in cell wall
  • aerobic, slow growing
  • nonspore, nonmotile
  • very small!
  • detected via acid-fast bacilli, fluorochrome dyes
    ex: M.tuberculosis complex (M.tuberculosis, M.bovis), M.avium complex, M.leprae, non-tuberculous mycobacteria (opportunistic inf from envt)
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38
Q

Detecting mycobacteria?

A
  1. Acid-fast bacilli stain - kinyoun stain - sputum smear
  2. *Culture: Mtb - slow up to 6wks; nonTM range; leprae not culturable in vitro.
  3. Nucleic acid amplification
  4. drug susceptibility testing - important for TB, MAC
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39
Q

Transmission of TB?

factors affecting:

A
  • airborne
  • inhale droplet nuclei that may have been there up to 2hrs before
  • large droplets and surface contaminations NO risk

*susceptibility - immune of host
infectiousness - smear positive, culture positive, other disease, coughing > aerosols
envt: poor ventilation, overcroding
exposure: higher duration, prox, freq

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40
Q

Pathogenesis of TB:

A

inhalation > *1ry focus = middle and lower lung zone > macrophage ingest > lymph nodes (Ghon complex) > *2ry focus = upper lungs, nodes, vertebral bodies, meninges > lympho and mono > tubercles & caseous necrosis

Primary disease dx within months -5% > immune failures
Latent TB: 95% - + tuberculin test. fibrosis, calcification.
>5% reactivation (10% chance over lifetime. usually first 2yrs)
» Pulmonary** or extrapulmonary

**only those with pulmonary > SPREAD
(proliferate > spread to other lung sites > infectious droplets)

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41
Q

Latent vs Active Pulmonary TB:

A

Latent:
-no symptoms, no spreading, + tuberculin test, normal CXR, sputum

Active:

  • symptoms, spread, +tuberculin,
  • maybe normal chest x-ray
  • maybe positive sputum smear and culture
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42
Q

How does Type 4 hypersensitivty occur with TB?

A

-Th1 cells activated > cytokines : IL2, IFNgamma, TNFalpha
> fever, wt loss, night sweats
-if no Th1 profile > IL10 > suppress immune > disease progression!

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43
Q

How does tuberculin skin test work?

A

-purified protein inject intracutaneously
-rxn read 48-72hrs later
-+: >10mm induration or 5mm in immunocomp
*latent or active with no pulmonary symptoms or vaccination
-2 steps: booster effect for 1st time testing
most useful for latent: sensitivty 75-90%
issues: FN - immunocompromised or immune system react deep under skin
FP: crossrxns

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44
Q

What is Interferon gamma release assay?

A
  • IGRA: in vitro, T cells exposed to TB antigen and IFNgamma
  • no crossrxn, 1 time test
  • only good for latent
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45
Q

Management of TB

A
  • at least 2 drugs: ISONIAZID, RIFAMPIN, PYRAZINAMIDE, ETHAMBUTOL 6-9months
  • resistance issues; liver toxicity side effects
  • DOT - direct observed treatment
  • isolation
  • N95 resp

for latent: ISONIAZID for 9 months

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46
Q

Vaccine for TB?

A

BCG: bacille calmetter-guerin

  • live attenuated M.bovis
  • DOES NOT prevent infection
  • helps prevent progression and dissemination
  • give to skin test -ve ppl
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47
Q

What is Leprosy?

A
  • Mycobacterium leprae
  • acid fast bacilli
  • NOT culturable in vitro
  • replicates in macrophages - escape phagocytoic killing
  • likes cold T’s : mouth, nose
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48
Q

Transmission of leprosy?

A
  • unclear. airborne? NOT contact

- repeated exposure

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49
Q

Tuberculoid vs Lepromatous Leprosy?

A

T: red blotchy lesions, increase sensation b/c nerve damage. Type 4 hypersensitivity.
-less freq. can be self limiting

L:

  • not due to hypersensitivity
  • skin, nerves, disfigurement, profuse growth of bacteria
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50
Q

Ex of mycobacteria

resevoir, virulence, disease, spread in human?

A
  1. M.tuberculosis. humans. high virulence > TB.
  2. M.bovis. animals. high virulence >TB
  3. M.avium complex: envt, birds. low virulence > TB like or disseminated IN AIDS. NO ppl transmission
  4. M. marinum: water, fish. low virulence. > skin granuloma. transmit via water not via ppl.
  5. M.laprae. human. high virulence. > leprosy.
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51
Q

Fungi

types?

