A Brief Synopsis of AFP's "Evaluation of Primary Immunodeficiency Disease in Children"

A brief synopsis of :
Evaluation of Primary Immunodeficiency Disease in Children 
CARIN E. REUST, MD, MSPH, University of Missouri School of Medicine, Columbia, Missouri 
Am Fam Physician. 2013 Jun 1;87(11):773-778 
http://www.aafp.org/afp/2013/0601/p773.pdf

     According to this article, there are over 180 primary immunodeficiency diseases that have been identified. The types that will be reviewed here are antibody (B cell), combined B and T cell, phagocytic, and complement disorders.  Antibody disorders are the most common. They are categorized by the presence or absence of B cells, and the quality of the B cells if present.  Patients with this type of disorder will have recurrent or severe encapsulated bacterial infections of the ears, lungs and sinuses. They include S. pneumoniae and H. influenzae. Agammaglobulinemia is a complete absence of B cells. A decrease in all immunoglobulin subtypes may be seen in testing as well. The infant patient may present with an absence of tonsils or lymph nodes. In hypogammaglobulinemia, some or all of the immunoglobulins may be at low or at deficient levels. Some examples of hypogammaglobulinemia are CVID, IgA deficiency, and IgG subclass deficiency. The patient may have an abnormal response to vaccinations. They may present with GI symptoms (diarrhea, malabsorption, IBS symptoms) or ear, sinus and pulmonary infections. They can be caused by C. difficile, Giardia, Salmonella, Campylobacter, and Yersinia. These patients will have problems with vaccine effectiveness. Titers should be checked in these patients. 
     T-cell disorders can have an absence of T-cells (such as in SCID) or T-cells and B-cells combined. Patients may present with  diarrhea, failure to thrive, and infection. Bloodwork will show lymphocytopenia or lymphocytosis. An absolute lymphocyte count of less than 3000/mm3 in a newborn is a good indicator. Patients will not have a response to a delayed hypersensitivity skin test. 
     Phagocytic disorders are due to problems with neutrophils and monocytes. They will have neutropenia (neutrophil count less than 1500 per mm3) and abnormalities in lysosomal granules.  One example is chronic granulomatous disease. It presents in a patient by the age of 5 with pneumonia, adenitis, omphalitis, and GI infections. The bacteria that invade are catalase positive, such as S. aureus, B. cepacia, Nocardia, Aspergillus, or Candida. Patients with leukocyte adhesion deficiency type 1 may present in infancy with prolonged separation of the umbilical cord, perianal ulcers, or omphalitis.
     Complement disorders involve infections with encapsulated organisms. A C3 deficiency will have recurrent pyogenic infections from S. pneumoniae or H. influenzae. A deficiency in C5-C9 are associated with N. meningitidis. The complement levels can be checked with a CH50 assay. 
     When determining whether to evaluate a patient for a primary immunodeficiency disease, look for children with recurrent ear, sinus and pulmonary infection, diarrhea, and failure to thrive. Infections in multiple anatomic locations are an important clue, especially if there are serious infections from unusual pathogens.  Three warning signs to look for are a positive family history, sepsis that needed IV antibiotic treatment, and failure to thrive. 

A Brief Synopsis of AFP's "End-Stage Renal Disease: Symptom Management and Advance Care Planning"

A brief synopsis of:
End-Stage Renal Disease: Symptom Management and Advance Care Planning
NINA R. O’CONNOR, MD, Arkansas Hospice, Little Rock, Arkansas, AMY M. CORCORAN, MD, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania
Am Fam Physician. 2012 Apr 1;85(7):705-710.
http://www.aafp.org/afp/2012/0401/p705.pdf

     End stage renal disease has three components; initiation of dialysis, symptom management, and advance directives. According to this article, dialysis has not shown survival benefit over conservative management.   Conservative management consists of proper fluid balance, diet, blood pressure control,  anemia treatment, and electrolyte management (potassium, calcium, phosphorus, and those causing acidosis). There does not appear to be a benefit in early adoption in dialysis so delayed onset of treatment is valid. Patients who discontinue dialysis will have a life expectancy of 1-2 weeks on average.
     Pain is a common symptom in patients on dialysis, especially if they have comorbid conditions (which is more commonplace with the increased availability of treatment centers). Calciphylaxis is an illness exclusively in dialysis patients. Altered metabolism of calcium and phosphorus causes skin ischemia and vessel calcification. Symptoms include a painful rash and overt necrosis (I had a patient with calciphylaxis on my first day as a medical student in the hospital. The poor woman was in so much pain when the hair on her leg got stuck to the adhesive on the wound-vac).  For mild pain, acetaminophen can be used safely. NSAIDs should be avoid because it may cause GI bleeding in a patient with platelet dysfunction from the uremia.  Tramadol can be used for moderate to severe pain, but is must be dose and interval adjusted. Fentanyl or methadone can be used for those needing opioids. Codeine, hydrocodone, morphine and meperidine are not recommended. Hydromorphone and oxycodone should be used with caution. Gabapentin is widely used for neuropathic pain, although the evidence of effectiveness is controversial. TCAs should be avoided. 
    Other symptoms seen in renal failure patients include fatigue, pruritus,  drowsiness, dyspnea, dry mouth, myalgia, RLS, anorexia, constipation and edema.  Pruritus can be managed with phosphate binders, emollients, antihistamines, ondansetron and naltrexone. Fatigued patients should be assessed for edema and depression. Nausea can be managed with ondansetron, metoclopramide and haloperidol. Encouraging physical therapy can help the dyspnea and fatigue. 
     Patients with end stage renal disease have a limited life expectancy. Patients who fill out an advance directive are more likely to talk with their family about end-of-life intervention. As far as hospice is concerned, end stage renal disease is not covered by medicare. Patients with a comorbid terminal condition can get hospice care with dialysis benefits under medicare.

A Brief Review of AFP's "Acute Kidney Injury: A Guide to Diagnosis and Management"

Acute Kidney Injury: A Guide to Diagnosis and Management
MAHBOOB RAHMAN, MD, MS, Case Western Reserve University School of Medicine, Cleveland, Ohio, FARIHA SHAD, MD, Kaiser Permanente, Cleveland, Ohio, MICHAEL C. SMITH, MD, Case Western Reserve University School of Medicine, Cleveland, Ohio
Am Fam Physician. 2012 Oct 1;86(7):631-639.
http://www.aafp.org/afp/2012/1001/p631.pdf

     Acute kidney injury is a common inpatient problem, occurring in 7% of hospitalized patients and 33% of ICU patients.  Patients with acute injury have a higher chance of developing chronic injury in the future. Risk factors include age greater than 75 years, diabetes, heart failure, liver failure, or sepsis.  The patient will have an elevated creatinine and reduced urine output within a 48 hour period  Dialysis may be necessary.  The three categories of acute kidney injury are prerenal, intrinsic, and postrenal.
      Prerenal injury is due to some type of volume loss. The patient will have decreased intravascular volume or decreased arterial pressure, which leads to a reduced GFR.  FENa will less than 1%. FEurea will be less than 35% if the patient is on diuretics. Causes include heart failure, sepsis, vomiting or diarrhea. Medications that can cause prerenal kidney injury include ACEIs, ARBs, and NSAIDs. A patient may have signs of volume loss such as orthostatic hypertension, poor skin turgor, ascites (decrease intravascular, but increased extravascular), increased thirst, decreased fluid intake, heart disease or liver disease.
     Postrenal injury is due to some type of blockage after the urine leaves the kidney. It can be by an enlarged prostate, a neurogenic bladder, mass or a stone causing an obstruction. The patient may complain of hematuria, urgency, hesitancy, or bladder distention. Ultrasound should be done in this case to find or rule out the cause. 
     Intrinsic injury has to due with part of the anatomy of the kidney. The FENa should be greater than 2%. Intrinsic injury can be broken down into four parts: tubular, glomerular, interstitial, or vascular. Acute tubular necrosis is either ischemic (hypotension) or nephrotoxic (drugs, contrast). It may also be from rhabdomyolysis (trauma). On UA, there may be renal tubular cells, tubular casts, or pigmented casts.  Glomerulonephritis is due to a systemic issue. Common causes are lupus, HCV, goodpasture's, HIV, and wegener's. It is a nephrotic syndrome so there will be heavy proteinuria, as well as RBC casts. Diagnosis of the specific cause may be done through biopsy, or other disease specific testing. Acute interstitial nephritis will produce WBC casts and eosinophils on UA. It is commonly caused by medication use, including antibiotics or PPIs. Patients may present with fever, rash or joint pain. Renal atheroembolic disease is the most common cause of vascular injury. The patient will be on anticoagulation. There may also be flank pain, recent trauma, recent vascular surgery, or recent vessel catheterization. 
     Hospitalized patients should have their volume status assessed and maintained on isotonic fluids, or diuretics if the patient is overloaded. Hypotensive patients may need vasopressors if it is severe. Hyperkalemic patients may need insulin and dextrose if it is above 6.5 mmol/L. Calcium gluconate may be added to reduce the risk of cardiac arrhythmias. Kayexalate has a role in hyperkalemia as well. Nephrotoxic medications should be discontinued, including metformin. Contrast media use should be avoided as well.  A conformational biopsy may be needed before treatment is started if the treatment itself is toxic. Patients may ultimately need dialysis if they have treatment refractory hyperkalemia, treatment refractory volume overload, uremic pericarditis, uremic pleuritis, encephalopathy, acidosis or intoxications form lithium or ethylene glycol. 

