Friday, June 28, 2013
A Blast From Step 1 "Hepatitis B Serology"
Here is a quick cheat to determine what phase of HBV infection your patient is in. Step 1; check the surface antigen. If it is positive, then the patient is either recovered or vaccinated. If there is nothing else positive, then he is vaccinated. If anything is positive (especially IgG), then he has recovered from a past infection). If the surface antigen is negative, then check the core antigen (it will be positive, but you need to know if it is IgG or IgM) If its it IgM positive, then you know it is an acute infection (just like when any disease is acute). If its IgG, then its chronic. Writing it out helps me remember it .
A Synopsis of AFP's "Gastroenteritis in Children: Part II. Prevention and Management"
Gastroenteritis in Children: Part II. Prevention and Management
CATHERINE A. CHURGAY, MD, Hope Medical Clinic, Ypsilanti, Michigan, ZAHRA AFTAB, MD, St. Luke’s Hospital/University of Toledo, Maumee, Ohio
Am Fam Physician. 2012 Jun 1;85(11):1066-1070.
http://www.aafp.org/afp/2012/0601/p1066.pdf
The most important part of gastroenteritis treatment is dehydration prevention. First line therapy is oral rehydration therapy (ORT). The composition of the solution is:
50 mEq/L Na,
25 g/L dextrose, and
30 mEq/L bicarbonate.
Fluids such as water, apple juice, watered down formula, soda, or chicken broth, are not recommended because they are hyperosmolar and do not contain proper electrolyte replacement. Recommended solutions include Pedialyte, Rehydrate, Infalyte, and Naturalyte.
In mild to moderate dehydration, patients should be given 50 ml per kg of ORT. This can be done at home by giving the patient 1 ml of solution per kg every five minutes for three to four hours. Take a short break if the patient vomits. An additional 10 ml per kg should be added for each loose stool or vomiting episode.
In moderate to severe dehydration, hospital admission may be required, especially if the patient is having intractable vomiting, profuse diarrhea, not getting adequate oral hydration, or not getting better after 24 hours. In this case, infants should get 30 ml per hour ORT, toddlers should get 60 ml per hour, and older children should get 90 ml per hour. 10 ml/kg can be added for each loose stool or vomiting episode. Ondansetron has been helpful in vomiting patients. If IV fluids are required, NS or RL can be used. A bolus of 10-20 ml/kg should be given first, followed by a maintenance fluid. Maintenance fluids are based on weight:
100 ml/kg for the first 10 kg
50 ml/kg for the next 10 kg
20 ml/kg for the next 10 kg
Regular diet can be continued once patient is adequately hydrated. Probiotics have shown promise in reducing the effects of gastroenteritis. They work by degrading and modifying the dietary antigens. They also regulate the inflammatory effects of cytokines. They do not colonize the gut flora, but leave the system within 1-2 hours. Antidiarrheals, such as loperamide should not be used and may increase nausea and constipation. Handwashing is very beneficial in preventing disease spread. Antibacterial soap is not better than regular soap.
Rotavirus vaccine has made a big impact on the prevalence of the infection. It is a live, oral vaccine given at two, four, and six months after birth and thus discontinued. The current vaccine is recommended and safe, although some studies note a small increase of intussusception with Rotateq as well.
CATHERINE A. CHURGAY, MD, Hope Medical Clinic, Ypsilanti, Michigan, ZAHRA AFTAB, MD, St. Luke’s Hospital/University of Toledo, Maumee, Ohio
Am Fam Physician. 2012 Jun 1;85(11):1066-1070.
http://www.aafp.org/afp/2012/0601/p1066.pdf
The most important part of gastroenteritis treatment is dehydration prevention. First line therapy is oral rehydration therapy (ORT). The composition of the solution is:
50 mEq/L Na,
25 g/L dextrose, and
30 mEq/L bicarbonate.
Fluids such as water, apple juice, watered down formula, soda, or chicken broth, are not recommended because they are hyperosmolar and do not contain proper electrolyte replacement. Recommended solutions include Pedialyte, Rehydrate, Infalyte, and Naturalyte.