A

-eukaryotic, uni/multicellular
-mostly asexual
-rigid cell wall: chitin, glucans, mannoproteins, ERGOSTEROL
-aerobic, requires organic carbons
Types: yeast, mould, dimorphic = yeast and mould

52
Q

saprophytic vs symbiotic vs parasitic?

A

fungi

sap: use nonliving organic material
sym: use living - mutally beneficial
para: harming living org when using resources

53
Q

Yeasts?

ex:

A

-single, budding
-blastoconidium - budding spores
-cultures: colonies, smooth, creamy, bacteria-like, slimy, capsule = halos
ex: Cryptococcus neoformans
Candida

54
Q

Moulds?

ex?

A
  • mycelium, filamentous
  • hyphae - septae

ex; Aspergillus fumigatus, Scopulariopsis brevicaulis

55
Q

Dimorphic fungi?

A

yeast or mould form depending on T, nutrients, O2

  • yeast: in vivo or in vitro @ 37
  • mould: in vitro in 22-25C
  • fatal!

ex: Bastomyces dermatitidis; Histplasma capsulatum; Sporothrix schenkii

56
Q

Types of fungal infections (4)

A

Mucocutaneous
-moisture, warmth, disrupt normal flora, decrase neutrophils, lymphocytes
ex: Candida albicans
>diaper rash

Superficial
-outermost layer of skin/nails; likes keratinized tissues
ex: Dermatophytoses: Tinea (ringworms); Microsporum, Tirchophyton, Epidermophyton
> athelete’s foot, ringworms

Subcutaneous
-on foot from envt
> Chromoblastomycosis: soil moulds> chronic nodular lesions
>mycetoma: chronic nodules, sinus trast, discahrge caused by black moulds, fungus-like bacteria

Systemic

  • dimorphic mycoses: lung issues, can be fatal
  • opportunistic mycoses: all fungi can cause dissemination by getting into bloodstream
    ex: candida, cryptococcus, aspergillus
57
Q

Blastomyces dermatitidis?

A
  • dimorphic fungi
  • endemic in ON
  • inhalation of CONIDIA from envt > convert to yeast > disseminate through out body from lungs
58
Q

Drugs for Fungi infections?

A

Polyene: binds sterol, interferes with cell membrane
use for: systemic disease, superficial candidiasis

Azole: inhibits ergosterol synthesis > cell membrane
use for: superficial candidiasis, systemic disease

Allylamine: inhibits ergosterol synthesis > cell membrane
use for: dermatophytosis

Echnocandin: inhibits glucan synthesis > cell wall
use: systemic disease

59
Q

Helminths?

classifications:

A
  • Flatworms : Trematodes (flukes); Cestodes (tapeworms)

* Roundworms: Nematodes (filarial vs non filarial)

60
Q

transmission routes

A
  • contact: through skin; faecal-oral is common

- grows in guts, lays eggs > stool > grows in envt/intermediate host > infect next

61
Q

diagnostic of helminths and protozoa?

(6) ex of helminths

A
  1. Direct examination (stool helminths - look for eggs)
  2. culture (Strongyloides)
  3. Antigen (Blood flukes; filaria)
  4. Host Ab detection/serology (invasive worms)
  5. Nucleic acid amp/PCR (some)
  6. Radiologic (tapeworms)
62
Q

How do host respond to helminths?

A 
>cytokines
>Th2 response
>eosinophils and mast cells degranulation
>macrophages
>nitric oxide production
>Ab: neutralize, enhance phagocytosis
63
Q

Define infectious hosts: direct vs indirect. Intermediate.

A

Direct: 1 host
Indirect: >1 host
Intermediate: larval, juvenile, non-sexual stages develop in

64
Q

How do helminths harm host?

A
  • mechanical - obstruct, barrier
  • compete for resources
  • cytotoxicity
  • inflammation
  • immune-mediated injury
  • malignant transformation
65
Q 
Ex of helminths and what they cause:
Ascaris
Filaria
Tapeworms
Hookworm
Flukes
A

Ascaris: intestinal obstruction
Filaria: obstruct lymphatics, immune-mediated injury
Tapeworms: takes VitB12 > anemia
Hookworm: takes iron > anemia
Flukes: goes through liver tissue; inflammation, immune-mediate injury, squamous bladder cancer

66
Q

Treatments for helminths? HEADS

A
  • Herbs/Plant extracts (ex: pumpkin seeds for tapeworm)
  • Endoscopic removal (ascaris in bile duct)
  • Anti-parasites (all)
  • Drainage (hydatid cyst)
  • Surgical excision (hydatid cyst, filaria)
67
Q

