Recently I was counseling a pt with dyslipidemia, who wanted to try diet and exercise, that they might try fish oil supplementation for the omega three fat content. At which point The MD I was working with interjected that flaxseed may be a better choice, so I decided to take a closer look.

As discussed in a posting above, fish oil can be beneficial both in the lipid profile and subsequent prevention of cardiovascular disease, i.e. in the outcome that matters avoiding heart attack. Similarly flaxseed has been shown to have a beneficial role in dyslipidemia. (see this citation from Nutrition Review 2004). These findings may be due to the omega three fat content in flaxseed. However fishoil contains EPA and DHA while flaxseed contains precursor fat ALA and other purportedly beneficial stuff such as lignans and phytoestrogen.

Flaxseed has the highest levels of ALA known of any food source. If you are interested to read in some biased but useful information from the flaxcouncil about the contents of flaxseed check out this pdf.

There is some question however whether the ALA is in fact converted to EPA and DHA (see this citation).

Given this it may turn out that flaxseed and fishoil are working in slightly different ways and that their effects are independent. So for the time being at least I will advocate a little helping of both.

Earlier this week, a 10 year old boy came into the clinic with his father for a medication checkup for his Straterra.  The boy was initially diagnosed with ADHD by his primary care physician after his father reported behavioral problems at school and home.  (Click here for more information on ADHD.)  Particularly, at home, the child was constantly defying his parents by staying up late at night, agitating his sister, and destroying things at home.  At school, his behavior was no better - with sudden outbursts in the classroom and difficulty paying attention to the teacher.  Ultimately, his lack of control had affected adversely at home and at school, especially in terms of his grades.

Over the last year, the parents and the doctor have tried different anti-ADHD drugs to find a balance that would offer a way to "control" his behavior.  Finally, with the administration of Strattera, over the last 3 months, the parents have noticed a significant improvement in the behavior of the child.  Most particularly telling has been his improvement in school.  His grades had improved and his teachers have written several notes commenting on the amazing progress he has made.

As the school year winds down, the child's dad has become particularly interested in taking the child off the medication during the summertime - placing him on a "drug holiday."

The number one reason that a doctor or parent would suggest a drug holiday is the side effects profile of the drugs being used.  (The side effects of the 4 major drugs used for ADHD are given here.)  However, other factors, such as the parents' desire to remove medication or the desire to see the child cope without an "artificial" means, are great motivating factors to remove the drug, especially on weekends and during summer vacation.

Although parents are eager to stop the drugs, research suggests that drug holidays are not recommended.  In fact, they may adversely impact older children.  Therefore, it seems that long-term treatment may be the most effective way of treating this disease.  This evidence requires practitioners to state to parents and children that treating ADHD is a continuing process that does not get "cured" from just a few months.  Although behavior may improve after some time, medications over longer duration of time will provide the framework by which the child may improve both neurologically and behaviorally (see article subheading entitled, "Effects of Long Term Treatment").

I recently had a patient ask to go over her pathology results from a recent breast biopsy.  This young women explained that she had several breast lumps removed , found to be "not cancer", but since this time the surgical site have continued "to leak."  She thought her breasts were infected and presented to her physicians' office to have them looked at.  A biopsy was done and the results stated a benign tumor called a seroma.  The patient asked me to explain this to her and as I began  realized I did not know what a seroma truly was. 

Harrisons was no help as seroma is not in the glossary and the section on nonmalignant tumors did not offer much if anything.  A quick google search lead to my information and my comforting explanation to the patient. 

Briefly, a seroma is a collection of serum (yellowish fluid of blood after the removal of RBC's and WBC's.)  This collection usually occurs at the site of a surgical incision where lymphatic circulation has been compromised thus fluid drainage from the wound area is deficient. Untreated most seromas will resolve on there own in several months time.  Treatment is elementary, involving insertion of drains to remove the collecting fluid.

The following website is a medical research page directed at animal welfare research but offers the best explanation and indepth information of a seroma that I have found.

It is interesting that my patient repeatedly spoke or her breast as infected but this is quite false.  An abscess, quite similar but different than a seroma, is a collection of serum with addition of WBCs, bacteria, and degenerate products of both.  A referral was done to a breast surgeon in the area and informed of the likely insertion of drainage tubes. 
 

(if there's too much damn typing here just go look at impression and plan for some asthma management...)

    A 25 year-old Female with chronic asthma presents for follow-up of a continuing intermittent feeling of eye-fatigue, blurryness, and dizzyness.
    The patient first noticed this almost a month ago, when she was having the heavy eyelid sensation every day.  She went to a walk-in clinic where she ws diagnosed with sinusitis and given a 10-day course of Omnicef.  It is now resolving, only happening once or twice a week.

    The patient recently had a fairly severe exacerbation of her asthma, the worst ever, and went to the emergency room - 4 days after her visit to the walk-in.  She was given a nebulizer treatment and sent home.  She was seen by us the next day and given a 4-day prednisone taper which worked very well and cleared her chest right up.  She is currently on Advair but doesn't feel that it is helping.  Her chest is still tight at night.  She has no wheeze now but reports one every morning.  Also, every morning she wakes up with muscle pain in her arms, shoulders, and back.  This improves with a shower and stretching, and is resolved by early-afternoon.

    In the interim an opthalmologist has given her a clean bill of health from his perspective (which is to say she doesn't need glasses, uhh thanks dude).  The patient is also complaining of all-over muscle pain for several weeks, however she denies any double vision, tunnel vision, headaches, or loss of consiousness.

    On physical exam this is a pleasant young woman in good apparent health, and no acute distress.  Her lungs were CTA bilaterally and no wheezes, rales, or rhonchi were appreciable.  She has a cough with scant clear sputum production.  During this visit we had her perform a trial of spirometry.  Her FEV was 64% of predicted and her FEV1 was 76% of predicted.  She is snuffling her nose and appears to still be suffering some post-nasal drip.  There is minimal mucus discharge on the posterior wall of her oropharynx.

Impression and Plan:

    She's got asthma, real bad, and it's poorly controlled.  From a further history we found out that she lives in a basemant apartment and just noticed some mold on one wall.  The landlord promptly painted over the mold after she pointed it out (nice slumlord, good slumlord).  She also just bought a brand new feather comforter.  We also did a quick chart review and found that theis was the third year in a row that she was showing up around April with these complaints.  So,

1. Sinusitis:  This wasn't resolved with Omnicef, a cephalosporin that inhibits cell wall synthesis, which is inactive against MRSA and organisms resistant to penicillins.  We gave her Bactrim DS (1 tab PO Bid, 24 days) for broad butt-kicking URI coverage.
2. Acute Asthma: This obviously needs to be better controlled.  We increased Advair to 500/50 and added Allegra 180 D and Singulair (10mg PO QDay).  Advair has a corticosteroid (fluticasone) component and a B2-adrenergic bronchodialtor (salmeterol).  Allegra adds a H1-histamine receptor antagonist (fexofenadine).  Singulair is a leukotriene receptor antagonist to slow down them mast cells.
   
3. Chronic Asthma:  Move out of the basement;  get a HEPA filter;  sorry about that expensive new comforter (actually you can buy hypoallergenic duvet covers)...  We advised her to come in in March next year, before her asthma acts up, so that we can address this prophylactically.
4. Chief complaint:  The symptoms of fatigue, heavy eyelids, and blurry vision, along with the myalgias will improve once we get the combination of sinusitis and asthma under control.  This was ultimately my point for using this case.  The symotoms could have pointed to just about anything, however common things being common,...  We will follow up with her in a month to see how she's doing.
   

ps. yeah that stuff about the mold and the down comforter belongs in the HPI not the I&P...  I know that... don't you think I know that? Sheesh.

A patient came to the office this week with a question about a scar, she wondered what she could do so the scar was less noticeable.  My preceptor suggested that time would heal all wounds, so to speak, and 4-6 months was required to see maximum cosmetic healing.  He also mentioned Vitamin E or aloe as possible adjunct therapy.  I brought up Mederma, which I used with good result myself, and have heard other physicians recommend.  Mederma is moderately expensive ($29/50g tube) even though it is available OTC and my preceptor wanted to know what the evidence was to support it's use.

I could only find one RCT on Pubmed that tested the product. The Mederma website lists a couple of studies, but I could not get to the full text to determine whether I would consider them valid.  I did find one review article that suggested the evidence was lacking for Mederma and other natural cream products.  They found that silicone patches or silicone applied to scars daily had reasonable effect.  Interestingly, Vitamin E has not been shown to improve the outcome of scars and in many cases can illicit a dermatitis.

Given my research, I suppose that I will not be able to recommend Mederma to patients, though I am not planning on throwing away my own tube.

In response to the comments: This patient's scars were three hypopigmented fully healed puncture wounds, ~1x1 mm each, and level with the surrounding skin.  Not anything I would ever be concerned about medically or cosmetically, but it was a possible litigation situation since it was a bite from the neighbor's dog, and her father was concerned she would be upset with the scars later in life.

I have seen several patients in the past few weeks with rheumatoid arthritis and although the patients I saw had already been diagnosed years before, I was interested in the clinical evaluation of a patient with suspected arthritis, and the best way to differentiate among the different types.

