How One Patient Pharmacist Relationship Can Change Your Life

One patient can completely change your life.  Brenda was her name.   The website where there is an online cemetery mirroring how it looks in real life.  There are moments in my career where I sit back and remember the impact she had on my life.  Not only was she so vibrant (even over the phone) but she was also inspiring.  We were in the same generation though my life was about a young man I had met (and later married) and hers was about fighting for her life.  I was her pharmacist while she was at home battling breast cancer.  She had a boyfriend with the same maiden name as me, and well it was cool Brenda and I had the same initials. pharmacist patient relationshipI always want to connect with patients, but unfortunately my current job does not afford me the opportunity very often.  I lingered outside one patient's room at the hospital yesterday wanting to go in and introduce myself letting him know I wished him the best with his new situation and just say hello.  I have to do this more often.  There is nothing at work keeping me from opening the door and saying hello.  I guess I worry the patients are bothered enough all day and night by nursing and physicians and lab techs and all.  They get little rest, and they are sick.  Perhaps some would want a friendly face just saying hello and asking them if they need anything.

It was a little easier for me in home health because I had to call to find out how they were doing on their supplies, how nursing was handling things with the home IV antibiotics or TPN and it made it easier for me since I have this southern accent that sounds more southern even TO a southerner.  Ha!  That in itself was always an easy icebreaker.  "Where are you from?"  It always went from there.

Brenda wanted to go to Florida and jet ski.  With her pain pump.  We made it happen.  I'm proud of that memory.  I'm proud that I finally went out to meet her in person though I should have gone earlier when she was not in the final stage of life.  I saw a picture of her healthy.  Beautiful and full of life... same as most of us now.  We just can't waste this life we have!

I may have blogged about her before.  I haven't gone back to look because today I am thinking about her... it's been ten years, but I still think about how her life focus shifted with knowing she had little time left.  I am guilty of complaining quite a bit about my current job at times.  There are so many things that bug me mostly dealing with how things are handled, how pharmacists have those in control snowed, and how there's very little incentive (promotion, opportunities, salary increases, etc...) to even go above and beyond.  A new schedule comes out and I think why in the hell did I decide to do this job?  I mean, yes, it could be worse.  I know this.  But, could it not be better?

I think I am going to try to make these interactions with patients happen more often somehow.  If you have any ideas on how I can at the hospital, let me know... or if you have made it happen let me know.  These moments define major influences in my life (in the past), and I don't want to lose them by allowing my current situation to completely stifle who I am as a pharmacist.  Don't let your job dumb you down professionally or personally.

 

ACCP: Update in Therapeutics (my thoughts)

Well, here I sit in the Reno airport waiting on my flight to LAS.  My brain hurts a bit, but really enjoyed my stay at the Peppermill with my friend.  She is taking the exam for the first time, and if you have been following me for any amount of time know its my second attempt at this certification.  I feel what the in-person attendance vs the audio recordings can provide is the dedicated time to only listen to pharmacy all day for four days.  I really have my days mixed up so forgive me if I quoted that wrong.  The instructors for the most part were more than adequate presenting their material save for the always dry statistics lecture that made more sense since it's probably my 21st time hearing it. I can quote that infectious disease lecture almost verbatim at this point.  Maybe even in Dr. Smith's accent.

I enjoyed the changes in cardiology.  The material seemed much more organized and flowed better.

What my plan is for the next few months is to really learn the guidelines and as soon as the new lectures arrive (CDs), I will be the soccer mom in a van not listening to Top 40 but the lectures ad nauseum.  I guess there comes a point where all of this material coalesces and makes sense.  It was such a treat, I might add, to see Shannon Finks present since we attended UT Memphis School of Pharmacy together.  I love seeing UT students make such huge impacts in our profession.

So for now, I am reviewing cardiology at the moment.  And my friend and I did spend some time in the hotel room listening to the High Yield Med Reviews online lectures.  The stats one, she remarked, made more sense of the ACCP material... if that helps any.  I also purchased a couple of books.

Good luck to all of you who are now going to study like never before.  Do NOT wait.  Start now.  We have 5-5.5 months left.  That's really just around the corner considering I just received last years results 4 months ago.  Time flies.

And, I got the great opportunity to meet the winner of the giveaway -- Yvonne!  Like me, she sees the value in getting this, especially if you have been out of pharmacy school for any amount of time.  Jobs are more scarce, guidelines change and if you don't show that you have kept or are keeping up (demonstrated by passing this test), then you may be in trouble.  Just do it!!!

BCPS 2013: Some Pharmacoeconomics

Pharmacoeconomics are on the test more than I would have thought.  Some notes for you.  Enjoy! Definitions

A. Pharmacoeconomics—the description and analysis of the costs and consequences of pharmaceuticals and pharmaceutical services and its effects on individuals, health care systems, and society. These costs and consequences typically include both economic and humanistic assessments.

1. A division of outcomes research; however, NOT all outcomes research is pharmacoeconomic research.

B. Outcomes research—broadly defined as studies that attempt to identify, measure, and evaluate the end results of health care services in general

1. Clinical effects as well as economic & humanistic outcomes (i.e. functional status, well-being, satisfaction w/ care).

2. Proposed that evaluation of drug therapy and related services should always include assessments of economic, clinical, and humanistic outcomes.

 

A. Economic, clinical, and humanistic outcome (ECHO) model

1. Economic outcomes—direct, indirect, and intangible costs compared with the consequences of medical treatment alternatives.