A BRIEF Synopsis of AFP's "Interstitial Cystitis/Painful Bladder Syndrome"

A BRIEF SYNOPSIS of: Interstitial Cystitis/Painful Bladder Syndrome 
LINDA M. FRENCH, MD, University of Toledo College of Medicine, Toledo, Ohio, NEELAM BHAMBORE, MD, University of California–Davis Medical Group, Sacramento, California
Am Fam Physician. 2011 May 15;83(10):1175-1181.
http://www.aafp.org/afp/2011/0515/p1175.pdf

     Interstitial cystitis (AKA painful bladder syndrome) consists of painful symptoms such as dyspareunia, dysuria, urgency, frequency, suprapubic and pelvic pain. It affects women more than men. The cause is unknown, but it is thought that damage to the urothelium produces cytokines and puts excess K into the bladder interstitium.  This causes mast cell activation and degranulation. 
     The differential diagnosis is broad and there is no standard test for interstitial cystitis. There are two screening questionnaires (O'Leary-Stant Symptom and Problem index and the Pelvic Pain and Urgency/Frequency Symptom Scale [PUF] ). A physical exam (bimanual pelvic or DRE) may show pelvic floor spams, rectal spasms, or subrapubic tenderness. 
     As far as laboratory testing is concerned, a UA and urine culture can be done to rule out infection and other illnesses. An intravesical potassium sensitivity test is a commonly used procedure to diagnose interstitial cystitis. Basically, water is inserted into the bladder with a catheter. It is drained out after 2-3 minutes and a second infusion is added. The second infusion is water with 40 mEq of K. If the potassium infusion causes increased pain, then the test is positive for cystitis.  The anesthetic bladder challenge (where an anesthetic solution is added to the bladder) that relieves pain is an indication that the bladder is the cause.  Direct visualization of the urothelium may be helpful in documenting the bladder inflammation. 
     Treatment effectiveness for interstitial cystitis is limited, thus it is important to set realistic goals and expectations with the patient. Dietary triggers, such as coffee, alcohol, citrus fruits, and spicy foods, should be removed. Pentosan polysulfate sodium is supposed to repair the urothelium. Hydroxyzine is supposed to control mast cell degranulation. TCAs are supposed to inhibit neuronal activation. These three can be taken orally. Intravesical therapies include dimethyl sulfoxide, pentosan polysulfate sodium (hello again!) and hyaluronic acid (not approved in the US-sad face). Physical therapy to treat pelvic floor spasms may also be helpful.

A Synopsis of AFP's "Pelvic Inflammatory Disease"

A synopsis of
Pelvic Inflammatory Disease, MARGARET GRADISON, MD, MHS-CL, Duke University Medical Center, Durham, North Carolina
Am Fam Physician. 2012 Apr 15;85(8):791-796.
http://www.aafp.org/afp/2012/0415/p791.pdf

     PID is an infection of the upper genital tract in women. It can lead to infertility (from tubal scarring) and  ectopic pregnancy. The patient may present with lower abdominal pain, pelvic pain, vaginal discharge, fever, chills, cramping, dyspareunia, nausea and vomiting. On pelvic exam, the patient may have cervical motion, uterine, or adnexal tenderness. There are no specific clinical finding to diagnosis PID definitively. There is no specific bug that causes PID. The most common bugs are Neisseria gonorrhoeae, Chlamydia trachomatis, Trichomonas, Gardnerella, Mycoplasma genitalium, and others! There are no specific lab tests for diagnosing PID, thus, clinical judgement should lead the way to treatment. Treatment should be done empirically.
     As far as testing is concerned, there are some tests that can be done (but should not delay treatment). PCR and other nucleic acid tests of vaginal or endocervical samples can be done for chlamydia and gonorrhea. Saline microscopy of vaginal discharge may reveal Trichomonas or bacterial vaginosis. PID is less likely without the presence of WBC's in the microscopy. Other diagnostic tests that are available include transvaginal ultrasonography, MRI, endometrial biopsy, laparoscopy, and CT.
     Treatment is empiric. Chlamydia and gonorrhea treatment is part of the regiment regardless of culture results. Treatment for Gardnerella is controversial and recommendations state treating for it only if the studies are inconclusive. Treatment is not directed against Mycoplasma, which has been associated with treatment failure.  There are many different treatment regimens depending on local resistance patterns (including fluoroquinolone resistant N. gonorrhoeae). According to this article, the first line therapy is IM ceftriaxone with 14 days of PO doxycycline. Cefoxitin or another third generation cephalosporin can be used instead of ceftriaxone. Metronidazole may be added to the therapy as well. Parental treatment and hospitalization may be needed if the patient cannot tolerate PO meds, if there is no response from the outpatient treatment, if they are pregnant, or if they have severe symptoms. Patients may need extended hospitalization if a tubo-ovarian abscess is found.
     Patients should improve within three days of treatment initiation. Male partners within the last 60 days may need evaluation. Patients should be checked for reinfection after 3-6 months. HIV and syphilis should be checked as well. Patient with an IUD have an increased risk of PID for three weeks following device insertion. Screening is recommended for all sexually active women younger than 25 and for those above 25 with increased risk.

A Synopsis of AFP's "Evaluation of First Nonfebrile Seizures"

A synopsis of-Evaluation of First Nonfebrile Seizures
JESSICA A. WILDEN, MD, and AARON A. COHEN-GADOL, MD, Indiana University School of Medicine, Indianapolis, Indiana
Am Fam Physician. 2012 Aug 15;86(4):334-340.
http://www.aafp.org/afp/2012/0815/p334.pdf

     The three components of an epileptic seizure are the clinical signs, the specific onset and offset, and the  electrical brain activity. The three types of epileptic seizures are provoked, unprovoked, and progressive.  Provoked (or situational) seizures are usually due to an underlying cause which affects brain and/or metabolic activity. Causes include alcohol, DM, viral infections, cancer, dehydration, liver or kidney disease, progressive headaches, or drug use. Unprovoked seizures do not have a precipitant. The possible causes include mental retardation, preeclampsia, prior TIA, CP, family history of seizure, or an old head injury. It is more common in older men. 
     Nonepileptic seizures have transient symptoms and no electrical brain disturbances. The two types are psychogenic and syncope. Psychogenic nonepileptic seizures may present with resistance to medications, multiple seizures per day, depression, or anxiety. Causes include physical or sexual abuse, childhood trauma, PTSD, history of self harm, and others.  Syncope may present with lightheadedness, chest pain, palpitations or nausea, followed by a loss of consciousness and motionlessness. There may be a brief jerking motion which may resolve within seconds. Causes include CAD, HTN, PVD, chest pain, cardiomyopathy, and others. 
     Evaluation of a patients' first seizure should include the events right before the seizure, the number of seizures over the last day, focal aspects,  length of time the patient is postictal, and how long the seizure lasted. A full neuro exam should be completed as well. A CT with and without contrast should be done in all patients experiencing a first seizure. If the patient has returned to baseline, or did not present in the ER, the CT can be done as an outpatient. It may not be needed if the patient is older than one, without any risk factors, and did not go to the ER.  Depending on the history and exam, a glucose, LP, serum sodium, or pregnancy test may be drawn. An elevated serum prolactin may be seen 10-20 minutes after a seizure if the etiology is tonic-clonic or focal, rather than psychogenic. 
     An EEG can be performed on all patients with seizures of unknown cause. It should be done within 24-48 hours. It should also be done during sleep and while awake. Sleep deprived EEG (up to 3 days) may be helpful as well. The EEG may find focal lesions not seen on CT or MRI. Such lesions may be associated with a high recurrence risk. 
     Treatment of epilepsy may help slow down the recurrence rate, but will not affect the time to remission. Patients with a high risk of recurrence should be considered for treatment.  Treatment may also be helpful for patients who become too stressed from the thought of a second seizure in public.The may be in a position of high public scrutiny. Driving privileges may be affected from a seizure.

