Leukemia: An Overview for Primary Care
MONICA D. MEAD, MD, University of California–Los Angeles, Los Angeles, California
Am Fam Physician. 2014 May 1;89(9):731-738.
Leukemia is caused by an uncontrolled stem cell proliferation in the bone marrow. The four subtypes include acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), chronic lymphocytic leukemia (CLL), and chronic myelogenous leukemia (CML). Risk factors include radiation exposure (as little as a couple of CT's), Down syndrome, neurofibromatosis, benzene, or household pesticides exposure in utero or in the first 3 years of life.
ALL is most common in children and young adults. Signs and symptoms include fever, lethargy, bleeding, muscle aches, and enlargement of the spleen, liver or lymph nodes. Blast cells are seen on peripheral smear or bone marrow aspirate. AML is mostly in adults. Symptoms include fever, fatigue, weight loss, shortness of breath, chest pain, bruising, nosebleeds, and menorrhagia. Pain is not common.
Chronic leukemia is often discovered incidentally and is more common in adults. CLL may present with an enlarged liver, spleen or lymph nodes. CML may present solely with splenomegaly. Bleeding and bruising are rare in chronic leukemia.
Leukocytosis is the first laboratory indication of possible leukemia. The type of WBC proliferation will help guide diagnosis. Monocyte predominance is seen in chronic infections, such as connective tissue disorders or TB. Basophilia is common in viral infections or inflammatory conditions. Lymphocytosis is seen in EBV, CMV, TB, pertussis, or asplenia. Eosinophilia is seen in parasitic, allergic or connective tissue disorders. Neutrophil predominance can be due to inflammation, stress, drugs, or infection.
The criteria to order a peripheral smear includes leukocytosis, WBC count >20,000/uL, enlarged liver, spleen or lymph nodes, constitutional symptoms (fatigue, fever, night sweats) or anemia thrombocytopenia, or thrombocytosis.
Acute leukemia will have an increase in hematopoietic precursor blast cells. AML will have auer rods on peripheral smear or with immunophenotyping (which is done using flow cytometry or cytogenetic testing). Chronic leukemia will present with a clonal expansion of B lymphocytes (>5000/uL). Bone marrow aspiration is not necessary. CML will have the Philadelphia chromosome on immunophenotyping.
Treatment of leukemia should be left up to the heme-onc specialists. Tumor lysis syndrome can occur with treatment. The destroyed cancer cells can cause electrolyte disturbances and renal injury. Patients who receive immunosuppression therapy may present with a neutropenic fever, prompting the use of broad spectrum antibiotic therapy. Survivors of leukemia have an increase risk of other cancer subtypes, especially ALL later in life. Children also have an increased risk of joint osteonecrosis.
Medicine changes every day. Every day is an opportunity to become better than the day before.
Thursday, June 12, 2014
Wednesday, June 11, 2014
A Synopsis of AFP's "Neglected Parasitic Infections: What Every Family Physician Needs to Know"
Neglected Parasitic Infections: What Every Family Physician Needs to Know
DANA WOODHALL, MD; JEFFREY L. JONES, MD, MPH; PAUL T. CANTEY, MD, MPH; PATRICIA P. WILKINS, PhD; and SUSAN P. MONTGOMERY, DVM, MPH, Centers for Disease Control and Prevention, Atlanta, Georgia
Am Fam Physician. 2014 May 15;89(10):803-811
This article will focus on four parasitic infections; Chagas disease, toxocariasis, cysticercosis, and toxoplasmosis. Chagas disease is caused from the parasite Trypanosoma cruzi. The CDC lifecycle can be found HERE. In a nutshell, a "kissing" bug (triatomine) bites a human and infects him or her with the parasite that it contracted from biting another human. It can also be spread through blood transfusion, organ transplantation, contaminated food, or congenitally. It is endemic to Mexico, Central and South America. It is usually asymptomatic, but it can cause conduction problems, heart failure, megacolon, megaesophagus, stroke, or cardiac disease. Treatment consists of Benznidazole and nifurtimox. Pregnant patients should not be treated because of adverse side effects. Congenital infections include anemia, low birth weight, low Apgar scores, thrombocytopenia, myocarditis, encephalitis, or hepatosplenomegaly.
