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463 Cards in this Set

  • Front
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NRTI MOA
requires phosphorylation

competes for reverse transcriptase
prematurely terminates DNA elongation due to modified OH group
NRTI ADEs
lactic acidosis
pancreatitis
lipodystrophy/lipoatrophy
How are NRTIs eliminated?
All are renally eliminated
Zidovudine:
Class and ADEs
NRTI

bone marrow suppression, GI, H/A, myopathies, metabolic abnormalities (lipoatrophy, lipids, insulin resistance), mitochondiral toxicity
What NRTIs also have activity against Hepatitis B?
Lamivudine
Emtricitabine
Tenofovir
Lamivudine:
Class and ADE's
NRTI

None; well tolerated
Emtricitabine:
Class and ADEs
NRTI

Well tolerated
Skin hyperpigmentation
Which NRTIs should not be used in combination together?
Lamivudine and Emtricitabine

Very similar drugs
Abacavir:
Class and ADEs
NRTI

Hypersensitivity (more common in whites, driven by genetics)
*Never restart if hypersensitivity suspected
What test should be performed if abacavir therapy is considered?
HLA*B5701
How is abacavir eliminated?
Renally eliminated as an inactive metabolite

NO renal adjustment needed
Tenofovir:
Class and ADEs
NRTI

Well-tolerated
N/V
May cause renal dysfunction
Which NRTI is monophosphorylated? What does this mean?
Tenofovir

It is a nucleotide analogue
NRTI combos
Zidovudine + Lamivudine
Zidovudine + Lamivudine + Abacavir
Lamivudine + Abacavir
Emtricitabine + Tenofovir
NNRTI MOA
bind noncompetitively to reverse transcriptase --> conformational change

Does not require phosphorylation
Do not compete with endogenous deoxynucleotides
How are NNRTIs metabolized?
Cyp450 = multiple drug interactions
NNRTIs half-lives
Very long
NNRTIs ADEs
rash
LFT increases
Efavirenz:
Class and ADEs
NNRTI (1st gen)

rash(mild), CNS effects (dizzy, drowsy, vivid dreams), increase LFTs, increase lipids, teratogenic
How/when should efavirenz be given?
Bedtime

On empty stomach
Efavirenz and P-450
Efavirenz is a P450 substrate and inducer
Nevirapine:
Class and ADEs
NNRTI (first. gen)

Rash, Stevens Johnson, hepatitis, increased LFTs
When should nevirapine be avoided?
Women with CD4 > 250
Men with CD4 > 400

Patient with increased risk of hepatitis
Nevirapine and P-450
Nevirapine is a P450 autoinducer and inducer of other drugs
Delavirdine:
Class and ADEs
NNRTI (first gen)

rash, increased LFTs, H/A
First generation NNRTIs
efavirenz
nevirapine
delavirdine
Second generation NNRTIs
etravirine
rilpivirine
Etravirine:
Class and ADEs
NNRTI (second gen)

rash, Stevens Johnson, N
Etravirine and P-450
Multiple drug interactions

Substrate for P450 3A4, 2C9, 2C19
Inducer of 3A4
Inhibitor of 2C9 and 2C19
Etravirine is only currently approved for what patients?
Only approved for antiretroviral experienced patients only
Rilpivirine:
Class and ADEs
NNRTI (second gen)

rash, depression, insomnia, H/A, increased QT interval
How should rilpivirine be taken?
Must be taken with a meal (at least 500 calories)
Which NNRTI is contraindicated with PPI use?
Rilpivirine

acid-dependent absorption
Drug interactions with acid-reducing agents
Rilpivirine and P-450
P450 substrate
When should rilpivirine NOT be used?
In patients with HIV-1 RNA > 100,000 copies/mL
Rilpivirine is currently only approved for what patients?
Only approved for antiretroviral naive patients only
What does NRTI stand for?
Nucleoside Reverse Transcriptase Inhibitor
What dose NNRTI stand for?
Non-Nucleoside Reverse Transcriptase Inhibitor
Protease Inhibitors MOA
Blocks HIV maturation process

Results in production of immature, noninfectious virions
How are Protease Inhibitors metabolized?
All are metabolized by CYP450

Multiple drug interactions
Protease Inhibitors ADEs
GI, lipodystrophy, hyperlipidemia, hyperglycemia, pancreatitis, LFT increases common
Ritonavir:
Class and ADEs
PI

GI
Most potent CYP450 inhibitor
Ritonavir
What is ritonavir now only used for?
Now only used for "boosting"
Atazanavir:
Class and ADEs
PI

GI, hyperbilirubinemia, nephrolithiasis
What PI has drug interactions with acid reducing agents?
Atazanavir

Acid-dependent absorption
T/F
Lipid abnormalities are common when using atzanavir "unboosted."
False.

No documented lipid abnormalities
Which PIs should not be used if a patient has a sulfa allergy?
Darunavir
Fosamprenavir
Tipranavir
Darunavir:
Class and ADEs
PI

GI

**SULFA moiety**
Lopinavir/ritonavir:
Class and ADEs
PI

GI
Fosamprenavir:
Class and ADEs
PI

GI

**SULFA moiety**
Tipranavir:
Class and ADEs
PI

GI, increased LFTs

**SULFA moiety**
Tipranavir is currently only approved for use in what patients?
Only approved for antiretroviral experienced patients
Entry Inhibitors MOA
Inhibits fusion of HIV with CD4 cells
Enfurvitide:
Class (MOA) and ADEs
Entry Inhibitor
Fusion Inhibitor

Injection site reactions
Maraviroc:
Class (MOA) and ADEs
Entry Inhibitor
CCR5 receptor antagonist

Hepatotoxicity +/- systemic allergic reaction (pruritic rash, eosinophilia, elevated IgE)
Maraviroc is currently only approved for what patients?
Only approved for antiretroviral naive or experienced patients who have CCR5 tropic virus
Maraviroc and P450
Maraviroc is a P450 3A4 substrate
How is maraviroc dose determined?
Dose depends on coadministered drugs
Integrase Inhibitors MOA
Prevent covalent bonds from forming between integrase and host DNA

HIV integrase unable to incorporate viral DNA into CD4 cell chromosome

Prevents strand transfer and viral replication
Raltegravir:
Class and ADEs
Integrase Inhibitor

No ADEs in clinical trials, well-tolerated

Post-marketing reports: skin rashes (including Steven's Johnson) and severe hypersensitivity
Raltegravir and P450
NO P450 metabolism

Glucoronidated by UGT1A1

Worry about interaction with Rifampin
Which HIV medication is metabolized by UGT1A1 glucoronidation?
Raltegravir
HIV drug most likely to cause yellowing of the skin and eyes
Atazanavir
What antiretroviral(s) should be avoided in patients with history of Stevens Johnson syndrome?
Darunavir
Fosamprenavir
Tipranavir
What antiretroviral(s) should be avoided with PPI use?
Rilpivirine
Atazanavir
If a patient is planning on getting pregnant or is currently pregnant, which antiretroviral(s) should be avoided?
Efavirenz
What antiretroviral(s) should be avoided in patients with CNS conditions (schizophrenia, bipolar disorder)?
Efavirenz
What antiretroviral(s) should be avoided in patients with higher CD4 counts?