A Synopsis of AFP's Approach to Acute Headache in Adults

A synopsis of 
Approach to Acute Headache in Adults
 BARRY L. HAINER, MD, and ERIC M. MATHESON, MD, Medical University of South Carolina, Charleston, South Carolina
Am Fam Physician. 2013 May 15;87(10):682-687.
http://www.aafp.org/afp/2013/0515/p682.pdf

     When a patient walks in with an acute headache, it must first be determined if the headache is life threatening.  Some illnesses that require prompt evaluation include SAH, hypertensive emergencies, closed angle glaucoma, or a vertebral artery dissection. Some red flags are focal neurological signs (unilateral pronator drift or extensor plantar response), neck stiffness, papilledema, temporal artery tenderness, or having "the worst headache of ones life". Something like this will call for a more extensive evaluation, including neuroimaging, blood tests, or an LP (do the CT first regardless of symptoms). 
     The three most common types of (primary) headaches are tension (40%), migraine (10%) and cluster (1%). Tension headaches are usually bilateral and found more often in women. Infrequent tension headaches occur less than once per month.  Frequent tension headaches can have up to 15 episodes per months. Criteria includes having at least 10 episodes,  headaches lasting 30 minutes to 1 week, nausea and vomiting, and photophobia or phonophobia. The patient must also have at least two of the following: bilateral, pressing or tightening quality, and not aggravated by exertion. 
     Migraine headaches have symptoms that can be remembers by using the "POUND" mnemonic (Pulsatile,  4-72 hours lOng, Unilateral, Nausea and vomiting, Disabling [4/5 for the criteria]). Migraines may or may not have an aura. An aura may be flickering lights, loss of vision, pins and needles, numbness or speech changes.  This usually occurs before a headache and will last less than an hour. 
     Cluster headaches have a unilateral orbital, superolateral, of temporal location. They last from 15-180 minutes and are associated with ipsilateral autonomic symptoms, such as conjunctival injection, lacrimation, congestion. rhinorrhea, sweating, ptosis, miosis, restlessness or aging. They can be sharp, pulsating or pressure-like. Patients may have associated depression, sleep apnea, restless leg syndrome or asthma.  Chronic cluster headaches last for one year at a time, and remission will last for less than one month. Episodic cluster headaches will last 7 days to 1 year, with remissions lasting longer than a month. 

A Synopsis of AFP'S "Hepatitis C: Diagnosis and Treatment"

A Synopsis of 
Hepatitis C: Diagnosis and Treatment
THAD WILKINS, MD; JENNIFER K. MALCOLM, DO; DIMPLE RAINA, MD; and ROBERT R. SCHADE, MD, Medical College of Georgia, Augusta, Georgia
Am Fam Physician. 2010 Jun 1;81(11):1351-1357.
http://www.aafp.org/afp/2010/0601/p1351.pdf

     Today is a fun day because I'm working on a Saturday, so I have to blog from my iPhone. Anyway, the girls up front were asking me all these questions about hepatitis C, so I figured this would be a good time to review the topic.

     Hepatitis C is a single-stranded RNA virus transmitted through exposure to infected blood. This includes dirty needles from IVDA, unsterilized syringes, unprotected sex, accidental needle sticks, etc. Transmission through blood transfusion occurs three times per 10,000 units transfused. Blood was not screened for Hep C until after 1992. Immunoglobulin has not been shown to be effective as a treatment in these situations.There is no vaccine available and the USPSTF does not recommend screening in asymptomatic low risk patients. 

     Symptoms are nonspecific and include fatigue, nausea, anorexia, myalgias, arthralgias, weakness and weight loss. Most patients are asymptomatic. Hepatitis C can lead to cirrhosis, causing portal hypertension, hemorrhage, and hepatocellular carcinoma. Risk factors are being male, immunosuppression, coinfection with HIV or HBV, or age greater than 40. Daily alcohol use can greatly accelerate the severity of damage. Median survival of hepatocellular carcinoma is eight months.

    Diagnostic tests are used to diagnose HCV. The screening test is the enzyme linked elisa test, which detects viral antibodies. The two confirmatory tests are the RIA (for antibodies against the HCV antigens) and PCR (for HCV RNA). If they are both negative after a positive screen, then it was a false positive. If all three tests are positive, then the patient is experiencing a current infection. If the screener and RIA are positive but the PCR is negative, then it signals an old infection.  Quantitative viral load is used to document the progress of the infection and the effectiveness of treatment. Surveillance of hepatocellular carcinoma should be considered as well.

    the goal of treatment is to slow down the progression of fibrosis and cirrhosis. Fibrosis can be predicted with a scoring system using platelet count and AST. Biopsy is another way to assess fibrosis. The standard therapy is pegylated interferon (alfa-2a and alfa-2b) and ribavirin.  Interferon can cause leukopenia, thrombocytopenia, and thyroiditis. Ribavirin can affect the kidneys (its renally excreted). HCV phenotypes 1 and 4 are treated for 48 weeks. Genotypes 2 and 3 are treated for 24 weeks. Therapy effectiveness is measured by sustained viral response. If the virus is undetectable after 4 weeks, this shows a rapid and sustained viral response and the treatment may be discontinued earlier than expected. If it is undetectable after 12 weeks, treatment should be continued until week 48.  A 100-fold reduction in viral load after 12 weeks is predictive of a partial response. The load should be recheck after another 12 weeks to determine if the therapy should be continued for another 48-72 weeks. If the treatment fails to decrease the load by 100-fold after week 12, or if the load is stable, the therapy can be discontinued. 

A synopsis of AFP's "Ulcerative Colitis"

A synopsis of:
Ulcerative Colitis, STEPHEN M. ADAMS, MD, University of Tennessee College of Medicine, Chattanooga, Tennessee, PAUL H. BORNEMANN, MAJ, MC, USA, Tripler Army Medical Center Family Medicine Residency Program, Honolulu, Hawaii
Am Fam Physician. 2013 May 15;87(10):699-705.
http://www.aafp.org/afp/2013/0515/p699.pdf

    Ulcerative colitis (UC) is inflammation of the colonic mucosa. If it affects the entire colon, it is referred to as pancolitis. Symptoms of UC consist of hematochezia, diarrhea, and abdominal pain. The onset can be gradual or sudden. Extraintestinal manifestations such as arthritis, uveitis, AS, psoriasis, and erythema nodosum can occur in up to a third of patients. Smoking or having had an appendectomy have a protective effect. Those with a previous infection from Salmonella or Campylobacter have a 10x higher chance of developing UC. A diet high in sugar, fat and meat have an increased risk. A diet rich in vegetables have a lower risk. People also say that living in such a "sterile" society (the hygiene hypothesis) decreases exposure to "bacterial and helminth antigens", which makes our immune system more open to illness such as UC. 
     Endoscopic biopsy will give a definitive diagnosis. P-ANCA and ASCA (anti-Saccharomyces cerevisiae antibodies) will be positive in UC.  Fecal calprotectin and lactoferrin are sensitive tests, but they may delay diagnosis. The difference between UC and Crohn's disease is that inflammation from UC is limited to the colonic mucosa, whereas in Crohn's, the inflammation can be anywhere. UC is a contiguous inflammation, crohns has unaffected areas of mucosa between diseased areas (skip lesions). Other diseases to rule out include dysentery, bacterial and C. diff colitis, ischemic colitis, and microscopic colitis. Biopsy will tweeze out most of these diseases. 
      Treatment is based on severity of the disease. The goal is to induce remission and prevent relapse. If the disease is distal to the colon, 5-ASA enemas can be used for 4-6 weeks. Suppositories are preferred in proctitis. Oral 5-ASA can be considered if remission does not occur, or if the colitis is more extensive than just distally. At this point, the patient can be maintained on their current medication if remission occurs. If the disease is ongoing, oral steroids may be tried for 4-6 weeks. If remission occurs now, the patient can be maintained on azathioprine. If remission has not occurred, infliximab can be started.  If the disease is still continuing, the patient may try IV steroids, cyclosporine, or a colectomy. Those who present with severe or fulminant colitis should be admitted and started on a 3-5 day regimen of IV steroids. Transition to azathioprine can happen it remission occurs at this point. If not, the patient can be given a trial of cyclosporine or infliximab. Colectomy can be considered at this point as well.  Probiotics (lactobacillus or E. coli/mutaflor) have been shown to be as effective as 5-ASA maintenance therapy.
     UC can increase rates of osteoporosis, colorectal cancer, and abnormal pap smears. 

A Three Second Synopsis of AFP's "Sick Sinus Syndrome: A Review"

A synopsis of  "Sick Sinus Syndrome: A Review", MICHAEL SEMELKA, DO, and JEROME GERA, MD, Excela Health Latrobe Hospital, Latrobe, Pennsylvania, SAIF USMAN, MD, University of Missouri–Kansas City School of Medicine, Kansas City, Missouri
http://www.aafp.org/afp/2013/0515/p691.pdf
Am Fam Physician. 2013 May 15;87(10):691-696

     Sick sinus syndrome is a problem with the SA node appropriately pacing the heart to the patients physiological needs. It can cause arrhythmias such as sinus bradycardia, sinus pause/arrest, SA exit block, or alternating brady/tachyarrhythmias. Patients can develop atrial fibrillation or flutter, whuch may lead to an embolic stroke. They could also develop an AV block, There are intrinsic and extrinsic causes. The intrinsic causes include degenerative fibrosis or remodeling of the SA node, connective tissue diseases, hemochromatosis, sarcoidosis, atherosclerosis of the sinus node artery, and amyloidosis  Some of the extrinsic causes include hypothyroidism, hypokalemia, hyperkalemia, hypocalcemia, hypothermia, and medications such as beta blockers, calcium channel blockers, digoxin, and lithium. 