2. Clinical outcomes—medical events that occur as a result of disease or treatment

3. Humanistic outcomes—consequences of disease or treatment on patient functional status, or quality of life, measured along several dimensions, e.g., physical functioning, social functioning, general health perceptions and well-being.

B. The ECHO model recognizes intermediary outcomes

1. Economic intermediaries à introduced from the clinical and humanistic side of the model.

a. Clinical à direct costs of medical care assoc’d with each treatment, not just the direct cost of the pharmaceutical products (i.e. lab testing, ED visits, inpt hospitalizations, and costs of retreatment from product failure)

b. Humanistic à

i. Indirect, or productivity costs assoc’d with the time lost from work

ii. Direct nonmedical costs à transportation to the hospital, or physician’s office for treatment

2. Humanistic intermediaries à affect the indl’s subjective evaluation of outcomes

a. Examples: side effects; efficacy/effectiveness; patient’s willingness or ability to pay; adherence to drug regimen (compliance); patient’s knowledge; drug dosing schedules

Economic outcomes assessment

**Balance cost vs consequences

A. Costs

1. Direct medical costs—costs incurred for medical products and services used for the prevention, detection, and treatment of a disease.

a. Examples: hospitalization, drugs, laboratory testing, supplies

i) Fixed costs represent overhead costs

ii) Variable costs—vary as a function of volume

2. Direct nonmedical costs—costs for nonmedical services that are the result of illness or disease, but do not involve purchasing medical services.

b. Examples: special food, transportation for health care, family care

3. Indirect costs—costs of morbidity and mortality resulting from illness or disease.

a. Examples: lost productivity, premature death

4. Intangible costs—costs of pain, suffering, grief, and other nonfinancial outcomes of disease and medical care

5. Incremental costs—additional costs incurred to obtain an additional unit of benefit from an alternative strategy.

6. Opportunity costs—the value of the next best use that is forgone

B. Consequences

1. Positive versus negative

a. Full evaluations must measure both desirable and undesirable outcomes.

2. Intermediate (“surrogate outcomes”) versus final

a. Intermediate outcomes are commonly used to demonstrate clinical efficacy because their usage reduces the costs and time required to conduct a clinical trial.

C. Perspectives: The pharmacoeconomic question being asked usually determines the appropriate perspective or viewpoint to be used.

1. Patient—costs are what they pay for a product or service (the portion not covered by insurance).

2. Provider—the health care professional or care organization; costs are the actual costs of providing a product or service, regardless of the charge

3. Payer—insurers, government, or employers; the costs are the charges for health care products and services allowed (reimbursed) by the payer.

4. Society—costs include patient morbidity and mortality costs, and the overall costs of giving and receiving medical care (**PREFERRED FOR CEA)

 

Economic Assessments

A. Full economic evaluation helps to assess the economic benefit of a program, service, or treatment

a. Requires (1) comparison of  >2 treatment alternatives and (2) BOTH costs and consequences of the alternatives are examined

Methodology

Cost Unit

Outcome Unit

Example

COI

$

Not assessed

Yields total cost of a disease

CMA

$

Comparative groups assumed to have = outcomes

Determine the least costly alternative

CBA

$

$

Net cost or benefit usually* or cost:benefit ratio

Used to decide how to allocate scarce resources

CEA

$

Natural units or units of effect

Used to compare competing programs or tx alternatives that differ in therapeutic outcome**

CUA

$

QALY

Used to compare txs or programs using terms of patient preference, quality of health care, or when outcomes can’t be expressed in monetary terms

COI = Cost of illness, CMA = Cost-minimization analysis; CBA = Cost-benefit analysis; CEA = Cost-effectiveness analysis; CUA = Cost-utility analysis; QALY = Quality-adjusted life years

*Example: if cost for treatment is $100 and value of outcome of treatment is $1000, cost-benefit ratio is:

benefit ÷ cost = $1000 ÷ $100 = 10/1 benefit of $1 million and cost of $100,000 also yields cost-benefit

ratio of 10/1 VS. net benefit = $900 ($1000 - $100)

**Results are expressed as average cost-effectiveness ratios, or as the incremental cost of using one alternative

over another.

Example: drug A has 90 percent cure rate, drug B has 95 percent cure rate; drug A costs $50,000 to

treat 100 patients, drug B costs $100,000 to treat 100 patients

-Calculation of average cost-effectiveness ratios:

drug A costs $50,000/100 patients ÷ 90 cures/100 patients = $555/cure

drug B costs $100,000/100 patients ÷ 95 cures/100 patients = $1053/cure

-Calculation of incremental cost-effectiveness ratio:

$100,000 - $50,000

95 cures - 90 cures      = $10,000/additional cure with drug B

 

Techniques for analysis

A. Discounting

1. Definition—an analysis that adjusts (reduces) future costs and consequences to reflect present fiscal value.

2. Discounting costs—based on the time value of money; because the value of money decreases over time, future costs must be adjusted (discounted) to present time values.

3. Discount rate of 3–8 percent should be used (often reflective of current interest rates used by banking institutions). Health care uses 5%.

B. Sensitivity analysis

1. Definition—an analysis that tests robustness of study conclusions; sensitive variables (or assumptions) are varied over a range of plausible results and the impact on study results is observed.

2. Variables include percent efficacy (or effectiveness), incidence of specific adverse drug reactions, and dominant costs.

C. Incremental cost analysis

1. Definition—an analysis that examines the extra cost of one program or treatment alternative relative to the additional effect provided by that alternative.