The history is an important part of the process, as always. The age and sex of the patient may first make certain diagnoses more or less likely. Also, the pattern of joint involvement is important - symmetry, large vs. small joints, locations, and migratory disease. Finding out how long the pain has been going on and whether the pain is worse in the morning and gets better with activity (inflammatory arthritis) or if there is no pain at rest and is precipitated by activity (osteoarthritis and nonarthritic musculoskeletal problems). Constitutional symptoms may be present in autoimmune disease and infection.

On physical exam, the joints in question must be examined for active and passive range of motion and also for joint deformity or effusion. The patterns of joint involvement is very important, as many diseases have very specific patterns. Rheumatoid arthritis almost always presents as involvement of the wrist and MCP joints, which is rare in osteoarthritis. The distal interphalangeal joints are almost always involved in inflammatory osteoarthritis and psoriasis. Ankylosing spondylitis and other spondyloarthropathies may be found by assesssing the axial skeleton.

Laboratory testing should involve synovial fluid analysis, because this helps to distinguish inflammatory processes from non-inflammatory. Patients with RA would likely have > 10,000 WBCs and a predominance of PMNs.  Rheumatoid factor is found in the blood of 80-90% of patients with RA, but also in many other rheumatic diseases, chronic infection and malignancy. Thus, the presence of rheumatoid factor is neither necessary nor sufficient to make the diagnosis of RA.

Radiographic studies in patients with RA would show erosive disease of the small joints of the wrist, the MCP joints, the PIP joints, the ulnar styloid and the small joints of the foot. The erosions seen in erosive psoriatic arthritis, however, are described as "telescoping of joints" or "pencil in cup" lesions.

Treatment for RA is based on maintaining function of the joints and decreasing the pain. NSAIDS are helpful for the pain, but do not act to reverse or slow the underlying process. Another class of drugs being used are called disease modifying antirheumatic drugs (DMARDs) or also slow-acting antirheumatic drugs (SAARDs), such as methotrexate, hydroxychloroquine, cyclosporine and also oral gold and gold salts. Methotrexate is the most widely used of this class, because it is has relatively low toxicity and is the fastest to act of this class. Corticosteroids can also be used to decrease inflammation, but should be used only when necessary and even then in low doses.

Physical therapy and occupational therapy can help these patients to improve muscle strength and maintain joint mobility.

This is a good website that I found for patient eduation on rheumatoid arthritis, but my computer hates me and won't let me hyperlink it, so I'll just give you the URL. It's http://www.medicinenet.com/rheumatoid_arthritis/article.htm 

Sorry about that. Hope it works.

 We had a tearful young woman come into the office this afternoon who was very distraught.  She complained of panic attacks that began 4 days prior and were not coming with any set frequency but did not exceed 4 per day.  The first attack presented itself while she was smoking marijuana of which she admits addiction and use of at least one joint per day for the last 3 years.  This has been an escalating habit up to $100/week.  She denies the use of other drugs or alcohol.  The attacks are debilitating in the sense that she is unable to leave her home and has not been to work in three days for fear of something happening to her.

The articles that I researched, including an Up To Date article on frequent marijuana use point to paranoia associated with occasional use and panic attacks, although rare, with chronic abuse such as in our patient.  One patient went to the emergency department many times with palpitations, diaphoresis, and sinus tachycardia.  He was diagnosed with panic disorder without agoraphobia.

The previous patient sounds a lot like ours.  A lengthy conversation revealed no significant changes in our patient's life but that she had been "down" for a number of weeks for no apparent reason. We decided to try a week of Prozac to see if it alleviates what my attending believes to be underlying depression manifesting in these panic attacks.  She is to call back in one week or prn if she does not feel the depression or panic attacks are improving.

Just another question you should be screening for in people with cp, tachycardia and diaphoresis.

Article abstract 1

Article abstract 2

   An ederly diabetic dialysis patient presented with intermittent bilateral lower back pain, rated at 6/ 10.  She was unable to further describe the type of pain, elucidate when the pain began, describe anything that made the pain better or worse, and could not remember if she had tried any medication with/ without relief.  Fortunately, her husband accompanied her on her visit and was able to give a little more insight into the complaint.  This incident highlights the complexities in evaluating and treating dementia patients.

   Since an adequate history is often difficult to attain in these patients, physical exam becomes very important.  PE should not only be focused on the chief complaint, but should also include a mental status and neurological exam.  On exam, it is also important to identify other problems that may also interfere with the patient's ADL's, including hearing/ vision loss, orthopedic problems, etc.

   Dementia is a very common finding in family medicine offices, with a prevalence of 50% after the age of 85.  Although most cases of dementia are irreversible, it is important to consider the full differential since some causes are reversible.  The differential includes Alzheimer's dementia (about 50% of cases), multi- infarct dementia, Lewy body dementia, depression, normal pressure hydrocephalus, thyroid disorders, B12/ folate deficiencies, syphilis, HIV, medications, MS, Parkinson's, Huntington's, Down's, and intoxication. 

   Diagnostic evaluation should focus on recognizing potentially treatable causes of dementia and identifying any co- existing illness that may also be contributing.  Recommended tests include CBC, SED rate, electrolytes, calcium, albumin, BUN, creatinine, LFTs, TSH, Vit B12/ folate, and urinalysis.  Also useful are hearing and vision tests, CXR, EKG, and neuroimaging.

  Outside of the medical management of dementia patients, it is of utmost importance to educate the family and caregivers about how best to create a safe, familiar environment for the patients.  Due to the incredible stress of caregivers, they also need to be informed of local support groups .

We had a patient call the office for a refill on her prescription of Metrogel (topical metronidazole) that she uses for treatment of her rosacea.  In discussing this with my preceptor I 1) wondered why an antibiotic that is usually used for anaerobes would be effective and 2) I didn't know a that much about rosacea even though I've seen a few patients with the skin disease who presented for different complaints.

Rosacea is a common, but often overlooked, skin condition of uncertain etiology that can lead to significant facial disfigurement, ocular complications, and severe emotional distress.  I found it interesting in my research that although the exact etitology of the disease remains debated, the primary first line treament is various classes of antibiotics, including oral antibiotics, such as tetracycline, doxycycline, and metronidazole  as well as topical metronidazole (cream [MetroCream] or gel [MetroGel]) I thought the article I linked above was a good overview of diagnosing, treating and most  importantly recognizing this disease that can cause serious disfiguriement in adults. Hope it helps, I'm sure you guys have seen patients with this disease too.

 

A pt in her low 30s came to the office for a BP check.  She has had BPs in the 140-150s/80-90s.  She was obese, I forget the BMI, but remember she was somewhere around 35.  She has tried to lose weight through Slim Fast (a shake for breakfast and lunch, and then a "sensible dinner").  She has lost around 10 pounds over the past 2mo, but we discussed how this is a difficult diet to keep up for the long term. 

The physician came in and agreed that we needed to teach her healthier eating habits which she could keep up for the rest of her life.  She recommended the DASH diet (Dietary Approaches to Stop Hypertension).  This is a diet by the NHLBI that is low in saturated fat, cholesterol, and total fat, and suggests eating more fruits, veggies, and lowfat dairy foods.  It is low in red meat and sweets, but suggests eating more whole grains, fish, poultry and nuts.  Clicking on the link above gives you a great pdf file that you can print out and give to your pt (our pt was very excited to get the info!). 

What is interesting about the DASH diet, is it was not designed to decrease weight, but to lower BP.  Studies have shown that the DASH diet does lower BP and there is a recent review article which discusses some of these studies.  The DASH pt handout does have some suggestions on how to modify the diet to help decrease total caloric intake (to lose weight).  Also, it should be noted that the DASH diet with a behavioral intervention was shown to reduce systolic BP by only 4.3mmHg.  This is helpful, but our pt was hoping for a larger decrease in BP.

We discussed the importance of lowering her total caloric intake (she was eating bags of chips for dinner!).  Then went over the DASH pt handout with her to help her understand how she could change her diet and still have it fit into her busy lifestyle. 

We started our patient on HCTZ in addition to putting her on the DASH diet.  A 4.3mmHg reduction was just not enough for us or the patient and she was acceptable to the idea of taking medication to help her lower her BP.  Obviously, our pt wanted to decrease her risk or morbidity and mortality associated with obesity and HTN, but at this point she just wanted something to help her lower her BP and help lose weight.  She didn't need data on how this will extend her life, she already assumed that it would.

It was asked what she does for exercise...Actually, the reason she came in for a BP check was because she started a new exercise program and felt her BP was going way too high during and after her workouts with a trainer.  This probably wasn't the case, but it seemed that she was over-exerting herself for an obese woman who never exercised before.  She actually stopped going to the gym because of this.  This is something we need to mention to our pts, it is important to start out slow with exercise because not only can they get injured, but if it is too difficult for them, they will only get discouraged.  Starting with 5-10min a day and working up is a good way to keep them motivated.

A woman in her thirties presents with chief complaint of peri-menstrual migraine headaches.  She is requesting medication she can take at onset of migraine, and also wants to know of alternative treatment and prophylaxis options. 

The triptan class of medications has been shown to be effective in treating migraine headaches; this article suggests that rizatriptan taken via nasal spray offers more rapid absorption compared to the oral route. Therefore, this option was suggested to the patient as a way to provide faster relief in the face of an acute migraine.  In addition, a new fast disintegrating/rapid release formulation of sumatriptan has been developed which can be used in the acute treatment of migraine so patients can return more rapidly to normal functioning.