    The patient is often asymptomatic, but the disease is progressive. Symptoms incluse fainting spells, syncope, lightheadedness, palpitations, GI symptoms, CHF or stroke. These all arise from cerebral or end-organ hypoperfusion. sinus bradyarrhythmia, such as a SA pause of 3 seconds or more, SA  block, or sinus arrest, is required for diagnosis. Tachyarrhythmias are often seen as well, but not necessary for diagnosis. If you suspect sick sinus syndrome becaseu of the presentation but ypou cannot documetn the EKG findings, the patient may need prolonged cardiac monitoring. This can be done with a holter monitor,  inpatient telemetry monitoring, or an implantable loop monitor. 
 Treatment starts with correcting the extrinsic cuase, whether it is an electrolyt abnormality or a medicaiton reaction. Pacemakers are often implanted for symptomatic relief and improved quality of life. They do not, however, affect survival rates. 

A Quick rundown of AFP's " Management of Hyponatremia "

A synopsis of: Management of Hyponatremia 
KIAN PENG GOH, M.R.C.P., Alexandra Hospital, Singapore
http://www.aafp.org/afp/2004/0515/p2387.pdf
Am Fam Physician. 2004 May 15;69(10):2387-2394.

     I came across a bunch of questions about hyponatremia while studying, so I figured I would see what AFP has to offer on the subject. So in the immortal words or Eddie Vedder, "and away we go!"
     Hyponatremia is diagnosed when the plasma Na drops below 135 mEq/L. Neurologic and gastrointestinal symptoms (such as headache and nausea) occur when it drops below 120 mEq/L.  There are three classes of hyponatremia: hypervolemic, hypovolemic, and euvolemic. 
     Hypervolemic hyponatremia is an excess of total body water, causing edema. The common causes are CHF, liver cirrhosis, and renal disease. These causes should be apparent from the history and physical.  The BUN/creatinine will be prerenal (>20). Hypovolemic hyponatremia means that the patient is volume depleted and sodium depleted. Euvolemic hyponatremia bus means that the total body volume is normal and the sodium is low. To differentiate between the hypo- and euvo- you need to figure out the plasma osmolarity and the urine sodium concentration.
     Patients with hyponatremia and normal osmolarity (280-300) may have pseudohyponatremia or post-TURP syndrome.  Pseudohyponatremia occurs when the relative concentration or sodium does not change, but  "other" particles (protein, fats, etc) skew the percentages. The post-TURP syndrome cause of hyponatremia is still uncertain. 
     Hyponatremic patients with increased osmolarity can be from hypoglycemia. An increase in blood glucose draws water from the intracellular space, thus diluting the sodium concentration. When the glucose gets to the kidney tubules, it creates an osmotic diuresis and hypovolemia. 
    If the patient is hyponatremic with a decreased plasma osmolarity (<280), then the urine sodium concentration is needed to determine the cause. A high urine sodium here is due to renal, endocrine, SIADH, drugs, or medications. Common renal disorders here are polycystic kidney disease, pyelonephritis, ischemia, and renal artery stenosis. Endocrine disorders include addison's, hypothyroidism, and reset osmostat syndrome. When the urine concentration of sodium is low, consider vomiting (as the cause, don't actually consider vomiting), diarrhea, burns or water overload (but I think some of these causes,  like burns, should be pretty obvious...)
     The two most common medications that cause hyponatremia are diuretics and SSRIs. Most medications will cause euvolemic hyponatremia, like in SIADH. 
     Treatment can be broken down into urgent or non-urgent  Patients with neurologic symptoms need to be treated urgently to avoid cerebral edema or encephalopathy. They would be given hypertonic saline at 1-2 mmol/l/hr with a return to baseline to take 48 hours (slowly!!). Non-urgent treatment focuses on correcting the underlying cause. Fluid restriction (1-1.5L/day) should help as well. Demeclocycline can be used in some situations of severe, persistent hyponatremia. 
    So in summary, when you have a hyponatremic patient, check the BUN/cr, if it is less than 20, then check the plasma osmolarity, If it is low, then check urine Na concentration. 

A Brief Synopsis of AFPs "Diagnosis and Treatment of Acne"

A brief synopsis of: Diagnosis and Treatment of Acne
STEPHEN TITUS, MD, and JOSHUA HODGE, MD, Fort Belvoir Community Hospital Family Medicine Residency, Fort Belvoir, Virginia
http://www.aafp.org/afp/2012/1015/p734.pdf.
Am Fam Physician. 2012 Oct 15;86(8):734-740

     Acne is an inflammatory disorder of the skin. The pathophysiology starts with an increased production of sebum from the sebaceous glands. Hyperkeratinization of the follicles and colonization by Propionibacterium acnes leads to the inflammatory reaction.  Acne should first be characterized into mild, moderate, or severe, depending on the amount of inflammation, as well as the presence or absence of papules, pustules and nodules.  There is no "best" grading system.  If the patient only has comedones, they can be started on topical retinoid. If it is effective, then they they can be maintained on it. If there is mild inflammatory papules and pustules, they can be given the topical retinoid with benzoyl peroxide.  If it is effective, then need only be maintained on topical retinoid. If it is not effective or the patient has moderate inflammatory papules and pustules, they can be started on the topical retinoids, benzoyl peroxide and topical antibiotics (clindamycin or erythromycin).  Benzoyl peroxide is beneficial here because it reduces the  bacterial resistance of the other antibiotics.  If it is effective, they can be maintained on topical retinoid.
     If the patient has moderate inflammation with nodules or severe inflammation without nodules, the patient can use the topical retinoid, benzoyl peroxide  and oral antibiotics, such as doxycycline, minocycline, or tetracycline. TMP/SMX can be used as an alternative. If it is effective, then they can be maintained on topical retinoid and benzoyl peroxide.  If the patient has severe acne with nodules, the patient can be started on oral isotretinoin. Do to the teratogenicity of isotretinoin, it is imperative that the patient agrees to be on OCP concomitantly. A signed contract is done to impress the importance of this to the patient. They are also given graphic pamphlets to read. If the isotretinoin is effective, then they they can be maintained on topical retinoid, benzoyl peroxide, with or without topical antibiotics.  Topical retinoids have been shown to reduced relapses once oral antibiotics are discontinued.

A Brief Synopsis of AFP's "Chronic Fatigue Syndrome: Diagnosis and Treatment "

A brief synopsis of:
Chronic Fatigue Syndrome: Diagnosis and Treatment, JOSEPH R. YANCEY, MD, Fort Belvoir Community Hospital, Fort Belvoir, Virginia, SARAH M. THOMAS, MD, Fairchild Air Force Base, Washington
http://www.aafp.org/afp/2012/1015/p741.pdf
Am Fam Physician. 2012 Oct 15;86(8):741-746

     Chronic fatigue syndrome is one of the tougher diseases to deal with as a physician. We don't know what causes it, and don't have any real great way to treat it. It is seen more commonly in women over 40 years old. The CDC has created a list of criteria. The patient will have severe fatigue for at least six months, plus at least four of the following symptoms; a new headache, pain in multiple joints (without swelling or redness), myalgia, malaise after a period of exertion (which lasts at least 24 hours), short-term memory or concentration impairment, sore throat, unrefreshing sleep, and lymph node tenderness.
     The history and physical exam should focus on the patients' most bothersome symptoms. The patient should also be evaluated for depression, which is present in almost half of CFS patients. Lab work (UA,CBC, CMP, Ph, TSH, CRP) is used to rule out other causes of fatigue.  THERE IS NO TEST FOR CFS. There is no need for viral titers. Red flag symptoms including chest pain, focal neurological defects, inflammation, weight loss, lymphadenopathy, or dyspnea,  may indication a serious underlying illness.
     The etiology is confusing and complex. It is either immune, viral, adrenal, genetic, biopsychosocial,  sleep or nutrition based. Or it could be mixed. Research is ongoing.
     There is no great treatment for CFS since all the medications that have been tried in the past don't really do much. Obviously, the physician wants to treat the patient by managing the symptoms. The most common ones are sleep, depression and pain. As far as treatment for the CFS itself, the two evidence based treatments are CBT and graded exercise therapy. CBT helps the patient realize that the fear of the fatigue and malaise can actually perpetuate the symptoms.  The therapy needs to be individualized on a case by case basis by an expert. Graded exercise therapy is done by having the patient slowly work up to a goal of mild exercise of 30 minutes for 5 days a week. Overexertion should be avoided. Many patients choose walking for their exercise. Patients may benefit from regular visits by a physiotherapist. Effects of either of these therapies is moderate at best, with resolution unlikely.

