A Brief Synopsis of AFPs "Clinical Management of Urinary Incontinence in Women"

A Brief Synopsis of:
Clinical Management of Urinary Incontinence in Women
LAUREN HERSH, MD, and BROOKE SALZMAN, MD, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania 
http://www.aafp.org/afp/2013/0501/p634.pdf

Am Fam Physician. 2013 May 1;87(9):634-640.
     The five types of incontinence in women are urge, stress, mixed, overflow and functional.  Urge incontinence is due to detrUsor overactivity (U for urge!). The patient has an "urge" to pee. There may have frequency and nocturia. It is common in neurologic issues such as spinal cord injuries or stroke. Stress incontinence is from intrinsic Sphincter dysfunction (S for sphincter ) and increased urethral mobility.  The patient losses urine during an increase in intraabdominal pressure (laughing, coughing, sneezing). Mixed is mixed. The last two are less common. Overflow is due to anatomic obstruction or impaired detrusor contractility (Just a reminder that the detrusor is the contractile part of the bladder wall and the sphincter it the little hole at the bottom where the pee pee comes out of). When the detrusor does not contract, the bladder fills to the top. There is also incomplete emptying.  Urine dribbles out as the bladder overflows. A common cause of functional incontinence are anticholinergic drug side effects. The patient may ultimately need catheter drainage as treatment,  In functional incontinence, the patient is unable to get to the toilet due to a functional, cognitive or physical impairment.
    The treatment for urge incontinence starts with behavioral training. Bladder training and pelvic floor strengthening are good first line therapies.  Bladder training starts with rapid pelvic muscle contractions and mental distractions during periods of urgency. relaxation techniques are also effective. The point is to increase the time from onset of urgency to voiding. Kegels are the same as pelvic floor exercises. This is only effective in urge incontinence. Other behavioral techniques are  habit training  scheduled voiding, and prompted voiding. Electric modulation with vaginal or anal stimulators can affect the reflex pathway. Stimulating the posterior tibial nerve (which shares the same nerve root as the bladder) is as effective as medication.
     Medication is effective in conjunction with other modalities. Selective anticholinergics (M2/M3) such as darifenacin or solifenacin are preferred.  Non selective anticholinergics (oxybutynin, tolterodine, fesoterodine) have a worse side effect profile. They are all contraindicated in dementia, narrow angle glaucoma, GI obstruction and gastric retention. The anticholinergic effects may counteract the procholinergic effects of the cholinesterase inhibitors used for the treatment of dementia. Beta adrenergic agents (mirabegron) act on B3 receptors to relax the detrusor. Side effects are nausea, vomiting  diarrhea, constipation, headaches, and increased blood pressure.  Botox injected into the detrusor muscle has been another treatment. It lasts 3-6 months at a time. Estrogen has not been effective.
     Stress incontinence can be seen in patients with obesity, childbirth, chronic cough,  and previous pelvic surgery. Weight loss and pelvic floor exercises are first line therapies. Patients need to learn the proper technique  either through biofeedback or by palpating the the pelvic muscles during contraction. Electric stimulation of the pelvic floor muscles is beneficial in patients unable to contract the muscles on their own. Vaginal inserts (pessaries and incontinence tampons) compress the bladder neck and urethra, reducing urine loss. Urethral plugs have a similar effect. No medications have FDA approval for treatment of stress incontinence, although duloxetine has shown to be helpful. Radiofrequency denaturation is another available treatment. It reduces compliance of the bladder neck and proximal urethra. Patients can also have bulking agents (collagen, fat, carbon beads) injected  into the bladder neck. For surgery, slings and urethropexy are commonly performed. It supports the bladder neck and urethra, which helps with urethral closure. Tension free vaginal tape is a new type of sling that is very effective, and can be done on an outpatient basis.

A Quick Review of AFPs "Evaluation of Nausea and Vomiting"

A quick review of;
Evaluation of Nausea and Vomiting
KEITH SCORZA, MD, AARON WILLIAMS, DO, J. DANIEL PHILLIPS, MD, and JOEL SHAW, MD  Dewitt Army Community Hospital Family Medicine Residency, Fort Belvoir, Virginia
http://www.aafp.org/afp/2007/0701/p76.pdf
Am Fam Physician. 2007 Jul 1;76(1):76-84.
     All throw-up is not the same. Vomiting is the forceful expulsion of stomach contents through involuntary contractions. Regurgitation does not have the "forceful expulsion", but food does come back up.  Rumination is voluntary regurgitation. Nausea and vomiting (N/V) are symptoms that could mean a lot or nothing. The differential is three pages long in this article. Medications can cause N/V at onset. Common medications that cause N/V are chemotherapeutic agents, alcohol, antibiotics, opiates, anticonvulsants, digoxin, hormones and illicit substances. Infectious agents, such as staphylococcus or B. cereus are self limiting, lasting up to 1-2 days.
     There is a three step approach to evaluating N/V. First, the consequences of the N/V should be addressed, such as dehydration or electrolyte issues. Then, the underlying cause should be diagnosed and treated. Lastly, empiric therapy should be started if the cause cannot be determined or if treatment is an ongoing process. A proper history and exam will reveal most the clues. Labs and imagining should be led by the initial evaluation. Emergent situations (such as chest pain, CNS problems, fever, hypotension, severe dehydration, and severe abdominal pain) should be properly evaluated. Pregnancy is a common cause of N/V. It can lead to morning symptoms or hyperemesis gravidarum.
     There is a really nice list of the possible diagnosis in this article based on history , so let me try and break it down a bit. If the onset is abrupt, think food poisoning, drugs medications, pancreatitis, gastroenteritis, or cholecystitis. It may also be infectious or iatrogenic. If the onset is subtle, consider GERD, pregnancy, gastroparesis, medications or metabolic disorders. If the timing of the N/V occurs right after eating, it may be psychiatric. If its 1-4 hours after eating, consider a gastric outlet obstruction. Symptoms before breakfast could signal pregnancy, uremia, alcohol or increased ICP. If there is associated abdominal pain, the location can also play a part in the diagnosis. 
     As far as the physical exam is concerned, the patient initially should be evaluated for dehydration, by looking at skin turgor, mucus membranes, orthostatic changes or hypotension/ tachycardia.  Fingertips, parotid gland enlargement, laguno and teeth enamel can be evaluated for signs of forced vomiting.  Loss of tooth enamel can also be from GERD. Distention can be from obstruction, but bloating may be from gastroparesis. Increased bowel sounds could be a sign of obstruction. Decreased sounds are a sign of ileus. Scars, hernias or evidence of previous surgeries can also be an important discovery.  An cranial nerve exam (including the eye) could point towards a brainstem lesion or increased cranial pressure.
     Lab tests can reveal inflammation, pregnancy, thyroid issues, pancreatitis or electrolyte abnormalities.  X rays (supine and upright) can show an obstruction. An EGD can detect mucosal lesions in the stomach and small intestine. A small bowel follow-through can see as far as the terminal ileum. Enteroclysis can see some of the smaller lesions that may be missed by the former procedures. Gastric motility studies can help diagnosis gastroparesis, gastric arrhythmias, or other motor disorders. Since these tests are somewhat controversial, a trial of a prokinetics and antiemetics may be a better place to start. 
     Fluid and electrolyte replacement is a cornerstone of treatment, as well as a proper diet. While you are working on the diagnosis and trying to figure out the underlying cause, you can start the patient on a phenothiazine or metoclopramide (prokinetic agent). Ondansetron is more effective than the first two, but it is cost prohibitive. There are many types of antiemetics available, but some have side effects to watch for.  Scopolamine is an anticholinergic, which may cause drowsiness, dry mouth and vision problems. Phenothiazines and metoclopramide have extrapyramidal side effects, such as dyskinesia and dystonia. 
 