2. Formula: _Cost B – Cost A_

Effect B – Effect A

 

Applied Pharmacoeconomics

A. Definition—putting pharmacoeconomic principles, methods and theories into practice to assess the value of pharmaceutical products and services used in “real-world” practice settings

B. Primary application—to inform local decision making. Examples:

a. Formulary management

b. Clinical guidelines

c. Drug use policies

d. Service or program evaluation

e. Individual patient treatment decisions

What is REMS?

A Risk Evaluation and Mitigation Strategy (REMS) is a strategy to manage a known or potential serious risk associated with a drug or biological product. A REMS will be required if the Food and Drug Administration (FDA) determines that a REMS is necessary to ensure the benefits of the drug or biological product outweigh its risks. A REMS can include a Medication Guide, Patient Package Insert, a communication plan, elements to assure safe use, and an implementation system. This resource center contains information for pharmacists, patients, and other healthcare professionals about REMS, and the specific requirements for drugs that require a REMS. The Food and Drug Administration Amendments Act of 2007 gave FDA the authority to require a Risk Evaluation and Mitigation Strategy (REMS) from manufacturers to ensure that the benefits of a drug or biological product outweigh its risks.  Additional REMS Information.

Check out this FDA website to obtain more information.

BCPS 2013: Geriatrics

Geriatric pharmacy is a field that will continue to grow due to the aging population.  Not only do you need to remember the physical changes that geriatrics experience, but the current guidelines.

Know your guidelines!

PK/PD

Organ System Physiologic Change with Aging Resulting Effect on PK
GI ↑ stomach pH

↓ GI blood flow

Slowed gastric emptying & GI transit

absorption of basic drugs and nutrients

↓ in 1st-pass metabolism

Rate of absorption may be prolonged

Skin Thinning of dermis

Loss of SQ fat

↓/↔ to drug reservoir formation with transdermal formation
Body Composition total body water

↓ lean body mass, ↑body fat

↑ α1-acid glycoprotein

↓/↔ serum albumin

↑ VD and accumulation of lipid soluble drugs (i.e. BZDs)

 

↑ free fraction of highly bound acidic drugs and ↓ free fraction of basic drugs

Liver ↓ liver mass

↓ blood flow to the liver

↔ in phase II drug metabolism

↓/↔ phase I metabolism

↓/↔ CYP450 enzymes

↑ half-life and ↓ CL of drugs with high 1st-pass metabolism

Renal ↓ GFR and renal blood flow

↓ tubular secretion

↓ renal mass

↓ renal elimination of many meds

↑ half-life of renally eliminated drugs and metabolites

Salts of acid drugs: sodium (sodium naproxyn), calcium (atorvastatin calcium), potassium (penicillin G potassium)

Salts of basic drugs: HCl (tetracycline HCl), sulfate (atropine sulfate)

Medications to AVOID in the elderly

  • Beer’s List: includes consensus drugs only
  • Anticholinergic medications (anti-SLUDGE)

 

DEMENTIA

Delirium

Dementia

Depression

SUDDEN, RECENT ONSET

Lasts hrs to weeks

Look for changes in meds, setting, and infection; often reversible

Slow, progressive onset

Irreversible, memory impairment

In the present, with you in the moment (good attention)

Slow or recent onset

Withdrawn and/or sad

Flat affect but emotional

Answers with “I don’t know”

Medication causes of mental status change (reversible):

 

  • Anticholinergics
  • Opioids
  • Glucocorticosteroids
  • BZDs and other sedative/hypnotics
  • Antiparkinsonian med

 

MMSE (mini-mental status exam) Scores:

  • Normal cognitive function= > 24 (out of 30)
  • Mild Alzheimer’s Disease= 21-24
  • Moderate AD= 10-20
  • Severe AD= <10
  • Expected point decline in untreated pt= 2-5 points/year

Also assess a patient’s function (IADLs) and global assessment (CIBIC-Plus)

 

AD Pharmacological Treatment:

1st line: cholinesterase inhibitors (CIs); all equal efficacy; risk of bradycardia and syncope increased for all CIs

  • Donepezil (Aricept): 5mg/d (10mg-23mg/d); also ODT tabs; mild-mod AND severe AD
  • Rivastigmine (Exelon): 1.5-6mg tabs BID [also 9mg (delivers 4.6 mg/d) and 18mg (delivers 9.5 mg/d) patches]; ADRs of  N/V/D more intense than w/ other CIs; mild-mod AD & mild-mod dementia with PD
  • Galantamine (Razadyne): 4-12mg BID or 8-24mg/d (ER formulation); administer with food; syncope at high doses

2nd line/adjunct: glutamatergic therapy (NMDA antagonist; blocks glutamate)

  • Memantine (Namenda): 5mg/d up to 10mg BID; mod-severe AD, may be used in combo w/ Aricept; well tolerated but sometimes confusion seen

**NOTE: CIs and memantine show stat sig improvement in cognition, global assessment, and ADL in high-quality studies but NOT clinically significant!