(women > 250 or men > 400)
Nevirapine
What antiretroviral(s) should be avoided in patients with a positive HLA*B5701 test?
Abacavir
If a patient also has Hepatitis B, which 2-NRTI comb is preferred?
Emtricitabine/tenofovir
What NRTI should be avoided in patients with a history of chronic renal insufficiency?
Tenofavir
What antiretroviral(s) should be avoided in patients with a risk of renal dysfunction? (uncontrolled HTN, DM, CAD)
Tenofavir
If a patient has uncontrolled dyslipidemia, what PI is preferred?
Atazanavir

lower risk of hyperlipidemia
Protease Inhibitors and Statins
CYP450 3A4 inhibition by PIs

Leads to increased concentration of statins
What statins are contraindicated with PI use?
simvastatin
lovastatin
Possible clinical consequences of PI + statin use
Rhabdomyolysis
inreased LFTs
What statin(s) should be recommended if given with PIs?
Pravastatin
Low dose atorvastatin
Protease inhibitors + fluticasone
CYP450 3A4 inhibition by PIs

Leads to increased concentration of fluticasone
Possible consequence of PI + fluticasone use
Cushing's syndrome
What inhaled steroid(s) can be used with PIs instead of fluticasone?
Any other inhaled steroid

Beclomethasone, triamcinolone, budesonide, mometasone
Atazanavir + high dose PPI (> omeprazole 20mg equivalent)
Atazanavir needs acid for absorption

Decreased concentration of atazanavir in presence of PPIs
Consequences of atazanavir use with PPIs
Possible viral failure of atazanavir
What should be used with atazanavir instead of PPIs?
H2 blockers, antacids or can use a different PI
Protease inhibitors + trazodone
CYP450 inhibition by PI

Leads to increased concentration of trazodone
Consequences of PI use with trazodone
Increased sedation
Recommendation for PI + trazodone use
Start with lowest possible trazodone dose and tirate up
Protease inhibitors (or NNRTIs) + warfarin
Unpredictable CYP effect on warfarin metabolism
Consequence of PI or NNRTI use with warfarin
Increased or decreased INR

Monitor closely
Rilpivirine + PPIs
Rilpivirine needs acid for absorption

Decreased levels of rilpivirine in the presence of PPIs
Consequences of Rilpivirine use with PPIs
Viral failure with rilpivirine
Recommendations for rilpivirine use with PPIs
Can take H2 blockers 12 hours before or 4 hours after rilpivirine

Can take antacids 2 hours before or 4 hours after rilpivirine
What antiretroviral should be used if P450 interactions are to be avoided?
Raltegravir

glucuronidation via UGT1A1
Starting therapy of antiretroviral naive patients
1 NNRTI + 2 NRTIs
OR
PI (preferably boosted with ritonavir) + 2 NRTIs
Or
Integrase Inhibitor + 2 NRTIs
NNRTI-based regimens
Efavirenz (NNRTI) + tenofovir + entricitabine
When should efavirenz be avoided?
Do NOT use during pregnancy (especially during first trimester) or in women with high pregnancy potential

Caution in patients with poorly controlled mental status
When should tenofovir therapy be used with caution?
Use with caution (or use alternative agent) in patients with underlying renal disease
Protease Inhibitor-based regimens
Atazanavir boosted with ritonavir + tenofovir/emtricitabine
OR
Darunavir boosted with ritonavir + tenofovir/emtricitabine
When should a PI-based regimen be avoided?
With patients who require high-dose PPIs
Integrase Inhibitor-based regimens
raltegravir + tenofovir/emtricitabine
Preferred regimen for Pregnant women
2 NRTIs: zidovudine + lamivudine

Boosted PI: lopinavir/ritonavir
Baseline evaluation of antiretroviral therapy
Plasma HIV RNA (viral load)
Chem-7
CD4 count
LFTs
CBC/diff
fasting lipids
Genotypic resistance testing if HIV RNA is > 500-1,000 copies/mL
HLA-B*5701 genetic screening (if considering abacavir)
Evaluation of antiretroviral therapy after 2 weeks
Monitor side effects, adherence

Can obtain viral load and CD4 count
After 2 weeks, how much should a patient's viral load decrease?
at least 0.5 log
Evaluation of antiretroviral therapy after 4-6 weeks
Monitor side effects, adherence

Obtain viral load, CD4 count
After 4-6 weeks, how much should a patient's viral load decrease?
at least 1 log
How often should a patient return for routine visits once they are HIV stable?
Every 3-6 weeks
Evaluation of antiretroviral therapy during routine visits after patient is HIV stable
Viral load, CD4 count, LFTs, CBC, Chem-7
Virologic Suppression
A confirmed HIV RNA level below the limit of assay detection

<48 copies/mL
Virologic Failure
The inability to achieve or maintain suppression of viral replication

(to an HIV RNA level < 200 copies/mL)
Incomplete virologic response
Two consecutive plasma HIV RNA levels > 200 copies/mL after 24 weeks on an antiretroviral regimen

Baseline HIV RNA may affect the time course of response, and some regimens will take longer than others to suppress HIV RNA levels
Virologic rebound
Confirmed detectable HIV RNA (to > 200 copies/mL) after virologic suppression
Persistent low-level viremia
Confirmed detectable HIV RNA levels that are < 1,000 copies/mL
Virologic blip
After virologic suppression, and isolated detectable HIV RNA level that is followed by a return to virologic suppression
Causes of treatment failure
Adherence
Tolerability
PK causes
Virologic failure
Immunologic failure
Clinical Failure
Intolerable toxicity
Immunologic failure
Failure to achieve and maintain an adequate CD4 response despite virologic suppression

Increases in CD4 counts in antiretroviral naive patients with initial antiretroviral regimens are approx. 150 cells/mm3 over the first year
Clinical failure
Occurrence or reoccurrence of HIV-related events (after at least 3 months on HAART)
Cervarix Efficacy
Prevents HPV types 16 and 18 (cause 70% of cervical cancer)
Gardasil Efficacy
Prevents HPV types 6, 11, 16, and 18 (cause 90% of genital warts)(also protects against cancers of the anus, vagina, and vulva)
Cervarix and Gardasil Dosing
3-dose series over 6 months (second and third dose given 2 and 6 months after the 1st dose)
Cervarix and Gardasil Schedule
Routinelyfor 11 and 12 year old girls; can be started at age 9

Catch-up vaccination is recommended for ages 13-26 who have not completed the series
Cervarix use in males
Not approved
Gardasil use in males
May be given, ages 9-26