A Quick Review of AFP's "Complications of HIV Infection: A Systems-Based Approach "

A brief synopsis of:Complications of HIV Infection: A Systems-Based Approach  
CAROLYN CHU, MD, MSc, and PETER A. SELWYN, MD, MPH Albert Einstein College of Medicine of Yeshiva University, Bronx, New York 
Am Fam Physician. 2011 Feb 15;83(4):395-406. 
http://www.aafp.org/afp/2011/0215/p395.pdf

     HIV doesn't kill you. Its the complications that do. Managing patients with HIV includes monitoring antiretroviral therapy, preventing and treating opportunistic infections, and treating related chronic complications. A careful review of preexisting conditions, current CD4 count, medication list, and recent exposures/ behaviors is an important part of management. This article will discuss the neurological,  cardiopulmonary, and gastrointestinal  complications.
     CNS problems are considerations in the HIV patient. The most common infections are toxoplasmosis, cryptococcus neoformans, JC virus, CMV, HSV,  and syphilis.   The symptoms vary widely, but most include focal neurological deficits, headache, fever and confusion. The CD4 count is a good place to start the differential. Neurosyphilis can invade when the CD4 count drops below 350. The typical tests (CSF VDRL, treponemal) are employed. The CSF will show elevated proteins and increased mononuclear pleocytosis. At 200, the JC virus or HSV can be involved. The JC virus can cause progressive multifocal leukoencephalopathy. CT or MRI show single or multiple white matter lesions with no edema, mass effect, or enhancement. HSV will show diffuse edema, as well as frontal or temporal necrosis. At 50, CMV, toxoplasmosis, and cryptococcal meningitis come into play. CMV will show periventricular enhancement on MRI. The cryptococcal antigen will be positive in the serum and elevated in the CSF of cryptococcal infected patients. Toxoplasmosis patients will have a ring enhanced lesion and edema on head imaging. Serum IgG will also be positive. Other than infections, lymphoma can cause CNS symptoms. Imagining may show a solid white matter mass with edema and mass effect.
     Dementia is an AIDS-defining condition. Diagnosis requires abnormalities in motor or behavioral function that impairs ADLs, along with a deficit in any two of the following areas; memory, attention and concentration. Psychiatric and substance abuse are also prevalent.
     Radiculopathy and neuropathy are elevated in HIV patients. Radiculopathy presents as radiating neck pain, leg weakness, leg sensory loss, bowel or bladder issues. Neuropathy presents as paresthesia, dysesthesia, or bilateral peripheral numbness.  The physician should evaluate this through testing deep tendon reflexes, vibration, EMG, NCV or MRI.
     Atherosclerosis and myocardial infarction should also be evaluated. HIV can increase cytokine levels, vascular inflammation, and endothelial dysfunction. Antiretroviral medications, such as abacavir, can cause cardiotoxicity. Elevated cholesterol combined with HIV and antiretroviral medications can affect the cardiovascular system.
     Pneumonia from Pneumocystis jiroveci presents with fever, dyspnea and cough. It arrives when CD4 counts drop below 200. Imaging will show bilateral interstitial infiltrates. If empiric treatment fails after 4 -5 days, then atypical causes should be investigated, such as Legionella.
    HIV patients who smoke have an increased risk of emphysema over non-infected patients. COPD is increased as well. HIV associated pulmonary hypertension is another complication that exists. The evaluation is the same as in non HIV infected patients.
      The oral cavity and esophagus can be a battlefield for infection as well. Candidal colonization is common, causing thrush. At CD4 count below 200, CMV and HSV can produce aphthous ulcers, oral ulcers and esophagitis. Patients should be checked for oropharyngeal cancer in this case.
     Diarrhea is a common symptom in HIV related gastrointestinal complications. HIV can directly affect gut motility,  causing enteropathy ( at a CD4 <200). CMV and cryptosporidium are seen when the CD4 drops below 100. Diarrhea can also be from protease inhibitors or intestinal malignancies. Protease inhibitors can also cause pancreatitis and nephrotoxicity.  Renal disease can also be HIV associated. Renal function should be assessed early in the diagnosis of HIV. Worsening renal function can be addressed with (non-nephrotoxic) antiretrovirals, ACEIs and steroids. Kidney transplantation may be an option.
     Endocrine complications are also seen in HIV. Antiretroviral therapy can affect glucose metabolism, lipid metabolism, and fat distribution. Patients need to be screened for glucose and lipid disorders at diagnosis. Choosing medications that don't affect these situations can be helpful. Adjusting medications for the other illnesses is also a good idea. Using pioglitazone, metformin or thiazolidinediones may be beneficial. Other endocrine disorders include adrenal insufficiency, testosterone deficiency, and hypogonadism.
     Osteopenia and osteoporosis have also been a side effect of antiretroviral medication. Bone ischemia from the virus can also lead to osteomalacia and osteonecrosis. Myopathy may be seen when the medications are given with statins, calcium channel blockers or antiepileptics. Myopathy from nucleoside analogues is no longer an issue since the development of newer treatments. 

A brief synopsis of AFPs "Acute Pancreatitis: Diagnosis, Prognosis, and Treatment"

A brief synopsis of 
Acute Pancreatitis: Diagnosis, Prognosis, and Treatment
JENNIFER K. CARROLL, MD, MPH, University of Rochester School of Medicine, Rochester, New York, BRIAN HERRICK, MD, University of California at San Francisco, San Francisco, California TERESA GIPSON, MD, and SUZANNE P. LEE, MD, University of Rochester School of Medicine, Rochester, New York
Am Fam Physician. 2007 May 15;75(10):1513-1520. 
http://www.aafp.org/afp/2007/0515/p1513.pdf

     Acute pancreatitis is basically an inflammation of the pancreas. The outcomes can vary widely, from a brief hospital stay to a trip to the ICU. Common risk factors include gallbladder disease or chronic alcohol use, but other risk factors including hypercalcemia, infection, drug side effects, or hyperparathyroidism could be the culprit.  If you remember the mnemonic "GET SMASHED",  it stands for gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion stings, hyperlipidemia/ hypercalcemia/ hypothermia, ERCP, and drugs [1].  The patient will have symptoms of abdominal pain, nausea and vomiting. He or she may seem restless and present in a hunched over position.  More serious findings may be fever, hypotension,  guarding, tenderness, and respiratory distress.
     Common labs that are ordered include amylase, lipase, CBC, BMP, triglycerides, UA and an ABG. Lipase is more specific and sensitive than amylase, especially during board exams (ha ha). Newer labs, including trypsinogen activation peptide,  procalcitonin, phospholipase A2, IL-6, IL-8 and CRP have been investigated, but have limited usage so far. CRP, however, is commonly used in England. A level greater than 210 mg/L after the first four days, (or greater than 210 mg/L at the end of the first week) is evidence of a severe attack [2].
     There are many scales, criteria, and scoring systems to assess severity of pancreatitis. This article says that the CT severity index is better than the APACHE II, Imrie and Ransons. The APACHE II scale is done with an online calculator. The CT severity index is done by giving a point value according to what the CT looks like as well as the amount of necrosis seen. There are two mnemonics for ransons criteria. The first one is "GA LAW" which is used during admission. It stands for:
Glucose > 200 mg/dl
Age > 55 years
LDH > 350 U/l
AST > 250 U/l
WBC> 16,000/ul
After 48 hours the mnemonic is "C HOBBS", which stands for:
Ca < 8mg/dl
Hematocrit drop greater than 10%
Oxygen saturation less than 60 mmHg
BUN increase greater than 8 mg/dl
Base deficit grater than 4 meq/L
Sequestration of fluid greater than 600 ml
A ransons score of 0-2 indicates minimal mortality. A score of 3-5 indicates a 10-20% mortality. If the score is greater than 5, there is over a 50% mortality and may be associated with more systemic complications.  A score above 3 is considered severe pancreatitis.
     Imaging is very helpful in the diagnosis of pancreatitis. CT with contrast should be used for patients with mild, uncomplicated illness when the patient appear to be getting worse during the treatment. It is also needed for the Ct severity index. It is good if you are looking for necrosis, abscess  psuedocyst, or fluid collection. ERCP is helpful to see the pancreatic duct and should be done emergently in cases of biliary sepsis, obstruction, cholangitis, elevated bilirubin, worsening jaundice, or worsening pain.  It is also helpfull in evaluating less common causes, including sphincter of oddi problems  pancreatic divisum and duct strictures. MCRP can asses the degree of pancreatic damage, find pancreatic cysts, and find gallstones (larger than 4mm). It is also used when an ERCP is not possible. 
     As far as treatment is concerned, aggressive volume repletion and pain management are key.  It was often considered standard practice to keep the patient NPO. This article advises that total enteral nutrition has shown clear benefits in severe cases of pancreatitis. It will prevent morbidity and mortality, as well as reducing infectious necrosis. The best route has not yet been determined  Antibiotic prophylaxis has shown mixed results in recent studies. Surgery may be an option after two weeks. 