In mild to moderate dehydration, patients should be given 50 ml per kg of ORT. This can be done at home by giving the patient 1 ml of solution per kg every five minutes for three to four hours. Take a short break if the patient vomits. An additional 10 ml per kg should be added for each loose stool or vomiting episode.
In moderate to severe dehydration, hospital admission may be required, especially if the patient is having intractable vomiting, profuse diarrhea, not getting adequate oral hydration, or not getting better after 24 hours. In this case, infants should get 30 ml per hour ORT, toddlers should get 60 ml per hour, and older children should get 90 ml per hour. 10 ml/kg can be added for each loose stool or vomiting episode. Ondansetron has been helpful in vomiting patients. If IV fluids are required, NS or RL can be used. A bolus of 10-20 ml/kg should be given first, followed by a maintenance fluid. Maintenance fluids are based on weight:
100 ml/kg for the first 10 kg
50 ml/kg for the next 10 kg
20 ml/kg for the next 10 kg
Regular diet can be continued once patient is adequately hydrated. Probiotics have shown promise in reducing the effects of gastroenteritis. They work by degrading and modifying the dietary antigens. They also regulate the inflammatory effects of cytokines. They do not colonize the gut flora, but leave the system within 1-2 hours. Antidiarrheals, such as loperamide should not be used and may increase nausea and constipation. Handwashing is very beneficial in preventing disease spread. Antibacterial soap is not better than regular soap.
Rotavirus vaccine has made a big impact on the prevalence of the infection. It is a live, oral vaccine given at two, four, and six months after birth and thus discontinued. The current vaccine is recommended and safe, although some studies note a small increase of intussusception with Rotateq as well.
Thursday, June 27, 2013
A Synopsis of AFP's "Gastroenteritis in Children: Part I. Diagnosis"
Gastroenteritis in Children: Part I. Diagnosis
CATHERINE A. CHURGAY, MD, Hope Medical Clinic, Ypsilanti, Michigan
ZAHRA AFTAB, MD, St. Luke’s Hospital/University of Toledo, Maumee, Ohio
Noninflammatory diarrhea is watery without blood, mucus or fever. It commonly involves the small intestine and does not destroy the lining. Inflammatory diarrhea will have blood and leukocytes in the stool. It commonly involves the large intestine and may be associated with pain, tenderness, fever or vomiting.
Diarrhea lasting more than 14 days may be due to a parasite. Diarrhea with neurological changes may be to toxins. Bacterial and viral bacterial may have systemic symptoms such as weakness, arthritis, fever, or jaundice.
The history and exam should focus on the patient's hydration status. Clinicians should ask about urination quality and quantity, bowel moments, vomiting, oral intake, stool quality, presence of fever, mental status, and history of other illnesses. Weighting the child can help assess the volume status of the patient. The degree of dehydration can be classified into none (less than 5%) , mild/moderate (5-10%), and severe (10% or more). Factors that may signal dehydration may be overall appearance, capillary refill time greater than two seconds, absence of tears, and dry mucus membranes. Two of these factors would be present in a patient with at least 5% dehydration. Presence of three of these features would be seen in a patient with 5-10% dehydration. A patient with more than 10% dehydration would have four of these factors. Dehydrated patients may have hypercapnia and acidosis. Urine specific gravity, serum electrolytes. and BUN are not very helpful. A bicarbonate level can give certain clues as to if the patient will need to be admitted (a bicarb less than 13). Stool for ova and parasite need only be ordered in cases of persistent diarrhea (greater than 2 weeks) or if there is evidence of an outbreak.