Approved for prevention of anal cancer and genital warts

Not yet routinely recommended
Cervarix Contraindications
Hypersensitivity to any vaccine component
History of anaphylaxis to latex
Moderate/severe acute illness
Pregnant
Gardasil Contraindications
Hypersensitivity to any vaccine component
Hypersensitivity to yeast
Moderate/severe acute illness
Pregnant
Urethritis
Discharge of purulent/mucopurulent material from the urethra, and burning upon urination
Commonly asymptomatic
Urethritis bacterial pathogen of importance in males
Neisseria gonorrhea
Gonococcal urethritis
Organism, Presentation, Onset
N. gonorrhea
More purulent (white/yellow color) discharge
Onset: few days
Nongonococcal urethritis (NGU)
Organism, Presentation, Onset
Chlamydia trachomatis
More mucous-like (clear) discharge
Onset: > 6-7 days
Diagnosis of urethritis
> (or =) 5 WBC/hpf on Gram-stain of swab
OR
Evaluation of 1st urine void with + leukocyte esterases or > (or =) 10 WBC/hpf
What appears on a Gram stain with N. gonorrhea and Chlamydia?
N. gonorrhea: Gram - intracellular diplococci (kidney bean)

Chlamydia: see nothing on Gram stain
Preferred treatment of uncomplicated gonococcal infection of cervix/urethra/rectum
Ceftriaxone 250 IM single dose
PLUS (if chlamydia not ruled out)
Azithromycin 1 g PO single dose
OR
Doxycycline 100 mg PO BID x 7 dyas
Alternative treatment of uncomplicated gonococcal infection of cervix/urethra/rectum
Cefixime 400 mg PO single dose
OR
Single dose injectable cephalosporin
Preferred treatment of uncomplicated gonococcal infection of the pharynx
Ceftriaxone 250 mg IM single dose
PLUS (if chlamydia not ruled out)
Azithromycin 1 g PO single dose
OR
Doxycycline 100 mg PO BID x 7 dyas
Signs/symptoms of Disseminated Gonococcal Infections (DGI)
chills, fever, arthralgias, skin lesions, tenosynovitis of small joints, septic arthritis
Disseminated Gonococcal Infections (DGI)
Results from gonococcal bacteremia that disseminates into skin, joints, CNS, heart
Preferred treatment of DGI
Initial therapy: Ceftriaxone 1 g IM/IV q24h until 24-48 hrs after improvement begins
Continued therapy (outpatient): Cefixime 400 mg PO BID

At least 1 week of total therapy
Preferred treatment for gonococcal endocarditis and meningitis
Ceftriaxone HIGH DOSE IV 1-2 g IV q12h
Meningitis: treatment 10-14 days (inpatient only)
Endocarditis: minimum of 4 weeks (may set up to go home)
Consequences of PID
Infertility
Ectopic pregnancies
Chronic pelvic pain
When should empiric treatment of PID be initiated?
Sexually active women
Women at risk for STDs if they are experiencing pelvic or lower abdominal pain
If no cause for the illness other than PID can be identified
AND if cervical motion tenderness OR uterine tenderness OR adnexal tenderness is present on pelvic exam
Inflammatroy disorder comprising PID
Endometritis
Salpingitis
Tubo-ovarian abscess
Pelvic peritonitis
Organisms responsible for PID
Often polymicrobial
GNRs
anaerboes
Chlamydia trachomatis
N. gonorrhoeae
Mycoplasma hominis
Ureaplasma urealyticum
Preferred Inpatient PID Treatment
Cefotetan 2 g IV q12h OR cefoxitin 2 g IV q6h
PLUS doxycycline 100 mg PO or iV q12

OR

Clindamycin 900 mg IV q8h + gentamicin
PID Duration of therapy
Continue IV therapy for at least 24 hours after first signs of clinical improvement
Continue doxycycline (or clindamycin) for 14 days total treatment
Preferred Outpatient PID Treatment
Ceftriaxone 250 mg IM single dose
OR
Cefoxitin 2 g IM + probenecid 1 g PO single dose (give concurrently)
OR
Ceftizoxime/cefotaxime (3rd gen. ceph) IV

ALL + doxycyline 100 mg PO BID x 14 days
ALL +/- Metronidazole 500 mg PO BID x 14 days
Which STD(s) are characterized by genital ulcers?
Syphilis and herpes
T/F
Genital ulcers have shown to increase risk for HIV
True
Organism responsible for syphilis
spirochete: treponema paalidum

highly infection, esp. in early stages
Primary syphilis
incubation = 21 dyas
chancre develops as site of inoculation as a painless papule which becomes ulcerated and indurated; nontender and filled with spirochetes
How long does primary syphilis last? Does it resolve on it's own?
1-5 weeks
Resolves on its own
Secondary syphilis symptoms
rash (hands, feet), lymphadonopathy, alopecia, H/A, weight loss
FEVER
How long does secondary syphilis last?
2-6 weeks
When is syphilis most infectious?
1st year of disease
Latent syphilis symptoms
No clinical manifestations
Serologic evidence only
Early latent syphilis
< one year duration
infectious
Late latent syphilis
> 1 year duration
not infectious
Tertiary syphilis
late manifestations (skin, bones, CNS, heart)
may be asymptomatic or accompanied by manifestations
must examine the CSF with a lumbar puncture to see if CNS is involved
Early syphilis definitive diagnostic test
Direct fluorescent antibody (DFA) test of lesion exudates or tissue
Serologic tests to diagnose syphilis
Nontreponemal tests
Treponemal tests
Nontreponemal tests
venereal disease research laboratory (VDRL)
Rapid plasma reagin (RPR)
Treponemal tests
Fluorescent treponemal antibody absorbed (FTA-ABS)
T. pallidum particle agglutination (TP-PA)
What changes in syphilis tests are considered clinically significant?
4-fold change in titer, equivalent to a change in 2 dilutions (1:16 to 1:4 or 1:8 to 1:32)
When is syphilis often more aggressive?
HIV + patients
T/F
Syphilis can be transferred through the placenta.
True
PCN G and syphilis
Recommended for tertiary syphilis
PCN V and syphilis
Never used for the treatment of syphilis
Benzathine PCN G
Duration is up to 30 days (longer than procaine PCN)
Used for the treatment of syphilis because the spirochetes grow and multiply slowly (want a long-acting drug)
Procaine PCN and syphilis
Not the recommended therapy option for shyphilis
Benzathine/procaine PCN G and syphilis
Not recommended for syphilis
Treatment for Early (primary, secondary, or latent < 1yr) syphilis
Benzathine penicillin G 2.4 million units IM single dose
Treatment for Late (>1 year duration, unknown duration, late-latent) syphilis
If no abnormal CSF findings:
Benzathine PCN G 7.2 million units total, administered as 3 doses of 2.4 million units IM each at 1 week intervals (q week x 3 weeks)
Neurosyphilis (asymptomatic or symptomatic) treatment
Aqueous PCN G 18-24 million units IV per day, administered as 3-4 million units IV q4h or continuous infusion x 10-14 days