A Brief Synopsis of AFP's "Diagnosis and Management of Osteomyelitis"

A synopsis of: Diagnosis and Management of Osteomyelitis
JOHN HATZENBUEHLER, MD, and THOMAS J. PULLING, MD, Maine Medical Center, Portland, Maine
 http://www.aafp.org/afp/2011/1101/p1027.pdf
Am Fam Physician. 2011 Nov 1;84(9):1027-1033.

     I was gonna read a different article today, but in the spirit of twitter, I am going to read the article the AFP just tweeted the link to...
     Osteomyelitis can be separated into acute or chronic, and also by mechanism of infection. Acute osteomyelitis presents within the first two weeks after an infection. Inflammatory changes are seen. In chronic osteomyelitis, necrotic bone is seen after 6 weeks. The infection can come from an open wound, exposed bone, or hematogenous spread. The most common bug is Staphylococcus aureus, followed by Group A strep, Streptococcus pneumoniae, and Kingella kingae. Groups B strep is seen mostly in newborns. Some other notable bugs are S. epidermidis,  P. aeruginosa, S. marcescens, E. coli,  as well as fungi and mycobacteria.
     Acute hematogenous osteomyelitis is most common in children (5 years old and younger) due to bacterial seeding of the highly vascular metaphyseal bone. Patients will present with systemic symptoms such as fever irritability, swelling, erythema, or tenderness over the infected bone. It will occur about two weeks after onset.  These patients usually require a shorter course of antibiotics (4 days IV, then 4 weeks PO). Immunocompromised patients may need up to 6 weeks of treatment.
     Chronic osteomyelitis will be seen with exposed bone, open fractures, bacteremia, and soft tissue infections. These are common in patients who are bedridden, in diabetic neuropathy, peripheral vascular disease, or condition with slow wound healing. This takes about three months to be an issue. It is rare for a prosthetic joint to be infected. The recurrence rate of chronic osteomyelitis is about 30%  a year. Those infected with P. aeruginosa have an even high recurrence rate. Parenteral antibiotics are recommended for 4-6 weeks in patients with chronic osteomyelitis. They will then be transitioned to oral medications for another two weeks.
     Hematogenous osteomyelitis is seen with patients who have an underlying disease, such as diabetes, chronic renal disease, IVDA or cancer. It is more common in adults. It affects the vertebrae, long bones, pelvis, and clavicle.
    Symptoms of osteomyelitis include fever, irritability, and lethargy. On physical exam, there should be a site of infection with swelling, bony tenderness, or erythema.  The lab work will show elevated WBC, CRP and ESR. Blood cultures may or may not be positive. Wound cultures are often times polymicrobial. A bone biopsy that correlates with the blood culture would be nice, but it happens less than half of the time.
 Imaging can be helpful. X ray will show osteomyelitis or a periosteal reaction after about 2 weeks and 50% bone loss. MRI can detect osteomyelitis within 3-5 days of infection. It can find necrotic bone, sinus tracts, and abscesses. Three-phase technetium-99 bone scintigraphy can also find osteomyelitis within a few days of disease onset. PET is affective as well, but expensive and not widely available.
   Treatment would ideally be driven by culture results. Often times this information is not available and broad spectrum empiric antibiotics are used. Children should be covered for S. aureus, or MRSA, if suspected. S. aureus can be treated with nafcillin, oxacillin, or cefazolin. MRSA can be treated with vancomycin. Clindamycin can be used in anaerobes. Ticarcillin/clavulanate can be used for enterobacteriaceae (E. coli) and anaerobes. Piperacillin/tazobactam can be used for enterobacteriaceae and P.aeruginosa. Fluoroquinolones are used in patients with penicillin allergies or diabetic foot ulcers.


   

A Synopsis of AFP's "Cutaneous Cryosurgery"

A Synopsis of; Cutaneous Cryosurgery
ETHAN E. ZIMMERMAN, MD, and PAUL CRAWFORD, MD 
Nellis Family Medicine Residency, Nellis Air Force Base, Nevada
http://www.aafp.org/afp/2012/1215/p1118.pdf
Am Fam Physician. 2012 Dec 15;86(12):1118-1124

     Cryotherapy is basically using liquid nitrogen to freeze part of your body to death. At low temperatures (-60'C) ice crystals form in the cells, break open, and the toxins and electrolyte come out.  It has excellent cosmetic results, low risk of infection, minimal aftercare, and can be used in pregnancy.  It can be very painful, so it should not be used on children younger than 7 years old. Topical lidocaine can be used to help relieve the pain. It is relatively contraindicated in patients with multiple myeloma, agammaglobulinemia, immunosuppression, raynaud disease and certain blood dyscrasias. 
     When using a spray gun, it should be held at a 90 degree angle about 1-2 cm away from the skin. There are different techniques, including tracing a spiral or going back and forth like using a paint brush. A cone shield can be used to avoid treating sensitive tissue that is in close proximity. 
     To treat a benign, superficial lesion, a Q-Tip dipped in liquid nitrogen is effective. When using the nitrogen spray, a continuous spray technique is used to minimize the depth of the tissue affected. When treating a malignant lesion,  it is important to freeze deep tissue. By using an intermittent spray technique,  an "ice ball" is created. An ice ball can penetrate down  up to 1 cm into the tissue.
     Cryotherapy has been very successful in treating genetal warts. Plantar warts and warts that are very large may need a longer treatment course. Cryotherapy may be combined with other therapy, such as salicylic acid, shaving down the lesion, intralesional steroids, or topical keratolytics.  Although cryotherapy has been used on molluscum contagiosum, patients should be aware that the lesions will resolve without treatment (in 6 months to two years).
     Actinic keratosis, bowen's disease, and keratoacanthoma (premalignant lesions) can be treated very effectively with cryotherapy. Biopsy should be performed beforehand. Lentigo maligna should be treated with excision if possible. Freezing pigmented nevi can cause atypical regrowth, which will need surgical excision anyway. It is difficult to differentiate melanoma form pigmented cells that were frozen. Referral to a dermatologist should be considered in difficult cases. 
     Treatment of a malignant lesion should be referred to a dermatologist.  Treatment of basal cell carcinoma and squamous cell carcinoma with low risk features may be undertaken.  A shave excision or curettage may need to be done beforehand. A 5 mm margin and depth is necessary for treatment to be considered successful. 
     After the therapy  the patient may experience bleeding, blisters, edema, pain, syncope or headaches. A dressing is not needed but if the area is large, then it may need daily cleansing with soap and water. The blister should turn into an echar in about 1-2 weeks. The area should be completely healed in about 4-6. The patient may end up with hypopigmentation, hair loss or permanent scarring in the area, but it is rare.

A Brief Synopsis of AFPs "Syphilis: A Reemerging Infection"

A brief synopsis of "Syphilis: A Reemerging Infection"
PETER L. MATTEI, MD, 87th Medical Group, Joint Base McGuire-Dix-Lakehurst, New Jersey, THOMAS M. BEACHKOFSKY, MD, 8th Medical Group, Kunsan Air Base, Republic of Korea, ROBERT T. GILSON, MD, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, OLIVER J. WISCO, DO, Harvard Medical School, Boston, Massachusetts
http://www.aafp.org/afp/2012/0901/p433.pdf
Am Fam Physician. 2012 Sep 1;86(5):433-440.

     Syphilis has been on the rise over the last decade, especially in men who have sex with men. It is spread by the transmission of Treponema pallidum through sexual contact. Primary syphilis is characterized by a single painless genital chancre, which develops about a week after infection.  Sometimes, (if the syphilis didn't read the micro book in disease school) the chancre may show up in the mouth, fingers, or nipple. There are times when more than one chancre appears (the nerve of that bug!).It is possible for the chancre to go undetected. 
     Secondary syphilis will occur 6-8 weeks after primary syphilis. Pinkish red macules and papules will appear on the face, trunk, mouth, and extremities. The patient may also develop syphilitic alopecia, which presents as "moth eaten"  hair. Occasionally the alopecia is the only symptom. Cutaneous mucosal papules can become macerated, warm, moist, flat and ulcerated. A sample from these cutaneous manifestations can reveal treponema under dark-field microscopy.
     Untreated secondary syphilis can progress to a latent stage, where the patient will appear symptomatic.  If the patient is in the latent stage for more than a year, it is classified as late latent, less than a year being classified as early latent. In the early latent phase, the patient can still infect others, whereas in the late phase, it appears that the patient cannot. 
     About a third of latent staged patients will progress to tertiary syphilis. It can present as either neurosyphilis, cardiovascular syphilis, or late benign syphilis. Neurosyphilis occurs when the treponema crossed the blood brain barrier. It can cause paresis, memory defects, or a cerebrovascular accident. It can cause changes in the posterior column of the spinal cord, causing tabes dorsalis (sensory ataxia of the legs). Patients infected with HIV have a greater risk of getting neurosyphilis.  Cardiovascular syphilis can affect the ascending aorta or similar vessels. Late benign syphilis occurs in about half of all patients with tertiary syphilis. It appears as granulomas, gummas, and psoriasiform plaques. 
     Transplacental transmission or direct contact with lesions during birth can cause congential syphilis. Two thirds of infected babies are symptomatic at birth.  Early signs (by age 4 years) are hepatosplenomegaly  fever, rash, seizures, a bulging fontanelle, or cranial nerve palsies. Common late signs (age 4-20 years) are hutchinson teeth (peg shaped upper central incisors), higoumenakis sign (unilateral enlargement of the proximal clavicle), mulberry moles (additional cusps on first molar), saddle nose (diminished nasal cartilage), or olympian brow(frontal bossing of forehead).
     Screening for syphilis is done with VDRL and RPR (nontreponemal serologic)  tests. They detect antibodies to cardiolipin in the blood. The test will not be positive until about a month after being infected.  IgM antibodies can be detected 2-3 weeks after being infected. Dark field microscopy can be used to directly visualize the pathogen within the lesion.  Patients who are positively screened should have a confirmatory test, such as the fluorescent treponemal antibody absorption assay or the T.pallidum particle agglutination test. If the screening test is negative, but there is strong clinical indication, a screen can be repeated in 2 weeks. Patients found to have syphilis should also be tested for HIV. Male patients who have sex with men should be tested for syphilis annually. 
     Treatment has not changed. In primary, secondary, and early latent syphilis, a single injection of penicillin G benzathine is given. Late latent or tertiary syphilis patients can be treated with three injections, one per week. Neurosyphilis requires IV aqueous crystalline penicillin G every four hours for up to two weeks.
     Within the first day of treatment, the patient can develop a Jarisch-Herxheimer reaction. The reaction is a acute fever in result of an increase of inflammatory cytokines from the pathogen lysis. within 3-6 months, the RPR/VDRL titer should decrease by fourfold. The pate will eventually seroconvert but if they don't it is called a serofast reaction. 
     