Alternative therapies for migraine have also been researched, including acupuncture and herbal remedies such as fever-few.  Acupuncture, in this study, was found to be no more effective than sham acupuncture in reducing migraine headaches.  But this article analyzes evidence-based information regarding alternative prophylactic treatment of migraine, and it finds that current clinical data supports the use of fever-few, butterbur, magnesium, and riboflavin in migraine prophylaxis. 

Studies are limited, and more rigorous methodologies and larger sample sizes are needed to further support the safe and effective use of these alternative treatments.  It is important for us to be aware of these alternative therapies to appropriately advise our patients. 

 

A 52 year-old obese female presented to the office for treatment of heel pain of her right foot.  The pain had started a few weeks ago and is only mildly relieved by Tylenol.  She has been working at a supermarket for over a year now, where she is on her feet for hours, but reports that the heel pain started recently.  She does not recall any recent injuries or increase in activity.  She is otherwise healthy, with her hypertension and diabetes well managed with medication, diet and exercise.  Physical exam revealed tenderness of the plantar surface of the right heel and foot.

Diagnosis: plantar fasciitis 

Heel pain is a common orthopedic complaint, and plantar fasciitis is the most common cause.  Plantar fasciitis is, not surprisingly, an inflammation of the plantar fascia resulting in degenerative changes.  The plantar fascia runs from the tuberosity of the calcaneus to the five toes and provides arch support.  Classically, patients complain of pain with the first few steps in the morning.  However, some may complain of pain only at the beginning of certain activities or, in severe cases, worse pain at the end of the day.  A characteristic finding on examination is local point tenderness along the fascia from heel to forefoot while dorsiflexing the patient's toes to pull the plantar fascia taut.  Other diagnostic testing is not necessary, although an x-ray may reveal a heel spur, which is often seen in conjunction with plantar fasciitis, but is not the cause of the pain (plantar fasciitis is commonly referred to as "heel spurs," which is a misnomer).

Differential diagnoses include: 

- Posterior tibial nerve entrapment (tarsal tunnel syndrome) - parasthesia, numbness

- Ruptures plantar fascia - sudden onset of pain, ecchymosis

- Bone pain from stress fracture of calcaneus - pain increases with weight bearing

- Bone pain due to osteomyelitis or neoplasm - constant pain with nocturnal worsening, MRI is diagnostic

- Posterior tibialis tendonitis - tenderness along course of tendon

- Painful heel pad syndrome - seen in marathon runners, pain localized to heel pad, not along plantar fascia, no increase in pain with dorsiflexion of toes     

 There are many risk factors for plantar fasciitis, over-use being more common than functional or anatomical risk factors.  Functional risk factors include tightness and weakness of the gastrocnemius, soleus, Achilles tendon and intrinsic foot muscles.  Some anatomical risk factors are pes planus (flat feet), pes cavus (high arches) and overpronation.  Over-use is seen in athletes, such as runners and ballet dancers, as well as those who stand on their feet for long hours.  Obesity is also a risk factor simply because of the amount of weight the arches must bear.  

Eighty percent of cases resolve completely in six to 18 months with rest, ice packs, ibuprofen and improvement of modifiable factors, such as weight loss.  Wearing properly padded shoes with good arch support, and exercises, such as calf-plantar fascia stretches, foot/ankle circles and toe curls, will also aid in improvement.  If these conservative therapies fail, cortisone injections are also effective, but carry a 10% risk of plantar fascia rupture and fat pad atrophy.  Custom made orthotics may also be helpful in difficult cases.  Surgery (plantar fasciotomy/fasciectomy) is reserved for the most recalcitrant cases (2-5%), but has a 70-90% success rate.  I must note, however, that there is very little data regarding the effectiveness of many plantar fasciitis treatment modalities. 

This article provides a link to a pamphlet that you can print out for patients, as well as having great information for providers.  
 
 

Patient is a young boy presents with a 3 weeks history of a papules rash on his back, trunk, and thigh.  Rash is not pruritic and patient has no systemic symptoms of fever, diarrhea, nausea/vomiting.  Patient is not taking any medication and is up to date with his immunization.  Patient has no recent illness or sick contact and no recent travel history.  There were no physical exam finding except for the rash.  A presumptive diagnose of Mucha-Habermann disease was made.  Mucha-Habermann or pityriasis lichenoides is a rare skin disorder that is self-limited.  It is of unknown etiology and can present as an acute or chronic condition.  Patient was referred to a dermatologist for a possible punch/shave biopsy to confirm the diagnosis.

Man in his 50's came in for a full physical.  He hadn't seen a physician in over 5 years because he hadn't been sick but his wife made him come in now.

Quick and dirty relevant info:  PMHx-No surgeries/hospitalizations.  Did have a normal colonoscopy in 2001.  Fam Hx-HTN on both sides of family, some uncles died of some kind of cancers (he didn't know exactly).  No meds.  Social- pack a day smoker for 40+ years.  ROS:  Some SOB with exertion. 

PEx:  Normal except for the DRE.  http://www.nlm.nih.gov/medlineplus/ency/article/007069.htm

My 2nd DRE ever, but there were 2 soft, mobile pea sized bumps on the walls of the rectum.  I don't think they were on the prostate.  Hemoccult was negative.  What the heck were they?!?! 

Differential for abnormal findings on DRE:  hemorrhoids, polyps, or abscesses. http://my.webmd.com/hw/colorectal_cancer/hw4404.asp

He wasn't referred for a colonoscopy at that time because of the prior normal history less than 5 years ago.  He did  get his blood drawn after the exam:  CBC, cholesterol, PSA.  My physician said that common things being common, the lumps were probably hemorrhoids.  He'd had a normal colonoscopy in the past and he wasn't febrile or complaining of pain, so the polyps and abscess were unlikely. 

This past week I saw a patient with complaints of amenorrhea.  The patient had been on Depo Provera for approximately three years, which is longer than the current recommendation of two years due to bone density issues.  Her last shot was in the early spring of 2004.  The patient's menstrual cycle had resumed in late summer of 2004 - about 6 months after her last shot of Depo Provera.  The patient's menstrual cycle had been normal for several months and then had stopped in early 2005.  The patient's menstrual cycle prior to and after the Depo Provera had been about 28 days.  Her LMP was normal but had occurred about 70 days prior to this visit.  The patient admitted sexual intercourse without barrier or other forms of protection a few weeks after her LMP but none since then.    

The patient's ROS was negative.  On physical exam the patient was overweight, VS were normal, with no abdominal or suprapubic tenderness.  The remainder of the exam was unremarkable.  The urine beta-HCG was negative. 

There are many methods to work up amenorrhea.  First, it should be noted that every year approximately 5 percent of menstruating U.S. women experience 3 months of secondary amenorrhea.  Lab studies should start with a beta-HCG which was done.  Other tests and the order in which to perform them, depends on the history and physical.  The levels of prolactin, FSH, LH, estradiol, testosterone, or TSH can be measured and inappropriate levels of these hormones are known causes of amenorrhea.  Imaging studies such as ovarian ultrasound or pituitary/hypothalamic MRI can be helpful.  Other tests such as the progesterone withdrawal test can also be used.  This test although not recommended by the authors of this paper was prescribed for this patient.  A positive test, i.e. bleeding after progesterone withdrawal, indicates that the ovaries are producing estrogen and the uterus is responsive to estrogen and progesterone.  Furthermore, a positive test indicates that there is a failure to menstruate due to a failure to ovulate.  This test was not recommended because a negative or positive test is not definitive and may delay "diagnosis of potentially serious disorders."

The recommended algorithm for evaluation of secondary amenorrhea is as follows: 1.) pregnancy test 2.) TSH and prolactin levels  3.) Progestin challenge  4.)  FSH and LH  5.)  MRI. 

In this patient, it was suspected that although her menstrual cycle had resumed since her last injection of Depo Provera, the Depo Provera may have still have been affecting her menstrual cycle and causing the secondary amenorrhea.  Additionally, the patient is overweight, which is known to cause amenorrhea and menstrual cycle dysfunction.  Follow up was scheduled for two weeks following the progesterone withdrawal.  

 

The helpful links:

http://www.emedicine.com/ped/topic2779.htm

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15589863

http://www.fda.gov/bbs/topics/ANSWERS/2004/ANS01325.html

http://www.emedicine.com/med/topic117.htm

http://www.amcstudents.com

A young woman came in for a routine physical with no complaints.  She has had no major illnesses, no significant past medical history, and no surgical history.  When asked about her menstrual cycles, she said that they were heavy at times and very irregular.  Some months there was two weeks inbetween cycles and other times she would not have a period for 2-3 months.  She had never really given this much thought and had not discussed this with her mother.  She began menstruating at age 11 and is now 17.  Her only other complaint was that she wanted to lose some weight.  She denies regular exercise and admits to a diet consisting of daily soda, some fast food, minimal fruits and vegetables, and candy/cookies.  

On physical exam she is obese, displays mild hirtuism on the upper lip, and has evidence of some acne on her face.  She does not have acanthosis nigrans.  The rest of the PE is benign. 