Following treatment: Benzathine PCN G 2.4 million units IM qweek x 3 weeks
Syphilis treatment in pregnancy
Treat according to stage
must desensitize if patient is pregnant and is allergic to PCN
Syphilis treatment ADEs
Jarisch-Herxheimer reactions within 2-3 hours of PCN injection
Jarisch-Herxheimer reaction sypmtoms
acute, febrile reaction (A/A, myalgias) within 24 hours after treatment of syphilis
Are Jarisch-Herxheimer reactions allergic reactions? How do you treat them?
Not an allergic reaction
Supportive treatment (APAP, fluids)
Tuberculosis Causing Organism
Mycobacterium tuberculosis
What is the most common risk factor for active TB?
HIV
HIV and TB
work synergistically making each disease worse than it might otherwise be
Mycobacterium tuberculosis
aerobic, non-spore-forming bacillus
thrives in environments where oxygen tension is relatively high (apices of the lung, renal parenchyma, growing ends of bones)
Mycobacterium tuberculosis and Gram stain
Resists decolorization by acid alcohol after staining with basic fuchsin (often referred to as an acid-fast bacillus)
Mycobacterium tuberculosis replication:
Fast or Slow
Slow
TB transmission
Tubercle bacilli are transmitted through the air by aerosolized droplet nuclei (person coughs, sneezes, speaks, sings)
Can TB be transmitted by inanimate objects like dishes, clothing, or bedding?
NO
Who is most at risk for contracting TB?
Family household contacts
Persons working or living in an enclosed environment
People with impaired immune systems
Development of TB infection
1. Tubercle bacilli inhaled, settling into bronchioles and alveoli of lungs
2. Initial organism multiplication
3. Phagocytosis by macrophages
4. Spreading via lymphatic system to lymph nodes and other body organs
5. T lymphocyte-mediated immune response
6. Further replication is inhibited
7. Granulomas are formed, limiting multiplication and spread of the bacilli
Latent TB
Most patients asymptomatic
No radiographic evidence of infection
Positive PPD
Is latent TB infectious?
NO
When is the risk highest for latent TB to develop into active TB?
first 2 years of infection
Risk factors for active TB
Immunosuppresion
HIV
Chronic renal failure
Diabetes
Old age
Adolescents
Children < 2 yo
Alcohol abuse
IV drug use
Diagnosis of active TB (signs/symptoms)
Cough (gradually becomes more productive)
Night sweats
Weight loss/anemia
Fever
Pleuritic chest pain
Objective findings with TB
Nodular infiltrates (apical or posterior segments of upper lobes)
Positive sputum smear for AFB
Positive PPD
Leukocytosis (increase in monocytes/eosinophils)
Anemia
What does PPD stand for?
Purified Protein Derivative
How long before a PPD will be positive after TB infection?
2-12 weeks after initial infection
PPD Test
1. 5TU injected intradermally
2. Sensitized T cells recruited to skin site, release cytokines
3. Induration/raised area occurs via local vasodilation, edema, fibrin deposition
4. Measure diameter of induration
When is max induration (raised area) seen after a PPD test?
48-72 hours after
When may PPDs give a false positive result?
History of bacillus of Calmette-Guerin vaccine (BCG)
When will a PPD result be >/= 5 mm?
Positive result
Recent history of close contact with someone with active TB
Fibrotic changes on CXR consistent with old TB
Organ transplant patients
> 15 mg of prednisone for at least one month
HIV infected
When will a PPD result be >/= 10 mm?
Diabetes, silicosis, chronic renal failure, leukemia, lymphoma, gastrectomy, jejunoileal bypass, weight loss > 10% of IBW, recent immigrant, injection drug user, resident/employee of high-risk setting, mycobacteriology lab personnel, children < 4 yo, infants/children/adolescents exposed to adults in high-risk categories
When will a PPD result be >/= 15 mm?
No known risk factors
Definitive diagnosis of TB
1. Isolation of M. tuberculosis from site of infection (positive culture)
2. AFB smear
When are AFB smears best obtained?
Early in the morning on at least 3 consecutive days
T/F.
A negative AFB smear rules out TB.
False.
Patient may still have a + culture
What is anergy?
decreased ability to respond to antigens
Causes false-negative PPD
What causes anergy?
old age, severe debility, immaturity in newborns, high fever, sarcoidosis, corticosteroids, immunosuppressive drugs, hematologic disease, HIV, overwhelming TB, recent viral infection, live-virus vaccination, malnutrition
What should you do if anergy is suspected?
Control skin tests should also be placed in the contralateral arm (candida, mumps, trichophyton)
If control tests are + and PPD is - TB is less likely
How often do PPDs produce a false negative result?
25% of the time
Isoniazid Duration of Treatment
Initial: 8 weeks
AND
Continuation Phase: 18 weeks (4 months)
Isoniazid's role in therapy
Kills rapidly multiplying organisms during initial phase of therapy
Isoniazid:
Class and ADEs
Anti-TB

hepatitis, increased LFTs, peripheral neuropathy, somnolence, seizures, psychosis (levels high), arthritic symptoms, SLE, dry mouth, CNS stimulation/depression, hemolytic anemia, agranulocytosis
Risk factors for isoniazid-induced hepatitis?
alcohol use
> 35 yo
other hepatotoxic drugs
liver disease
Black/Hispanic women
Postpartum women
GI symptoms of hepatitis
abdominal pain
N/V
anorexia
viral illness
jaundice
hepatomegaly
Which anti-TB drug causes peripheral neuropathy?
Isoniazid

Interferes with vit. B6 metabolism
What metabolism does isoniazid interfere with?
Metabolism of vit. B6
What must be given concurrently if a patient is on isoniazid?
Vit. B6
Symptoms of an isoniazid allergic reaction
skin rash, fever, tongue swelling, arthralgia
Isoniazid and P450
Izoniazid is a potent inhibitor of CYP 450 (2C9, 2C19, 2E1)
Minimal effects on 3A4
Rifampin:
Class and ADEs
Anti-TB
Flu-like symptoms, increased LFTs, thrombocytopenia, N/V, fever, rash, drug-induced lupus, acute renal failure, turn fluids red/orange
Rifampin MOA
inhibits RNA synthesis by binding to RNA polymerase and inhibiting RNA transcription
When should TB patients not wear contact lenses?
If on rifampin
T/F.
If a patient experiences thrombocytopenia while taking rifampin, it is ok to discontinue therapy and then restart again later.
False.

Restarting is contraindicated because reaction will recur
Rifampin Duration of therapy
Initial: 8 weeks
AND
Continuation phase: 18 weeks (4 months)
Rifampin and P450
Rifampin is the most potent inducer of Cyp450 3A4 and glucuronidation

Interactions with MANY drugs
Most potent inducer of Cyp450
Rifampin
Pyrazinamide duration of therapy
Initial phase ONLY = 8 weeks

Give only if patient is adherent and organism is susceptible
When is pyrazinamide most effective?
Against organisms in acidic environment within macrophage or areas of tissue necrosis
Most effective in first 2 months of treatment
Pyrazinamide MOA
converted to pyrazinoic acid in M. tuberculosis which lowers pH of environment
Pyrazinamide:
Class and ADEs
Anti-TB

Malaise, N/V, arthralgias, hepatitis (esp. in combo with rifampin)
When is pyrazinamide induced hepatitis especially common?
When used in combo with rifampin
Ethambutol duration of treatment
Initial phase ONLY = 8 weeks