1. http://www.mnemonic-devices.info/blog/example-real-world-mnemonics/get-smashed-medical-mnemonic-for-pancreatitis/

2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2503457/?page=1

A Brief review of AFP's "Transfusion of Blood and Blood Products: Indications and Complications"

A Brief review of : Transfusion of Blood and Blood Products:  Indications and Complications
SANJEEV SHARMA, MD; POONAM SHARMA, MD; and LISA N. TYLER, MD 
Creighton University School of Medicine, Omaha, Nebraska
Am Fam Physician. 2011 Mar 15;83(6):719-724.

http://www.aafp.org/afp/2011/0315/p719.html

     In honor of lab week, and also because I think AAFP tweeted a link to this article on Tuesday, I will be reviewing the implications and complications of blood product transfusion. Packed RBCs are whole blood that has had 250 ml of plasma removed from it. It is then filtered to remove leukocytes (which lowers the chances of a febrile nonhemolytic transfusion reaction).  It is used to treat sickle cell crisis, acute blood loss (greater than 1500 ml), or symptomatic anemia. Recent studies say that a transfusion should be done if the hemoglobin drops below 7 g/dL, and maintained between 7-9 g/dL, 8.5-9.5 g/dL in children who are stable in intensive care. Keep in mind that a unit of blood (500 ml) will increase the hemoglobin by 1g/dL and the hematocrit by 3%. Studies have shown that this aggressive approach and a strict criteria for transfusion has been effective for the patient.  
     There are two types of plasma; FFP and thawed plasma. They both contain coagulation factors, but the FFP can be used to reverse the effects of anticoagulants, whereas the thawed plasma has less factor V and VIII ( these factors are unstable when "thawed"). Many labs use it interchangeably, but you would rather use FFP for a consumption coagulopathy, such as DIC. Regardless, plasma is used in active bleeding in a patient with an elevated INR, reversal of warfarin during a hemorrhage (major or intracranial), reversal of warfarin before surgery, in microvascular bleeding during a massive transfusion, in TTP, HUS, or hereditary angioedema (when C1 esterase inhibitor is not available).
     Platelets are use to prevent hemorrhage in a patient with thrombocytopenia. It is contraindicated in TTP and HIT. A prophylactic platelet transfusion is given in stable, non bleeding patients when the platelet count is less than 10 (x 10 [to the third] per ul). If the patient has a fever above 100.4C or undergoing an invasive procedure e, we transfuse at 20 or less.  It there is no fever, but an invasive procedure or major surgery is planned, we would transfuse at less than 50. If a patient is undergoing ocular or neurosurgery  a transfusion can be considered if the count is 100 or less. 
     Cryoprecipitate is simply the precipitate that comes out when FFP is thawed. It is high in factor VIII (makes sense since it is low in thawed plasma) and fibrinogen. It is used when a patient is low in fibrinogen (duh). This happens in massive hemorrhage, Factor VIII or XII deficiency,  vWD, surgical bleeding, congenital fibrinogen deficiency, or hemorrhage after cardiac surgery.
     Transfusion reactions can be either acute or delayed, or infectious. Transfusion related infections are very rare to to the screening and preventative measures in place today. 
     Acute hemolytic reaction is caused when the patient's antibodies attack the donor RBCs.  This occurs within 24 hours or transfusion. It can occur extravascularly when the donor RBCs, coated with IgG or complement, are attacked in the liver or spleen. The more severe form, intravascular hemolysis, is due to ABO antibodies within the vessels. Symptoms include fever, chills, nausea, vomiting, dyspnea, anuria, oliguria,  dialysis, and DIC. 
     A patient could have an allergic reaction of hives or itching. An anaphylactic reaction could also occur if the patient was previously presensitized to some of the proteins (immunoglobulin, complement, etc.) in the donor plasma. The risk can be reduced by avoiding these products or having the products "washed" to remove the proteins. 
     Patients may get noncardiac pulmonary edema from a transfusion, known as TRALI (transfusion related acute lung injury). Certain antibodies will activate the immune system  causing pulmonary edema and tissue damage from proteolytic enzyme secretion.  Using male donated plasma may reduce this risk. 
     Repeated transfusions or previously pregnant patients are at increased risk of FNHTR (febrile nonhemolytic transfusion reactions). As the name states, the patient will develop a fever of at least 1C (1.8F) above normal within 24 hours of transfusion. They may show signs of rigor, chills, or discomfort.  This occurs because of cytokine release (IL-1, IL-6, IL-8, TNF), and/or antigen mediated endogenous pyrogen release. This diagnosis should be considered only after all other causes of fever have been excluded.
     If a patient gets too much product too fast, they can get "transfusion associated circulatory overload (fitting name). They present with tachycardia, cough, dyspnea, hypotension, elevated CVP, increased wedge pressure, and a widened pulse pressure. Cardiomegaly and pulmonary edema may also be seen. 
     The main form of delayed reaction is "transfusion related graft vs host disease". The tissue and organs are attacked by the donor lymphocytes. It if often fatal. High risk patients are those who are  immunocompromised, have been of fludarabine, chemotherapy, cytotoxic drugs, have had hodgkin's disease, a stem cell transplant, or are receiving blood from a relative.  Gamma irradiation of the blood products can reduce the risk. 

A Brief Synopsis of: AFP's "Management of COPD Exacerbations"

A brief synopsis of: Management of COPD Exacerbations
ANN E. EVENSEN, MD, University of Wisconsin School of Medicine and Public Health, Verona, Wisconsin
Am Fam Physician. 2010 Mar 1;81(5):607-613
http://www.aafp.org/afp/2010/0301/p607.pdf

     Proper management of COPD can really help the quality of life in a suffering patient.  Exacerbations can be caused by infection, tobacco smoke. occupational exposure or ozone. There are many times when the  cause cannot be identified. Symptoms of an exacerbation are most commonly cough, dyspnea, and  increased sputum production. Other symptoms such as tachycardia, confusion, wheezing, fatigue and fever are just a few.  COPD exacerbations can be classified into three stages of severity. Mild exacerbations can be controlled by increasing the dosage of medication. Moderate exacerbations require treatment with antibiotics or systemic steroids. Severe exacerbations require hospitalizations, or a least a trip to the ER.
     When evaluating a patient for an exacerbation, taking a proper history, previous chest x rays, ABGs and spirometry will help to determine baseline function. All patients should have a pulse oximetry, ABG, chest x ray, BNP, and cardiac enzymes ordered when they arrive to the ED. A CBC, echo, and BMP can be considered depending on the severity.  If the patient is in, or at risk of, respiratory distress, hospitalization should be considered.
     The patient should have an oxygen saturation over 90%. If oxygen supplementation through cannula or high flow mask is not adequate, NIPPV can be used. If the pH is less than 7.36 and the CO2 is greater than 45 mmHg  on ABG, the patient needs to be intubated. 
   The medications used for a COPD exacerbation are beta agonists (long acting) and anticholinergics. The medication most commonly used are albuterol and ipratropium. Combivent is a "combo" of both of these medications. Short courses of corticosteroids can help by shortening hospital stay, improving hypoxemia, increasing FEV1, and decreasing rate of treatment failure. There is no benefit of using corticosteroids for longer than two weeks compared to eight weeks, and treatment is the same regardless if the medication is oral or parenteral.
     Antibiotics can be used if the patient is not getting better with the above therapy and the exacerbations are of moderate or severe intensity. Broad spectrum antibiotics that correlate with local resistance patterns should be chosen. The length of time the antibiotic should be give is unclear, but long term prophylaxis has not been shown to be effective. Commonly used antibiotics are cephalosporins, quinolones and macrolides.
     The patient may be considered for discharge if they do not need albuterol more frequently than every 4 hours, their oxygen partial pressure on the ABG is above 60 mmHg for 12 hours, and they are clinically y stable. Patient education, at home support (oxygen, nebulizers), and close follow up should be in place upon discharge.
     