 

> 50% of pts with dementia have psychosis and agitation

1. Determine cause

2. Non-pharmacological interventions (i.e. educate caregivers, have routine, improve environment)

3. Pharmacologic

A. CIs: ? efficacy; can increase agitation; 1st line for psychosis in Lewy body dementia

B. Atypical Antipsychotics (APs): NO FDA-APPROVED AP for tx of dementia-related psychosis

  • No clear standard on when to use, use for shortest time possible
  • Cochrane review suggests olanzapine and risperidone have most evidence for use in psychosis and aggression; however, use quetiapine if pt has comorbid PD or Lewy body dementia
  • High rate of ADRs: sedation, orthostasis, ↑ risk of stroke/death (OR 1.54 (CI 1.06-2.23), p=0.02)

URINARY INCONTINENCE

Type

Description

Drug-induced causes

Drug Tx

Comments

Urge or Overactive Bladder Loss of mod amts of urine w/ an ↑ in need to void; can result from CNS damage from stroke Cholinergic agents (stimulate bladder; i.e. CIs) Anticholinergic agents (i.e. darifenacin, oxybutynin, solifenacin, tolterodine) -1st line agents

-Oxybutynin has highest CNS effects

Stress incontinence Loss of urine w/ ↑ ab pressure (i.e. sneezing, coughing) α-blockers α-agonists (i.e. PSE and phenylephrine)

Topical estrogens and Duloxetine

-All variable efficacy

-SURGERY normally 1st line

Overflow incontinence Loss of urine b/c of excessive bladder volume caused by outlet obstruction or an acontractile detrusor Anticholinergics, CCB, opioids ↓ detrusor contractions α-blockers (outlet obstruction)

Add-on 5-α reductase inhibitors or bladder antispasmodics (i.e. oxybutynin, tolterodine) à advanced BPH or refractory sxs

Cholinomimetic (bethanechol)

Functional incontinence Inability to reach toilet due to mobility constraints Sedating meds cause confusion; diuretics Remove barriers and obstacles, provide toilet scheduling; assist pt on/off toilet
Mixed incontinence UI w/ >1 cause; usually stress and overactive bladder   Focus on dominating symptoms

Reversible causes of UI: DIAPERS (Delirium, Infection, Atrophic vaginitis and urethritis, Psychiatric disorders, Excessive urine output, Restricted mobility, and Stool impaction)

 

BPH Treatment:

1st line: α-blockers (↓ smooth muscle contraction in urethra); all can cause hypotension!

  • Nonspecific α-blockers: doxazosin (Cardura), prazosin (Minipress, not FDA-approved for BPH), and terazosin (Hytrin)
  • Selective α1-blocker: tamsulosin (Flomax)- less hypotension but ↑rate of ejaculatory dysfunction
  • Selective post-synaptic  α1-blocker: alfuzosin (Uroxatral)

2nd line: α-reductase inhibitors (prevent conversion of testosterone to DHT, DHT stimulates prostate growth)

  • Finasteride (Proscar) and dutasteride (Avodart); decreased libido
  • DO NOT IMMEDIATELY REDUCE SXS! At least 6 mo’s needed for benefit
  • Need baseline PSA to monitor for prostate cancer

Combo therapy for men w/ lower urinary tract symptoms, larger prostate size (>40g) and elevated PSA

  • Dutasteride w/ tamsulosin FDA-approved

Saw palmetto- conflicting efficacy data; may decrease efficacy of reductase inhibitors if used together

Surgery- for severe sxs and those with mod sxs not responding to meds

 

OA

Weight-bearing joints, unilateral, increased with age

Treatment

1st line: APAP up to 4 g/d (< 2.6 g/d if EtOH abuse); 2nd line: opioids, NSAIDs should seldom be used

Other options with ?efficacy: gabapentin (if neuropathic pain), baclofen if muscle spasms, topical agents (i.e. capsaicin, licocaine 5% patch), glucosamine +/- chondroitin

 

RA

Autoimmune disease, common in women (3:1 vs men) and younger people; bilateral inflammation in small joints of hands, wrists, and feet; (+) RF, ESR, C-reactive protein, and normochromic normocytic anemia

Treatment: goal = control inflammation à disease remission

  • 1st line tx: methotrexate (7.5-15mg/week) or potentially other DMARD; 3 months of use before effects seen!
    • For IMMEDIATE tx of pain and inflammation: NSAIDs (analgesic effects w/in hrs, antiinflammation 1-2 weeks) and glucocorticosteroids…both used SHORT-TERM
    • 2nd line if methotrexate does not work: TNF (etanercept, infliximab, adalimumab, etc) or IL inhibitor

 

Canada Pharmacy Reviews from Best Price RX Pharmacy

BCPS 2013: Asthma (a refresher of guidelines)

BCPS AsthmaThe BCPS Test contains questions the ACCP calls Ambulatory Care which has a few subtitles, one of which is asthma.  Charts and charts and memorization for the BCPS 2013:  Asthma.  Fun stuff right?  I do remember questions detailing patient has this many night symptoms and this many weekly, what category and what treatment.  So know these charts (embeded PDF files) Asthma is a chronic inflammatory disorder of the airways characterized by paroxysmal or persistent symptoms, such as shortness of breath, wheezing, cough, sputum production, and chest tightness, accompanied by variable airway hyper-responsiveness and degrees of airway obstruction.

Asthma diagnosis is confirmed by spirometry which includes an improvement in obstructed FEV1 by >/= 12 % from baseline and 200 mL at 5 minutes after using inhaled short-acting beta-2 agonist OR an increase > 10% of predicted FEV1 after inhalation of short-acting bronchodilator.

Acute or chronic?

Severity is determined by lung function and frequency and duration of symptoms (including at night).  Classification to determine treatment regimen.  Once asthma is well controlled, severity may be judged by determining minimal treatment needed to maintain acceptable control.