Only if patient is adherent and organism is susceptible
Ethambutol: bacteriostatic or bactericidal
static at low doses
cidal at high doses
What is ethambutol mainly used for?
To prevent resistance
Ethambutol sterilizing activity
little sterilizing activity
Ethambutol MOA
RNA synthesis inhibition
Ethambutol:
Class and ADEs
Anti-TB

optic neuritis
Which anti-TB drug causes optic neuritis? What is it?
Ethambutol

decreased visual acuity, loss of green color vision
Do ethambutol doses need to be adjusted for renal dysfunction?
Yes b/c excreted as unchanged drug
Pyrazinamide and P450
No Cyp450 interactions
Which anti-TB drug's absorption is decreased if taken with aluminum salts?
Ethambutol
What med and dose should be administered with isoniazid?
Pyridoxine 25 mg/day (vit. B6)
TB monitoring parameters
CBC, LFTs, visual exam
Sputum cultures, AFB smears
CXR
Adherence
How often should sputum cultures and AFB smears be collected in TB patients?
every 2-4 weeks initially
then monthly after sputum cultures are negative
After cultures negative, need one more smear and culture at completion of therapy
Candidates for latent TB treatment
have + PPD
at risk for reactivation of active TB
Preferred treatment for latent TB
Isoniazid x 9 months
In what population may TB signs/symptoms be absent?
Elderly
Treatment of active TB in elderly
Same as others

Isoniazid, Rifampin, Pyrazindamide, Ethambutol
Extra cautions with side effects
Treatment of latent TB in elderly
Same as others

Isoniazid x 9 months
Use cutoff of >/= 15 mm for persons >35 yo so benefitis of isoniazid outweigh risks or hepatotoxicity
What is MDR-TB?
Resistant to isoniazid and rifampin
Primary TB resistance
Patient harbors a resistant strain before treatment (got resistant strain from someone else)
Acquired TB resistance
Resistant subpopulation are selected by inappropriate therapy, nonadherence, inadequate doses, or malabsorption
When should a single drug be added to a TB regimen?
NEVER
What populations are at risk for MDR-TB?
HIV
persons in institutionalized settings
How do you decide what drugs to begin with MDR-TB therapy?
Use at least 3 previously unused drugs to which there is in-vitro susceptibility
One agent must be injectable
How many drugs should a new MDR-TB regimen contain? What options do you have?
At least 4

Options: fluoroquinolones, para-aminosalicylic acid, cycloserine, ethionamide, injectable agents (streptomycin, amikacin, capreomycin)
Treatment of latent TB with HIV patients
Same

Isoniazid x 9 months
Treatment of active TB with HIV patients
Same 4 drugs (isoniazid, rifampin, pyrazinamide, ethambutol)

If patient on PI, rifampin contraindicated (sub. rifabutin)
When is rifampin use contraindicated? What should be used in it's place?
Contraindicated in HIV patients on PI

Replace with rifabutin
T/F.
Benefits of TB treatment during pregnancy do not outweigh the benefits so should be avoided.
False.
How long should TB treatment during pregnancy last?
9 months
Which anti-TB drug(s) should be reserved in pregnancy for cases of suspected drug resistance?
Pyrazinamide
Which TB regimen drug(s) should be avoided during pregnancy? Why?
Streptomycin

Causes ototoxicity
Is TB an indication for termination of pregnancy?
NO
Is breast feeding contraindicated with TB?
NO
Which anti-TB drug(s) is not used routinely in children? Why?
Ethambutol

Difficult to assess visual acuity in children
Which anti-TB drug(s) should only be used in children if resistance is suspected?
Ethambutol
Possible sites of extrapulmonary TB
bone/joint
military TB
meningitis
How long does TB treatment last with extrapulmonary TB and TB meningitis?
at least 12 months
Therapy for solid organ transplant patients
Standard therapy

Isoniazid, rifampin, pyrazinamide, ethambutol

Drug interactions with immunosuppressives
Primary HSV infection
mucocutaneous lesion
How long does it take for a primary HSV infection to resolve?
2-3 weeks
How does HSV change from primary to latent?
virus moves into ganglia --> latency period
When is HSV most severe?
1st episode
What symptoms are associated with the 1st episode of HSV?
flu-like systemic symptoms
When do HSV symptoms start? What are they?
Start after 1 week after initial exposure

Prodromal symptoms
Tingling, itching, burning
Progression of HSV
Prodromal stage --> vesicles appear --> vesicles erupt --> painful genital ulcers
How long does the prodromal stage of HSV last?
hours to days
When do HSV lesions mature?
Mature as they ulcerate

Can lead to secondary infection
Primary HSV infection signs/symptoms
local pain
itching
urethral/vaginal discharge lasting 11-14 days
How long does it take for HSV lesions to completely disappear?
3-6 weeks
When can HSV be spread?
when the virus is shedding
HSV contagious period
virus is spreadin
HSV prodromal stage
hours-days before lesions appear
When is HSV most contagious?
Ulcerative stage
HSV treatment: First clinical episode
acyclovir
famiciclovir
valacyclovir

x 7-10 days
How do HSV treatment agents work?
Shorten symptomatic period by 2-3 days
Decrease the severity of symptoms
Decrease viral shedding
HSV Treatment: Episodic recurrent infection
Acyclovir
Famciclovir
Valacyclovir

x 1-5 days
HSV Episodic recurrent infection
episodes shorter in duration
more localized
If meds are started within 48 hrs: decrease symptoms by 1 day, decreased viral shedding by 1 day
HSV Treatment: daily suppressive therapy (patients with >/= 6 recurrences/year)
Acyclovir
Famciclovir
Valacyclovir

Use daily
When should HSV therapy be stopped to re-evaluate infection with daily suppressive therapy?
Once a year
HIV-infected patient with episodic HSV: Treatment
acyclovir
famciclovir
valacyclovir

x 5-10 days
HIV-infected patient with suppressive HSV: Treatment
acyclovir
famciclovir
valacyclovir

used daily
T/F.
Condoms protect 100% from HSV transmission.
False
When is an infant especially at risk for contracting HSV from it's mother?
when passing through the birth canal

especially if mom is having 1st episode
Is mother-to-child HSV transmission risk the same no matter what stage the infection?
No
Less risk with recurrent episodes
Less risk with latent herpes
T/F.
Latent herpes indicates the need for a C-section.
False. Method of delivery up to physician.
Bacterial vaginosis
polymicrobial clinical syndrome resulting from replacement of the normal H2O2-producing lactobacillus sp. in vagina with high conc. of anaerobic bacteria
What is the most prevalent cause of vaginal discharge or malodor?
bacterial vaginosis
How often is bacterial vaginosis symptomatic?
50%
What is bacterial vaginosis associated with?
Multiple sex partners
New sex partner
Douching
Lack of vaginal lactobacilli
T/F.
Women who have never had sex are rarely affected by bacterial vaginosis.
True
Is treatment of male sex partners beneficial in preventing recurrence of bacterial vaginosis?
No
Diagnostic test for bacterial vaginosis
Gram stain
Diagnosis of bacterial vaginosis
thin, white discharge that smoothly coats the vaginal walls
presence of "clue cells" on microscopic exam
pH of vaginal fluid >4.5
fishy odor of vaginal discharge before/after addtion of 10% KOH (whiff test)
Bacterial vaginosis Preferred Treatment
Metronidazole 500 mg PO BID x 5 days
OR
Metronidazole gel 0.75%, 5g/1 applicator, intravaginally qhs x 5 days
OR
clindamycin cream 2% 5g/1 applicator, intravaginally qhs x 7 days
Alternative treatment of Bacterial Vaginosis
Metronidazole 2g PO single dose
OR
Clindamycin 300mg PO BID x 7 days
OR
Clindamycin ovules 100mg intravaginally x 3 days
Causative organism of trichomoniasis
protozoan trichomonas vaginalis
Trichomoniasis symptoms
Men: some asymptomatic, some have non-gonococcal urethritis