We suggested several things at the conclusion of her exam: take some blood to test for androgen levels (total testosterone, free testosterone), cortisol levels, random glucose, and thyroind function tests and  refer her to a nutritionist for a review of her diet to help her with weight loss.  As far as she knows, there are no other family members that have been diagnosed with PCOS.

Her history and PE findings suggest PCOS.  Classic PCOS has been defined as an association of amenorrhea with polycystic ovaries and, variably, hirsutism and/or obesity.  A good webiste that has some of the latest information on PCOS for both doctors and patients is  http://www.obgyn.net/pcos/pcos.asp . 

Although there is no cure for PCOS, there have been some advances in trying to treat patients with this syndrome.  Typically the first line treatment is OCPs to control the ovulatory dysfunction and dermatological manifestations of PCOS.  GnRH agonists can be given to those patients who can not tolerate OCPs.  Hyperinsulinemia and insulin resistence is common in patients with PCOS causing both weight gain and contributing to the hypersecretion of androgens. Metformin has been studied and appears to have some utility in the management of weight loss by suppressing appetite. 

The results of this patient's labs are currently pending.

An elderly female came in with a nodule distal to her DIP joint.  She reported that the nodule was painless and denied any oozing.  The only thing she could remember was banging her finger a few times in the same place.  Upon further questioning, she also rememberred gardening several times before the nodule appeared, but denied any punctures from thorns.  On physical exam, she was afebrile and the nodule was superficial, non-erythematous, mobile, and non-purrulent.  It had the appearance of a blister. 

My differential included sporotrichosis because of the gardening history.  I excluded rheumatoid arthritis and other bony changes, because the nodule was more superficial.

At this point, we decided to drain the cyst with a needle.  Upon its puncture, a clear, mucinous fluid oozed out.  No further treatment was needed at this time.

After seeing the mucinous drainage, the diagnosis of mucinous cyst was made.  It probably developed due to repeated trauma to her finger.  It was explained to me that Sporotrichosis was ruled out because of the lack of inflammation.

Migraine in Children

A 14 y/o male patient presented in the clinic with a history of a sore throat in the morning, followed by a headache, and cyclical vomiting during a period of one day.  This pattern also occurred in the late fall of 2004.  The only other positive symptoms found during a complete history and review of symptoms was that during these episodes he was under more stress than usual at school, and that he was most comfortable during these episodes in a dark, quiet room during these periods.  In addition, his mother took his temperature and found it slightly elevated at 99. The only pertinent positive on physical examination was 2+ tonsilar erythema.  The patient was given a presumptive diagnosis of a migraine.  

After seeing this interesting presentation of a migraine I was curious as to whether or not a sore throat was possibly an atypical presentation of a migraine aura.  Upon reviewing the literature I found that an acute onset migraine in most children is accompanied with an upper respiratory tract infection. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10759922

These results correspond with the patient's history of a recent increase in stress and a sore throat.  Stress is associated with both an increased risk of an infection and a migraine.  It is very possible that he had a low grade URI.  In addition, he brought a progress note from a visit to another clinic.  The Nurse Practitioner clearly noted that the patient looked physically unwell after the episode which also supports this theory.  On both occasions the headache, sore throat, and vomitting cleared up after one day but were followed by a short period of fatigue.  It would be interesting to ask him on another visit if he commonly has these symptoms with upper respiratory infections.

Treadmill stress tests are performed every Wednesday morning at one of the outpatient clinics. In the past two years I have worked at several Family Practice clinics, each routinely conducted treadmill stress test. A review of treadmill testing is provided at the American Academy of Family Physicians website (you can read the article if you like, but the tables are self explanatory and tell you most of what you need to know in a fraction of the time).

The treadmill test requires individuals to walk or run on a treadmill that inclines to a slope of 14-16%. Therefore, any patient seeking a treadmill test needs to be able to walk and have relatively good balance. If this is not the case, tests such as and adenosine-thallium or dobutamine stress test are more applicable to these patients. These tests mimic a treadmill test by stimulating the heart, but have no exercise component. The patient's history is taken to determine a pre-test probability of coronary artery disease (charts are available for this). The pre-test probability is determined by gender, age, and symptoms (typical angina, atypical angina). The patient's max heart rate is also determined (220-age). The desired goal is to reach 85% of the patients max heart rate during the test.

Indications for a treadmill stress test (Table 2) include symptoms of coronary artery disease, presence of typical anginal symptoms of chest pressure or pain with or without exercise, shortness of breath or dyspnea with exertion, following surgical intervention for coronary artery disease, or after an MI.

Absolute contraindications (Table 5) include acute MI, unstable angina, acute cardiac inflammation (pericarditis, endocarditis, myocarditis), severe CHF, uncontrolled ventricular arrhythmias, symptomatic supraventricular arrhythmias, high-grade block, severe hypertension (systolic pressure >200 mm Hg or diastolic >110 mm Hg), active thrombolic process, and poor candidate for exercise. As previously mentioned the treadmill inclines to a slope of 14-16%. Go to the gym and try this out. Regarding the blood pressure limits one needs to remember that many of these patients have HTN for which they are receiving medication. Since b-blockers and Ca⁺⁺ channel blockers affect the test, patients are counseled to go off these medications prior to the test. Due to this a patient showed up this week with a BP of 248/138.

What to look for, the indications of a positive test (Table 8 and Figure 1). This can be divided into clinical findings and ECG findings. Clinical symptoms suggesting ischemia include exercise induced hypotension, exercise induced angina, or the appearance of S₃, S₄, or murmurs. Figure 1 illustrates some positive ECG findings. In general one looks for ST segment changes, typically ST segment depressions. Many clinicians use a 1mm depression as the cut off for a positive result. However, there are some who recommend using a depression of 0.5mm as a positive result. The argument is that this increases the sensitivity of the test. However, we all know from EBHC that this in turn will decrease the specificity.

Mom brought 6 yo pt in who had developed acute onset right ear pain in 2 days.  The pain is intermittent, and fleeting at times. The patient had no fevers, no other constitutional symptoms, and has otherwise been a healthy 6 yo. On physical exam, both tympanic membranes were erythematous and the right side seemed to bulge more than the left, but without effusion, and negative insufflation. No other positives on physical exam or review of systems.  Would you treat?  I said "yes".  American Academy of Pediatrics said "no".   

I thought this a useful lesson to share.  With the concerning over-prescription of antibiotics, and different perspectives of pediatric care, AAP makes a valid and potentially good argument for one to bring up with office staff and attendings. Their management plan and reasoning is summarized below, but the link with complete recommendations is found here.

Age	Certain Diagnosis	Uncertain Diagnosis
<6 mo	Antibacterial therapy	Antibacterial therapy
6 mo to 2 y	Antibacterial therapy	Antibacterial therapy if severe illness; observation option if nonsevere illness
2 y	Antibacterial therapy if severe illness; watchful waiting if non-severe illness	Watchful waiting

However, their recommendations for observation are appropriate only when follow-up can be ensured and antibacterial agents started if symptoms persist or worsen. Non-severe illness is defined as mild ear pain and fever <39°C in the past 24 hours. Severe illness is moderate to severe pain or fever 39°C. A certain diagnosis of acute otitis media meets all 3 criteria: 1) rapid onset, 2) signs of middle ear effusion , and 3) signs and symptoms of middle-ear inflammation.

In a nutshell, there evidenced based guidelines come from the following studies and reviews. A placebo-controlled trial of acute otitis media showed most children did well without antibacterial therapy. Between 7 and 20 children was the range of number needed to treat for 1 child to benefit, and after the first day after diagnosis, 61% of patients had decreased symptoms regardless of antibiotic treatment.

The likelihood of recovery without antibacterial therapy differs depending on the severity of signs and symptoms at initial examination. In another placebo controlled trial, treatment failure was approximately 4% with placebo for non-severe cases versus approximately 14% for severe cases when compared with amoxicillin treated patients. Also, there has been poorer outcomes in younger children due to decreased immune system strength when compared to older children, increased number of penicillin-resistant strains of pneumococci in those younger than 18 months, and thus antibiotic treatment is justifiably warranted. Current evidence does not suggest increased risk of mastoiditis when AOM is managed only with initial symptomatic treatment without antibacterial agents, nor does routine antibacterial treatment for otitis media prevent bacterial meningitis.

So, this patient was sent home with reassurance and instructions to call if symptoms worsen, fevers develop, or patient does not get better in 72 hrs. If this mom was not to be trusted with close observation or transportation was a problem, she would have received a prescription Amoxicillin (80 to 90 mg/kg per day).

Drug resistance and over-prescription is a HUGE problem these days, so next time your attending is pulls out his/her prescription pad, make sure the latest guideline recommendations support the treatment being written.

    An anxious appearing woman in her 40's presents with intermittent, unilateral headache.  The onset of each episode is very rapid, and the duration is very short.  However the episodes occur every 45-60 minutes.  The pain is deep, continuous, and excruciating, although it is NOT the worst headache in her life.  These episodes are not accompanied by any vision changes, dizzyness, or LOC.  The patient felt better if she worked through these episodes, even continued physical exercise through one.  She noted one occasion of trismus (lockjaw in the vernacular) with a headache, but no extra-cephalic symptoms.

    Differential: Subarachnoid hemorrage, migraine, temporal arteritis, cluster headache.

