Q: In regards to the the lipid management, once we initiate a statin, when do we ask for a lipid profile to see if the statin was effective? And if the statin was effective at hitting the threshold, do we ask for a lipid profile once every year to make sure it's stable?

A: Yes - once a statin is initiated, would suggest repeating the lipid profile 3 months post initiation. Then, once on statin, lipid profile should be checked yearly.

Q1: Should family physician's be starting the PCSK9 inhibitors or icosapent ethyl on their own, or does this warrant a referral to cardiology? I work in Quebec if that provides any context.
A1: Family physicians can definitely start PCSK9 inhibitors and icosapent ethyl on their own. The use of these agents are now part of robust national guidelines for best practice in the right patient where these medications are indicated. At present, many specialists (primarily Endocrinology and Cardiology) are often initiating these agents, although as we become more familiar and comfortable, it is encouraged that any clinician (primary care or specialty) seeing a patient where these meds are indicated educate and initiate to prevent clinical inertia and delaying therapy that reduces residual CV risk.

Q2: Can fibrates be started with a statin on board already? Seems controversial on UptoDate.
A2: In general, fibrates can be started with a statin on board already, although with caution since concurrent administration has been associated with myopathy, rhabdomylosis and acute renal failure. Fibrates may be considered concomitantly with a low-or moderate-intensity statin only if the benefits from atherosclerotic CV risk reduction and TG lowering (i.e. when TG>10 to reduce risk of TG-related pancreatitis) outweigh the potential risks for adverse events. It is important to instruct patients to report any unexplained muscle pain, tenderness or weakness. If muscular symptoms develop, monitor serum creatine kinase (CK) levels and renal function.

Q1: Can you use depo provera long term in the depressed patient?
A1: Certainly depression is not an absolute contraindication or at all a predictable side effect of Depo-Provera but we have so many other better long-acting birth control methods the Depo-Provera is really limited to very few patients these days. Because if it’s long-acting nature it wouldn’t be my first choice in such a patient.

Q2: I am very interested in the implant. The other long acting, progestin-only, non-IUD contraception that we are familiar with is depo-provera. How does the implant compare to depo-provera with regards to weight gain associated with the product?
A2: No contest here. Depo-Provera is associated with 4-5pounds of weight gain in the first year of use and up to 11 pounds by two years it’s even written on the product monograph. None of the other long term reversible methods like the IUD or the implant are associated with any significant weight gain. No contest.

Q: I have a 76 yrs old female patient with controlled bp on coversyl and asa. I saw her for regular checkup and discussed the risks of asa in [pro\mary prevention and the risk/benefit ratio. We stopped the asa and 2 weeks later she had a stroke which affected her R side mildly and she was aphasic. Thankfully she recovered her hemiparesis and her speech is mildly slurring.I have good notes and she was not upset

A: This is indeed very unfortunate case scenario. However the data at least statistically still support that there is little to no evidence to support decreasing vascular risk and clearly an increased risk to major bleeding. We still have grey zone as the people enrolled in clinical trials were all naive to the use of ASA. As mentioned in the talk and the Guideline there is no randomized trial of people already on ASA and what there risk of a vascular event is after discontinuing ASA which is why we suggested shared decision making. There is some literature that MAY suggest that there may be a thombotic rebound effect after discontinuing ASA. That being said if it were my Mom I would have stopped the ASA as this family Doctor did. Was a cause for the stroke ever found??? PAF, Carotid stenosis etc..?

Q: Any recommendations re: young adults who have high-normal blood pressure, on stimulant ADHD medication? I have a patient in her 20's who is on both Concerta 27 DIE and Ritalin 10 DIE PRN -- decreasing the dose would greatly affect her studies.

A: I would suggest trying another class to see how the BP react. If BP remains a concern, you can consider treating the high BP and maintain stimulants the same dosage. There was a study done with Dr Timothy Wilens with Adderall XR. Hope this helps.

Q1: Varicocele in a young man -- would you recommend referring to Urology, since it could affect fertility?
A1: Varicocele management among pediatric urologists remains a controversial subject. They have a hard time deciding if they should wait until they are old enough to do a semen analysis before offering surgery. For young patients who have no pain from varicoceles (if they do have pain, varicocele repair is indicated), my approach is to inform them (including parents or partners) the risk of future infertility. I lean more towards repairing varicoceles mainly because the micro-surgical varicocelectomy or embolization (done by interventional radiologists) have low risk of complications.