CATHERINE A. CHURGAY, MD, Hope Medical Clinic, Ypsilanti, Michigan
ZAHRA AFTAB, MD, St. Luke’s Hospital/University of Toledo, Maumee, Ohio
Am Fam Physician. 2012 Jun 1;85(11):1059-1062.
http://www.aafp.org/afp/2012/0601/p1059.pdf
Acute gastroenteritis in children is most commonly due to infection. Diarrhea (3 or more loose or watery stools in 24 hours) is often seen with gastroenteritis. It is due to virus (rotavirus) 85% of the time, bacteria (Campylobacter, Shigella, Salmonella) 15% of the time, travelers diarrhea (E. coli enterotoxin) 10% of the time, and parasites (Giardia, Cryptosporidium) less than 5% of the time. The differential diagnosis includes IBD, intussusception, membranous colitis, food allergy, sepsis, pneumonia, meningitis, UTI and others.http://www.aafp.org/afp/2012/0601/p1059.pdf
Noninflammatory diarrhea is watery without blood, mucus or fever. It commonly involves the small intestine and does not destroy the lining. Inflammatory diarrhea will have blood and leukocytes in the stool. It commonly involves the large intestine and may be associated with pain, tenderness, fever or vomiting.
Diarrhea lasting more than 14 days may be due to a parasite. Diarrhea with neurological changes may be to toxins. Bacterial and viral bacterial may have systemic symptoms such as weakness, arthritis, fever, or jaundice.
The history and exam should focus on the patient's hydration status. Clinicians should ask about urination quality and quantity, bowel moments, vomiting, oral intake, stool quality, presence of fever, mental status, and history of other illnesses. Weighting the child can help assess the volume status of the patient. The degree of dehydration can be classified into none (less than 5%) , mild/moderate (5-10%), and severe (10% or more). Factors that may signal dehydration may be overall appearance, capillary refill time greater than two seconds, absence of tears, and dry mucus membranes. Two of these factors would be present in a patient with at least 5% dehydration. Presence of three of these features would be seen in a patient with 5-10% dehydration. A patient with more than 10% dehydration would have four of these factors. Dehydrated patients may have hypercapnia and acidosis. Urine specific gravity, serum electrolytes. and BUN are not very helpful. A bicarbonate level can give certain clues as to if the patient will need to be admitted (a bicarb less than 13). Stool for ova and parasite need only be ordered in cases of persistent diarrhea (greater than 2 weeks) or if there is evidence of an outbreak.
Wednesday, June 26, 2013
A synopsis of AFP's " Causes and Evaluation of Chronic Dyspnea"
Causes and Evaluation of Chronic Dyspnea
STEVEN A. WAHLS, MD, Oregon Health & Science University, Portland, Oregon
Am Fam Physician. 2012 Jul 15;86(2):173-180.
http://www.aafp.org/afp/2012/0715/p173.pdf
Breathing is regulated by chemoreceptors in the brain and vascular system, mechanoreceptors in the chest wall and diaphragm, and vagal receptors in the pulmonary system. Chronic dyspnea is a shortness of breath lasting at least one month. It is subjective and varying in intensity. Causes of dyspnea include asthma, congestive heart failure, myocardial ischemia, COPD, interstitial lung disease, pneumonia, and psychogenic disorders.
Clinical presentation alone is sufficient information to allow the clinician to make a correct diagnosis in more than half of the cases. Patients with asthma present with chest tightness. Those with heart failure may have shortness of breath on exertion, a sensation of suffocation, or "air hunger". Patients having sputum production with cough and dyspnea should may need spirometry. A questionnaire will ask how often is mucus produced with cough, how often are chest sounds audible, how often is there dypnea on exertion, age, and smoking history. Patients with intermittent dyspnea may be suffering from reflux or aspiration. Fever may be associated infection, inflammation, or malignancy.
Physical exam can give other clues to support the diagnosis. Paradoxical pulse may suggest asthma or COPD. JVD may suggest CHF. A pleural rub may indicate effusion. Murmurs may indicate an ASD or a valve problem. A chest X ray and ECG can be considered if there are signs of heart failure. Spirometry can be performed to diagnose a restrictive or obstructive lung disease. BNP and N-terminal pro-BNP can be drawn do distinguish between cardiac and pulmonary causes of dyspnea.