[embed]http://theblondepharmacist.com/asthmaclassification.pdf[/embed]

[embed]http://theblondepharmacist.com/asthmacontrol.pdf[/embed]

[embed]http://theblondepharmacist.com/5-11yearoldasthma.pdf[/embed]

[embed]http://theblondepharmacist.com/inhaledcorticosteroids.pdf[/embed]

There's also a great resource for guidelines that are relatively cheap if downloaded digitally.  Here's the asthma one!

 

High Yield Med Reviews: A Giveaway!

I am so excited to be teaming up with High Yield Med Reviews to offer one of my readers a free subscription to their BPS (can be BCPS, BCACP or BCPP) Online Review Course!  See the value below.  We will make this easy!  Just retweet or share this post on your facebook or twitter and you will have an entry into the contest!  Post you did in the comments, and a random generator will decide who the lucky reader is!  The winner will be announced on April 1st! Comment on the post to confirm you have shared and you are entered automatically!

High  Yield Med Reviews

Pills, Thrills and Methadone Spills!

I have an exciting giveaway to mention!  A fellow twitter pharmacist has written a book available on amazon kindle!

Mr Dispenser is  a community pharmacist from England and has written a funny book about pharmacy called ‘Pills, Thrills and Methadone Spills: The Adventures of a Community Pharmacist’.
It’s a collection of the best blogs, tweets and anecdotes about the wonderful world of pharmacy.
There is a chapter of American anecdotes in there.

Get your Kindle version here: Paperback copy 

5% of sales are going to  Pharmacist Support which is a UK pharmacist charity.

Want to follow the author?

Blog

Facebook Page

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Retweet this post or share on Facebook for a chance to win a free copy!  Winner will be decided this coming Monday at noon!  Post a comment on THIS POST saying you retweeted or shared.  Drawing will be random!

 

BCPS 2013: Infectious Diseases

My infectious disease review.  I've already talked about pneumonia and may be revising these to go from the direction of the bugs and then the drugs again.  One thing I will say:  Invanz is not active against MRSA, ampicillin-resistant enterococci, Pseudomonas aeruginosa or Acinetobacter species.  Hear me?  :)

BCPS ID Review

Pneumonia

CAP

HAP

Organisms M. pneumonia, S. pneumonia, H.flu, C. pneumonia, Legionella, Viruses S. aureus, Pseudomonas, Enterobacter, Klebsiella pneumo, Candida, Acinetobacter, Serratia, E.coli, S.pneumonia
Treatment Healthy no Abx in previous 3 months

Macrolide (clarith or azith) OR doxycycline

Cormorbidity or Abx in previous 3 months

FQ (moxi, gemi, levo 750mg)

Macrolide (or doxy) + [High-dose amox 1g

tid OR amox/clav 2g bid OR ceph ]

(ceftriaxone, cefuroxime, cefpodoxime)

Early onset (< 5 days)

3rd ceph (ceftriaxone, cefotaxime)

FQ (levo, moxi, cipro)

Amp/sulbactam

Ertapenem

Late onset (> 5 days or RF for MDR)

   Ceftazidime OR cefepime + AG or FQ (cipro, levo)

Imi, mero, or dori + AG or FQ (cipro, levo)

Pip/taz + AG or FQ (cipro, levo)

   + Vanco/linezolid only if MRSA risk factors

Duration At least 5 days 7 days (14 days for Pseudomonas)

 

Influenza: Type A (Annual, H1N1, H1N2), Type B

Prophylaxis:  if outbreak and cannot receive vaccine

1. Amantadine, Rimantadine 5-7 weeks

2. Neuraminidase inhibitors: Oseltamivir 75-150mg daily x6wks; 75mg daily x7days within 2 days of contact

Zanamivir 10mg daily through inhalation x4wks

Treatment: only if severe symptoms or at risk for complications

1. Amantadine, Rimantadine- only against Type A, decreases symptoms 1 day  *do NOT use for at risk for complications

Dosing: 100mg bid x3-7 days [Elderly 100 daily]; ADJUST FOR RENAL DISEASE (amantadine> rimantadine)

AE: CNS, GI, peripheral edema, orthostatic hypotension

2. Oseltamivir- decreases symptoms 1-1.5 days

Dosing: 75mg bid x5days [CrCl <30 75mg daily]

AE: GI

3. Zanamivir- decreases symptoms 1-1.5 days

Dosing: 2 inhalations (5mg/inhalation) bid x5days

AE: bronchospasm, cough

 

UTIs Treatment Other Comment
Uncomplicated cystitis Nitrofurantoin 100mg bid

     X 5 days

TMP/SMX DS bid x 3 days

Or Fosfomycin 3 gm once

Duration: 3 days vs 5

Alternatives:

Amox-clavulanate, cefdinir, cefaclor, or cefpodoxime x 3-7d or FQ x 3 d

 
Pregnancy Amoxicillin

Nitrofurantoin

Cephalexin

TMP/SMZ

Duration: 7 days

AVOID:

FQ

Tetracyclines

AG

TMP/SMZ (esp 3rd trimester

Pregnant women should be screened for UTI even if asymptomatic
Recurrent cystitis Relapse: treat 2-6 weeks Reinfection

<2/yr: pt initiated x3days

3+/yr: post-intercourse

TMP/SMZ SS, cephalexin 250mg, nitro 50-100mg

3+/yr: daily or 3x/wk

3+/yr other can also use TMP 100mg, or Norfloxacin 200mg
Uncomplicated Pyelonephritis Not requiring hospital:

Cipro 500mg BID x 7d

Cipro ER 1000mg daily x 7d

OR Levo 750 mg daily x 5d

OR TMP-SMX DS bid x 14d

 

Hospitalized:

IV FQ

Aminoglycoside with or w/o ampicillin

OR extended-spectrum cephalosporin or an extended-spectrum pcn with or without an aminoglycoside or carbapenem

 

Not requiring hospital:

Or Oral beta-lactam (less effective) plus initial IV ceftriaxone 1gm OR IV 24-hour dose of aminoglycoside

 

For pts without N/V and not immunocompromised
Complicated UTIs FQ levo x 5 days

AG x 5-14 days

Extended spectrum Beta lactam  
Catheter-related UTIs Symptomatic pts x 7-10 days and cath removal Assymptomatic pts should NOT be treated E.coli, Candida, Enterococcus, Pseudo, Kleb pneumo, Enterobacter
Prostatitis Acute: Duration 4 weeks TMP/SMZ

Cephalosporins

FQ

Chronic: 1-4 months

TMP/SMZ

FQ

 
Epididymitis >35 yr: TMP/SMZ, FQ

x 10 days- 4 weeks

< 35 yr: Ceftriaxone 250mg IM AND doxycycline 100mg bid

x 10 days

 

Skin and Soft Tissue Infections

Cellulitis Nafcillin, Oxacillin, Dicloxacillin x5-10 days Alternatives: Clinda, BL combos, 1st ceph Vanco/Linezolid for MRSA

PCN G if streptococcal

Erysipelas Penicillin G, Clindamycin

x 7-10 days

   
Necrotizing Fasciitis B lactam combo + clinda  + cipro

Carbapenems

Cefotaxime + clinda OR metron

Streptococcal: High dose IV PCN + clindamycin ABX not curative, surgical debridement necessary!
DM Foot Infection Deep:  1-2 weeks

Amp/sulbac, Ticar/clav, Pip/taz

Ertapenem

FQ + [clindamycin OR metron]

Cefoxitin

3rd ceph + [clinda OR metron]

Shallow: treat like cellulitis

PCN, 1st ceph, etc.

Topical: Becaplermin 0.01%

Human platelet derived growth factor, improves healing from 35-50%

 

Surgery also important

 

Osteomyelitis: treat for 4-6 weeks (chronic IV 6-8 weeks + 3-12 months PO)

1. Neonates: Nafcillin + [cefotaxime OR AQ]

2. Infants: Cefuroxime OR ceftriaxone OR [Nafcillin + cefotaxime]

3. Peds (>3yr): Nafcillin OR Cefazolin OR Clindamycin

4. Adults: Nafcillin OR Cefazolin OR Vancomycin

5. Pts with Sickle Cell Anemia: Nafcillin + Ampicillin

6. Prosthetic Joint Infections: Vancomycin + rifampin OR Nafcillin + rifampin

 

CNS Infections: Meningitis

Empiric: 7-14 days

1. Neonates: Ampicillin + AQ OR + cefotaxime

2. 1 month- 50 yrs: 3rd ceph (cefotaxime, ceftriaxone) + Vanco

3. >50 yrs: 3rd ceph +Vanco + ampicillin

4. penetrating head trauma: Vanco + cefepime, ceftazidime, meropenem

Pathogen Known: MOSTLY PCN G 4mill units IV q4h OR Ampicillin 2g q4h, alt: 3rd ceph, vanco, mero, FQ

Corticosteriods: Dexamethasone 0.15 mg.kg q6h x2-4 days; give 10-20 mins before (or at time of ) Abx

Benefit in: Peds with H.flu and Adults with S. pneumo

Brain Abscess: Treat based on source: mostly metron + 3rd Ceph                               Unknown source: Vanco + Metron+ 3rd ceph

 

Endocarditis: Strep, Staph, Entero, HACEK    Duration: 4-6 weeks (8+ weeks with VRE)

Strep: PCN G ± gent, Ceftriaxone ± gent, Vanco

Staph: Oxa/nafcillin ± gent (+ rifampin if prosthetic valve), Cefazolin ± gent (+ rifampin if prosthetic)

MRSA: Vanco (+ rifampin if prosthetic); may also use Vanco in severe PCN allergy

Entero: [PCN G or ampicillin or vanco]  + [gent or streptomycin]                 VRE: linezolid, Quin/Dalf

HACEK: ceftriaxone, Amp/sulbactam, FQ

PPx: dental and resp tract procedures: Amoxicillin 2g PO 1 hr prior                          PCN Allergy: Clinda, azith/clarith

Perotonitis/ Intra-Abdominal Infections

Mild-Mod: cefoxitin, Ticar/clav, ertapenem, moxifloxain,tigecycline;  [cipro/levo +metronidazole],

[cefazolin/ cefuroxime/ceftriaxone/cefotaxime + metronidazole]

Severe, healthcare acquired, High-risk: Pip/Taz, [ceftazidime/cefepime +metronidazole], imi/cil, mero, dori, [cipo/levo +

metronidazole (not for healthcare acquired)]

Duration: 4-7 days, [injuries repaired in 12hr can be treated for only 24 hr]

 

C. difficile: diagnose by presence of endotoxins

Initial TherapyMild to moderate initial episodeMetronidazole 500mg PO/IV tid x 10-14days OR Vanco 125mg PO QID x 10-14days