What is neurocysticercosis?
organism
symptoms
tx

A

by: pork tapeworm: Taenia solium
- parasite in CNS > mass effect, inflammation
- siezures, headaches, hydrocephalus, cysts in brain
1. -grows in guts > eggs in stool > pigs eat stool > larve grows > humans eat raw pork with the larvaes > grows up to 15 ft
2. if humans eat the stool with larvae = intermediate host&raquo_space; CYSTICERCOSIS

tx: Antiparasitics: ALBENDAZOLE, PRAZIQUANTEL, prednisone; endoscopic removal from ventricles

68
Q

What is cutaneous larva migrans?
organism
symptoms
tx

A

-eggs in feces from dogs/cats > hatch in envt. Worm penetrate skin of humans > pruritus
tx; Antiparasitics: ALBENDAZOLE, IVERMECTIN

69
Q

Lioasis?

A

-type of filariasis (neomotode, roundworm)
-worm crawling around
-obstruct lympathatics
from deer fly > human > mature and moves around and makes microfilaraie in blood > deer fly bites and take micro
dx: microscopy, skin nips, blood film, antigen, ab serology, nucleic acid amp, radiologic for lymphs

tx: Doxycycline (antibiotic)
anti-parasitic: Diethylcabamazine, albendazole, ivermectin
surgery - remove from eyes

70
Q

How to classify protozoa? (4)
using what?
ex

A

by moving mechanism

  1. amoebae: pseudopods (E.histolytica)
  2. flagellates: flagella (Trypansoma)
  3. ciliates: cilia (Balandidium)
  4. apicoplexans: gliding (Plasmodium)
71
Q

How are protozoa transmitted?

A

contact: fecal-oral; ingestion directly
or indirectly : vector-borne

GI symptoms, diarrhea, abscess (pus in nonantomical cavity)

72
Q

How do protozoa harm? ex?

A
  • Mechanical - Giardia > barrier to fat absorption but coating wall; plasmodium infect RBC > clog vessels
  • Competition for resources > plasmodium: glucose comp
  • cytotoxcicity: E.histolytica: abscess in liver
  • inflammation - plasmodium > cytokine storm
  • immune mediated - Leishmania: activate T cells . ulcers
    malignant: none we know
73
Q 
How to diagnose:
stool protozoa
Plasmodium > malaria
Leishmania
E.histolytica
Trypanosomes
Amoebic liver abscess
A
  • Plasmodium > malaria: examine in blood; Rapid Diagnostic test for antigen
  • Leishmania: culture, radiology for liver abscess
  • E.histolytica: stool protein test for antigen; host Ab
  • Trypanosomes: Ab
74
Q

Treatment for protozoa?

ex?

A
  • antibiotics: Giardia, Plasmodium (doxycycline)
  • antifungals: Leishmania
  • antiparasitics: all
  • herbs/plants: quinie tree bark for plasmodium
  • elements: Leishmania - antimony (Sb)
  • drainage (E.histolytica abscess)
75
Q

Cutaneous Leishmaniasis?

A

by: Leishmania - flagellate. Protozoa, vector-borne. Indirect.
-bite of sand fly > mobile form into blood > mature and mutiple > exits via fly bite
> ulcers
dx: biopsy, culture, host ab, nucleic acid amp
tx:
antibiotics: Azithromycin, paromomycin
antifungals: fluconazole, amphotericin
garlic
pentavalent antimony

76
Q

What is malaria?

A

-Plasmodium: falciparum (deadly), vivax (most common), malariea, ovale
-protozoa, vector-borne (night-biting anopheles mosq), indirect
>odd shaped RBC, obstruct capillaries > headache, chills, abdo pain, cough, FEVER from the tropics!
-Dx: direct exam of BLOOD SMEAR with Giemsa stain (thick for diagnosis, thin for species); Rapid diagnostic test (antigen in urine stick), PCR good if smear is negative since it can detect small amounts
-Tx: antibiotics - Coxyclicine, clandamycin
antiparasitics - Choloroquine, Mefloquine
Herbs: Artemisinin, quinine (tree bark)
(meds attack erythrocytic cycle

77
Q

What are common symptoms from travelers?

What are common infections? from where most often?

A

-fever, rash, acute diarrhea, chronic diarrhea, GI

Infections: 
Malaria - africa
dengue - SEA, caribbean 
rickettsiosis - africa
typhoid - south asia
mononucelosis -south asia
78
Q

Approach to fever in returned traveller?