    Ok, without going into too much detail (and given that I know what happened to her), it's not the worst HA of her life and it has been coming and going 15-20 times per day for three days, so subarachnoid hemorrage is pretty low  on the differential.  There are no auras or visual disturbances and the onset, duration, and frequency are wrong for migraine.  We're left with temporal arteritis and/or cluster headaches.
    Temporal arteritis (Giant Cell Arteritis - GCA) presents with gradual onset headaches in the region between the temple and ear.  They are often accompanied by temporal artery tenderness to palpation, constitutional symptoms like fever or weight loss, and jaw claudication.
    Cluster headaches have a rapid onset and creschendo in minutes.  The duration is usually from 30 minutes to an hour, and the frequency is often 1-3 attacks per day for several weeks at a time.  The patients often prefer to remain active through these headaches as opposed to in migraines where they would like to find the nearest cave.
    In this case the patient had findings that were consistent with both diagnoses.  She described tenderness from the temple to just above her ear, and had at least one episode of trismus, an exaggerated form of jaw claudication.  However the onset and duration of her pain was much better described as cluster headaches.  There was one additional consideration.  Cluster HA'a appear more often in men, and occur 1-3 times a day.  There is a subset of cluster HA's that is pretty rare, however it happens up to 20 times a day predominantly in women.  This zebra is called chronic paroxysmal hemicrania, or by it's older name "indomethacin responsive headache".
    We decided to treat for cluster headaches and started the patient on 4L O2 by nasal cannula.  Indomethacin is an NSAID, so we then gave her Toredol, another NSAID, as a trial.  Both of these measures are reported to abort the HA cycle.  They worked, the patient left the office feeling better and was instructed to report back in the morning if the HA's returned.  They didn't, she didn't, and so I'm done here.  There's only a few last things...

to rule out Temporal Arteritis - try a trial of prednisone, if steroids don't fix it it probably isn't GCA.  Also get an ESR.  ESR<30 is associated with a likelihood ratio of GCA of only 0.02 (umm that's damn small).

Cluster headache can be prophylaxed against with verapamil (Ca-channel blocker), prednisone (steroid), lithium, indomethacin (NSAID), or ergotamine (halucinogenic possibly responsible for the Salem witch trials among other weird and wonderful historic anomalies).

As part of the family center, gynecologic clinics are held on two afternoons for the purposes of performing colposcopies or loop electrosurgical excision procedures (LEEP). The referral for colposcopy or LEEP is based on a set of published guidelines/algorithms. The patients seen in the clinic range in age from the late teens to women in their 40's. The cervical cytologic abnormalities include low grade intraepithelial lesions (LSIL), high grade intraepithelial lesions (HSIL), and atypical squamous cells of undetermined significance (ASCUS). While ASCUS still appears on many cytologic reports, newer terminology subdivides this into ASC-US (same as before) and ASC-H (atypical squamous cells in which HSIL cannot be excluded). ASC-H have a much greater probability of demonstrating HSIL on biopsy then does ASC-US. This terminology recommendation was made in what is referred to as the 2001 Bethesda System.

Due to advances in technology, testing and understanding of the progression of cervical changes and the causative agent (high risk human papilloma virus), The Ameican Society of Colposcopy and Cervical Pathology (ASCCP) held a meeting in September 2001 in Bethesda, MD to come up with evidence-based consensus guidelines for the management of cervical cytologic abnormalities. The Consensus Guidelines for the Management of Women with Cytologic Abnormalities was published in JAMA 2002. The guidelines are more easily viewed as algorithms that are available in PDF format from the ASCCP.

The guidelines address the following scenarios:

Management of women with ASC-US. Due to the lower potential for cervical intraepithelial neoplasia (CIN), a repeat PAP in 4 to 6 months, HPV DNA testing in 12 months or colposcopy are acceptable treatments. Three normal PAP's are required before returning to routine yearly testing. If the PAP returns abnormal or the HPV DNA testing is positive, colposcopy is recommended. If CIN is detected in colposcopy biopsies, a second set of guidlines and algorithms published by the ASCCP regarding the management of women with histologic abnormalities is employed. These guidlines involve the use of ablation procedures (cryotherapy) or diagnosic excision procedures, such as LEEP.

Management of women with ASC-US in special circumstances. This category involves post menopausal women with evidence of vaginal atrophy. These women can be referred to immediate colposcopy or HPV DNA testing. However, it is also acceptable to start these women on estrogen therapy and repeat a PAP after completion of therapy.

Management of women with ASC-H. As mentioned previously, ASC-H has an increased risk for HSIL as compared to ASC-US. Therefore, unlike with ASC-US, the sole recommended initial treatment is colposcopy.

Management of women with LSIL. Women with LSIL are referred for colposcopy. Biopsies are taken if necessary. If CIN is detected the above mentioned algorithms regarding ablation or excision are employed.

Management of women with LSIL in special circumstances. This category includes adolescents. Since LSIL is relatively common in the adolescent population and the presence of CIN is infrequent, it is acceptable to follow these patients with a repeat PAP in 6 months or HPV DNA testing in 12 months. As with women with LSIL, colposcopy is also an acceptable option.

Management of women with HSIL. Because up to 3% of women with HSIL have invasive cancer colposcopy with endocervical sampling is required. HPV DNA testing in 12 months is considered unacceptable. This scenario, however, can become complicated when biopsy reports come back as LSIL or even normal. This has occurred several times at the center. Since this is not an infrequent occurrence it is addressed within the algorithm. One is required to review the information and make a clinical judgment on whether to uphold the initial diagnosis, requiring subsequent ablation or excision, or whether to down grade the diagnosis and follow up with HPV DNA testing or a PAP. With conflicting data, this is not necessarily a straight forward task. Today a woman was seen that had HSIL on her PAP, but her biopsies came back normal and her HPV DNA testing was negative for HPV. The question is whether to perform a LEEP due to the known risks associated with HSIL.

I have had the opportunity to see various patients presenting with different stages of lyme disease.  Most patients in the early stage, however, do not present with the targetoid rash (erythema chronicum migrans) that is so often referenced in the texts.  Rather, the rash is ovaloid, erythematous, macular with non-discrete borders.  On further eval. (in my short experience) it has tended to have a sandpaper like texture that is not apparent with simple observation. The article linked addresses the different dermatologic presentations of lyme disease. 

There is some controversy as to how to treat lyme disease.  Many clinicians do not opt to treat until the tick has been identified as a deer tick that has fed for at least 24 hours (the minimum feeding time needed for transmission).  Other clinicians treat empirically with doxycycline 100mg bid for 21-28 days or amoxicillin 500mg qid for 21-28 days.  On the other hand, a single 200 mg dose of doxycycline given withing 72 hours after an I. scapularis tick bite has been reported to be effective in preventing the development of Lyme disease.  The problem with this approach is that most patients present with no recollection of a tick bite or with a tick embedded in the skin for an unknown amount of time.  The article talks about these treatments.

Finally, I have seen a surprising amount of post-Lyme disease depression.  Unfortunately, it does not respond to antibiotics because it is not caused by on-going infx.  The article talks about the long-standing neuro-psych issues associated with lyme disease.

Finally, prevention through proper clothing, inspection/treatment of pets, permethrin cream and, as mentioned earlier, prophylactic antibiotic treatment of tick bites are all helpful.  The article suggests some other ways to prevent infx.  Lyme disease is extremely common this time of year and should not be ruled out simply due to no history of tick bite or rash.

A patient in her 40s came into the office complaining of nausea almost to the point of being "knocked to the ground."  She noticed that this sensation came over her for the first time when she was bending down to shave her legs n the tub.  Upon standing up, she found herself extremely dizzy and needing to steady herself to prevent herself from falling.

In the following days, she has found herself getting extremely dizzy when turning her head quickly while driving and when walking briskly.  However, if she keeps her head steady, she feels fine.  Hearing this history in conjunction with her physical exam, she was diagnosed with benign paroxysmal positional vertigo (BPPV).

BPPV may occur due to the following:

• head trauma
• severe cold
• aging (average age of onset is 54 years, range 11-84)

Clinical manifestations include lightheadedness, dysequilibrium and sometimes nausea, vomiting, pallor and sweating.

To understand how this occurs, it helps to understand the workings of the ear.  However, in short, BPPV most commonly occurs when loose otoconia settle within the posterior semicircular canal.

Typically, this condition will resolve within 4-6 weeks as the calcium carbonate crystals within the inner ear (otoconia) dissolve or fall into the vestibule.

However, for most patients, this can be a very debilitating condition, so treatment may involve symptomatic management until resorption of the crystals or may include complete relief through Semont or Epley maneuver. 

In our outpatient setting, the appropriate management for BPPV is meclizine, an antihistamine, that minimizes the effects of the vertigo until the crystals clear.  However, this drug is quite sedating which may not be appropriate for a patient who works.  Other symptomatic drugs may be found here.

For patient looking for "instant" relief, they may prefer the Semont or Epley procedure.  More recently, modified versions of the original maneuvers have been found to be extremely effective, especially the modified Epley procedure (MEP).  As written in this article in Neurology, 95% of patients who were followed up 1 week after the MEP were found to have resolved BPPV compared to only 58% on the modified Semont maneuver (MSM).