Toxocariasis is caused by roundworms Toxocara canis and T. Cati. The CDC lifecycle can be found HERE. Humans become infected by either eating contaminated, undercooked meat, or by ingesting soil that has been contaminated with parasitic eggs from infected dogs or cats. Most patients are asymptomatic (covert toxocariasis). Young children (2-4 years old) present with visceral toxocariasis, an inflammatory response characterized by fever, wheezing, coughing, abdominal pain, anorexia, and fatigue. Older children (5-8 years old) may present with ocular manifestations including strabismus, granulomas, granulomatous masses, vision loss, or granulomas with traction bands. Serological testing is available. Treatment includes albendazole and mebendazole, with steroids it there is inflammation.
Cysticercosis is caused by an infection from the parasite Taenia Solium. The lifecycle can be found on the CDC website HERE. There are two cycles to this parasite. Humans can be infected by eating infected, undercooked pork, which manifest as intestinal tapeworms. Humans can also be infected through fecal-oral contact with the feces of other infected humans (which will contain eggs). The eggs with hatch and develop cysterci in various organs, including muscle, brain, and eyes. Symptoms include cysterci lumps under the skin, seizures, meningitis, headaches, intracranial hypertension, or hydrocephalus. Diagnosis is done with serology and imaging. Treatment consists of symptomatic control, steroids, and albendazole.
Toxoplasmosis is due to an infection with Toxoplasma gondii. The CDC chart can be found HERE. Humans are infected through ingestion of raw, contaminated meat, contaminated water, or fruits and vegetables contaminated with cat feces (in the soil). Cats can shed parasites in their feces (we have all heard about pregnant women and litter boxes). Most patients are asymptomatic, but some may present with flu-like symptoms or encephalitis. Congenital toxoplasmosis can result in a miscarriage. Testing includes immunoglobulin serology and a toxoplasma avidity test. Amniotic fluid can be tested as early as 18 weeks gestation. Treatment is usually not necessary, but when it is, Pyrimethamine, sulfadiazine or leucovorin are used.
DANA WOODHALL, MD; JEFFREY L. JONES, MD, MPH; PAUL T. CANTEY, MD, MPH; PATRICIA P. WILKINS, PhD; and SUSAN P. MONTGOMERY, DVM, MPH, Centers for Disease Control and Prevention, Atlanta, Georgia
Am Fam Physician. 2014 May 15;89(10):803-811
This article will focus on four parasitic infections; Chagas disease, toxocariasis, cysticercosis, and toxoplasmosis. Chagas disease is caused from the parasite Trypanosoma cruzi. The CDC lifecycle can be found HERE. In a nutshell, a "kissing" bug (triatomine) bites a human and infects him or her with the parasite that it contracted from biting another human. It can also be spread through blood transfusion, organ transplantation, contaminated food, or congenitally. It is endemic to Mexico, Central and South America. It is usually asymptomatic, but it can cause conduction problems, heart failure, megacolon, megaesophagus, stroke, or cardiac disease. Treatment consists of Benznidazole and nifurtimox. Pregnant patients should not be treated because of adverse side effects. Congenital infections include anemia, low birth weight, low Apgar scores, thrombocytopenia, myocarditis, encephalitis, or hepatosplenomegaly.
Toxocariasis is caused by roundworms Toxocara canis and T. Cati. The CDC lifecycle can be found HERE. Humans become infected by either eating contaminated, undercooked meat, or by ingesting soil that has been contaminated with parasitic eggs from infected dogs or cats. Most patients are asymptomatic (covert toxocariasis). Young children (2-4 years old) present with visceral toxocariasis, an inflammatory response characterized by fever, wheezing, coughing, abdominal pain, anorexia, and fatigue. Older children (5-8 years old) may present with ocular manifestations including strabismus, granulomas, granulomatous masses, vision loss, or granulomas with traction bands. Serological testing is available. Treatment includes albendazole and mebendazole, with steroids it there is inflammation.
Cysticercosis is caused by an infection from the parasite Taenia Solium. The lifecycle can be found on the CDC website HERE. There are two cycles to this parasite. Humans can be infected by eating infected, undercooked pork, which manifest as intestinal tapeworms. Humans can also be infected through fecal-oral contact with the feces of other infected humans (which will contain eggs). The eggs with hatch and develop cysterci in various organs, including muscle, brain, and eyes. Symptoms include cysterci lumps under the skin, seizures, meningitis, headaches, intracranial hypertension, or hydrocephalus. Diagnosis is done with serology and imaging. Treatment consists of symptomatic control, steroids, and albendazole.