A
  1. pre-travel vaccines, malaria prophylaxis: Yellow fever, Hep A, Hep B, typhoid, meingococal, Japanese encephalitis
  2. Itinerary of trip: urban/rural, timing, accomodations
  3. Exposure hx: water, flooding, insects, bites, sex, dairy
  4. Hx, PE
  5. Lab tests accordingly
79
Q

Back from tropics for longer than 7 days and have fever?
NOT ___?
long incubation period = think which?

A 
NOT DENGUE (incub period: 3-5days)
think:
malaria
TB
viral hep
schistosomiasis
80
Q

4 things to know to treat malaria?

A
  1. fever = assume malaria because it kills fast. if malaria, which species?
  2. if plasmodium falciprum, what is the load?
  3. Is it resistant to CHLOROQUINE?
  4. is it severe malaria?
81
Q

Drugs for malaria

A
  • Malarone = uncomplicated malaria
  • Artsunate for severe
  • chloroquine is 1st antimalarial
82
Q

Dengue?

A

-Flavirus
-vector borne: day-biting Aedes mosquitoes
-caribbean and SEA, urban
-short incub: 3-5days!
-fever, headache, pain, nausea/vomitting, rash, hemorrhagic shock
-Dx: CBC for WBC, platelets, liver enzymes
serology, IgG, PCR
-Tx: IV fluids, antipyretics,
AVOID salicylates, NSAIDS

83
Q

Typhoid?

A

-bacteria: Salmonella typhi (gram -ve bacillus)
-fecal-oral
-South Asia
>FEVER, headache, abdo pain, constipation, diarrhea, cough, sore throat
Dx: blood culture, gram stain, CBC, travel hx, rule out malaria
Tx:
-CEFTRIAXONE (3rd gen cephalosporin)
-Azithromycin/Cefixime
AVOID fluoroquinolones b/c of resistance

84
Q

Rickettsiosis?

A

Tick bite fever

  • R. africae; R.conorii
  • southern Africa, India, Mediterr
  • FEVER, adenopathy, rash, tache noire = bite looks like a cig burn)
85
Q

Other common causes of fever but non-tropical?

A

-pneumonia, pyelonephritis, gastroenterisits, influenza, meningitis

86
Q

Travel to:
South asia
fever
gram -ve bacteria

A

Typhoid

87
Q

Travel to: South africa
fever
cig burn lesion

A

Rickettsiosis

88
Q

Travel to:
carribean, SEA
fever within 3 days of coming back
sore muscles, better quick

A

Dengue

89
Q

Respiratory infection cluster includes: 5 syndromes

A

POMPS

  • pharyngitis
  • otitis media
  • pneumonia
  • meningitis
  • sinuisitis

Bugs: pneumoccus, H.influenzae, meningoccous, chlamydophila pneumoniae, mycoplasma pneumoniae, Group A strep

90
Q

Intra-abdo cluster6 syndromes

A

DIPPDC

  • diverticulitis
  • abscess/periotonitis
  • pyelonephritis
  • pelvic inflammatory disease
  • diabetic foot infection
  • cholecystitis

bugs: Gram -ve bacilli aerobes
anaerobes
enterocci

91
Q

Skin cluster: 3

A

ACE
-abscess, cellulitis, erysipelas

bug: Group A strep, Staph aureus

92
Q

Organization of drugs:

A

3 big families: Penicillins, FQ, Cephalosporins (C)
4 pretty big families:
>2 outpatients MT: macrolides (S), tetracyclines (S)
>2 sick inp AC: cabapenems (C), aminoglycosides (S or C)

5 singles: VTNMC
vancomycin (C)
trimethoprim-sulfamethoxazole (C)
nitrofuantoin (C or S)
metronidazole - anaerobes (C)
clindamycin (S)
93
Q

What is bacterial meningitis?

tx?

A

-fever, neck stiffness, altered mental state, headache
>ICP > edema, seizures, death
-usually people have 2/4
-BRUDZINKI’s: neck flexion > knee flexion
-Kernig’s sign: hip
-due to: Strepto pneu, meningococcus, gram -ve bacilli
Tx: according to age group
-IV dexammethasone
-ampillicin, vancomycin, ceftriaxone, cefotaxime

94
Q

When to LP? what is included in analysis?

A

LP only if no sign of mass effect. CT first!

  1. cell count, differential
  2. glucose, protein
  3. gram stain, culture, infectious stuff
  4. cell count, differential with xanthochromia
95
Q

What is necrotizing fasciitis?
what causes it?
tx?