For our patient, her wishes i(n spite of the evidence for the beneficial effects of the modified Epley maneuver) were for pharmacologic symptom relief.  Therefore, our patient was given a 30 day course of meclizine and was advised to follow-up in one month to see if her vertigo had resolved.

     The other day in the office there was a lively discussion between a doctor and a nurse on whether a DRE and fecal occult blood test should be performed on every adult patient who comes in for an annual physical who is asymptomatic.  The argument was that these were two easy and fast procedures that may save a life in the future by detecting colon cancer early.  While we would all do a DRE on any patient who has blood in their stools or is otherwise symptomatic, is there any need to submit the average adult with no risk factors to this procedure before the recommended guidelines?

      Current guidelines put out by the U.S. Preventative Services Task Force recommend that screening begin at age 50 in the adult with average risk factors.  In fact, they state that "neither digital rectal exam nor the testing of a single stool specimen obtained during DRE is recommended as an adequate screening strategy for colorectal cancer". Screening tests options put out by the American Cancer Society include the following:

1.  Colonoscopy performed every 10 years, or

2.  Flexible sigmoidoscopy or double-contrast barium enema every 5 years, or

3.  Fecal occult blood test, FOBT (the take home multiple sample method) or fecal

     immunochemical test (FIT)  every year combined with the sigmoidoscopy every 5 years, or

4.  FOBT or FIT test every year.  Least preferable option.

   

     The colonoscopy is the most sensitive and specific test for detecting cancer and large polyps but it is also costly and has higher risk of bleeding and perforation.  The problem with the single hemoccult test is that it misses cancer 95% of the time according to a recent study and therefore cannot be used to reassure a patient.

To be done correctly, stool needs to be collected on 3 consecutive days with the multiple sample method.  Even so, the false positive rate for the FOBT is 80%.  In A systematic review of the effects of screening for colorectal cancer using the faecal occult blood test, Hemoccult; the false positive rate was 80% and this study was performed on asymptomatic adults over 40.  The meta-analysis of 4 randomized control studies showed that if 10, 000 people were offered FOBT screenings then 8.5 deaths from colorectal cancer would be prevented over the next 10 years but between 20 to 800 colonoscopies or sigmoidoscopies per life prolonged would be performed.

This means if we were to apply the DRE and single FOBT to all adult patients on their annual physicals we would be subjecting an even greater number of people to unnecessary colonoscopies and the potential harm associated with them. 

     The DRE and FOBT should be reserved for symptomatic patients and screening for colorectal cancer should begin at 50 unless otherwise indicated.      

   Last week, an obese 50- year old woman presented with complaints of chronic lower back pain for the past 1 year, which would not improve with over the counter Tylenol.  She rated the pain as dull and constant, rating an 8/ 10 for the past year; however, she never seeked treatment before.  She denied any recent injuries, but admits to being under increased stress recently due to her demanding job at the post office.  Her past medical history was also significant for depression 3 years ago, but denies despression currently.  She refuses diet modification and exercise, and states that her pain will only will improve with oxycodone. 

   After a negative physical exam and negative imaging, she was reassured, and encouraged to seek counseling for stress reduction.  She was also given a referral to a pain management specialist, per her adament request.  And that ended her 15 minute office appointment.

   Later that same week, 2 more patients came into the office with similar complaints of lower back pain, and my preceptor expressed the challenges in treating patients with chronic pain.  The differential diagnosis is vast, with the most common etiologies including lumbar disk disease, spinal stenosis, trauma, spondylolisthesis, osteoarthritis, vertebral metastases, infection, immune disorders, osteoporosis, visceral diseases, etc.  Management is complex and not amenable to a simple algorithmic approach.  Treatment is based on upon the identification of the underlying cause; and when no specific cause is found, conservative management is necessary.  For an excellent review article on this common topic, please refer to this article from the NEJM.

A 56 year old patient with diabetes mellitus type 2 (DM 2), hypertension (HTN) and hyperlipidemia came to the office for his annual physical exam.  He has been very compliant with his medications (metformin, lisinopril, hydrochlorothiazide, Lipitor) and his efforts are evident in his well-controlled blood glucose levels, blood pressure and cholesterol and triglyceride levels.  The patient has also been following a healthy, low fat diet and walks 30 minutes a day, five to seven times a week.  Although he has made every effort to reduce his risks of coronary vascular disease, he still wonders if there is anything he can do to reduce his risk of having a heart attack.  He has read that adding fish to his diet would help because they contain omega-3 fatty acids.  However, he does not like fish and also worries about mercury levels in the fish.  He asks for advice regarding omega-3 fatty acid supplements.

In short, omega-3 fatty acids are believed to reduce cardiovascular disease by slowing down the growth of atherosclerotic plaques by reducing inflammation, platelet-derived growth factor and adhesion molecule expression.  They are also antithrombogenic, lower blood pressure, decrease the heart's susceptibility to arrhythmias and reduce triglyceride levels.  Studies have shown that 1 to 3 grams of omega-3 fatty acids per day are effective in reducing cardiovascular disease for those who carry risk factors such as DM or have documented coronary heart disease.  This amount can be attained by eating fatty fish, such as salmon, albacore tuna, mackerel or lake trout, daily.  Mercury levels in some fish are concerning.  However, many selections of fatty fish have very low mercury levels and are not overly concerning, except for those who may be or become pregnant.  Patients who are unable to tolerate fish, cannot afford to buy fish, or do not have access to fish, will benefit from omega-3 supplements, such as fish oil capsules.  Since these capsules are fish-derived and thus may contain some mercury, patients should be informed to buy supplements that have been purified to remove as much mercury as possible.

Heart disease continues to be the number one killer of Americans who have comparatively less fish in their diet than those in other countries.  Many of our patients will benefit from adding a omega-3 fatty acid supplement to their diet.

 

A female patient in her 50's came in for a "med refill" visit, but turned out to have multiple conditions/diseases that she wanted to discuss in her "20 min" visit.  In addition to discussing her HTN, DM Type 2, COPD (and various other problems) she received a flyer in the mail from medicaid saying they would pay for smoking cessation therapy for her.  She is a pack a day smoker with a 30+ pack year history.  She wanted us to recommend a therapy for her, but when I suggested the nicotine patch, she said she had already tried it and it didn't work.  Then I went through the other therapies that I knew of, the nicotine gum or nicotine inhaler. Turns out she has tried those therapies as well and said none of it works.  She wanted something else.

I read her flyer from medicaid and it also mentioned covering Zyban or the nicotine nasal spray.  I mentioned Zyban to her and told her it was the same drug as Wellbutrin.  She has taken Wellbutrin in the past and told me it had horrible side effects for her and she didn't want to try it again.  THe only thing left was the nicotine nasal spray.   I told her I had never heard of it before and didn't know how effective it was.  She was willing to try it anyways she said and all we needed to do was write her a prescription.

Since I knew the other therapies have been shown to be effective, I thought I would look up info on the nasal spray to see if it is effective as well.  Unlike the patch, it seems to me that it would give people the quick nicotine "fix" that they crave when they first quit smoking.  The American Family Physician journal had an article that is 10 years old, but is a nice brief overview of the nasal spray.

THe article states that the nasal spray with group therapy, is more effective than a placebo with group therapy in helping people to quit.  It discusses a study that showed the percentage of subjects who were totally abstinent after the first two weeks of treatment and up to one year following the start of treatment was 27% in the active group, versus 15% in the placebo group.

There is a great patient handout on the AAFP website that discusses the pros/cons of each type of nicotine replacement therapy to help the patient choose what will owkr best for them.  There is even a link at the top of that site to take you to an article that reviews the evidence for nicotine replacement therapy for helping smokers quit (for all you EBM junkies!).  And yes, according to this article, "the review of 94 randomized control trials of NRT offers compelling evidence for the efficacy of NRT in the treatment of smokers with moderate to severe nicotine dependence."  Just help the pt choose a method that you both think will work best for them with the fewest barriers to quitting.

In the span of one week at my FP clinic three different people presented with a chief complaint of constipation.  These three people were each quite different: a young adolescent female, a middle aged female, and an elderly man.  The following link from last months Emergency Medicine magazine online is a great resource to learn all you need to know about constipation including the workup a physician would do.                       

There are many conditions associated with constipation  namely by class: structural, systemic, medications, muscle, neurologic, and functional.  The initial basic in-office exam would generally include a review of medications, change in diet, what they have tried before coming to the doctors followed by a physical exam for any perineal causes.  In depth studies are numerous and include: colonic transit study, anorectal manometry, colonoscopy, contrasted radiologic studies just to name a few.

Initial therapies include increasing fluids, increasing physical activity, increasing fiber which according to my find is adults 50 years or less 38 grams for men and 25 grams for women; adults greater than 50 30 grams for men and 21 grams for women.  This difference in numbers is attributed to older adults eating less food.  It is generally understood that achieving these fiber goals is difficult and underestimated by many.  Insight by the physician in increasing fiber should be done to aid the patient.  Laxatives, discussed at length in the above link, are not a first line treatment modality.  Patients are told to follow the above instructions and on follow up a reassesment is done to see what progress has been made.  Changes are made accordingly.

Although the overall prevalence of myotonic dystrophy is 1/20,000 worldwide, I saw two patients with this disorder this week, so it may be more relevant than you think.