Toxoplasmosis is due to an infection with Toxoplasma gondii. The CDC chart can be found HERE. Humans are infected through ingestion of raw, contaminated meat, contaminated water, or fruits and vegetables contaminated with cat feces (in the soil). Cats can shed parasites in their feces (we have all heard about pregnant women and litter boxes). Most patients are asymptomatic, but some may present with flu-like symptoms or encephalitis. Congenital toxoplasmosis can result in a miscarriage. Testing includes immunoglobulin serology and a toxoplasma avidity test. Amniotic fluid can be tested as early as 18 weeks gestation. Treatment is usually not necessary, but when it is, Pyrimethamine, sulfadiazine or leucovorin are used.
Monday, June 9, 2014
A Synopsis of AFP's "Surgical and Nonsurgical Management of Gallstones"
A Synopsis of:
Surgical and Nonsurgical Management of Gallstones
SHERLY ABRAHAM, MD; HAIDY G. RIVERO, MD; IRINA V. ERLIKH, MD; LARRY F. GRIFFITH, MD; and VASANTHA K. KONDAMUDI, MD, The Brooklyn Hospital Center, Brooklyn, New York
Am Fam Physician. 2014 May 15;89(10):795-802
http://www.aafp.org/afp/2014/0515/p795.pdf
Gallstones are made of cholesterol or calcium. Risk factors for gallstone formation include diabetes, obesity, metabolic syndrome, dyslipidemia, hyperinsulinemia, and high-calorie diets. Typical presentation includes abrupt, steady, right upper quadrant pain. Pain peaks within one hour and resolves after the stone passes (1-5 hours). Complications include acute cholecystitis (fever, leukocytosis, RUQ pain), cholangitis (charcot's triad is fever, jaundice and abdominal pain), and gallstone pancreatitis (sphincter of Oddi obstruction). Choledocholithiasis is an obstruction of the common bile duct. Risk factors include symptoms of cholangitis, a bilirubin level above 4 mg/dl, or a common bile duct wider than 6mm.
Ultrasound is the first line choice of imaging because of cost and low invasiveness. CT is superior to ultrasound, but it is more expensive and has radiation exposure. MRCP is a second line choice as well.
HIDA scan is used to visualize the biliary tree and assess liver and gallbladder function. The patient is given iminodiacetic acid which can be detected with a gamma camera as it travel through the liver and gallbladder in the bile. ERCP is diagnostic and therapeutic because is can be used to retrieve the stone, add a stent, or collect a biopsy.
Treatment depends on several factors. If the gallstone is asymptomatic, the patient can be followed clinically or sent for laparoscopic cholecystectomy. Symptomatic patients should be treated with NSAIDs or narcotics (meperidine or ketorolac). Scopolamine is not as effective. Complications (choledocholithiasis, cholecystitis, pancreatitis) may be referred to surgery as well. If the patient is not a candidate for surgery, treatments such as oral dissolution therapy or extracorporeal shock wave therapy can be considered. Oral dissolution therapy is best with gallstones 5 mm or smaller, although the therapy can take up to two years. Patients with calcified gallbladders, hemolytic anemia, stones larger than 3 cm, morbid obesity undergoing bariatric surgery, native american heritage, or bladder dysmotility are exceptions to expectant management.
Antibiotic prophylaxis is generally not required for laparoscopic cholecystectomy. High risk patients may benefit from a single dose of cefazolin.
Pregnant patients should not be given NSAIDs. Meperidine is appropriate. Ursodeoxycholic acid is another option. Surgery can be considered for patients in recurrent or intractable pain.
Friday, June 6, 2014
A Synopsis of AAFP's "Update on Latent Tuberculosis Infection"
Update on Latent Tuberculosis Infection
Hartman-Adams H, Clark K, Juckett G
June 1 2014 Vol. 89 Number 11
Tuberculosis affects about one third of the world's population. The classic symptoms include cough, hemoptysis, weight loss, fever, and night sweats. Approximately 10-15% of these people have latent infection. 5-10% of latent infections progress to active disease, which will occur within 2 years for half of these patients. Risk factors for progression include age less than 5 years, low body weight, diabetes, drug/alcohol abuse, GI bypass, immunosuppression, and others. Latent infection is noninfectious. Sputum AFB is negative.