Q2: Should we add testicular ultrasound in initial evaluation of infertility, in primary care?
A2: Currently, testicular ultrasound has not been accepted as part of the initial work-up for male infertility. The main issue is the cost effectiveness in finding significant pathology in the absence of any physical findings. If you do have suspicious findings such as mass, varicoceles, pain etc, then testicular ultrasound should definitely be included.

Q: Is chondrocalcinosis something we would see incidentally, on X-ray, even in asymptomatic patients?

A: The answer is yes. You can see chondrocalcinosis as an incidental finding on x-ray without the patient being symptomatic. The finding of chondrocalcinosis tends to increase with age and with osteoarthritis. It becomes a risk factor for having Pseudogout in the context of an acute inflammation in the joint.

Q1: Does a worsening BMD ie more than 5% on a biphosphonate allow us to use the RAMQ code for our patients to switch to denosumab? My understanding is that only an intolerance or contraindication is accepted in which case how can we get coverage in this situation?
A1: Worsening BMD does not meet the criteria for RAMQ reimbursement of denosumab. Physicians still do switch from a bisphosphonate to a parental form (denosumab or iv zoledronic acid) - however, I suggest you document clearly in your note why you are switching and that you have investigated the aetiology of this BMD loss. If nothing is found (ie compliance is good, it is a true loss and there is no evidence of secondary causes of bone loss), then I think it may be justified to switched invoking poor absorption or lack of response.

Q2: Wouldn’t we be able to indicate worsening BMD under ‘autre’ mallgré prise reguliere?
A2: Sure, you could. I just want to reinforce the importance of keeping clear information in the chart in case the MD gets audited. The problem is that there are no studies that have shown that prolia would provide better risk reduction if one’s BMD goes down while on bisphosphonate. Most of the time it is a question of the patient not taking the bisphosphonate properly or not at all. Hence it is as if the patient is not treated. One must remember that the RAMQ has access to prescription dispensation and they can verify if the patient is actually compliant with their bisphosphonate. As far as I know people have not been audited about this - but one never knows.

Q3: An older patient with high osteoporosis who was under biphosphonate for 8 years, and who does not want to switch to denosumab because of the duration of the treatement. Can we continue the biphosphonate?
A3: Bisphosphonates can be continued up to 10 years. However, one must be careful and monitor symptoms of atypical femur fractures such thigh pain or fatigue, specifically when going up the stairs or standing from the sitting position. After 10 years, one should definitely discontinue the bisphosphonate temporarily (2 to 3 years) as the risk of AFF does increase. One can then reassess the risk for fracture after that period of time and if still elevated, could resume the bisphosphonate.

Q4: After the first BMO control 2-3 years after starting the medication, do we need another control, if the medication doesn't change?
A4: Usually you do not need to repeat the BMD, since the medication would be expected to continue to be efficacious- unless new risk factors might have appeared; new Rx, decrease in renal function etc.

Q5: One of my patients was switched to Prolia. Although I have a better BMD score, the FRAX score calculated was worse. Should I bother?
A5: The FRAX score should not be monitored over time as it does tend to worsen (age is a being component of FRAX). Therefore, if the patient meets the criteria for treatment with denosumab, presumably because of a high risk for fractures, then you should continue the denosumab.

Q6.1: How do you decide when to use prolia vs forteo if not using a bisphophonate?
A6.1: Teriparatide can be used in patients who sustain a fracture while on an anti-resorptive agent (this is the criterion for RAMQ reimbursement). Usually if planning to use an anabolic agent, it is recommended the patient be referred to a specialist. Denosumab can be used in patients at high risk for fractures who have a contraindication to oral bisphosphantes (GI) or who have reduced creatinine clearance (below 35ml per min)

Q6.2: Until what age would you continue to screen with BMD?
A6.2: There is no age limit, so long as you will act on the the BMD results; ie it would change your management.

Q6.3: For a patient who is high risk, you suggested we do not need to do a BMD but would it not be important for documenting the degree of osteoperosis and response to treatment?
A6.3: You do not need to do a BMD prior to initiating treatment- however you can do one shortly after so to monitor response to treatment.