Pulmonary function tests have a role in dyspnea diagnosis. TLC is reduced in restrictive disease, but normal or elevated in obstructive disorders . V/Q scanning can rule out thrombosis. In the case of sarcoidosis, fungal infections, or interstitial diseases, lavage or biopsy can be done.
Tuesday, June 25, 2013
A Brief Review of AFP's "Diabetic Nephropathy—The Family Physician’s Role"
Diabetic Nephropathy—The Family Physician’s Role
MICHELLE A. ROETT, MD, MPH; SARAH LIEGL, MD; and YALDA JABBARPOUR, MD, Georgetown University Medical Center, Washington, District of Columbia
Am Fam Physician. 2012 May 1;85(9):883-889.
http://www.aafp.org/afp/2012/0501/p883.pdf
Diabetes is a leading cause of renal disease. Renal disease, cardiovascular events, and all-cause mortality are associate with increased microalbuminuria levels. Microalbuminuria is defined as 30-300mg of albumin in a 24-hour sample. Risk factors for microalbuminuria include hypertension, high glucose levels, high cholesterol, and smoking. In diabetes, microalbuminuria leads to macroalbuminuria, which leads to loss of GFR, which leads to ESRD. Patients diagnosed with IDDM (type 1) should be screened within five years of diagnosis. NIDDM (type 2) patients should be screened immediately. Yearly albumin levels can be used to track disease progression. During diagnosis, microalbuminuria should be confirmed at least two more times over the next three to six months. Microalbumin is a inflammatory marker for many diseases, so seeing it elevated over a long time period is a better determining factor than a once time lab. Patients with chronic kidney injury should have an ultrasound to rule out reversible causes.
Besides lifestyle management, ACEIs and ARBs have been shown to improve and prevent kidney disease progression, by lowering blood pressure and glycemic level. According to the ACCORD trial , the aggressive approach of lowering AIC level, although it may reduce the risk of microalbuminuria, will increase the amount of hypoglycemic events and increase all-cause mortality. Lowering blood pressure to below 130/80 with ACEIs or ARBs is beneficial too. Studies of aggressive pressure control have had adverse outcomes including hypotension, bradycardia, lower GFR, and elevated creatinine. Combinations of ACEIs and ARBS have no additional benefit.
The ADVANCE trial showed that perindopril and indapamide lower nephropathy, albumin, and mortality. It did not affect the rate of ESRD.
A low protein diet will be beneficial in these patients. Supplemental folic acid, vitamin B6 and cyanocobalamin should be avoided because they can affect GFR.
MICHELLE A. ROETT, MD, MPH; SARAH LIEGL, MD; and YALDA JABBARPOUR, MD, Georgetown University Medical Center, Washington, District of Columbia
Am Fam Physician. 2012 May 1;85(9):883-889.
http://www.aafp.org/afp/2012/0501/p883.pdf
Diabetes is a leading cause of renal disease. Renal disease, cardiovascular events, and all-cause mortality are associate with increased microalbuminuria levels. Microalbuminuria is defined as 30-300mg of albumin in a 24-hour sample. Risk factors for microalbuminuria include hypertension, high glucose levels, high cholesterol, and smoking. In diabetes, microalbuminuria leads to macroalbuminuria, which leads to loss of GFR, which leads to ESRD. Patients diagnosed with IDDM (type 1) should be screened within five years of diagnosis. NIDDM (type 2) patients should be screened immediately. Yearly albumin levels can be used to track disease progression. During diagnosis, microalbuminuria should be confirmed at least two more times over the next three to six months. Microalbumin is a inflammatory marker for many diseases, so seeing it elevated over a long time period is a better determining factor than a once time lab. Patients with chronic kidney injury should have an ultrasound to rule out reversible causes.
Besides lifestyle management, ACEIs and ARBs have been shown to improve and prevent kidney disease progression, by lowering blood pressure and glycemic level. According to the ACCORD trial , the aggressive approach of lowering AIC level, although it may reduce the risk of microalbuminuria, will increase the amount of hypoglycemic events and increase all-cause mortality. Lowering blood pressure to below 130/80 with ACEIs or ARBs is beneficial too. Studies of aggressive pressure control have had adverse outcomes including hypotension, bradycardia, lower GFR, and elevated creatinine. Combinations of ACEIs and ARBS have no additional benefit.