A

-flesh-eating: subcutaneous infection > destruction and necrosis of tissue, fascia, vasculature

Type 1: polymoicrobial - 1 anaerobe + 1 facultative anaerobe + enterobacteria
ex: bacteroides + non grou
p A strep + Ecoli
Type2: monomicrobial - *Staph pyogenes usually with staph aureus
-risk factors: drug use, DM, obesity, immunosupp, pvd
-FEVER, tachy, hypotn
>tense edema, disporptionate pain, blisters/bullae, necrosis, crepitus, subcaneous gas

Tx: Clindamycin, Pen G, IVIG, SURGERY
-prophalyxis for contacts

96
Q

Meningitis in >50yrs?

A

by: S.pneumoniae, Listeria monocytogenes, gram _ve bacilli

tx: Ampicillin, vancomycin, ceftriaxone/cefeotaxime
or meropenem and vancomycin

97
Q

Meningitis for kids and adults

A

by: S.pneumoniae, meningococcus, rarely H.influenzae

tx: vancomycin, cetraixone or cefotaxime +/- ampicillin
or meropenem and vancomycin

98
Q

Meningitis in neonates?

A

by: Group B strep, Ecoli, listeria, mram -ve/gram+

ampicillin and cefotaxime or gentamycin

99
Q

What 2 does penicllin cover?

A

Strep A

pneumococcus

100
Q

What does piperacillin cover?

A

more gram-ve

pseudomonas

101
Q

What does cloxacillin cover?

A

Strep A, pneumococcus

-and Staph aureus

102
Q

First gen Cephalosporins?

A

Blactam

po: CEPHALEXIN
iv: CEFAZOLIN
- cover gram +ve aerobes (NOT enterococci)
- some gram- bacilli (ecoli, klebsiella, proteus mirabilis)

103
Q

2nd gen cephalosporins?

A

CEFUROXIME

  • cover gram +ve aerobes (NOT enterococci)
  • some gram- bacilli (ecoli, klebsiella, proteus mirabilis)
  • Hemophilus influenzae
104
Q

3rd gen cephalosporins?

A

CEFIXIME
CEFTRIAXONE
*gram-ve bacilli and cocci
good for pneumococcus

105
Q

3 major FQ?

A

CIPROFLOXACIN - gram- bacilli, esp UTI, abdo
LEVOFLOXACIN - resp, pneumonia
MOXIFLOXACIN - resp, pneumonia

106
Q

Macrolides?

A
  • gram +ve aerobe cocci
  • if allergic to penicillin
  • resp infections
  • Azithromycin - some -ve coverage (gonorrhea, traveler’s diarr)

Erythromycin
Clarithromycin

107
Q

Tetracyclines?

A
  • ex: DOXYCYCLINE

- for resp inf, chlamydia, other usual

108
Q

Aminoglycosides?

A

ex: GENTAMICIN, TOBRAMYCIN
- gram -ve bacilli
- seriously ill
* nephrotoxic, ototoxicity

109
Q

Carbapenems?

A
  • seriously ill pts; high resistant to others

- very broad spec

110
Q

Cystitis - bladder infection. use what?

A
  • Trimethoprim-sulfamethoxazole

- nirtrofurantoin

111
Q

Metronidazole

A
  • cdiff

- gram-ve

112
Q

Vancomycin?

A

gram positive aerobic cocci

MRSA resistant to others; or allergies

113
Q

Clindamycin?

A
  • anerobes from above diaphragm + gram+ve aerobe (like MRSA)

- but not enterococcus

114
Q

Drug for Group A strep

A

Penicillin
Ceph 1
macrolide

115
Q

Pneumoccus

A

Penicillin
Ceph 2, 3
Maroclide

116
Q

Enterococci

A

Ampicillin

Vancomycin

117
Q

Staph aureus, meth-sensitive

A

Cloxacillin

Ceph1, Vancomycin, TMP-SMX

118
Q

MRSA

A

Vancomycin
Clindamycin
TMP-SMX

119
Q

Ecoli

A

Ciprofloxacin (FQ), Ceph 1,2,3

Aminoglycosides

120
Q

Pseudomonas (gram-ve)

A

Ciprofloxacin (FQ)
Piperacillin
Aminoglycoside
Ceftazidime

121
Q

H.Influenzae

A

Ceph 2,3
Amoxicillin
Macrolide (A, C)
RFQ

122
Q

Meningococcus

A

Ceph 3

123
Q

Chlamydia

A

Azithromycin

Doxycycline

124
Q

Anaerobes

A

Metronidazole
Clindamycin
Moxifloxacin

125
Q

Gonococcus

A

Ceph 3

Azithromycin

126
Q

Legionella

A

Macrolide

RFQ

127
Q

Which STI is reportable to PH

A
  • gon
  • chlamydia
  • syphilis
  • hep B
  • trachomonas

MMMD 1 - QH (7 decks)

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