Women: diffuse, malodorous, yellow-green vaginal discharge with vulvar irritation
Do sex partners of patients with trichomoniasis need to be treated?
yes
How long should trichomoniasis patients avoid sex?
Until they and their sex partners are cured
(when therapy has been completed and patient and partner are asymptomatic)
Trichomoniasis Preferred Treatment
Metronidazole 2g PO single dose
Epidermis
nonvascular layer of skin
Dermis/hypodermis
connective tissue, blood vessels, lymphatics, nerve endings, sweat glands, sebaceous glands, hair follicles, smooth muscle fibers
Fascia
separates skin from underlying muscle
Is skin conducive to bacterial growth? Why or why not?
No, resistant to infection

dry surface, cont. renewal of skin cells, sebaceous secretions inhibit growth of many bacteria/fungi
Risk factors for infection
high conc. of bacteria (>10^5 bacteria)
excessive moisture of the skin
inadequate blood supply
availability of nutrients
damage to stratum corneum allowing for bacterial entry
Normal flora of exposed areas (face, neck)
staphylococcus epidermis
Normal flora of moist areas (axilla, groin)
GNRs (acinetobacter sp.)
Primary SST infection
usually involve areas of previously healthy skin and are typically caused by one pathogen
Secondary SST infection
usually occur in areas of previously damaged skin and are often polymicrobic
Examples of primary SSTIs
erysipelas
impetigo
lymphangitis
cellulitis
necrotizing fasciitis
Examples of Secondary SSTIs
diabetic foot infections
pressure sores
bite wounds
burn wounds
Bacteria responsible for impetigo
staphylococcus aureus
group A streptococcus
What is impetigo?
superficial infection of stratum corneum
Who is most likely to be infected by impetigo?
children, those with poor hygiene
Clinical manifestations of impetigo
purulent, localized vesicles/lesions (starts as rash)
mild pain, pruritis
Where is impetigo most likely to appear?
Exposed areas
Bullous impetigo
fluid filled sac greater than 1 cm in diameter
Impetigo treatment first-line
wash affected areas daily with soap and water
Antibiotic treatment for impetigo with localized lesions
Mupirocin ointment TID x 7 dyas
Antibiotic treatment for impetigo with extensive/nonresponsive lesions
Cephalexin 250 mg PO QID x 10 days
OR
Amox/clav 875/125mg PO BID x 10 days
Furuncle
infection of the hair follicle that usually extends through the dermis into subcutaneous tissue resulting in small abcess
Carbuncle
inflammatory nodule that extends through multiple adjacent follicles
Treatment of small furuncles
moist heat to promote drainage
Treatment of large furuncles and carbuncles
Incision and drainage required
systemic antibiotics usually unnecessary
Who usually gets erysipelas(lymphangitis)?
really young and really old
Risk factors for erysipelas (lymphangitis)
breaches in skin
pre-existing skin infections
inflammation
What part of the body is most commonly affected by erysipelas (lymphangitis)?
Legs
Bacteria responsible for erysipelas (lymphangitis)
erysipelas: group A strep
lymphangitis: group A strep (maybe staph aureus)
Presentation of erysipelas (lymphangitis)
raised, erythematous lesions with clear line of demarcation
typically associated with intense burning
orange peel appearance
often presents with systemic symptoms (fever, malaise)
Treatment of erysipelas (lymphangitis)
Penicillin IV/PO (depends on severity) x 14 days

If staph suspected, anti-staph B-lactam or first gen. cephalosporin x 21 days
DOC for erysipelas (lymphangitis)
Penicillin
Cellulitis
involves the deeper dermis and subcutaneous fat
Risk factors for cellulitis
middle-aged and older patients
breaches in skin
obesity
Presentation of cellulitis
erythematous, nonelevated lesions without defined margins
affected areas are edematous and warm to the touch
systemic symptoms
lymphatic involvement
Cellulitis Treatment (MSSA)
anti-staph B lactam or first gen. cephalosporin

if PCN allergic, use FQ
Risk factors for MRSA cellulitis
crowding, frequent skin contact, compromised skin, sharing contaminated personal care items, lack of cleanliness
minor trauma, close contact, peds pts with dermatologic conditions, adults who smoke/have diabetes, dermatologic conditions
Presentation of MRSA cellulitis
erythema and edema of the skin
lesion hot, painful and nonelevated with poorly defined margins
malaise, fever, chills, and leukocytosis can be present
lymphatic involvement possible
Treatment for MRSA cellulitis: minor skin infections or secondarily infected skin lesions
Topical mupirocin 2% may be effective
MRSA cellulitis treatment: cutaneous abscesses
incision and drainage
When are antibiotics recommended for MRSA cellulitis treatment?
abscess PLUS one of these:

severe or extensive disease/rapid progression
S/Sx of systemic illness
comorbidities/immunosuppression
extremes of age
abscess in area difficult to drain
lack of response to incision/drainage
Antibiotic outpatient MRSA cellulitis therapy
TMP/SMX (2 double strength tabs BID)
tetracyclines (minocycline, doxycycline)
clindamycin
linezolid
rifampin (used in combo)
Antibiotic inpatient MRSA cellulitis therapy
severe infections require hospitalization
vancomycin (DOC)
linezolid
tigecycline
daptomycin
DOC for inpatient MRSA cellulitis therapy
vancomycin
Duration of treatment for MRSA cellulitis
7-10 days
Traditional cellulitis vs. MRSA cellulitis
MRSA: purulent drainage from necrotic lesion and/or presence of abscess
Bacteria causing cellulitis
group A strep
S. aureus
occasionally other gram + cocci, gram - bacilli and/or anaerobes
Bacteria causing necrotizing fasciitis
Type 1: anaerobes, facultative bacteria (strep, enterobacteriaceae)
Type 2: group A strep
Necrotizing fasciitis
rare subcutaneous infection that spreads rapidly along fascial planes
results in progressive destruction in subcutaneous fat, fascia, muscle compartments
Necrotizing fasciitis risk factors
DM
penetrating truama
crush injuries/interrupted blood supply
Presentation of necrotizing fasciitis
skin necrosis or ecchymosis with associated severe, constant pain
systemic toxicity manifested by fever, leukocytosis, delirium, renal failure
Type 1 necrotizing fasciitis
mixed anaerobes, gram - bacilli, enterococci
mortality: 20%
Type 2 necrotizing fasciitis
group A strep
associated systemic toxicity
Mortality: 20-60%
Treatment of necrotizing fasciitis
antibiotic therapy based on gram stain/culture
type 1: amp/sulb +/- FQ
type 2: clindamycin