A Breif Synopsis of AFP's "Chlamydia Trachomatis Infections: Screening, Diagnosis, and Management"

A brief synopsis of:
Chlamydia Trachomatis Infections: Screening, Diagnosis, and Management
RANIT MISHORI, MD, MHS; ERICA L. McCLASKEY, MD, MS; and VINCE J. WINKLERPRINS, MD Georgetown University School of Medicine, Washington, District of Columbia 
http://www.aafp.org/afp/2012/1215/p1127.pdf 
Am Fam Physician. 2012 Dec 15;86(12):1127-1132.

     Chlamydia trachomatis is a gram negative bacteria. It is the most common (or at least most commonly reported) STD in the USA and the leading cause of infectious blindness in the world. It affects young adults (more often women) with multiple sex partners.  Most people are asymptomatic. Women may have discharge, vaginal bleeding, cervical friability and dysuria. Men may rarely have symptoms, which are pruritus, discharge, and dysuria. Patients who participate in anal sex may get a rectal infection and those who engage in oral sex may get a pharyngeal infection. Although patients diagnosed with gonorrhea are also treated for chlamydia, those infected with chlamydia are not also treated for gonorrhea. Complications include PID, infertility, and Fitz-Hugh-Curtis syndrome. Infection during pregnancy can cause miscarriage  PROM, preterm labor, low birth weight, and infant death.  Complications for men include epididymoorchitis and infertility. Patients may also get Reiters syndrome and chlamydia-induced reactive arthritis.
     The most sensitive test for diagnosis is nucleic acid amplification tests (NAATs) of a sample from the infected area or even from the urine. Rectal or oralpharyngeal swabs can be used as well. A wet mount will be positive for >10% WBCs/hpf for chlamydial or gonococcal infections. 
     Uncomplicated chlamydia can be treated with azithromycin, doxycycline, erythromycin, levofloxacin, or ofloxacin. Pregnant women can use azithromycin, amoxicillin or erythromycin.  They should also be rechecked after 3-4 weeks. If they are in their first trimester, they can be rechecked in the third trimester. 
     Sexual partners should be notified, treated, and referred for evaluation. They should contact anyone they have had sexual contact with in the last 60 days. They should also abstain form intercource for seven days after the medication is complete. patients can be retested within a year.
   It is recommended that all sexually active women 24 years and younger be screened for chlamydia. Women 25 years and older who have had multiple sexual partners or who have a new sexual partner should be screened as well. All pregnant women should be screened at their first prenatal visit. Men should only be screened if they are in a setting of high prevalence, such as prison or an STD clinic. Men who participate in risky behavior, such as having sex with other men, should also be screened (for genetial and rectal infection if necessary). Urine screening can be done annually in men who have had insertive (rather than receptive) anal intercourse within the last year.
     C. trachomatis can also cause lymphogranuloma venereum (LGV). It presents as a unilateral, tender node in the inguinal or femoral area. It can also cause proctocolitis, rectal discharge, pain, constipation, fissures, strictures or tenesmus. Treatment consist of doxycycline or erythromycin. 
     Neonatal pneumonia can affect infants born to mothers with active chlamydia during labor. It will occur 1-3 months after birth. Symptoms consist of tachypnea and a staccato cough. DIffuse bilateral infiltrates and hyperinflation may be seen on x ray. Lab work may show eosinophilia. Treatment consists of erythromycin. 
     There are three types of ocular infections caused by chlamydia. Neonatal conjunctivitis/ophthalmia neonatorum will present in up to one third of child of chlamydia infected mothers during labor. The patient will have conjunctival injection, discharge, and swollen eyelids. Culture is taken from the everted eyelid. Treatment consists of oral erythromycin or ethylsuccinate. (Silver nitrate protects against gonorrhea, not chlamydia).  Adult inclusion conjunctivitis is a mucopurulent infection associated with the genitourinary infection. The everted eyelid should be cultured. Treatment is with doxycycline or azithromycin. Trachoma is a chronic or recurrent eye infection. it can cause abnormal positioning of the eyelash and lead to scarring of the eyelids. It is the largest cause of blindness worldwide. It is spread through poor hygiene, direct contact and flies. Treatment consists of erythromycin, azithromycin, or doxycycline.

A Synopsis of AFPs "Failure to Thrive: An update"

Failure to Thrive: An Update
SARAH Z. COLE, DO, Mercy Family Medicine Residency, St. John’s Mercy Medical Center, St. Louis, Missouri, JASON S. LANHAM, MAJ, MC, USA, Eisenhower Army Medical Center, Ft. Gordon, Georgia
http://www.aafp.org/afp/2011/0401/p829.pdf
Am Fam Physician. 2011 Apr 1;83(7):829-834.

     Failure to thrive (FTT) is defined as a child's lack of appropriate growth or growth maintenance when values are plotted on standardized growth charts. There are common criteria to diagnose FTT. The parameters are:

< 5%ile of BMI, weight, weight velocity, OR length for age,
Weight gain dropping past 2 major %ile lines,
Weight < 75% of median weight for age OR length.

A child with true FTT should have a combination of more than one of the above criteria. Weight for length is the best indicator for nutritional treatment. Some patients, such as premature infants, those with small parents, or who were LGA babies may deviate from the charts. 
     The most common cause seen in the office is due to inadequate calorie intake. Inadequate absorption and excessive caloric expenditure are also issues. Inadequate caloric intake can be due to improper breastfeeding technique, problems transitioning to solid food, insufficient calorie consumption, excessive juice drinking, or parents not giving high calorie foods (baby diets).  GERD, IBS, or improper formula preparation can also be the culprit. Parents may not be knowledgeable about proper nutrition, not capable of understanding nutrition, or simply not being able to afford it. Neglect or abuse could also be the cause. Inadequate calorie absorption can occur through emesis, celiac disease, chronic diarrhea, food allergies, or inborn metabolic errors. Excessive caloric expenditure could be from thyroid disease, chronic pulmonary disease, congenital heart disease, malignancy or immunodeficiency.
     A detailed history is as important as with any other patient. Questions should be asked about eating habits, proper latching techniques, and a quantification as to how much the patient consumes during breast feeds. If the patient is a toddler, it is important to differentiate between a picky eater and a toddler who is refusing food.  Food journals and measuring caloric intake can be helpful as well.  A review of symptoms that detects recurrent infections, respiratory problems, vomiting, diarrhea, may be due to an organic problem. Red flag signs for an organic cause include:

cardiac findings, 
developmental delay, 
dysmorphic features,
failure to gain weight even with proper calorie intake,
recurrent respiratory, urinary or mucocutaneous infections,
or recurrent vomiting, diarrhea, or dehydration.