Screening is based on risk stratification. Factors include recent immigration from a high risk area (especially Asia), being a health care professional, working in an "institution", and being homeless. Low-risk patients should not be tested due to possible false positive tests. The two testing options are the Tuberculin skin test (TST) and the interferon-gamma release assay (IGRA). They cannot distinguish between active and latent infection. TST is more sensitive and IGRA is more specific. High risk patients with negative TST can have a confirmatory IGRA. Low risk patients with a positive TST should have a confirmatory IGRA to avoid unnecessary treatment. ***PEARL OF THE ARTICLE** Apparently, having the BCG vaccine within 10 years can in fact create a false positive TST test 20% of the time. Board question writers.. start your engines! In this case, IGRA is preferred over TST. It is also preferred in patients who may not return to have the test read. TST is the test of choice in patients younger than 5 years old. For patients with recent exposure, a patient may not show positive conversion with either test for 3 months. High risk patients with recent exposure should get "window prophylaxis" until a screening test can be reliably performed. Sometimes a patient may need a second TST to get a positive reaction (booster effect- ***another BOARD REVIEW PEARL**).
There are four treatment regimens. Isoniazid can be given for 9, 6, or 4 months. The longer the treatment, the more effective, more expensive, more patient compliance, and more liver toxicity. A new regimen of 12 weekly doses of isoniazid and rifapentine are as effective as the 9 month long dose of isoniazid. It has better compliance but is more expensive.
Hartman-Adams H, Clark K, Juckett G
June 1 2014 Vol. 89 Number 11
Tuberculosis affects about one third of the world's population. The classic symptoms include cough, hemoptysis, weight loss, fever, and night sweats. Approximately 10-15% of these people have latent infection. 5-10% of latent infections progress to active disease, which will occur within 2 years for half of these patients. Risk factors for progression include age less than 5 years, low body weight, diabetes, drug/alcohol abuse, GI bypass, immunosuppression, and others. Latent infection is noninfectious. Sputum AFB is negative.
Screening is based on risk stratification. Factors include recent immigration from a high risk area (especially Asia), being a health care professional, working in an "institution", and being homeless. Low-risk patients should not be tested due to possible false positive tests. The two testing options are the Tuberculin skin test (TST) and the interferon-gamma release assay (IGRA). They cannot distinguish between active and latent infection. TST is more sensitive and IGRA is more specific. High risk patients with negative TST can have a confirmatory IGRA. Low risk patients with a positive TST should have a confirmatory IGRA to avoid unnecessary treatment. ***PEARL OF THE ARTICLE** Apparently, having the BCG vaccine within 10 years can in fact create a false positive TST test 20% of the time. Board question writers.. start your engines! In this case, IGRA is preferred over TST. It is also preferred in patients who may not return to have the test read. TST is the test of choice in patients younger than 5 years old. For patients with recent exposure, a patient may not show positive conversion with either test for 3 months. High risk patients with recent exposure should get "window prophylaxis" until a screening test can be reliably performed. Sometimes a patient may need a second TST to get a positive reaction (booster effect- ***another BOARD REVIEW PEARL**).
There are four treatment regimens. Isoniazid can be given for 9, 6, or 4 months. The longer the treatment, the more effective, more expensive, more patient compliance, and more liver toxicity. A new regimen of 12 weekly doses of isoniazid and rifapentine are as effective as the 9 month long dose of isoniazid. It has better compliance but is more expensive.
Thursday, June 5, 2014
A Synopsis of AAFPs "Salivary Gland Disorders"
A Synopsis of:
Salivary Gland Disorders
KEVIN F. WILSON, MD; JEREMY D. MEIER, MD; and P. DANIEL WARD, MD, MS, University of Utah School of Medicine, Salt Lake City, Utah
Am Fam Physician. 2014 Jun 1;89(11):882-888.
http://www.aafp.org/afp/2014/0601/p882.pdf
The salivary glands include the parotid, submandibular, sublingual, and some minor ones that line the mouth. The three types of disorders include obstruction, neoplasm, and infection. The initial typical symptom is inflammation. If there are systemic findings (fever, joint pain) then the inflammation may be due to sjogren's syndrome, lymphoma, fungal, or mycobacterial. Acute localized inflammation may be either viral or bacterial. Recurrent localized inflammation will need to be evaluated for duct obstruction.