A Brief Synopsis of AFP's "Diagnosis of Chronic Obstructive Pulmonary Disease"

A brief synopsis of:  Diagnosis of Chronic Obstructive Pulmonary Disease
MARK B. STEPHENS, CDR, MC, USN, and KENNETH S. YEW, CAPT, MC, USN
Uniformed Services University of the Health Sciences, Bethesda, Maryland 
Am Fam Physician. 2008 Jul 1;78(1):87-92.
http://www.aafp.org/afp/2008/0701/p87.pdf

     COPD is a serious disease because it is preventable in many instances. It is an inflammatory disease caused mostly by smoking. It is associated with chronic bronchitis (cough and sputum production for at least 3 months in two consecutive years) and emphysema (destruction of the alveolar-capillary membrane). COPD can also be caused by alpha1-antitrypsin deficiency, environmental, and occupational pollutants. 
     The pathophysiology is that the smoking causes airway irritation, inflammation,  mucus production, decreased clearance and lung scarring. This leads to obstruction, dyspnea, and infection. Interestingly, women are more susceptible than men, due to differences in lung size and the fact that a woman's lung is more hyperresponsive to irritants. Other symptoms may be wheezing, chest tightness, weight loss, and waking up more often at night. If the patient is a smoker, determining the number of "pack-years" is helpful. Multiplying the number of packs smoked per day by the number of years smoked is the formula. 
     On the physical exam, the patient may be seen with lung hyperinflation, barrel chest, hyperresonance on percussion, or diminished breath sounds. There may also be signs of cor pulmonale,  such as JVD, hepatomegaly  peripheral edema, or a loud S2.  Other signs may be pursed breathing, increased use of accessory breathing muscles,  and increase time of expiration. 
     COPD can often be confused with asthma. They are both obstructive lung disease with similar symptoms. COPD is often seen in smokers over age 35 years old with progressive symptoms. These features are variable in asthma. The cough is productive in COPD and non productive in asthma. Asthma has a stronger family history and diurnal variation in symptoms than COPD. 
    The two measurable factors in COPD are dyspnea and spirometry. The Medical Research Council (MRC) dyspnea index can be used to assess the severity. Dyspnea is graded from one to five. A grade of one is seen if the patient becomes dyspneic only during strenuous exercise. A grade of two will be given if the patient becomes short of breath while walking up a small hill. If the patient needs to catch their breath when walking at a normal pace and walks more slowly than others, then the patient is at a grade three. A grade four is given if the patient needs to stop and catch their breath when walking 100m. A patient with level 5 dyspnea  becomes too short of breath to even leave their home or do normal ADLs.
    The two parameters in spirometry are FEV1 and FVC. To review, FEV1 is the amount of air expired in one second after a full breath. FVC is the maximum amount of air exhaled after a full breath. A diagnosis of COPD is confirmed when the FEV1/FVC ratio is less than 0.7 and the FEV1 is less than 80% of the predicted value for the persons age, sex and height.  There are different staging categories based on the spirometry findings. A smoker with good values is at stage 0 (at risk). All of the higher stages have a FEV1/FVC ratio less than 0.7 and variable FEV1.  
At stage one (mild), the FEV1 is still above 80%.
At stage two (moderate), the FEV1 is 50-80%. 
Stage three (severe) is at 30-50%.
Stage four (very severe) is below 30%.
     Other useful tests are a chest x ray to look for nodules, masses, or fibrotic changes. Pulse oximetry, CBC, ECHO and ECG may also be considered to rule out anemia, polycythemia, and pulmonary issues. 
    

A Brief Synopsis of AFP's Medical Management of Stable Coronary Artery Disease"

A brief synopsis of; Medical Management of Stable Coronary Artery Disease
MATTHEW PFLIEGER, DO, Clinica Family Health Services, Denver, Colorado, BRADFORD T. WINSLOW, MD, Swedish Family Medicine Residency Program, Littleton, Colorado, KYLE MILLS, PharmD, Bend Memorial Clinic, Bend, Oregon, IRA M. DAUBER, MD, South Denver Cardiology Associates, Denver, Colorado
http://www.aafp.org/afp/2011/0401/p819.pdf
Am Fam Physician. 2011 Apr 1;83(7):819-826.

    Okay, so your patient survived an "event". Now what? Angina, MI, or a documented plaque is called coronary artery disease. This article discusses treatment for stable CAD. Before medication is given, the patient needs lifestyle modification. This includes tobacco cessation, alcohol reduction, a low salt and saturated fat diet, 2-3 servings of fruits and vegetables, exercise and weight loss. 
     Once your get the patient to improve their lifestyle the best they can, its' time for the drugs. Lipid therapy is a very important factor in CAD treatment. Statins are the first medication that should be used and it is effective in lowering LDL. Patients should try and get their LDL below 100 mg/dL. Those who are high risk should try and get it down to below 70 mg/dL.  Side effects are rhabdomyolysis and myalgia.  Triglycerides and HDL are also important parameters. Nicotinic acid can be considered if the triglyceride level stays above 200 mg/dL or if the HDL below 40 mg/dL. Fibrates and ezetimibe have had mixed results. It has been shown, however, that patients already on a statin who continue to have an LDL above 200 mg/dL and an HDL below 40 mg/dL may benefit from fenofibrate. 
     The JNC7 recommends a BP below 140/90 for patients with CAD. The AHA recommends a BP below 130/80. According to this article, beta blockers are a first line therapy. Beta blockers are effective because they lower heart rate, increase diastolic filling time, lower cardiac oxygen demand, and decrease contractility. Newer research has questioned the usefulness of beta blockers. 
     ACE inhibitors are another helpful medication. It prevents the conversion of angiotensin I to angiotensin II, reducing vasoconstriction, lowering peripheral vascular resistance, and preventing ventricular dilation.  It should be used in all CAD patients already on beta blockers. ARB's can be used as an alternative to ACE inhibitors. Using ACEIs and ARBs together can adversely affect the kidneys without any additional benefit.
     Ca channel blockers can be used if beta blockers cannot be tolerated. Short acting nifedipine should be avoided.  Long acting Ca channel blockers do offer benefit. They cause coronary vasodilation, decrease myocardial oxygen demand, and reduce anginal symptoms.
     Antiplatelet therapy is another important aspect of CAD therapy. Aspirin and clopidogrel are the two medications most commonly used. There is no benefit over one or the other. Aspirin is typical used first, with clopidogrel used if there is a contraindication or intolerance. Clopidogrel is  recommended when the patient had a recent MI or having stent placement. 

A Brief Synopsis of AFP's " USPSTF: Screening for Intimate Partner Violence and Abuse of Elderly and Vulnerable Adults: Recommendation Statement"

A brief review of:
U.S. Preventive Services Task Force: Screening for Intimate Partner Violence and Abuse of Elderly and Vulnerable Adults: Recommendation Statement
http://www.aafp.org/afp/2013/0415/od3.pdf
Am Fam Physician. 2013 Apr 15;87(8):online.

     Intimate partner violence is defined as  any harm (sexual, physical, or mental) done by a spouse or partner. Sexual intimacy is not required for this classification of this type of violence. Between 25-30 percent of people claim to have experienced some form of IPV. The numbers are likely higher due to underreporting. Patients may feel guilt, self-blame, or fear of retaliation which may contribute to the underreporting. Since there are no current standards for screening, this could also be a factor of the underreporting. 
    The USPSTF recommends screening of all women of childbearing age for IPV. Clinicians can use various screening tools including;
Hurt, Insult, Threaten, Scream (HITS),
Ongoing Abuse Screen/ Ongoing Violence Assessment Tool (OAS/ AVAT),
Slapped, Threatened, and Throw (STaT),
Humiliation, Afraid, Rape, Kick (HARK), 
Modified Childhood Trauma Questionnaire-Short Form (CTQ-SF), and
Woman abuse Screen Tool (WAST).

 For example, the four questions asked in the HITS assessment tool are 
"how often does your partner;
1. Physically hurt you?
2. Insult or talk down to you?
3. Threaten you with harm?
4. Scream or curse at you?"
Each question is scored from one to five, depending on frequency (never, rarely, sometimes, fairly often, or repeatedly). A score greater than 10 is positive. [1]  
     Patients who are victims of IPV often develop depression, PTSD, stress, anxiety, substance abuse, suicide, eating disorders, obesity, teen pregnancy, suicide and other conditions. Although studies are limited, there appears to be little harm in screening. Patients who screen positive need to be referred for intervention services. They can be counseled on safety behaviors, community resources, as well as emotional support, education on problem-solving strategies and parenting. Physicians need to be aware of state and local reporting laws.