When these red flags are seen, lab testing should be considered. Studies show that when an organic symptom was not found, almost all of the patients were determined to have a behavioral cause for the FTT. A psychosocial history is important from the caregiver and the child, if possible. 
     During a physical examination, proper weight and height measurements should be rechecked. The physician should have the infant undressed for an accurate weight and to observe for signs of abuse or neglect. Positive signs of malnutrition through neglect or abuse will necessitate a hospital admission. 
     Treatment consists of treating the organic cause of FTT. If there is no organic cause, the parent should be given guidance for catch up growth and counseling.  Calorie dense food or formulas, or formula supplementation in breast fed infants can help. The patient should avoid excessive juice or milk. Gravies, sauces, and butter can be added to increase calories to meals. Medications such as megestrol or cyproheptadine promote weight gain, but have not been studied for cases of FTT.
     If untreated, malnutrition can lead to developmental and cognitive problems. Low birth weight preterm infants with FTT have long term problems such as poor academic performance and lower cognitive abilities. They have a smaller statute as well. Results of whether normal birth weight infants who become FTT have long term issues are mixed. Some studies show poorer math skills and shorter statue, while others show no change in IQ. Regardless of the studies, proper prevention is the key to reducing long lasting effects in these patients.

A Synopsis or AFP's "Vaginitis: Diagnosis and Treatment"

 A synopsis of; Vaginitis: Diagnosis and Treatment
BARRY L. HAINER, MD, and MARIA V. GIBSON, MD, PhD, Medical University of South Carolina, Charleston, South Carolina 
http://www.aafp.org/afp/2011/0401/p807.pdf
Am Fam Physician. 2011 Apr 1;83(7):807-815.

     The three most common causes of vaginitis are bacterial, candidiasis, and trichomoniasis. Bacterial vaginosis is caused by the colonization of gardnerella, mycoplasma, or anaerobic bacteria such as prevotella or mobiluncus. A fishy odor will be present. It is unlikely that bacterial vaginosis is present without a perceived odor .The fishy odor is from the amines that are created by the anaerobic bacteria. The odor becomes more prevalent after menses or unprotected sex (sperm in the vagina) because of the increase in vaginal pH. The discharge may be clear, white or gray. There is no pain, pruritus  or inflammation. It is asymptomatic in up to half of those infected. It is associated with late miscarriages, PROM, preterm birth and increased risk of HIV transmission. Diagnosis can be done using the Amsel criteria. The four parts are:
-thin, homogenous discharge
-vaginal pH >4.5 (normal is 4-4.5)
-positive whiff test 
- > 10% clue cells
The whiff test is done by adding 10% KCl to the culture. A unique odor is produced. Clue cells are vaginal epithelial cells covered in coccobacilli, which obscures the cell border when placed on a wet mount. Three of the Amsel criteria are needed for it to be positive, but 2 of the criteria are just as sensitive. 
     Treatment consists of clindamycin or metronidazole. A one time dose of 2g metronidazole is no longer recommended. It should be given as 500 g twice a day for a week. Topical or oral medications can be used, depending on patient preference (metronidazole has an unpleasant, metallic taste). Screening pregnant women for asymptomatic bacterial vaginitis is not recommended. 
     Trichomoniasis causes dyspareunia, vaginal soreness, and dysuria. The patient may present with the classic "strawberry cervix". Whiff test will be positive. The vaginal pH will be >5.4. A wet mount should show trichomonads, which are a flagellated organism slightly larger than WBCs. Tricomonads can be found on examation of the vagianl fliud or in a centrifuged urine sample. PCR can be done as well. Treatment can be done with metronidazole, with the dosage and frequency individualized for patient comfort. Sexual partners need to be treated as well. Intercourse should be halted until treatment is complete and the patient is asymptomatic. Because of the risk of low birth weight infants, trichomoniasis can be treated in pregnant women after 37 weeks gestation. 
    Candidiasis is a common infection that most woman have in their lifetime. Symptoms consist of itching, burning, vaginal soreness, pain with sexual intercourse, and a thick, cheesy, white discharge. It is odorless. Vaginal pH is normal. Microscopic examination should show budding yeast. A rapid yeast detection test is also available and inexpensive. PCR is an expensive alternative. Treatment is categorised as either complicated or uncomplicated.  Uncomplicated illness is considered mild to moderate. The patient will have less than 4 episodes a year. Hyphae or pseudohyphae will be visible on microscopy. Complicated disease will be moderate to severe. There will be four or more episodes per year. On microscopy, only budding yeast will be seen. Complicated patients may also be pregnant, have diabetes, or be immunocompromised. Uncomplicated candidiasis will require a short course of antifungal medication, where as complicated patients will need a more intense, longer course of medication. 
    Atrophic vaginitis is due to estrogen deficiency. It can cause vaginal dryness, pruritus, discharge, irritation or pain during intercourse. Topical estrogen cream or the estradiol vaginal ring have been effective with minal side effects. 
    The last cause of vaginitis are allergic or irritant contact dermatitis. This can be from latex condoms, spermicide, feminine hygiene products, among many other causes. The cure is removal of the offending product. 

A Synopsis of AFP's "Heel Pain"

A synopsis of; Diagnosis of Heel Pain
PRISCILLA TU, DO, and JEFFREY R. BYTOMSKI, DO, Duke University, Durham, North Carolina
http://www.aafp.org/afp/2011/1015/p909.pdf
Am Fam Physician. 2011 Oct 15;84(8):909-916


      This is a review of an article discussing some of the mechanical causes of heel pain. It is broken up into plantar heel pain, posterior heel pain, and midfoot heel pain. The most common cause of plantar heel pain is plantar fasciitis. There is a more extensive review of plantar fasciitis in an earlier post (plug!). The pain occurs after a long rest or when first getting out of bed in the morning. Pain is worse with passive dorsiflexion of the foot or toes. Tenderness is found at the medial calcaneal tuberosity and plantar fascia. Ultrasound may show a heel aponeurosis of at least 5 mm. Treatment consists of rest, stretching, exercise, pain medication, anti-inflammatory meds, and ice. Orthotics, heel cups and night splints are available over the counter. Steroid injections or extracorporeal shock wave therapy are other options, as well as surgical transection of the plantar aponeurosis. If treatment is not working, a neuroma should be considered.  It presents similarly to plantar fasciitis, but the pain is characterized as burning or tingling. It may feel like a "painful lump" on palpation.
     Calcaneal stress fractures are the second most common stress fracture in the foot (metatarsal fracture is the first). Pain is seen with weight bearing activity or when walking on a hard surface. It is common in soldiers who do a lot of marching and in people who enjoy running on the road. Unlike plantar fasciitis, the patient will have pain at rest. There may also be swelling, point tenderness or ecchymosis on the posterior portion of the heel. Imaging will not show the fracture for about 2-3 weeks, when healing occurs. Treatment consists of not bearing weight on the area, and rest. Orthotic devices, such as heel pads or walking boots may help.
     Heel pad syndrome presents as a deep soreness upon palpation of the middle of the heel. It is worse when walking barefoot, on hard surfaces, or during periods of prolonged weight bearing. Treatment consists of rest, ice, anti-inflammatory medications, or pain medications. Taping, heel cups and proper footwear will help as well.
     HPV can present as a plantar wart. It should be evident on inspection. Treatment consists of topical medication, laser therapy, cryotherapy, or shaving it off.
     The causes of posterior heel pain are achilles tendinopathy, a haglund deformity, or sever disease. Achilles tendinopathy is pain at the insertion point or in the belly of the tendon. It can be caused by wearing high heels, fluoroquinolone use, running, or calf overuse. The pain may feel achy or sharp, and it will worsen with activity or with passive foot dorsiflexion. The tendon will be tender to palpation. Ultrasound may show thickening of the tendon. X ray may show calcification. Treatment can be done with pain and anti-inflammatory medications, orthotic devices, and muscle lengthening through eccentric stretching. Nitroglycerin patches and injections of platelet rich plasma can help as well. Surgery may be necessary if debridement is needed. Tendinopathies can also occur at the insertion of the posterior tibialis, flexor digitorum longus, flexor hallucis longus or peroneal tendons.  This would cause medial or lateral heel pain, depending on which tendon is involved. Treatment is the same as for the achilles.
     Haglund deformity is a bony prominence that forms on the posterior portion of the calcaneus. It is commonly called "pump bump" because young women who wear high heels or poorly fitting shoes develope inflammation and swelling in the area. It can lead to bursitis between the calcaneus and achilles tendon (retrocalcaneal). Treatment consists of turning in the heels for some open heeled shoes, corticosteroid injections, pain medications and anti-inflammatories. PT can also reduce the pain. Surgery may be needed to remove the deformity.
     Sever disease is where the achilles tendon pulls away from its insertion to the bone. It is more common in young, growing children. The combination of bone growth occurring faster than the muscles and tendons, with the repetitive running and jumping activities in a childs life, create microtrauma in the area. The patient will present with pain, swelling and tenderness at the insertion point of the tendon. Treatment consist of....you guessed it.... ice, pain meds, anti-inflammatories, stopping the offending activity, as well as stretching and strengthening the calf muscle.  Don't let me forget about orthotics!
     Along with tendinopathy, the midfoot heel pain syndromes are the tarsal tunnel syndrome and sinus tarsi syndrome. The tarsal tunnel is the the space consisting of the flexor retinaculum, medial calcaneus, posterior talus, and medial malleolus. Pain and numbness of the posteriormedial ankle and heel occurs when the posterior tibial nerve is compressed when passing through this tunnel. Pain is worse with standing, walking, or running. It is better with rest or with comfortable footwear. Patients who are flat footed (pes planus deformity) may be at increased risk. Tinel sign will be positive. Passively causing the nerve to stretch or flex may exacerbate the pain. Treatment consists of orthotics, anti-inflammatories, activity modification, steroid injections, TCA's and antiepileptics.
     The sinus tarsi is a tunnel that runs laterally to medially (or medially to laterally if you are are lefty) though your heel. The borders of the tunnel consist of the calcaneus,  talus, talocalcaneonavicular joint, and subtalar joint. Pain is located on the lateral part of the ankle. It is worse after exercise or walking on uneven surfaces. It can be exacerbated by multiple episodes of foot hyperpronation or lateral ankle sprains. You can only guess what the treatment is.