Severe initial episode:  Vancomycin 125 mg PO QID for 10-14 days

Severe complicated CDI: Vancomycin 500mg PO plus Metronidazole IV 500mg Q8H

Recurrences:  First recurrence:  Same as for initial episode

Second recurrence: Vancomycin tapered/pulsed

 

Medical/Surgical PPX

Procedure Treatment Comment
Gastric/duodenal Cefazolin 1-2g Indicated: morbid obesity, esophe obstruction, decreased gastric pH or motility
Biliary Cefazolin 1-2g Indicated with (without?): acute cholecystitis, obstr. jaundice, common duct stones, >70yr
Appendectomy Cefoxitin 1-2g

Cefazolin 1-2g  + metronidazole

OR amp/sulbactam

If perforated treat x 3-7 days
Colorectal Cefoxitin 1-2g

Cefazolin + metronidazole OR amp/sulbacam

Gent/tobra 1.5mg/kg + clinda 600mg/metron 0.5-1g

± neomycin +erythromycin/

metronidazole

PO/IV may be better bc PO only may cause Cdiff

Mechanical bowel prep is not recommended

Obstetrics/GYN Hysterectomy: Cefazolin/cefoxitin 1-2g

Caesarian: cefazolin 1-2g

 

Caesarian: administer AFTER cord clamped

Cardiothoracic Cardiac surg/Pulm resection:

cefazolin/cefur oxime 1-2g

Vascular surg: cefazolin 1g q8h x3doses

For all: Use Vanco if MRSA risk

 

Orthopedic Cefazolin 1-2g (or cefur or vanco) Indicated: surgery involves prosthetics
Head/Neck Cefazolin 1-2g

Amp/sul 1.5-3g

Gent 1.5mg/kg + clinda 600-900mg

Indicated: major surgery when incision through oral or pharyngeal mucosa
Urologic NOT recommended If (+) urine culture, treat then operate

Pseudomonas Putida BacteriaAnd because pseudomonas is always mentioned:

Pseudomonas aeruginosa
Drugs of Choice:  Piperacillin-tazobactam, Imipenem, Meropenem, Ceftazidime, Cefepime, Amikacin, Gentamycin, Tobramycin, Ciprofloxacin
Alternatives:  Timentin, Aztreonam, Levofloxacin
Third-Line agents: 
Comments:  (Gram-negative bacilli).   Consider using two agents from two different classes as empiric treatment in critically ill patients if P. aeruginosa is suspected. Once susceptibilities known, narrow to one drug according to susceptibility report. 

 

BCPS 2013: Cardiology II

More of what I was studying last week: Acute Coronary Syndromes

UA NSTEMI STEMI
CP +

CE –

ECG +

CP +

CE +

ECG + (ST depress, T wave ∆s)

CP +

CE +/– (90 min door to balloon, may not have dmg)

ECG + (ST elevation > 1 mm)

Risk factors → cath

Stress test

Cath 12-24 hrs Cath 90 min

Chest pain → atypical, typical (exertional, relief from SL nitro, shorter (min-hr), substernal, radiating left)

Cardiac enzymes → troponin, CK-MB

ECG changes → ST or T wave ∆s

Therapeutic goals

UA/NSTEMI: prevent total occlusion, control chest pain and other symptoms

STEMI: restore patency of infacted artery, prevent complications (e.g. arrhythmias), control CP and Sx

  UA NSTEMI STEMI
Morphine 1-5 mg IV

Oxygen (if O2 sat < 90%)

Nitroglycerin

Aspirin (chew 162-325 mg)

x x x
Beta blocker     x
Anticoagulation x x x
Antiplatelet x x x
IIb/IIIa If PCI If PCI If PCI
Fibrinolysis     If no PCI

 

UA/NSTEMI

  Early invasive (PCI < 12 hr) Delayed PCI (> 12 hrs) Early conservative (no PCI)
Anticoagulant UFH, enox, bival,

fonda (+ UFH w/ PCI)

UFH, enox, bival,

fonda (+ UFH w/ PCI)

Enox, fonda
Antiplatelet Clopidogrel or prasugrel

Abciximab or eptifib w/ PCI

Clopidogrel or prasugrel

Eptifib or tirofib w/ PCI if high or moderate risk

Clopidogrel

Abcix or eptifib w/ PCI if +stress test

 

STEMI PCI (w/in 90 min) Fibrinolysis (w/in 30 min, up to 12 hrs)
Anticoagulation UFH w/ abciximab (or eptifib or tirofib)

Bivalirudin alone

UFH 48 hrs or

Enoxaparin 8 days or

Fondaparinux 8 days

Antiplatelet Clopidogrel or prasugrel Clopidogrel

 

Dosing and duration of antiplatelet

  ASA Clopidogrel/Prasugrel
Initial 162-325 mg chewed CLO 300-600 mg LD (300 mg if w/ fibrinolytics)
Pre-PCI 75-325 mg CLO 300-600 mg LD or PRA 60 mg LD
No stent 75-162 mg/day indefinitely CLO 75 mg for 14 d to 1 yr

BMS

DES

 

162-325 mg 1 month

3 mo (siro), 6 mo (paclitaxel)

Then 75-162 mg/day infef.

CLO 75 mg/day or PRA 10 mg/day (5 mg if < 60 kg)

for 12-15 mo

 

See Table 8, 9, 10 for IIb/IIIa, anticoagulants, thrombolytics. See Table 11 for contraindications to thrombolytics.