1.http://www.orchd.com/violence/documents/HITS_eng.pdf
     

A Brief Synopsis of "Updated Guidelines on Outpatient Anticoagulation" from AFP

 A brief synopsis of "Updated Guidelines on Outpatient Anticoagulation"
PATRICIA WIGLE, PharmD, BCPS, and BRADLEY HEIN, PharmD, University of Cincinnati James L. Winkle ,College of Pharmacy, Cincinnati, Ohio, HANNA E. BLOOMFIELD, MD, MPH, University of Minnesota and Minneapolis VA Medical Center, Minneapolis, Minnesota, MATTHEW TUBB, MD, PhD, The Christ Hospital/University of Cincinnati Family Medicine Residency Program, Cincinnati, Ohio, MICHAEL DOHERTY, PharmD, BCACP, University of Cincinnati James L. Winkle College of Pharmacy, Cincinnati, Ohio

http://www.aafp.org/afp/2013/0415/p556.pdf
Am Fam Physician. 2013 Apr 15;87(8):556-566.

This is a very detailed article (see how many authors!)  that i reviewed and I suggest reading it for more information
     For many decades, warfarin was the only option for anticoagulation, besides aspirin.  Recently, newer medications have come on the market.
     Warfarin is an anticoagulant which inhibits vitamin K dependent clotting factors II, VII, IX, and X. Due to the half life of these clotting factors, warfarin can take several days to take effect. In the beginning stages of using this drug, there is a paradoxical increase in clotting risk due to the decrease in protein C and S. Heparin or LMWH is used at the onset of warfarin therapy due to this hypercoagulable state. It is continued until the INR is in therapeutic range for 24 hours. Heparin is eventually stopped and warfarin is used because warfarin is an oral medication and heparin is not.
     Warfarin can be started at 5-10 mg per day and then adjusted, depending on the INR. If it is elevated, but less than 4.5, the dosage can be lowered or held. With levels 4.5 to 10, one or two doses should be held, then resumed at a lower dosage once the INR is therapeutic.  If the INR is greater than 10, the patient may need vitamin K, in addition to holding the medication, to reverse the effects of warfarin. There are many drug and food interactions that can affect the effects of warfarin.  Amiodarone and rifampin, for example, can alter the INR long after the medication has been discontinued. Diet should be maintained while using warfarin  without and drastic changes, such as becoming a vegan.
     Unfractionated heparin works by inactivating factor IIa and Xa by binding to antithrombin. It also prevents the growth of clots. There is a risk of bleeding with this drug as well as an increased risk in HIT.
     The two LMWHs are lovenox and fragmin. It is given subcutaneously. Anti-factor Xa monitoring is not needed. Bleeding and HIT can be an issue, although less likely than unfractionated heparin.
     Fondaparinux is a synthetic analogue of heparin. It had no effect on thrombin formation and only works on factor Xa. It is given subcutaneously as well and does not need to be monitored.
     There are times when anticoagulation needs to be stopped. According to this article, if the patient is to have surgery, warfarin can be stopped 5 days before the procedure and restarted one to two days after. If there is only a low risk of bleeding, perioperative bridging may not be indicated. Otherwise it may be necessary to bridge the patient with LMWH or unfractionated heparin during the perioperative period.
     The biggest issue with warfarin is getting the dosage right, and the constant need for adjusting it. The advent of newer meds is very appealing, due to its ease of prescribing and lack of need for monitoring. Dabigatran is an anticoagulant that is effective in preventing embolism and stroke for patients with nonvalvular atrial fibrillation. Rivaroxaban is effective in prevention of DVT in patients having hip or knee replacement surgery, in treatment of DVT and PE, and prevention of embolism in nonvalvular atrial fibrillation.



   

A Brief Synopsis of AFP's "Evaluation and Diagnosis of Wrist Pain: A Case-Based Approach"

A synopsis of-
Evaluation and Diagnosis of Wrist Pain: A Case-Based Approach
RAMSEY SHEHAB, MD, Henry Ford Health System, Detroit, Michigan 
MARK H. MIRABELLI, MD, University of Rochester Medical Center, Rochester, New York
http://www.aafp.org/afp/2013/0415/p568.pdf
Am Fam Physician. 2013 Apr 15;87(8):568-573.


     Wrist pain can be classified as acute or chronic. Acute pain is typically due to trauma. Chronic pain can be neurologic, systemic, inflammatory, or from an old trauma. History, including the location, timing, and quality of pain can aid in the diagnosis. The diagnoses  that will be discussed here are scaphoid fracture  ulnar neuropathy, and De Quervain tenosynovitis. I will do my best not to use the words "brevis", "minimi", "longus" or "pollicis"
     The lunate and scaphoid are the two carpal bones that articulate with the ulna and radius, respectively. Scaphoid fractures are more common in the young because of the increased surrounding cartilage. The most common presentation is "falling on an outstretched hand". The wrist and anatomical snuff box may be swollen, with tenderness dorsally around the distal radius. Axial pressure on the first metacarpal bone will reproduce pain. With x ray imagining, its is important to order AP, AP in ulnar deviation, lateral, oblique, pronated oblique, and supinated oblique views. They may need to be repeated two weeks later to see if the fracture is healing. A bone scan or MRI may be needed if the x rays are not sufficient. Patients with suspected scaphoid fracture, but negative x rays, should be given a thumb spica cast and repeated in two weeks.
     In the wrist, the ulnar nerve passes through the guyon canal, to the anterior surface of the hand. The nerve splits off and innervates the sensory portion of the medial palm, the muscles of the pinky, and the muscles for thumb flexion and adduction. Compression of the ulnar nerve in the wrist is typically caused by repetitive trauma or a ganglion cyst. The entire length of the nerve should be investigated to rule out issues in the cervical spine, brachial plexus, and ulnar groove . The patient will complain of numbness and/or tingling in the 4th and 5th digits.  Tinel sign and Phalen sign should be part of the exam. X rays should be ordered first. Nerve conduction tests may uncover entrapment in acute injuries. EMG can be used if the issue is chronic. An ultrasound of the nerve may reveal compression. MRI can be a useful if other tests are inconclusive. 
     De quervain tenosynovitis is inflammation of the sheath that encompasses the the tendons of the lateral border or the anatomic snuffbox. Again, the wrist and tissue around the anatomical snuffbox may be swollen. Finkelstein test will be positive. Grind test should be negative (and positive in OA of the thumb MCP joint).  Injection of lidocaine into the joint can rule out arthritis. Appropriate labs may be drawn if an infection is suspected, and further imaging can be considered if needed.
     

A Brief Synopsis of AFP's Rational Use of Opioids for Management of Chronic Nonterminal Pain"

Rational Use of Opioids for Management of Chronic Nonterminal Pain
DANIEL BERLAND, MD, and PHILLIP RODGERS, MD, University of Michigan Medical School, Ann Arbor, Michigan
Am Fam Physician. 2012 Aug 1;86(3):252-258.
http://www.aafp.org/afp/2012/0801/p252.pdf


     Pain management is a large part of why people see their doctors. Most patients assume that all pain needs to be treated with opioids  Opioids are well know to be highly addictive and overused. It is now even more popular than illicit drug use. Overuse of opioids can cause opioid  induced hyperalgesia, where an increase in opioid use causes a paradoxical increase in pain. 
     Acute pain is different from chronic pain. Acute pain can be relieved with opioids while tissue recovery takes place. Chronic pain is from "complex CNS signalling" involved with biopsychosocial factors that will not resolve acute pain therapy. Opioid treatment should not be used in those with chronic central or visceral pain. These factors can be addressed with modalities such as physical therapy, massage, heat, steroid injections, topical lidocaine, or electric stimulations. Diet, exercise, and proper sleep can make a big impact on chronic pain as well. SSRI's are effective for neuropathic pain.  TCA's can be used if the neuropathy is concomitant with headaches, depression, panic disorder or tobacco addiction. Comorbid psychiatric illnesses such as anxiety, depression, or PTSD, should be treated accordingly.  After all these factors are dealt with, then opioids may be considered.
     The patient should have a comprehensive evaluation and their risk of potential abuse determined before beginning them on a trial basis.  The patient should understand that the goal of opioid therapy is to improve function, not decrease pain, per se. A written agreement should be set up instructing the patient not to be treated by multiple physicians or go to multiple pharmacies for the opioids.  Refill policies, "loosing prescriptions , regular drug testing, regular follow ups, and asking for refills early should all be incorporated into this agreement. 
     Morphine is a good first-line therapy because it is long acting, inexpensive, and reliable. Side effects include nausea, pruritus, constipation and drowsiness. Patients with a morphine allergy can be prescribed oxycodone, although it has a higher potential for abuse. Fentanyl patches or buprenorphine are an expensive alternative. Methadone may be an option because of its long action and lower tolerance rates, but it can cause arrhythmias such as prolonged QT syndrome. Multiple opioids should not be used simultaneously and the meds should be consolidated with a narcotic conversion calculator. Total opioid doses over 100 mg of a morphine equivalent is associated with an increased risk of overdose.
     In acute pain, the idea of giving a short acting medication PRN for "breakthrough pain" is common. It has been show that this concept has not improved outcomes and has only increased the risk of misuse and tolerance. Long acting, sustained-release preparations are preferred. 
     Once the therapy has run it course or has been deemed ineffective or unsafe, the medication should be tapered. A slow taper can be done by decreasing the dose by 10% every one to four weeks, and then by 5% for the last 20% of the original dose. Rapid tapering can be done by decreasing the dose by 25% every three to seven days. Therapy should not be continued for fear of withdrawal symptom because they are usually non life-threatening.  WIthdrawal can be tempered with clonidine or tramadol.