Q1: Are certain individuals more prone to concussions after having sustained a couple? For example, If we see prolonged recoveries and easier impacts causing the recurrence of symptoms… If they are more at risk, is it due to physiological alterations?
A1: Athletes in the same sport who have suffered a previous concussion are thought to be 4-6 times more likely to suffer future concussions. Athletes who have prolonged recovery from one concussion are also felt to be at high risk for prolonged recovery in the future. On average, subsequent concussions take longer to recover than previous concussions, remembering that each concussion is its own entity. Why athletes who have suffered a previous concussion are more at risk for future concussions may be because there are anatomical changes that occur, such as scarring. With newer imaging such as DTI, we can see scarring in the brain years after a concussion that we could not Identify previously. Other reasons may include that an individual athlete has a more aggressive style of play leading to more contacts, or that they may be more likely to volunteer his or her symptoms and thus be diagnosed with a concussion. It may also be that there is some anatomic predisposition on how the brain sits inside the skull which may either predispose or protect certain individuals from concussions. That may play a factor in why we see concussions occur frequently in some families.

Q2: If the athlete is reporting feeling off after exercising, but the injury happened over a year ago, should exercise still be done in a sub symptom way? If he has no symptoms while exercising but reports feeling terrible hours later and the increase in symptoms last days before returning to baseline, is it still considered exercise intolerance?
A2: Delayed onset of symptoms after exercise would depend on the symptoms. Brain related symptoms are usually exacerbated during exercise. Other symptoms which are often neck related usually improve during exercise and then can be exacerbated several hours later or the next morning. Although this is hard to do an in office, sometimes we have athletes come in and exercise on a stationary bike or exercise on a treadmill and gauge how other symptoms respond and examine them afterwards. Or they can be examined the next day when they feel worse. If we feel the symptoms are neck related, we will ask them to continue exercising while also treating the neck with therapy and sometimes injections to relieve any tightness of the muscles possible compressing the nerves in the occipital area.

Q3: What is the most effective medication used during persistent concussion symptoms of vestibular/ocular type? If the athlete has done vestibular therapy, neck treatments, ocular therapy, …, without noticing any positive results, is there any medication that can be prescribed that may help? I have tried amitriptyline in a patient with PPPD diagnosed 1 year post concussion with good reults ( 25 mg ) but the exercise intolerance persists and he is on a very slowly increasing exercise program but he has to stay at subthreshlod level or else experiences nausea and light-headedness 2-3 hrs post exercise that can last 3-4 days. Any suggestion to get the patient back to full capacity in training ( he is doing exercise bike with short intervals 6/10 intensity ) and when should the weaning process for the amitriptyline occur and at what rate?
A3: There are a lot of moving parts in this question. I do not know if I can give a simple answer. I am not a PPPD expert. PPPD is often treated by otolaryngologist with a specialty in "dizziness "or vestibular abnormalities. Other times it is treated by neurologists. I might suggest referring the pateint to the "vertigo/dizziness clinic " at the MUHC which is run by otolaryngologist with a specialty in vestibular abnormalities.

Q: Given the delays when ordering investigations should all pts with syncope be referred to ER?

A: Difficult question. Should rather send to ER if: -very brief prodrome (ie. no ability to put hands in front to prevent a fall) -significant trauma associated with the syncope -syncope associated with symptoms of “hypoxia” – brief shaking -known cardiac history -history of multiple medical comorbidities

Q: Do you recommend treatomg patients with elevated lipoprotein (>150 nmol/L) if they have no other CAD risk factors with a Framingham risk score <10%?

A: Elevated lipoprotein a (Lp(a)) is highly genetically determined and considered a cardiovascular risk modifier when assessing a patient’s CV risk. Essentially, one can conceptually think of an elevated Lp(a) almost increasing the calculated Framingham risk score up a risk category. Based on the guidelines, for FRS (5-9%/10 years), statins can be considered beyond health behaviour change if LDL-C ≥ 3.5 mmol/L (or non-HDL-C ≥ 4.2 mmol/L or ApoB ≥ 1.05 g/L), particularly with other CV risk modifiers (e.g., family history, Lp(a) ≥50 mg/dL [or ≥100 nmol/L] or coronary artery calcium score (CAC) >0 AU).