Post ACS:

1. Beta blockers,

2. ACEi or ARB,

3. ASA + CLO or warfarin,

4. Statin (LDL < 70-100 mg/dL)

 

Peripheral Artery Disease: vascular insufficiencies in noncoronary arteries 2/2 atherosclerotic occlusions

  1. Functional – due to spasms of vessels
  2. Organic – structural changes e.g. fatty buildup

Age > 50                 HTN

Smoking                 # homocysteine

Diabetes                                High sensitivity-CRP

HL                            Male

Family Hx

Symptoms: leg or hip pain, cold legs and feet, changes in skin color, pain reduced w/ resting, numbness or tingling

Ankle brachial index = ankle SBP ÷ arm SBP                  PAD risk factors

1-1.29 Normal
0.91-0.99 Borderline
0.41-0.9 Mild to moderate
0-0.4 Severe

 

Treatment: reduce risk factors

Diet, exercise, smoking cessation, HL drugs (goal LDL < 70), antihypertensives (goal BP < 140/90 or 130/80 if diabetic), diabetes control ( A1C < 7%), homocysteine, folic acid and B12, antiplatelet (ASA 75-325 or CLO 75)

Treatment of claudication: cilostazol 1st line, pentoxifylline 2nd line, IR for angioplasty or stents

Dyslipidemia

Fasting lipid panel (9-12 hrs)

LDL < 100

100-129

130-159

160-189

> 190

Optimal

Above optimal

Borderline high

High

Very high

HDL < 40

> 60

Low

High

TC < 200

200-239

> 240

Desirable

Borderline high

High

TG < 150

150-199

200-499

> 500

Normal

Borderline high

High

Very high

 

LDL goal

CHD risk equivalents: CHD (MI, CABG, PCI, ACS), atherosclerotic dx (PAD, AAA, carotid), DM, > 20% Framingham

Positive risk factors: smoking, HTN, low HDL, family Hx premature CHD (55m, 65w), Age (45m, 55w)

Negative risk factors: high HDL

 

Risk category LDL goal LDL to start Rx
CHD risk equiv, Fram > 20% < 100 (optional < 70) > 130, opt > 100 or < 100?
2+ risk factors, Fram 10-20% < 130 (optional < 100) > 130, opt > 100
2+ risk factors, Fram < 10% < 130 > 160
0-1 risk factor < 160 > 190, opt > 160

Non HDL goal = 30 + LDL goal

Lifestyle changes: weight loss, exercise, diet (plant sterols, soluble fiber, low cholestrol)

Low HDL: TG < 200, niacin safer combo w/ statins than fibrates, smoking cessation, exercise

TG 200-499 target non-HDL, TG > 500 target TG

High TG > 500: goal prevent pancreatitis

Low fat diet, fibrates or niacin, reduce TG before LDL

Pharmacotherapy

Statins (HMG-CoA reductase inhibitors)

$ LDL 24-60%, $ TG 7-40%, # HDL 5-15%. Reduce coronary events, CHD mortality, stroke, total mortality

AE: myopathy, elevated LFTs (check baseline, 3 month, yearly)

DI: SAL (simvastastin, atorvastatin, lovastatin) are CYP3A4. Fluva 2C9, Rosu 2C19, Pita 2C9. Avoid with inhibitors.

Myopathy risk higher with gemfibrozil than fenofibrate. Niacin lower risk than fibrates (careful if > 1g/day).

Efficacy

  5 mg 10 mg 20 mg 40 mg 80 mg
Fluvastatin     24 30 36
Pravastatin   24 30 36 40
Lovastatin   24 30 36 40
Simvastatin 24 30 36 42 48
Atorvastatin   36 42 48 54
Rosuvastatin 42 48 54 60  

Pitavastatin (1 mg = 30%, 2 mg = 36%, 4 mg = 42%). About 6% with each dose doubling and rank.

Bile acid sequestrants – inhibits bile acid recirculation. Liver converts cholesterol to bile acid

$ LDL 15-26%, # HDL 3-6%, reduce coronary events and CHD mortality.

Names: cholestyramine, cholestipol, colesevelam

AE: GI distress, constipation, may increase TG.

DI: decreased absorption of drugs (e.g. warfarin, BB, thiazides)

Niacin – inhibits mobilization of FFA from perif adipose tissue, reduces VLDL synthesis

$ LDL 15-26%, $ TG 20-50%, # HDL 15-26%, reduces coronary events, possibly reduces mortality

Formulations: IR Niacin, ER Niaspan, SR Slo-Niacin

AE: flushing, hyperglycemia, hyperuricemia, GI distress, hepatotoxicity (check LFTs base, q6-12wks, yearly)

Sustained release more hepatotoxic, less flushing (can give ASA 30 min prior to reduce flushing)

Fibrates – reduce lipogenesis in liver

$ LDL 5-20% (normal TG, may # TG up to 45% w/ high TG), $ TG 30-55%, # HDL 18-22%, reduce coronary events and progression of coronary lesions

Names: gemfibrozil, fenofibrate

AE: dyspepsia, gallstones, myopathy, # LFTs (check q3mo for 1st year, then yearly)

Ezetimibe – inhibits cholesterol absorption. Adjunct with statins.

$ LDL 18-20%, $ TG 7-17%, may # HDL 1-5%

AE: HA, rash

Omega-3 (Lovasa) – unknown mechanism

(may # LDL up to 45% w/ high TG), $ TG 26-45%, may # HDL 11-14%

AE: GI (burping, dyspepsia), inhibit plt aggregation, bleeding

Purple heart in the hands