A Quick Synopsis of AFP's "Diagnosis and Treatment of Plantar Fasciitis"

A Quick Synopsis of AFP's;
Diagnosis and Treatment of Plantar Fasciitis
JAMES D. GOFF, DO, and ROBERT CRAWFORD, MD, Summa Health System, Akron, Ohio
http://www.aafp.org/afp/2011/0915/p676.pdf
Am Fam Physician. 2011 Sep 15;84(6):676-682

     Plantar fasciitis is an injury, causing sharp pain on the bottom of the heal. It is a sports injury from overuse, running, or prolonged standing. Patients will complain of heel pain after standing up out of bed in the morning, or after prolonged sitting. Walking barefoot may also reproduce the pain. Sharp pain will be observed on the medial aspect of the heel during palpation.  Dorsiflexion of the first toe will also reproduce the pain. Imaging, although unnecessary (unless used to rule out other causes in the differential) will show a heel spur or a thickened plantar fascia. Risk factors include excessive foot pronation, flat feet, obesity, high arch, tight achilles tendon, sedentary lifestyle, and a job the requires prolonged standing or walking. 
     Regardless of treatment, plantar fasciitis should improve within a year. Initial treatment should include rest, activity modification, ice massage  stretching, NSAIDs, acetaminophen  and weight loss. In addition, patients may find relief with heel cups, orthotics, or anterior night splints, all of which can be found over the counter. 
     If the conservative therapy is ineffective, other therapies, such as eccentric stretching, deep myofascial massage, iontophoresis (using electricity to increase absorption of charged topical medicine through the skin), or steroid injections. Extracorporeal shock wave therapy, which is supposed to increase blood flow and healing, has had mixed results. Plantar fasciotomy is a last line therapy which has been effective, but is invasive.  These last two choices are typically reserved for chronic recalcitrant fasciitis, lasting six months or longer.

A "Brief" Synopsis of AFP's "Diagnosis of Urinary Incontinence"

A brief synopsis of; 
Diagnosis of Urinary Incontinence
CHRISTINE KHANDELWAL, DO, and CHRISTINE KISTLER, MD, MASc, University of North Carolina, Chapel Hill, North Carolina
Am Fam Physician. 2013 Apr 15;87(8):543-550.
http://www.aafp.org/afp/2013/0415/p543.pdf

     Urinary incontinence can be a embarrassing situation for patients of all ages. It is not something that comes with age. It is pathologic. The 5 types of urinary incontinence are stress, urge, mixed, overflow, and functional. Stress incontinence is due to sphincter weakness. The patient will lose small amounts of urine during physical activity or with increased intra abdominal pressure. Leakage will coincide with coughing. It is common in obese women and men after prostatectomy.
     Urge incontinence is due to detrusor overactivity due to bladder irritation (from cystitis, prostatitis, atrophic vaginitis, or bladder diverticuli), or loss of neurological bladder control (from dementia, stroke, spinal cord injury, or parkinson disease). Patients will report a sudden and severe desire to urinate and will "not make it to the toilet . Changes in body position or minor sensory stimulation may trigger bladder contraction. They will have a history of variable volume loss, frequency, nocturia, and urgency.
     Mixed incontinence is a mix of stress and urge. Patients report involuntary leakage with exertion, sneezing, coughing or urgency.
     Overflow incontinence is due to impaired detrusor contractility causing overdistention of the bladder. This causes dribbling, hesitancy  and inability to feel when the bladder is full.  This is commonly due to medication side effects or effects from other illnesses (diabetes, MS, BPH, or spinal cord illnesses).
     Functional incontinence will present with variable amounts of leakage caused by cognitive or physical impairment such as dementia, immobility, or mental health disorder
     When diagnosing incontinence, the physician should first rule out reversible (transient) causes  The mnemonic to remember the causes is "DIAPPERS", which stands for
delirium,
infection (UTI),
atrophic vaginitis,
pharmaceuticals ,
psychological disorders such as depression,
excessive urine output,
reduced mobility, and
stool impaction.
     Common pharmaceuticals that may cause this are antihypertensives, pain relievers  antidepressants, antihistamines, and anticholinergics. Once these causes are ruled out, then one of the chronic types of urinary incontinence should be considered. Along with a proper history, a quick questionnaire can be given which ask three questions. It asks if the patient has leaked urine in the last three months and if so, was physical activity, coughing, sneezing, a feeling of urgency, or inability to reach a restroom a contributing factor. It also asks which situations cause the most amount of leakage. A focused physical exam including looking for signs of volume overload, bladder distention, neurological or psychological impairment, will help with the diagnosis. post void residual volume can help determine they type of incontinence  Less than 50 ml is often seen with stress, urge or mixed incontinence. Volumes greater than 200 ml is often seen with overflow incontinence.  Laboratory tests and a "cough stress test (positive in stress incontinence)" may be considered. A voiding diary (of at least three days) documenting frequency of incontinent episodes, leakage, dribbling, fluid intake and nighttime activity is also helpful.
 

A Tachycardic Synopsis of AFP's "Common Types of Supraventricular Tachycardia: Diagnosis and Management "

A brief synopsis of:
Common Types of Supraventricular Tachycardia: Diagnosis and Management 
RANDALLA.COLUCCI, DO, MPH, Ohio University College of Osteopathic Medicine, Athens, Ohio
MITCHELL J. SILVER, DO, McConnell Heart Hospital, Columbus, Ohio
JAY SHUBROOK, DO, Ohio University College of Osteopathic Medicine, Athens, Ohio http://www.aafp.org/afp/2010/1015/p942.html 
Am Fam Physician. 2010 Oct 15;82(8):942-952.


     Besides atrial flutter and fibrillation, there are three common types of SVT. They are AVNRT (AV nodal reentrant tachycardia), AVRT (AV reciprocating tachycardia), and AT (atrial tachycardia). 
     Nodal reentry is the most common type. It is seen in young, healthy women. The reentry occurs inside the AV node itself. The signal takes a slow route down the node (antegrade), and then a fast path back up it (retrograde). A "retrograde P wave" may not be seen on the ECG, but if it is, it will appear as a "pseudo R wave in lead V1".
     AV reciprocating tachycardia occurs shen the impulse passes through the AV node but instead of going to the bundle of his and around the apex of the ventricle, it follows an accessory "short cut"  through part of the heart and back to the AV node. This creates a reentry circuit and a short RP interval, which will vary depending on the specific trail of the shortened path. A delta wave may be seen. The patient may also develop spontaneous atrial fibrillation. 
   AT is caused by a signal being created in a place other than the SA node, commonly "adjacent to the crista terminalis in the right atrium or the crista terminalis in the right atrium". It can also be multifocal. 
     The most common symptoms in SVT are chest discomfort, dyspnea, fatigue, lightheadedness, and palpitations  The palpitations are intermittent. The patient may be told that they have anxiety or panic disorder. Tachycardia may be the only sign in an otherwise normal patient. The history may show symptoms since childhood, onset with coffee, stress, or lack of sleep, or a positive family history. An ECG may show a narrow QRS complex, prolonged QT interval, or delta waves. A wide complex tachycardia may be associated with a bundle branch block. 
     Management can be divided into short and long term, depending on whether the symptoms come and go, or if they are more serious, causing syncope, hemodynamic instability or other dangerous symptoms. Short term management can be performed first by nonpharmacologic treatments such as the valsalva maneuver, vagal maneuvers, or carotid massage (unless the patient may have an atherosclerotic plaque). This will increase vagal tone and decrease heart rate. Pharmacologic treatments include adenosine or verapamil. Adenosine may cause ventricular fibrillation in patients with Wolff-Parkinson-White syndrome.  It is an AV node blocking agent and thus would not work with AT. Verapamil can be used if adenosine does not correct the SVT. It is a negative inotrope,  so it may cause bradycardia and vasodilation. If none of these treatments work, then referral to a cardiologist for treatment with flecainide or propafenone may be necessary. 
     Long term management is considered, depending on frequency, intensity, and quality of life. The options are radiofrequency catherter ablation or intermittent medication. If the patient only experiences episodes a few times a year, they can be given verapamil PRN, known as the "pill-in-a-pocket" method. Ablative therapy has recently been shown to be quite effective with better long term outcomes and cost.