Q: If the patient is taking antidepressant (I.e. Effexor) Is it possible to add contrave?

A: Contrave and Effexor should NOT be combined.  The bupropion part of the contrave can inhibit the metabolism of effexor and result in side effects, such as elevated blood pressure, anxiety, restlessness.  Some clinicians do combine Effexor and Bupropion, and monitor closely for this interaction, but I would avoid this if possible. If the patient is already on bupropion and effexor then you may be able to switch the bupropion for contrave and not have any adverse effects.  But technically the answer is not to combine them. I tend to avoid Contrave in patients on multiple medications, as looking up the interactions can become time consuming. The GLP1a have fewer drug interactions, the main one is to stop a DDP4i if you are starting a GLP1a.

Q1: Under what circumstances do you prescribe nasal steroids qd vs bid?
A1: My general rule of thumb is to follow the recommended dosage for each individual steroid spray, which is once daily for most, except mometasone, budesonide, and fluticasone/azelastine which can be taken twice daily. For these latter 3, I tend to prescribe them as bid dosing (for 6 months minimum) but recommend patient s to only use them once daily if symptoms are controlled and twice daily if symptoms are uncontrolled or for flare ups.

Q2: Is it wrong to use them when there is no hx allergy rhinitis or recurrent sinusitis?
A2: In my practice, they are prescribed for most causes of nasal congestion even if there is no history of allergy or sinusitis, because congestion is often multifactorial with a component of rhinitis that may respond to topical nasal steroids.

Q: I have a gentleman with chronic pain and cirrhosis. He is taking Dilaudid 2mgs QID for his pain. Should I switch him to another medication in view of his cirrhosis?

A: No. Hydromorphone is actually recommended for patients with cirrhosis. Just have to be careful when increasing the dose and monitor closely for adverse effets". We could provide him with this reference on the topic: https://www.uspharmacist.com/article/pain-management-considerations-in-cirrhosis

Q: Is the MMSE, MOCA as useful in young patients complaining of memory loss or are there other tools available to evaluate memory loss in younger people?

A: The simple answer is yes. The sensitivity and specificity of cognitive screening tool does not change with age. Furthermore, given that younger age is not associated with cognitive complaints (as opposed to normal cognitive aging in older adults), the predictive values of cognitive screening tests in a symptomatic young patient is probably higher than in an older individual. Nevertheless, we usually tend to send symptomatic young individuals for more specialized cognitive evaluations (neuropsychological testing) as the prevalence of atypical conditions (frontotemporal dementia, comorbidity with psychiatric conditions, etc.) increases.

Q: I was wondering what you advise parents about children who have AOM or OME and who have plane travel. Anything in particular that you tell the parents to do while on the airplane? ie. blowing with a straw, trying to drink during landing and take off? Are they at greater risk of tympanic perforation during air travel?

A: This is a common concern of parents. If a child is just starting an acute otitis media, then I do counsel about delaying travel more for the risk of developing complications of AOM in a foreign country where there may be difficulties in accessing healthcare. In terms of risk of tympanic membrane perforation, the highest risk is when there is an actual air fluid level seen or bubbles. If the ear is completely filled with fluid (as it often is in children) then there is very little risk of barotrauma / tympanic membrane perforation. Breast-feeding young children on take-off and landing is helpful. For older children, taking plenty of sips of water is similarly helpful.

Q: Frequently on abdominal ultrasound reports, there is mention of varying degrees of fatty liver. Please clarify how we should interpret this. And comment on appropriate f/up.

