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463 Cards in this Set
- Front
- Back
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 |
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Chronic acute sinusitis
|
sinusitis episodes lasting more than 3 months
|
|
Acute bronchitis
|
inflammation of large components of tracheobronchial tree
|
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Does acute bronchitis affect alveoli?
|
NO
|
|
Affect of acute bronchitis on secretions and mucociliary activity
|
increased bronchial secretions
impaired mucociliary activity |
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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 |
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When are antibiotics used with bronchitis?
|
pertussis
patients with persistent fever or respiratory symptoms for > 4-6 days |
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What antibiotics are used with bronchitis?
|
Macrolides (azith, clarith, erythro)
FQs (levo, moxi) |
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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 |