Acute suppurative sialadenitis is bacterial inflammation of the parotid gland. Risk factors include diabetes, hypothyroidism, use of anticholinergic medications, renal failure, and sjogren's. Treatment includes empiric antibiotics (amoxicillin-clavulanate), warm compresses, sialagogues, hydration, oral hygiene, and salivary gland massage.
Recurrent parotitis of childhood appears as fever malaise, pain, and swelling of the parotid gland. Treatment is the same as above.
Chronic sialadenitis is thought to be due to obstruction of the parotid gland. Treatment consists of sialagogues, hydration, massage and anti-inflammatory medication.
Sialolithiasis are stones in the submandibular gland. Symptoms include postprandial pain and swelling. A stone may be found through palpation (under anesthesia) or imaging. Stones in the parotid duct may require surgery.
Viral infections include mumps and HIV. Mumps occur mostly in children less than 15 years old. It is highly contagious and spreads through respiratory droplets. It is nonsuppurative and diagnosed through viral serology. Treatment is supportive. HIV is associated with cysts in the salivary glands and xerostomia.
Neoplasms present as painless, asymptomatic, and slow-growing. Diagnosis is made with biopsy and imaging. Pleomorphic adenomas are the most common tumor. They are found in the parotid gland and can become malignant with time. Warthin tumors are benign tumors found in older male smokers. Mucoepidermoid carcinoma is a low grade tumor with excellent prognosis if treated. Adenoid cystic carcinoma invades the nerves and can cause facial weakness. Treatment is resection.
Salivary Gland Disorders
KEVIN F. WILSON, MD; JEREMY D. MEIER, MD; and P. DANIEL WARD, MD, MS, University of Utah School of Medicine, Salt Lake City, Utah
Am Fam Physician. 2014 Jun 1;89(11):882-888.
http://www.aafp.org/afp/2014/0601/p882.pdf
The salivary glands include the parotid, submandibular, sublingual, and some minor ones that line the mouth. The three types of disorders include obstruction, neoplasm, and infection. The initial typical symptom is inflammation. If there are systemic findings (fever, joint pain) then the inflammation may be due to sjogren's syndrome, lymphoma, fungal, or mycobacterial. Acute localized inflammation may be either viral or bacterial. Recurrent localized inflammation will need to be evaluated for duct obstruction.
Acute suppurative sialadenitis is bacterial inflammation of the parotid gland. Risk factors include diabetes, hypothyroidism, use of anticholinergic medications, renal failure, and sjogren's. Treatment includes empiric antibiotics (amoxicillin-clavulanate), warm compresses, sialagogues, hydration, oral hygiene, and salivary gland massage.
Recurrent parotitis of childhood appears as fever malaise, pain, and swelling of the parotid gland. Treatment is the same as above.
Chronic sialadenitis is thought to be due to obstruction of the parotid gland. Treatment consists of sialagogues, hydration, massage and anti-inflammatory medication.
Sialolithiasis are stones in the submandibular gland. Symptoms include postprandial pain and swelling. A stone may be found through palpation (under anesthesia) or imaging. Stones in the parotid duct may require surgery.
Viral infections include mumps and HIV. Mumps occur mostly in children less than 15 years old. It is highly contagious and spreads through respiratory droplets. It is nonsuppurative and diagnosed through viral serology. Treatment is supportive. HIV is associated with cysts in the salivary glands and xerostomia.
Neoplasms present as painless, asymptomatic, and slow-growing. Diagnosis is made with biopsy and imaging. Pleomorphic adenomas are the most common tumor. They are found in the parotid gland and can become malignant with time. Warthin tumors are benign tumors found in older male smokers. Mucoepidermoid carcinoma is a low grade tumor with excellent prognosis if treated. Adenoid cystic carcinoma invades the nerves and can cause facial weakness. Treatment is resection.