A Brief Synopsis of AFP's "Hypothyroidism: An Update"

A brief synopsis of: Hypothyroidism: An Update,DAVID Y. GAITONDE, MD; KEVIN D. ROWLEY, DO; and LORI B. SWEENEY, MD, Dwight D. Eisenhower Army Medical Center, Fort Gordon, Georgia

Am Fam Physician. 2012 Aug 1;86(3):244-251.

http://www.aafp.org/afp/2012/0801/p244.pdf

     Hypothyroidism is caused by either thyroid gland failure (primary) or poor stimulation of the thyroid gland from the pituitary gland or hypothalamus (secondary). Primary gland failure can be congential, autoimmune, or  iatrogenic. Common symptoms of hypothyroidism are weight gain, fatigue, depression, constipation, cold intolerance, dry skin, or hair loss. In children and infants, the most common signs are lethargy and failure to thrive. Menstrual irregularities and infertility are a common feature in women.  Cognitive decline may be the only symptom present in older adults.  Common signs are peripheral edema, brittle hair, goiter, pleural effusion, megacolon, and pericardial effusion. Patients may have ECG abnormalities including bradycardia and flat T waves. Lab findings may include hyponatremia, hypercapnia,  hypoxia, hyperprolactinemia,  hyperlipidemia, and elevated CK.
    Although universal screening is not recommended, patients who are symptomatic, or have risk factors,  including a history of autoimmune disease, previous radioactive iodine therapy, or a positive family history, should have a serum TSH drawn. If the TSH is elevated, then a T4 should be checked. A low T4 is seen in primary hypothyroidism and a normal T4 is seen in subclinical hypothyroidism.  A low TSH and low T4 signifies secondary hypothyroidism. Since the TSH level fluctuates, its best to check it in the morning.
     Most patients require lifelong levothyroxine (synthetic T4). The typical patient is started on 1.6 mcg/kg/day, given in the morning 30 minutes before breakfast. Certain patients need different dosages. Older patients with coronary heart disease are given 25-50 mcg/day, and increased by 25 mcg each 3-4 weeks until the optimal dose is found (a full dose could cause tachyarrhythmia and ischemia). Pregnant patients should get an extra 2 doses during the pregnancy.
     Patients with persistent symptoms should be checked for alternative causes, such as adrenal insufficiency,  depression, liver disease,  obstructive sleep apnea or chronic kidney disease. It can also be from deficiencies in B12, iron, or vitamin D. It is important to know that switching between name brand and generic medications for hypothyroidism is a bad idea because they have different bioavailabilities. myxedema coma is an extremely rare situation and should be treated in a ICU by an endocrinologist.
  

A Brief Synopsis of AFP's "Diagnosis of Secondary Hypertension: An Age-Based Approach"

A brief synopsis of : Diagnosis of Secondary Hypertension: An Age-Based Approach, ANTHONY J. VIERA, MD, MPH, and DANA M. NEUTZE, MD, PhD, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina

Am Fam Physician. 2010 Dec 15;82(12):1471-1478. 

http://www.aafp.org/afp/2010/1215/p1471.html

     Hypertension is one of the most common illnesses seen today. It is a predictor of serious illness, which is why blood pressure is considered a "vital sign". Oftentimes, a cause can not be found, so the patient is given anti-hypertensive pills and sent on their way. Up to 10% of these patients have secondary hypertension, which can be corrected without anti-hypertensive medications. Depending on the age of the patient, different etiologies are more common than others for secondary hypertension. 
     First, when a patient presents with elevated blood pressure, it needs to be check two other times during two other occasions. Correct positioning of the cuff, cuff size, diet, and a full medication review should be performed to avoid chasing any zebras.  Common medications that can cause elevated hypertension are OCP's, steroids  diet pills, amphetamines  lithium, TCA's, decongestants, and several herbs, like ma huang and ginseng.  If the patient is a child, the onset of hypertension was rapid, or the history simply does not seem typical, investigating other causes of hypertension should be considered.
     Patients under 18 years old may have secondary hypertension from renal parenchymal disease or  coarctation of the aorta. Renal parenchymal disease includes glomerulonephritis, reflux nephropathy, and congenital abnormalities.  A BUN, creatinine, UA, urine culture, and renal ultrasound should be ordered. In aortic coarctation,  a murmur may be heard, or there may be a pressure difference between bilateral brachial, or brachial and femoral pulses.  Rib notching may be seen on x ray. MRI or transthoracic echocardiology can be done to rule out coarctation. 
     In patients between the ages of 19 to 39, common causes of secondary hypertension are renal artery stenosis, and thyroid dysfunction. In this age group, the renal artery stenosis is due to decreased renal perfusion from fibromuscular dysplasia   A high pitched, holosystolic, renal bruit may be heard. MRI with gadolinium, CT angiography, or doppler ultrasound can be used to diagnose this.  HypOthyroidism can cause an elevation in diastolic pressure. HypERthyroidism can raise systolic pressures. TSH can be tested in this age group, as well as any older subgroup.
     Patients between the ages of 40 to 64 may have elevated pressure from aldosteronism, obstructive sleep apnea, pheochromocytoma, or cushing syndrome. Patients with elevated aldosterone syndromes may have hypokalemia. The best test is to check morning aldosterone/renin levels. These patients may need to be referred for confirmatory testing.  In obstructive sleep apnea, a polysomnography or a clinical assessment tool with nighttime pulse oximetry may be positive. Pheochromocytoma patients will have the 6 P's (Pounding headaches, Palpitations, Palor, Panic, Pressue/Paroxysmal burst, and Perspiration) as well as the "rule of 10's (10% familial, 10% bilateral, 10% malignant, 10% calcify, 10% extramedullary). 24-hour urinary metanephrines or plasma free metanephrines should be checked. Cushing disease patients will present with a buffalo hump, central obesity, moon facies and stria, but I would bet that your cushing patient won't have any of these classic signs (unless your patient is a medical textbook model...) Tests to rule out this disease include a 24-hour urinary free cortisol, low-dose dexamethasone suppression test or late-night salivary cortisol test.
    In patients older than 65 years old with secondary hypertension, the most common causes are renal artery stenosis or renal failure.   Patients who develop hypertension late in life, those with atherosclerosis, or rapid deterioration of renal function when started on ACEI's or ARB's may have secondary hypertension. They can be imaged by MRi with gadolidium or CT angiography. Patients with suspected renal failure should get an ultrasound, GFR, and a UA with albumin level. 