Myotonic dystrophy is an autosomal dominant disorder that commonly presents with muscle weakness, usually of the distal leg, hands neck and face, myotonia and cataracts. DM-I (Type I) is associated with a CTG trinucleotide repeat in the DMPK gene and severity of the disease generally correlates with the number of repeats.

In terms of treatment, there is no specific treatment for the progressive muscle weakness. I learned in the office while managing these patients, that hypothyroidism and some meds for hyperlipidemia can exacerbate the muscle weakness and if this is remedied, the muscle strength can return. One of the main concerns with management of these patients is cardiac involvement, specifically conduction deficits. It is recommended that a baseline echo and yearly EKGs be done with these patients.

I found a website that talks about myotonic dystrophy, and gets into a lot of detail about the genetics and genetic counseling issues involved with this disorder. These are extremely important issues for a family doc to be aware of, as he/she is often asked these questions by the patient.

I learned a lot about this disease this week, so I hope this will be helpful to everyone.

I don't know about you guys, but I saw a lot patients with knee pain this past week.  Many were middle aged men with aches and pains that my preceptor mostly attributed to muscle strain and possible some mild osteoarthritis. One younger patient who worked in construction was having trouble walking after his knee "gave out" when carrying some cement upstairs.   He reported he got some relief with Advil and he also was given a diagnosis of muscle strain, given some samples of Celebrex and sent on his way.

One case of knee pain that I saw that triggered a faint recollection in the back of my head of some vague anatomy lecture from 1st year, when the doc I'm working with mentioned Baker's cysts.  The patient was a middle aged male who was with complaints of knee pain and trouble walking. The patient denied any recent trauma. No fevers, no history of arthritis or any other problems with the joint. On physical exam there was no redness, but the patient reported it was much more comfortable to extend his leg than sit with it flexed at the knee.  There was a fluid filled area in the popliteal fossa that was extremely painful to touch.  A posible diagnosis of a Baker's cyst was given.

Baker's cyst is an accumulation of synovial fluid that forms behind the knee after a herniation of the knee joint capsule occurs, out through the back of the knee (as often occurs in adults) or accumulation of fluid in the joint space 9as often occurs in children).  It is often seen in children but can be seen in adults as well. 

Foucher's sign is a term that came up in my research for this blog. It is a measurment of the change in pressure in the Baker's cyst with extension and flexion of the knee.  With extension, the gastrocnemius and the semimembranosus muscles approximate each other and the joint capsule compressing the cyst against the deep fascia, therefore causing the cyst to become hard. Opposite effects in flexion allow the cyst to relax. Just one more fun eponym for us to remember!

Because it is a fluid mass, a Baker's cyst will not be seen on Xray, but may be visualized on MRI.  However, since it is a relatively benign condition that usually improves with time, a MRI was not ordered of this patient.  He was told to continue to monitor for worsening symptoms, told to use some Advil for pain and to return if the pain got worse. At that time, he would most likely for refered to an orhopaedic surgeion for possible drainage. 

A woman in her late 20's came hobbling into the office complaining of low back pain.  In the room, she stood bent at the waist with her trunk supported by the exam table.  As she rocked back and forth on her heels, tears dripped off the end of her nose.  "I just want to talk to the doctor," she sobbed.  "You can be there, but I only want to talk with the doctor."

She had been in a motor vehicle accident 2 months ago and had visited the doctor on an almost weekly basis since then.  She worked as a nurse's aide in an adult facility.  In physical therapy the day before, the pain was worsened, which triggered this particular visit.

The doctor pressed on the patient's lower back during the physical exam.  The patient cried and groaned with every touch from the lumbosacral joint to the coccyx.  The pain was 12/10 bilaterally, with shooting pains down to the tips of her toes.  The doctor was so mean for pushing, esp. knowing that it would hurt the patient.

I was rather uncomfortable with this patient's presentation, so I looked up information on the acute management of back pain http://www.emia.com.au/MedicalProviders/EvidenceBasedMedicine/NHMRC_Bogduk_ALBP_Guidelines.pdf

There was an interesting section in Chapter 10 (starting on page 72) of this article which dealt with yellow flags or psychosocial factors that are associated with a poor prognosis.  The doctor didn't really address any of these items, but instead gave a script for more Lortab and wrote a note excusing the patient from work for 3 days. 

 

Recently a patient with a known sulfa allergy (to sulfamethoxazole in bactrim) who had hypertension and DM type 2 visited our office for routine care. The patient's glucose was under poor control and an additional drug was added. During the discussion of the possible choices the subject of cross-reactivity of sulfonylureas and the sulfonamide antibiotics came up.  For that matter what about sulfites and sulfates and preservatives in food.  Are there any problems with cross-reactivity with them?  Using a quick search I found some information on the subject which was very informative. 

Not all drugs which contain sulfur cross-react with the sulfonamide antibiotics.  In fact not all sulfonamides cross-react.  The sulfonamide antibiotics have the sulfur dioxide and nitrogen groups attached to a benzene ring as all sulfonamides do.  However they also have an arylamine at the N4 position whereas some other sulfonamides do not, accounting for their sporadic cross-reactivities.  Other medications and preservatives that contain sulfur but are not sulfonamides do not cross-react with the sulfonamide antibiotics. 

The product labeling and FDA recommendations for each sulfonamide varies.  For the most part the evidence consists of case reports or manufacturer testing.  However some sulfonamides are contraindicated for use in sulfonamide antibiotic allergy (see table page five in linked pdf document) while others have no recommendations or cautions. 

A 10-15 weeks pregnant patient presents with a positive PPD (> 15mm induration).  Patient has had negative PPD prior to this.  She recently came back from a trip outside of the US where she thinks she may have been exposed to TB.  Patient denies any symptoms and her physical exam is normal.  Typical TB management would be to do a chest x-ray to rule out active disease and start patient on Isoniazid 300mg daily (with pyridoxine for pregnant patient).  However, given that patient is in her first trimester of pregnancy, there are some controversy regarding the risk and benefit of doing a chest x-ray.  According to the Bureau of Tuberculosis Control of the NYC Department of Health patient can have chest x-ray done after the first trimester with appropriate lead shielding.    The US National Council on Radiation Protection believe that even an exposure of 5- 10cGy (typical x-ray is usually < 1cGy) pose no danger to the fetus/embryo.
The patient in question was referred to a TB clinic for further evaluation.   

A young boy presented to the office 2 weeks after initiation of antibiotic (amoxicillin) treatment for streptococcal infection.  He presents with facial/motor tics including pronounced blinking and puckering his lips repeatedly, and choreiform movements of his arms.  He has no past medical history of tics, Tourrette's, or other neuropsychicatric disorders. Family history is also negative for neuropsych problems. 

Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infection (PANDAS) is a syndrome in which pre-adolescent children have abrupt onset of tics and/or Obsessive-Compulsive Disorder (OCD) symptoms related to streptococcal infections.  There are five criteria for diagnosis: 1) obsessive-compulsive disorders and/or tics, 2) episodic course with abrupt exacerbations, 3) abnormal results of neurologic examination (choreiform movements), 4) temporal relation between GAS infection and onset of symptoms and 5) pre-adolescent age.  This article examines possible links between bacterial pathogens, autoimmune reactions, and neuropsychiatric symptoms. 

This is a controversial topic, however.  This article is one of the first studies performed to determine the risk of developing symptoms characteristic of PANDAS after GAS infection.  Interstingly, it concludes that children with GAS infection were not at increased risk for developing PANDAS symptoms.   

It will be interesting to see what future research will reveal about PANDAS.  The current view is that GAS infection in a susceptible host incites the production of antibodies to GAS that crossreact with neurons of the basal ganglia to produce tics and OCD symptoms. 

Current recommendations for treatment include penicillin treatment of each exacerbation with positive throat culture and more aggressive therapies (intravenous immunoglobulin or plasmapheresis) when symptoms are severe.    

An significant concern among breast cancer survivors on long-term adjuvent chemotherapy is quality of life.  Tamoxifen is a commonly used adjuvent and has some significant side effects.  One complaint among postmenopausal users of Tamoxifen is weight gain.  I did a search on the side effects of Tamoxifen since weight gain in itself is an important risk factor for breast cancer.  Most of the studies that I located reported no significant difference in weight gain between Tamoxifen and placebo. However, the frequency with which this question has been adressed in the literature alone suggests that there is still some concern that Tamoxifen may be associated with weight gain. There were a few studies that linked Tamoxifen with weight gain among users. Due to the discrepencies among the literature I consulted a multi-study, evidence based review of the side effects of Tamoxifen.  This particular study concluded that Tamoxifen is not associated with weight gain https://nsas1.amc.edu/get/uri/http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11773306.

A middle-aged woman presented with a "lump" in the midline of her neck.  This had been present and growing for the last six months.  She has not come to the physician because of personal tragedy.  In the last year, her sister (55), mother (76) and daughter (33) have all died of breast cancer.  She occasionally does self-breast exams (where she has not found any changes or lumps), but has not had a mammogram in over 3 years. 

On exam a middle-aged woman in NAD who looks well with a 2 x 2 cm symmetrical nodular thyroid at the midline.

Clearly, breast cancer runs in this family but why is she presenting with an enlarged thyroid?  And is this related to her family history of breast cancer? 

The answer to the previous questions are:  1: she probably has a goiter (either hyper or hypothyroid) and B: maybe.