surgical debridement, amputation
Bacteria causing diabetic foot infections
polymicrobial

staph, strep, enterococcus, E. coli, GNRs, anaerobes
Key factors in development of diabetic foot infections
neuropathy
angiopathy and ischemia
immunologic defects
Presentation of diabetic foot infections
depends on extent of damage

swelling and erythema of foot
Types of foot infection
deep abscesses
cellulitis
ulcers
Potential complication of diabetic foot infection
osteomyelitis
What can diabetics do to optimize wound healing?
glucose control
wound care
Antibiotic treatment duration for diabetic foot infections
Mild infection (outpatient): 10-14 days
Moderate infection (in/outpatient): 2-4 weeks)
Severe infection (in-->outpatient): 2-4 weeks
Antibiotics for MSSA diabetic foot infection treatment
Outpatient - mild severity

amox/clav
FQ
SMX/TMP + clindamycin
Doxycyline + clindamycin
Antibiotics for MRSA diabetic foot infection treatment
Inpatient - moderate/severe infection

amp/sulb
pip/tazo + aminoglycoside
Pip/tazo + FQ
+/- vancomycin
Imipenem
Osteomyelitis
infection of the bone
Organisms that cause osteomyelitis
staph aureus
coag. - staph
strep
enterobacteriaceae
pseudomonas
Most common organism causing osteomyelitis
staph

aggressive, invasive
Which organism causing osteomyelitis is usually associated with foreign material or implants?
coagulase-negative staphylococci
Which organism causing osteomyelitis may spread rapidly through soft tissue?
streptococci
Manifestation of osteomyelitis
pain, swelling, drainage after surgery or injury
Diagnosis of osteomyelitis
imaging
Labs: CBC, ESR, CRP
Cultures: wound swab, needle aspiration, bone biopsy
Treatment of osteomyelitis
Hard-line therapy
early surgical intervention
aggressive antibiotic therapy
Treatment for MSSA osteomyelitis
oxacillin or nafcillin
cephalosporins
clindamycin
Treatment for MRSA osteomyelitis
vancomycin
daptomycin
linezolid
Treatment for Enterobacteriaceae (E.colid, klebsiella) osteomyelitis
ceftriaxone (or another cephalosporin)
ciprofloxacin
Treatment for pseudomonas osteomyelities
pip/tazo
cefepime
ciprofloxacin
imipenem
Treatment duration for osteomyelitis
IV antibiotics 4-6 weeks
Bite wounds:
Organism and treatment
Pasteurella multocida
Use augmentin
Otitis media:
Pathogens
viral etiologies
Strep pneumo
H. influenzae
M. catarrhalis
Otitis media:
Presentation
ear pain, ear fullness, hearing impairment, middle ear effusion, bulging tympanic membrane, erythema of tympanic membrane, opaque/cloudy tympanic membrane
Otitis media:
Diagnosis
rapid onset of symptoms
middle ear effusion
inflammation indicated by otoscopic evidence (tympanic membrane)
Otitis media:
First line therapy
high dose amoxicillin
Otitis media:
alternative therapy
high dose amox/clav
2nd/3rd gen. cephalosporin (cefuroxime, cefdinir, cefpodoxime, ceftriaxone)
PCN/ceph allergic: use azithromycin, clarithromycin, TMP/SMX
Otitis externa:
pathogens
Bacterial: pseudomonas, staph aureus
Fungal: aspergillus, cadida
Non-infectious causes
Otitis externa:
Presentation
"swimmer's ear"
otalgia
otorrhea
Otitis externa:
Diagnosis
Inflammation, erythema of external auditory canal only
No tympanic membrane inflammation/redness (occasionally perforated)
Otitic externa:
Treatment
Antibiotic +/- steroid drops for bacterial otitis externa

cipro + hydrocortison
cipro + dexamethasone
ofloxacin
neomycin, polymyxin B, hydrocortisone
2% acetic acid solution +/- hydrocortisone
Pharyngitis:
Pathogens
Viruses are most common cause

Bacterial: strep. pyogenes = group A strep
Pharyngitis:
Viral Presentation
sore throat, conjunctivitis, coryza, cough, diarrhea
Pharyngitis:
Bacterial Presentation
sudden onset, sore throat, FEVER, H/A, N/V, abdominal pain, inflammation of pharynx/tonsils, tonsillar erythema, patchy discrete exudates, tender enlarged cervical nodes, patient aged 5-15 years, presentation in winter/early spring, history of exposure
Pharyngitis:
Diagnosis
Rapid antigen detection test (false negative unlikely)
Throat swab culture - gold standar
What is the gold standard for pharyngitis diagnosis?
throat swab culture
When is a negative rapid antigen detection test enough to warrant no treatment?
If negative in adults
When should a rapid antigen detection test be confirmed by a throat swab culture?
If RADT negative in peds/adolescents
Pharyngitis:
First line therapy
PCN V 500mg PO BID x 10 days
PCN G benzathine 1.2 mil U IM single dose
Amoxil 500mg PO TID x 10 days
Keflex 250-500mg PO QID x 10 days

If PCN allergy: Eryth, clarith, azithro
Pharyngitis:
Antibiotics for recurrent episodes
Clindamycin 600 mg/day PO in 2-4 doses x 10 days
Amox/clav 500mg PO BID x 10 days
PCN G benzathine 1.2 mil U IM single dose
+/- rifampin 20 mg/kg/day PO in 2 doses x 4 days
Acute sinusitis:
Pathogens
viral etiologies
strep pneumo
H. influenae
M. catarrhalis
Acute sinusitis:
Presentation
nasal discharge/congestion
facial pressure/pain
postnasal drainage
fever, cough, fatigue
maxillary dental pain
ear pressure/fullness
Acute sinusitis:
Diagnosis
no clinically proven tools/tests
difficult to decide viral vs. bacterial
How long does it take patients to recover spontaneously without any therapy from acute bacterial sinusitis?
7-14 days
Acute sinusitis:
Treatment - mild disease w/o recent antibiotic
First line: high dose amoxicillin

Alternative: amox/clav, 2nd/3rd gen ceph, azith, carith, TMP/SMX, doxy
Acute sinusitis:
Treatment - mild disease with recent antibiotic exposure (w/in 4-6 weeks)
amox/clav 4g/day
ceftiaxone 1g IM qd x 5 days
levofloxacin 500 mg/d
moxifloxacin 400 mg/d