A Synopsis of AFPs "Practice Guidelines: AUA Guideline Addresses Diagnosis, Evaluation, and Follow-Up of Asymptomatic Microhematuria"

Practice Guidelines: AUA Guideline Addresses Diagnosis, Evaluation, and Follow-Up of Asymptomatic Microhematuria
http://www.aafp.org/afp/2013/0501/p649.pdf
Am Fam Physician. 2013 May 1;87(9):649-653.


     Asymptomatic microhematuria is defined as the presence of 3+ RBC's per HPF. A positive dipstick by itself is not enough to call it asymptomatic microhematuria. Benign causes, such as infection, menstruation, exercise, trauma, or a recent procedure can be ruled out through a proper history and physical. Renal function can be assessed through a GFR, serum creatinine, and BUN. If proteinuria, cellular casts, or dysmorphic RBCs are found, then a further nephrogenic workup is in order.  Patients over 35 years old or those with risk factors (irritation with voiding, smoking, chemical exposure) should undergo a cystoscopy.
     Imaging with a multiphasic CT urography (with or without contrast) is the best choice. Magnetic resonance urography or combining CT with ultrasound can be used if needed. A retrograde pyelogram can be used to evaluate the entire upper tract.  Urine cytology, blue light cytology and urine markers are not recommended routinely. Patients with persistent microhematuria may find cytology helpful after a negative workup, especially if the patient has multiple risk factors. 
     If the workup is negative, but the patient is still having persistent asymptomatic microhematuria, yearly UA can be done. After two negative workups, the evaluation can be repeated after 3-5 years. 

An uncomplicated Synopsis of AFP's "Diagnosis and Management of Acute Diverticulitis"

A brief synopsis of:
Diagnosis and Management of Acute Diverticulitis, THAD WILKINS, MD; KATHERINE EMBRY, MD; and RUTH GEORGE, MD, Georgia Regents University, Augusta, Georgia
http://www.aafp.org/afp/2013/0501/p612.pdf

Am Fam Physician. 2013 May 1;87(9):612-620.

     Diverticulitis is simply inflammation of the colon. If there is an associated abscess, phlegmon, obstruction, bleeding, fistula, or perforation, then it is known as complicated diverticulitis. Asians more commonly have it in the ascending colon, whereas westerners have it in the sigmoid and descending colon. If there is no inflammation and only outpouching (diverticula), it is known as diverticulosis. There is a genetic prevalence in diverticulitis, but lack of dietary fiber, lack of exercise, aspirin use, NSAID use, and obesity are contributing factors. 
    The diverticulitis patient will present with constant, acute LLQ pain. The patient may also have fever, constipation, nausea, diarrhea, dysuria and anorexia.  Symptoms such as rebound tenderness, rigidity, and lack of peristalsis would suggest peritonitis over diverticulitis. Pregnancy should be ruled out, and a CBC can be done to look for an elevated WBC. An FOBT may be conducted to rule out occult GI bleeding. A CRP above 50 mg/L in a patient who isn't vomiting is highly suggestive of acute diverticulitis. A CT may show bowel wall thickening, fat stranding, free air, abscess, or inflammation. 
     If the severity is mild, without peritoneal signs,  and the patient can tolerate PO intake, then the patient can be treated on an outpatient basis. The patient would be given a clear liquid diet with a follow up appointment in 2-3 days. If the symptoms persist, then an antibiotic can be started, such as TMP/SMX, Augmentin, or fluoroquinolones. 
     If the patient is having moderate/ severe symptoms, peritoneal signs, or mild symptoms that are persistent,  suspicion of complicated diverticulitis may be in order. The patient may not tolerate PO intake.  At this point, the patient should be admitted.  IV fluids and antibiotics, such as Zosyn, Timentin, Invanz, Tygacil, or fluoroquinolones can be given. If the diverticulitis appears life threatening, Primaxin, Meropenem or Doripenem can be considered.  In about 2-4 days, the fever should resolve, pain should decrease, and WBC should normalize. Patients should be transitioned from IV to oral antibiotics once a clinical improvement is seen. If the patient is not improving and imaging shows abscess or obstruction, then a surgical consult may be in order  A localized abscess may need CT-guided drainage. Surgical colectomies have been on the decline, with laparoscopic drainage, washout or resection on the rise. A colonoscopy is recommended in complicated diverticulitis, 4-6 weeks after resolution. 
     Prevention includes increasing dietary fiber, more exercise, and weight loss in overweight patients. The theory that eating seeds, nuts, or popcorn increases the likelihood of diverticulitis has been debunked. 
    

A Two Minute Review of AFP's "Psoriasis"

A brief synopsis of
Psoriasis, NANCY WEIGLE, MD, Duke University School of Medicine, Durham, North Carolina, SARAH McBANE, PharmD, University of California, San Diego, Skaggs School of Pharmacy  and Pharmaceutical Sciences, La Jolla, California
http://www.aafp.org/afp/2013/0501/p626.pdf
Am Fam Physician. 2013 May 1;87(9):626-633.

     Psoriasis is a rather common skin condition presenting as red, itchy, painful, scaly patches. There is a genetic component, but it is an immune mediated disease. It can be associated with stress, smoking, trauma, obesity, alcohol, and recent infection. The most common type is plaque psoriasis. The rash is well circumscribed and often coalesces. It is found on the extensor surfaces of the arm, legs, scalp, trunk and buttocks. Inverse psoriasis is less scaly than the plaque version. It occurs on the flexor surfaces and skinfold areas of the inguinal, intergluteal, axillary and perineal area. Erythrodermic psoriasis is accompanied by systemic symptoms, widespread edema and plaques. A localized pustular psoriasis forms on the palms and soles. It can be acute and life threatening. Guttate psoriasis presents as fine scaling and small pink papules located on the trunk. It is seen in young patients and those with a recent staph URIs.
     Nondermatologic manifestations are also prevalent. The majority of patients will also have psoriatic onychodystrophy, a nail disease. This will present as pitting, separation from the nail bed, and hyperkeratosis. It is very resistant to treatment. Psoriatic arthritis is also common. It is a seronegative inflammatory syndrome that presents about 12 years after the onset of the skin manifestations. OH, yeah, it affects the joints.
     Patients with psoriasis have an increased risk of other illnesses. There is a psychologic component,  causing social isolation, depression, and an overall feeling of unattractiveness. Patients often feel like the physician has neglected them. There is also an increased risk of crohn's, UC, squamous cell carcinoma,  lymphoma, metabolic syndrome, obesity, and heart attack.
     Treatment can be divided between disease severity. Mild/moderate disease covers less than 5% of the total body surface. It does not affect the hands, feet, face, or genitals. Treatment includes topical preparations of corticosteroids, vitamin D analogs, tazarotene, and calcineurin inhibitors (tacrolimus and pimecrolimus).  Steroids can have adverse and systemic side effects such as skin atrophy, irritation, and impaired wound healing. The symptoms will return once the corticosteroids are discontinued. Calcipotriene and calcitriol (vitamin D analogs) take longer to kick in, but the effects last longer. They  may cause hypercalcemia and parathyroid hormone suppression. Tazarotene is a topical retinoid that is similar in effectiveness to steroids, with a longer lasting benefit. Tacrolimus is better than pimecrolimus.
     Severe psoriasis presents with involvement of more than 5% total body surface area. It may affect the hands feet, face or genitals. It can be treated with phototherapy and methotrexate, cyclosporine, or acitretin. "Second tier medications" include azathioprine, hydroxyurea, sulfasalazine, leflunomide, tacrolimus and thioguanine. Methotrexate should be taken with folic acid to reduce side effects. Cyclosporine has many drug interactions, but can be used as a bridge therapy due to its rapid onset. Acitretin is a retinoid that takes about 3-6 months to be effective. Because is is teratogenic, it may cause hyperlipidemia, mucocutaneous lesions, or live damage. 
     Newer biological therapy is effective in severe psoriasis. Thery are different TNF inhibitors, such as adalimumab, etanercept, and infliximab. Infliximab has the most rapid clinical response. Etanercept is often given with methotrexate. With biologic agents, it is important ti watch for serious infecions, such as TB. They could also result in lupus like syndromes, liver issues, demylenating disorders, or heart failure axacerbation.