Rarely (0.5-2%) breast cancer may metastasize to the thyroid (article) or pieces of a breast carcinoma may embolize and present as acute thyroiditis (article). 

The diagnosis of goiter upset the patient and she had to be consoled and counseled that nothing was final until some tests were run and a thorough exam (including a breast exam) was performed and unremarkable except for the goiter.  She was sent to the lab for a THS, FT4, and a screening/diagnostic mammogram.   

Just one more thing to think about when finding a goiter on a patient.

I saw a female patient with a history of Pap smears (three) that were negative for squamous cell changes but showed chronic inflammatory changes.  The physician had scheduled her for more frequent exams and sent a HPV test, which was positive, but had not decided whether her exam warranted colposcopy.  The patient was told at another clinic that the inflammation was due to having intercourse before her internal exams, which neither the nurse nor I had heard of before. 

I investigated this topic to determine if the patient had been given appropriate information and also to determine the appropriate follow-up for this patient.

I found a JAMA article (JAMA. 2002;287:2114-2119) that discussed the 2001 Bethesda system for grading Pap smear results, and several other sources (Cervix Low Female Genital Tract. 1989 Jul-Sep;7(3):207-12; Acta Cytol. 2001 Jan-Feb;45(1):5-8) which suggested that the inflammatory changes were most likely due to infection or birth control method.  None of my sources suggested that intercourse would change the outcome of the Pap smear.  They did suggest that given this woman's history of repeated inflammatory changes and HPV status that she should be scheduled for colposcopy (Int J Gynecol Cancer. 2003 Jul-Aug;13(4):518-21, J Fam Pract. 1995 Jan;40(1):57-62). 

I recently saw a patient with Neurofibromatosis Type 1 (aka von Recklinghausen disease) complaining that some of the neurofibromas were rubbing on his/her clothing/jewelry/accessories.  The patient asked if the neurofibromas could be removed in the office.  Before answering that question, I had to remember (aka look up NF1).
            NF1 is an autosomal dominant disorder affecting around 1 in 4000 individuals.  The NIH defined that the diagnosis of NF1 can be made when 2 or more of the following criteria are met:  more than 6 café-au-lait spots measuring at least 15 mm in adults and 5 mm in children, at least 2 neurofibromas of any type or at least 1 plexiform neurofibroma, freckling in the axillary or inguinal regions, optic glioma, two or more Lisch nodules, a distinctive bony lesion, or a first degree relative with NF1. 
            The neurofibromas on this patient were extensive from head to toe.  The size of the neurofibromas varied from a few millimeters to many centimeters.  Check out these images on Google of neurofibromas.  Interestingly, The Elephant Man was incorrectly diagnosed with neurofibromatosis. 
            Surgery is not curative for NF1, but can be performed to relieve symptoms of the cutaneous and subcutaneous tumors.  The use of intraoperative electromyography monitoring can reduce the risk nerve function loss due to surgery.  Additionally, radiation can be used to shrink the neurofibromas when there is increased risk of damaging nerve function.  If the AMC firewall worked properly, I may have been able to read this article, which appears appropriate for this clinical question.  After reviewing the various sites discussing surgical treatment for NF1, it looks appropriate to treat the patient with surgery while explaining that the neurofibromas can redevelop after being excised. 
 

A man in his 40's came in with complaints of lower back pain for a week and a half.  The pain was constant and radiated down both of his legs.  He did not have any associated weakness or urine or stool incontinence.  His lower back was also tender to palpation.  The patient had back pain before about 10 years ago, but it has never been this bad.  He took Ibuprofen and Aleve for the pain with no relief.  He attributes his pain to sacral agenesis. 

After hearing this, I wondered what the causes of sacral agenesis were and what sequelae it had. 

Sacral agenesis is a condition when part of the sacral segments are absent.  The absence of 3 or more segments usually results in nerve abnormalities.

Sacral agenesis occurs in 1:25,000 live births.  Most cases of sacral agenesis are sporadic.  However, there is an increase association with maternal diabetes during pregnancy.  Other causes include vascular anomalies with alteration of blood flow, infectious agents, teratogens (a case report suggested an association with the use of minoxidil solution for the prevention of hair loss during pregnancy), and a hereditary form (aut dom) has also been reported, which can occur with a presacral mass and with ano-rectal malformations (Currarino triad).

Conditions associated with sacral agenesis include hip dislocation, foot deformities, spina bifida, narrowing of spinal canal rostral to the last vertebral body, tethered cord with lipoma, teratoma, cauda equina cyst, fusion of caudal vertebral bodies, neurogenic bladder, anal atresia,  and malformation of genitalia.

We decided to treat the patient with Ibuprofen and Lortab (for breakthrough pain).  We also suggested putting orthotics in his shoes, since his work required him to stand on his feet all day.  For further evaluation of his back pain, we sent him for an x-ray.

Yesterday a patient in his 30's presented with a history of 3 episodes of blood in his semen following intercourse with his girlfriend.  On the second episode he noticed that there was a "clot-type" piece of tissue in the tip of the condom.  He denies pain with ejaculation, new lumps or bumps, warmth, or tenderness in his genital area.  The patient denied changes in urinary habits, pain or burning upon urination, or any abdominal pain.  Patient is consistent with condom use and denies any STDs or known exposure.  He denies having urethral discharge.

The patient is concerned about the possibility of cancer.

On physical exam, the patient was afebrile and BP was normal.  There were no lumps or swellings noted on or around testes.  There was no enlargement of the inguinal lymph nodes.  No lesions were seen.  There was no discharge noted from urethra.

Hematospermia, or blood in the semen, can be caused by inflammation, infection, blockage, or injury to the genital area.  (http://www.nlm.nih.gov/medlineplus/ency/article/003163.htm) It is important to rule out CA although this is very rare and one would typically see a mass and/or swollem lymph nodes.  Testicular cancer usually presents between ages 15-35 and is the most common solid malignancy affecting males in this age group. It is also important to note any urethral discharge to rule out infection.

A U/A was done on this patient which was negative and he was sent to a urologist to have a further work up done to rule out less likely causes such as cancer.

A patient with long standing history of rheumatoid arthritis came to the office for her follow up visit. She had numerous flare ups with her arthritis in the past, and was  prescribed numerous steroids, anti-inflammatory agents, and combinations of both, however, none seemed to truly help. Today, she appeared at the office for the first time, with absolutely no pain complaints. She attributed this to her 2 week start of Minocycline by her  new rheumatologist. Is this her cure or the placebo effect?

As some background, rheumatoid arthritis is a symmetric, peripheral polyarthritis of unknown etiology.  Many potential causes have been identified, namely genetic susceptibility, cigarette smoking, bacterial infections, viral infections, superantigens, heat shock proteins, and autoantibodies, but none proven to date. The disease usually progresses from the periphery to more proximal joints, and in patients who do not fully respond to treatment, results in significant locomotor disability within 10 to 20 years.

The management of the patient with RA is very individualized based upon response to previous treatment regimens, elimation of risk factors where possible, and universal preventive measures such as rest, exercise, physical, occupational dietary therapy, and general measures to protect bone structure and function. Although treatment regimens vary, most physician turn to disease modifying anti-rheumatic drugs (DMARDs) as soon as possible after disease onset. Those with more severe active disease and/or poor prognostic signs are usually  treated more aggressively than those with milder disease. The common endpoint of treatment is to increase the intensity of treatment until evidence for synovitis diminishes or disappears, or until drug-induced side effects become intolerable.

There are four main classes of drugs are currently used, and combination drug therapy from the different classes are frequently employed in treatment, as in the patient mentioned. Topical and oral analgesics ranging from capsaicin to oxycodone, are used to alleviate pain and help patients carry on with a functional life. NSAIDs or selective COX-2 inhibitors, such as celebrex, in patients at high risk for GI bleeds have both analgesic and antiinflammatory properties but do not alter disease outcomes. Glucocorticoids, namely prednisolone or prednisone are most commonly used to suppress inflammation, thereby relieving joint paint and tenderness, may be administered orally, intravenously, or by intraarticular injection. And lastly, a miscellaneous group of drugs termed slow-acting antirheumatic drugs (SAARDs) or disease-modifying antirheumatic drugs (DMARDs) have the potential to reduce or prevent joint damage, preserve joint integrity and function, reduce health costs, and maintain economic productivity. Such agents include, hydroxychloroquine, sulfasalazine, methrotrexate, leflunomide, and less often prescribed, gold salts, D-penicillamine, azathioprine, and cyclosporine.

As mentioned above, none on these drugs seemed to work for my patient.  The Minocycline prescribed for her has 2 potential mechanisms of action that may work in treating rheumatoid arthritis: 1) Inhibit/interferes with the activity of several inflammatory mediators such as metalloproteinases prostaglandins, leukotrienes, nitrous oxide synthase, and oxygen radicals that are involved in joint destruction by rheumatoid synovium, and 2)Antibacterial effect against the postulated Mycoplasma etiology of rheumatoid arthritis. Because of the lack of a gold bullet to cure RA, many physicians are now turning to alternative drugs such as Minocycline after more studies have shown efficacy and safety compared to placebo in patients with mild to moderate disease.

It's worked so far for this patient!

http://www.postgradmed.com/issues/1999/04_99/alarcon.htm