B-lactam allergy: respiratory FQ, clinda 600mg/day 2-4 doses
Chronic acute sinusitis
sinusitis episodes lasting more than 3 months
Acute bronchitis
inflammation of large components of tracheobronchial tree
Does acute bronchitis affect alveoli?
NO
Affect of acute bronchitis on secretions and mucociliary activity
increased bronchial secretions
impaired mucociliary activity
Most common causes of acute bronchitis
repiratory viruses: common cold, rhinovirus, coronavirus, influenze, adenovirus, RSV
Bronchitis:
Pathogens
mycoplasma pneumoniae
chlamydophilia pneumoniae
bordetella pertussis
Bronchitis:
Presentation
cough (progresses to mucopurulent sputum)
rhonchi
bilateral rales
headache, fever, malaise
Hallmark symptom of bronchitis
cough
Bronchitis:
Treatment
supportive: APAP, ibuprofen, cough suppreswsants (dextromethorphan, codeine), nasal decongestants
Antibiotics
When are antibiotics used with bronchitis?
pertussis
patients with persistent fever or respiratory symptoms for > 4-6 days
What antibiotics are used with bronchitis?
Macrolides (azith, clarith, erythro)
FQs (levo, moxi)
Chronic bronchitis
adult reporting coughing up sputum on most days for at least 3 consecutive months each year for two consecutive years
T/F
Chronic bronchitis is a component of COPD.
True
Can patients with chronic bronchitis progress to COPD?
YES
Acute exacerbation of chronic bronchitis
episodic worsening of chronic bronchitis with increased sputum volume, suputum purulence, and/or worsening of SOB in a previously stable patient
Pathogenesis of chronic bronchitis
chronic inflammation in walls and lumen of the airways resulting in increased mucus production and impaired lung defenses
Acute Exacerbated chronic bronchitis:
Pathogens
Viral pathogens: rhinovirus, coronavirus, adenovirus, influenza, parainfluenza
Bacterial pathogens: strep pheumo, H. influenzae, M. catarrhalis, C. pneumo, Mycoplasma pneumo, H. parainfluenzae, pseudomonas, enterobacteriacaea
Hallmark symptom of acute exacerbated chronic bronchitis
cough
AECB: Treatment
smoking cessation
chronic: long acting B agonists, long acting anticholinergics, inhaled corticosteroids
Acute exacerbation: Inhaled bronchodilators (SABA, SA anticholinergics), oxygen, systemic corticosteroids, antibiotics
AECB:
Antibiotics
Mild/moderate: amoxicillin, doxy, TMP/SMX, cephalosporins
Severe: amox/clav, azith, clarith, cephalosporins, levo/moxi
Pneuomonia
inflammation of the lower airways (alveoli) typically caused by viral pathogens

lower airways fill with pus and compromis air exchange
HCAP
pneumonia in patient who was hospitalized at least 2 days within 90 days of infection onset
HAP
occurs 48 hrs or more after admission and was not incubating at time of admission
How do microorganisms gain access to LRT?
inhalation as aerosolized particles
bloodstream
aspiration
Pneumonia:
Presentation
fever, chills, dyspnea, productive cough, leukocytosis, low O2 saturation

tachypnea, tachycardia, inspiratory crackles, diminished breath sounds over affected area
Pneumonia:
Diagnosis
Chest radiograph: dense lobar or segmental infiltrate
Expectorated sputum culture/stain
deep tracheal aspirate
blood culture
legionella urine antibody test (ICU, fialed OP treatment, alcohol abuser, travel w/in 2 weeks, pleural effusion)
bronchoscopy (bronchoalveolar lavage, protected brush specimen)
lung biopsy
Aspiration CAP:
Pathogens
oral anaerobes
enteric gram-negative
CAP with alcoholism:
pathogens
strep pneumo
oral anaerobes
Klebsiella pneumo
acinetobactor
mycoplasma tuberculosis
CAP with COPD/smoker:
pathogens
H. influenzae
pseudomonas
legionella
strep pneumo
M. catarrhalis
chlamydia pneumo
Influenza active in community:
pathogens
strep pneumo
staph aureus
H. influenzae
CURB-65
confusion
uremia
respiratory rate
low BP
age >/= 65 yo

scores >/= 2 --> hospitalization
CAP treatment
antibiotics while in ED
Criteria for clinical stability
temp < 37.8
HR < 100
RR < 24
systolic BP > 90
Ox saturation >90% or pO2>60mmHg on room air
maintain oral intake
normal mental status
Duration of CAP treatment
treat for at least 5 days
be afebrile for 48-72 hours
no more than one sign of clinical instability
CAP Outpatient treatment (CURB </=1)
1.macrolide or doxy
2. repiratory FQ
3. beta-lactam (high dose amox or high dose amox/clav) + macrolide
CAP non-ICU treatment (CURB = 2)
1. respiratory FQ
2. B-lactam (ceftriaxone, cefotaxime or amp/sulb) + macrolide
CAP ICU treatment (CURB >/= 3)
1. B-lactam (cefotaxime, ceftriaxone, or amp/sulb)
2. azithromycin or repiratory FQ

If PCN allergic: respiratory FQ + aztreonam
Early vs late onset HAP/VAP/HCAP
early: diagnosed within 4 days of hospitalization
late: 5 or more days after hospitalization
Risk factors for MDR pneumonia pathogens
antimicrobial therapy in preceding 90 days
current hospitalization of 5 days or more
resistance in comm/hospital
risk factors for HCAP
immunosuppressed
HCAP treatment: no risk for MDR pathogen (early onset)
ceftriazone 2g/day
OR
levo 750 mg/day
OR moxi 400 mg/day
OR
amp/sulb 3g q6h
OR
ertapenem 1g qd
HCAP treatment: risk for MDR pathogen (early onset)
combo therapy required

pip/tazo 4.5g q6h + cipro 400 q8h OR levo 750mg qd + vanc 15-20mg/kg q12h
vanc target trough: 15-20 mcg/mL
Flu manifestations
abrupt onset of H/A, fever, chills, myalgia, rhinitis, malaise, sore throat, cough
Resolution of flu symptoms
2-5 days
Who should be vaccinated (flu)?
all older than 6 months old
Vaccination for children 6 months-8 years
If receiving first seasonal flu vaccine - get 2 doses
Children 6 months-9 years of age who did not receive at least one dose last year, should get two doses this year
Who should not be vaccinated(flu)?
allergy to chicken eggs
had reaction to flu vaccine
Guillian-Barre syndrome within 6 weeks of getting vaccine
less than 6 months old
moderate/severe illness with a fever (wait until recover)
Trivalent inactivated influenza vaccine (TIV)
inactivated vaccine
IM
active against flu A/B, H1N1, H3N2
regular shot, high dose (>/= 65 yo), ID shot (18-64 yo)
Live attenuated influenza vaccine (LAIV)
live vaccine
nasal spray
active against influenza A/B, H1N1
approved if healthy and age 2-49
Contraindications to nasal flu vaccine
egg allergy
less than 2 yo or greater/= 50 yrs
underlying medical condition
chronic ASA therapy in children
pregnant
T/F.
Flu nasal spray must be readministered if patient sneezes after administration.
False
Treatment of flu
initiate within 2 days of illness onset
duration of 5 days
oseltamivir (>/= 13 yo)
Treatment of HSV1
acyclovir 400mg PO 5x/day x 5 days
famciclovir 1500 mg PO single dose
valacyclovir 2g PO q12h x 1 day
acyclovir 5% cream 6x/day x 7 days
docosanol 10% cream 5x/day until healed
penciclovir 1% cream q2h x 4 days
Varicella treatment
acyclovir 800 mg PO 5x/day x 7-10 days
famciclovir 500mg PO TID x 7 days
valacyclovir 1g PO TID x 7 days
+/- prednisone