A: Hepatic steatosis is due to the abnormal accumulation of lipids, particularly triglycerides within hepatocytes. It is important for the radiologist to mention this because steatosis can lead to fibrosis and cirrhosis. Diffuse hepatic steatosis is often idiopathic. It may be associated with: • alcohol abuse • non alcoholic fatty liver disease (NAFLD) which in turn is associated with insulin resistant diabetes obesity dyslipidemia • steroid intake • certain drugs: amiodarone, methotrexate, chemotherapy drugs such as tamoxifen • pregnancy (acute fatty liver of pregnancy) • metabolic disorders like glycogen storage diseases, and Wilson’s disease • radiation In ultrasound, steatosis manifests as increased echogenicity resulting in poor visualization of deep portions of the liver. It can be graded but grading is often not done because visual grading of hepatic steatosis is subject to a wide interobserver and intraobserver variability • grade I: diffusely increased hepatic echogenicity but periportal and diaphragmatic echogenicity is still appreciable • grade II: diffusely increased hepatic echogenicity obscuring periportal echogenicity but diaphragmatic echogenicity is still appreciable • grade III: diffusely increased hepatic echogenicity obscuring periportal as well as diaphragmatic echogenicity Radiologists mention it so that the referring physician realizes that the ultrasound evaluation of the liver may be limited and if a liver lesion is suspected another imaging modality may be required. Follow up is recommended because as long as hepatic fibrosis and cirrhosis have not developed, fatty change is reversible with modification of the underlying causative factor, e.g. alcohol, pregnancy, obesity, diet. Generally, actions for the referring physician to take are to search for a cause and understand the complications that can result.

Q: Someone asked a question about low dose contraceptif like Alesse. I would like to clarify if low dose contraceptif is contra indicated in teenagers because of the effet on the bone?

A: As per adolescent med, we avoid low dose OCP like Alesse and Lolo - not enough estrogen for optimizing bone mineral density.

Q1: What is your approach to enlarged occipital or cervical lymphadenopathy in infants and children? I would think this is most likely reactive to local infection, trauma, bites or scratches. If the nodes are mobile and soft, how long would you expect the nodes to last?
A1:Very common occurrence. In the absence of any systemic symptoms, I observe them indefinitely as they are likely to persist for years. Instruct the parents to see you again if there is any enlargement. Otherwise, repeat exam in 6 months, and if no change, you can discharge the patient. 

Q2:For umbilcal granulomas that are dry and not draining any fluid, do you need to treat with silver nitrate or could we just observe?
A2: They often will not fall off on their own, and they can epithelialize and become an umbilical polyp, so I typically still treat them.

Q: Can you give a link to the West Island SNAP program? I searched and could not find it, but did find an article from the Gazette 2019 that the West Island SNAP program is in desperate need of funding.

A: https://www.centrefamille.com

Q1: Questions regarding desensitization to peanuts. A two year old with moderate eczema, and mild peri-oral urticaria acutely after ingesting peanuts. Parents continue to expose child to peanuts with small amount ie. 1 peanut, which does not cause any acute reactions. Allergist told parents to continue with this...however, parents are wondering at which frequency? Child can tolerate 1 peanut well, but then has an eczema flare within the next 24 hr (possibly related to the peanut exposure?) The eczema flare seems to coincide with every exposure to peanuts. So my question is what to advise parents in terms of frequency of exposure to peanuts as they want to continue to desensitize, but at the same time they don't want their child to be continually having eczema flares. Is a monthly exposure to 1 peanut enough to desensitize over time?
A1: If 1 peanut ingestion is temporally associated with eczema flare, ideally you half the amount given (ie ½ peanut) and maintain the frequency. Monthly exposures is more likely to be sensitizing and thus not recommended. We do not know how frequently you need to induce and maintain food tolerance but I am uncomfortable, in these circumstances, if it is not at least every other day…but you can decrease the amount. Also it depends upon the severity of the flare-if mild I would treat with hydration creams and keep going. In the long term the eczema is predicted, in general, to be outgrown while food allergies are usually life long.

Q2: What is the youngest age you would order a skin test or Ige on a child? Would you only consider this if you have a positive oral challenge?
A2: There is no age limit for a skin test on a child. You must be guided by history as the false positive rate especially in the young is extremely high. The youngest child I have seen tested as age 5 weeks (history of anaphylaxis to bananas-why she was given this at 5 weeks is a question). Child was positive for banana and avoided for the first few months of life before it could be safely introduced. I almost never use serum specific IgE. Only in a child with a good history and either no skin to test on (rare) or needs antihistamines all the time-also rare. I will also use them occasionally to follow clinical resolution but for that skin testing has a better predictive value. Neither of these tests should be used as screening tools as they create disease more often than they prevent disease when used in this manner. Counselling safe introduction using small amounts of properly prepared foods (ie crushed peanut instead of peanut butter, eggs in a baked product, for example) is better than testing.