Tuesday, June 3, 2014
A Synopsis of "Evaluation and Treatment of Neonatal Hyperbilirubinemia"
Evaluation and Treatment of Neonatal Hyperbilirubinemia KAREN E. MUCHOWSKI, MD, Naval Hospital Camp Pendleton Family Medicine Residency Program, Camp Pendleton, California Am Fam Physician. 2014 Jun 1;89(11):873-878.
Severe neonatal hyperbilirubinemia can cause kernicterus in about 2% of infants, however it is usually benign. Symptoms include hypertonia, arching, retrocollis, opisthotonus, fever, and high pitched crying. Risk factors include cephalohematoma, bruising, exclusive breast feeding, and weight loss greater than 8%. Total serum bilirubin (TSB), transcutaneous bilirubin, or risk scores can be used to screen patients. Some institutions prefer to do universal screening. AAFP says that screening has no effect on clinical outcomes.
It is important for the old-timer docs to know that you can not visually predict bilirubin level though visual inspection. It is more accurate to plot the level on a nomogram HERE (BTW that was my first ever link on my blog- go me!" The treatment is typically phototherapy (at a frequency of 460-490 nm). There is no standard protocol for exact type or amount of light. Fiber optic lights are only about half as good as conventional. Adverse effects of phototherapy include separation from mom, increased blood draws, longer hospital stays, and more visits to health care professionals during infancy. Exchange transfusion is considered if the patient has a TSB above 25 ng/dL and signs of encephalopathy. Complications occur 5% of the time.
Hyperbilirubinemia is more a function of calorie deprivation rather than breastfeeding exclusivity. frequency needs to be increased in these children. Intake can be approximated by monitoring daily wet diapers (4-6 is adequate) and stools (3-4). Encouragement and continued maternal interaction by doctors and nurses is helpful in promoting breastfeeding throughout infancy.
Studies on long term effects have shown no difference in cognition or neurologic function between patients with RSB levels above or below 13. Those with a positive coombs test had lower cognitive scores. Infants with TSB above 19 have had an increased incidence of ADD.
Evaluation and Treatment of Neonatal Hyperbilirubinemia KAREN E. MUCHOWSKI, MD, Naval Hospital Camp Pendleton Family Medicine Residency Program, Camp Pendleton, California Am Fam Physician. 2014 Jun 1;89(11):873-878.
Severe neonatal hyperbilirubinemia can cause kernicterus in about 2% of infants, however it is usually benign. Symptoms include hypertonia, arching, retrocollis, opisthotonus, fever, and high pitched crying. Risk factors include cephalohematoma, bruising, exclusive breast feeding, and weight loss greater than 8%. Total serum bilirubin (TSB), transcutaneous bilirubin, or risk scores can be used to screen patients. Some institutions prefer to do universal screening. AAFP says that screening has no effect on clinical outcomes.
It is important for the old-timer docs to know that you can not visually predict bilirubin level though visual inspection. It is more accurate to plot the level on a nomogram HERE (BTW that was my first ever link on my blog- go me!" The treatment is typically phototherapy (at a frequency of 460-490 nm). There is no standard protocol for exact type or amount of light. Fiber optic lights are only about half as good as conventional. Adverse effects of phototherapy include separation from mom, increased blood draws, longer hospital stays, and more visits to health care professionals during infancy. Exchange transfusion is considered if the patient has a TSB above 25 ng/dL and signs of encephalopathy. Complications occur 5% of the time.
Hyperbilirubinemia is more a function of calorie deprivation rather than breastfeeding exclusivity. frequency needs to be increased in these children. Intake can be approximated by monitoring daily wet diapers (4-6 is adequate) and stools (3-4). Encouragement and continued maternal interaction by doctors and nurses is helpful in promoting breastfeeding throughout infancy.
Studies on long term effects have shown no difference in cognition or neurologic function between patients with RSB levels above or below 13. Those with a positive coombs test had lower cognitive scores. Infants with TSB above 19 have had an increased incidence of ADD.
Tuesday, May 13, 2014
ARE YOU MISSING ME???
Sorry I haven't called. Yes I miss you too....
I have been doing some intense studying for licencing and will be back JUNE 2nd !! I hope you are as excited as I am to get caught up on all the AFP journals!!
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