Death by Thrombus or exsanguination? A Brief Synopsis of AFP's "Perioperative Antiplatelet Therapy"

A brief synopsis of; Perioperative Antiplatelet Therapy

PIERRE GUY CHASSOT, MD; CARLO MARCUCCI, MD; and ALAIN DELABAYS, MD, University Hospital of Lausanne, Lausanne, Switzerland, DONAT R. SPAHN, MD, University Hospital of Zürich, Zürich, Switzerland

Am Fam Physician. 2010 Dec 15;82(12):1484-1489.

http://www.aafp.org/afp/2010/1215/p1484.html

     The decision whether or not to stop antiplatelet therapy is often an issue for the family physician who is managing a patient who need surgery. It is often debated between the surgeon and the primary care provider. The big question is, "is the patient more likely to throw a clot or bleed to death?"
     Antiplatelet therapy is used after a stroke, MI, ACS, and other thrombogenic situations. It is also important after coronary revascularization and stent placement.  These treatments "act as unstable plaques" until they either heal. Bare metal stents require 6 weeks to 3 months for smooth muscle and endothelium to cover it, respectively  It can take much longer  (up to 3 years) in drug-eluding stents. This is why clopidogrel treatment is given for 6 weeks with bare metal stents and a least a year with drug eluding stents.  It should be used for 2-4 weeks in angioplasty without stents, 3-6 months in an MI, and 6-12 months in an unstable ACS. Aspirin should also be used in these patients. Previous studies have shown that stopping aspirin, even two years later, can cause thrombosis. Thus, aspirin should be a lifelong medication in these patients.
    In general, there is a 20% increase in perioperative bleeding when on aspirin or clopidogrel.  The risk of hemorrhage is up by 50% (which isn't that much considering that the risk of hemorrhage in surgery is small to begin with). Whats interesting is, although it may take longer to get the bleed under control, the surgical mortality is the same. However, stopping antiplatelet therapy is associated with up to a 40% increase in MI and up to an 85% increase in mortality. Thus, the risk of thrombosis is higher than the risk of hemorrhage.
    Aspirin should be used forever in patients who use it for secondary prevention. The only time it may make sense to stop it is in diabetic patients using aspirin for primary prevention. Patients on dual antiplatelet therapy after stent placement should not have elective operations done during this time. If an emergency operation is needed and the clopidogrel must be stopped, the aspirin should be continued.

A Brief Synopsis of AFP's "Diagnosis, Initial Management, and Prevention of Meningitis"

A brief synopsis of: Diagnosis, Initial Management, and Prevention of Meningitis, DAVID M. BAMBERGER, MD, University of Missouri–Kansas City School of Medicine, Kansas City, Missouri

Am Fam Physician. 2010 Dec 15;82(12):1491-1498.

http://www.aafp.org/afp/2010/1215/p1491.html

     Considering the recent outbreak in upstate New York, I thought it would be appropriate to review meningitis (i'll save bird flu for next week). Meningitis is usually bacterial or viral (aseptic).  Bacterial is more rare and way more dangerous. The most common types of aseptic meningitis are enterovirus, HSV, HZV and Borrelia burgdoferi.  Enterovirus and arbovirus are prevalent in the summer and fall months. 
     In adults, most patients with bacterial meningitis will have either fever, neck stiffness, altered mental status or headache. Some will present with a recent history of otitis, sinusitis, pneumonia, or an immunocompromised state. A petechial rash may also be seen in meningococcal meningitis. Seizures, focal neurological findings, and altered consciousness is more commonly seen in pneumococcal meningitis. Younger adults are less likely to present with seizures and hemiparesis, but more commonly with headaches, nausea, vomiting, and nuchal rigidity. Younger children will present with lethargy, irritability and a history of a recent URI. They may also "catch" a seizure at this young age. So you get the point, right? we have a serious disease with high mortality, but subtle clinical findings. Thus, if you can't come up with an explanation for all the symptoms, you better evaluate that CSF.
     A lumbar puncture is generally a safe procedure. We all have fear that we will cause a brain herniation when we hear the "pop", but as long as the patient the patient does not have any neurological issues (shunts trauma, papilledema, etc), you will be safe. Of course, if the patient had a seizure or is impaired, a CT will be necessary. Regardless, you still need to get blood cultures and start empiric therapy before the CT. Sitting on therapy for as little as 2 hours could affect the outcome poorly. Starting therapy before the LP will decrease the amount of bacteria available to culture, and may affect the glucose level, protein level , and ability to culture the bug for antibiotic sensitivity testing. It will not affect the gram stain of PCR results. 
     For empiric therapy, give vancomycin and ceftriaxone. Add ampicillin if the patient is over 50 years old  and an alcoholic. If the patient had a penetrating trauma, a CSF shunt or is post surgery, switch out the ceftriaxone for cefepime. If the patient is less than a month old, try ampicillin and cefotaxime. If you suspect M. Tuberculosis or S.pneumoniae , you can add dexamethasone.
     Aseptic meningitis is a less serious infection. It can be diagnosed by PCR of the CSF. An RPR, VDRL, or HIV antibody test may be done if the history warrants.  Fungal and TB meningitis can be diagnosed with PCR as well. Cryptococcal is the most common fungal cause and can be treated with amphotericin b and flucytosine.

A Brief Synopsis of AFP's "Management of Chronic Tendon Injuries"

A brief synopsis of:

Management of Chronic Tendon Injuries

MARC A. CHILDRESS, MD, Fort Belvoir Community Hospital, Fort Belvoir, Virginia

ANTHONY BEUTLER, MD, Uniformed Services University of the Health Sciences, Bethesda, Maryland

Am Fam Physician. 2013 Apr 1;87(7):486-49

http://www.aafp.org/afp/2013/0401/p486.html

     Most chronic tendon injuries tend to be from overuse (and I have a left elbow to prove it). These areas typically have a poor blood supply with collagen separation and degeneration.  Rather than bleeding and inflammation, the pain is mediated by glutamate and non-prostaglandin pathways. NSAIDs are considered first line medication but there is little evidence to support this, and the side effects (GI, renal, and cardiovascular issues) outweigh the benefits. In general, steroid injections may provide short term pain relief, but long term benefit has not been proven.
     There are two types of Achilles tendinopathy; midsubstance and insertional.  Midsubstance tendinopathy is located approximately in the middle of the Achilles tendon. First line treatment is eccentric strengthening of the gastrocnemius and soleus. This article has a nice table and picture of the exercise, which appears to be a modified calf raise. The classic therapies (ultrasound, electric stimulation, massage, surgery and stretching) have not been shown consistently to improve long term function. Insertional tendinopathy is located distal to the midsubstance injury, near the insertion of the Achilles. Eccentric stretching is not as helpful, but has shown benefit in about 30% of these injuries. The patient should also be in a walking boot for 4-6 weeks.
     Eccentric exercise is a first line treatment for patella tendinopathy, which consists of a type of slow knee bend (please see figure 3 of this article). This has been shown to be of greater benefit than surgery or injections of sclerosing agents.
     Lateral epicondylitis is pain that can be reproduced by forearm extension and pronation against resistance. The best therapy here is wrist extensor strengthening and stretching. Steroid injection provide short term pain relief, but may affect long term cure rates. Studies have shown benefit with autologous blood and platelet-rich plasma injections, as well as nitroglycerin patch.
     Rotator cuff tendinopathy can be caused by repetitive actions of throwing, lifting, and overhead motions. Imagining is helpful to determine the extent of the injury and to rule out a possible tear. The main therapy is strengthening the rotator cuff, stabilizing the scapula, and increasing range of motion  Steroid injections can be used to help relieve pain during therapy, but the location of injection may not be important.
     Prolotherapy is the injection of irritants to induce healing. Examples are dextrose, autologous blood and platelet-rich plasma. Other therapies  such as lasers, phonophoresis, ultrasound and iontophoresis have had mixed results and are not a substitute for first line therapy.
   

A Quick Blurb of AFP's "AASM Updates Treatment Guidelines for Restless Legs Syndrome and Periodic Limb Movement Disorder"

A brief synopsis of :

AASM Updates Treatment Guidelines for Restless Legs Syndrome and Periodic Limb Movement Disorder BY CARRIE ARMSTRONG

Am Fam Physician. 2013 Feb 15;87(4):290-292.

http://www.aafp.org/afp/2013/0215/p290.html?printable=afp

     Restless leg syndrome is this uncontrollable urge to move your legs at night. You may have seen something similar on YouTube, but this has nothing to do with the Harlem hake. The most effective medication for moderate to severe RLS is pramipexole and ropinirole. The side effects (nausea and others) will resolve with stopping the medication. Levodopa can be used with intermittent RLS if daily medication is not recommended. Cabergoline can be used if the other medication are not effective, although cabergoline is not well tolerated. Medications such as gabapentin, pregabalin, carbamazepine, ans clonidine should no longer be used as first or second line medications due to the creation of the better alternatives described above. 
     Benzos, VPA, Valerian and Amantadine  have not been proven to be beneficial and really should not be considered at this time.
     This article does not recommend medications for periodic limb movement disorder.