The ADVANCE trial showed that perindopril and indapamide lower nephropathy, albumin, and mortality. It did not affect the rate of ESRD.
A low protein diet will be beneficial in these patients. Supplemental folic acid, vitamin B6 and cyanocobalamin should be avoided because they can affect GFR.
Monday, June 24, 2013
A Quick Synopsis of AFP's "Nongenital Herpes Simplex Virus "
Nongenital Herpes Simplex Virus
RICHARD P. USATINE, MD, and ROCHELLE TINITIGAN, MD, University of Texas Health Science Center, San Antonio, Texas
Am Fam Physician. 2010 Nov 1;82(9):1075-1082.
http://www.aafp.org/afp/2010/1101/p1075.pdf
It's really hot out up here in the Bronx, so i'm going to try and make this a brief, brief review. This article had some nice pictures so it is worth clicking the link above. HSV-1 is the "other" herpes virus. This is the one that is on the oral mucosa and lips. HSV-2 is the "genital herpes" disease. Its important to remember that type-2 can be found on the mouth and type-1 can be found on the genitals. The prevalence of HSV-1 is almost 60%. Transmission can occur through kissing, sharing a toothbrush or utensil, or sharing towels. It takes between two to 20 days for the infection to appear. The patient may have a fever, tingling, burning, paresthesia or itching before the lesions occur. Lymphadenopathy can appear in the cervical and submandibular area. The ulcers heal in about a week.
HSV-1 can also spread to the eye. Look for pain, photophobia, and dendritic ulcers on fluorescein staining. Scarring can be permanent. If it appears on the fingers and hands it is called herpetic whitlow. It can also cause erythema multiforme. Diagnosis can be done my culture, PCR, serology, antibody testing, or the Tzanck test.
As far as treatment is concerned, the topical treatments have not been shown to be effective, by maybe resolving the features by about half of a day faster. Oral treatment has been more effective. It can decrease pain, shedding, and healing time by about 50% in each category. The different types of protease inhibitors (acyclovir, famciclovir, valacyclovir) have been equally effective. They are relatively safe.
RICHARD P. USATINE, MD, and ROCHELLE TINITIGAN, MD, University of Texas Health Science Center, San Antonio, Texas
Am Fam Physician. 2010 Nov 1;82(9):1075-1082.
http://www.aafp.org/afp/2010/1101/p1075.pdf
It's really hot out up here in the Bronx, so i'm going to try and make this a brief, brief review. This article had some nice pictures so it is worth clicking the link above. HSV-1 is the "other" herpes virus. This is the one that is on the oral mucosa and lips. HSV-2 is the "genital herpes" disease. Its important to remember that type-2 can be found on the mouth and type-1 can be found on the genitals. The prevalence of HSV-1 is almost 60%. Transmission can occur through kissing, sharing a toothbrush or utensil, or sharing towels. It takes between two to 20 days for the infection to appear. The patient may have a fever, tingling, burning, paresthesia or itching before the lesions occur. Lymphadenopathy can appear in the cervical and submandibular area. The ulcers heal in about a week.
HSV-1 can also spread to the eye. Look for pain, photophobia, and dendritic ulcers on fluorescein staining. Scarring can be permanent. If it appears on the fingers and hands it is called herpetic whitlow. It can also cause erythema multiforme. Diagnosis can be done my culture, PCR, serology, antibody testing, or the Tzanck test.
As far as treatment is concerned, the topical treatments have not been shown to be effective, by maybe resolving the features by about half of a day faster. Oral treatment has been more effective. It can decrease pain, shedding, and healing time by about 50% in each category. The different types of protease inhibitors (acyclovir, famciclovir, valacyclovir) have been equally effective. They are relatively safe.
Friday, June 21, 2013
A Synopsis of AFPs "Pharmacologic Therapy for Acute Pain"
Pharmacologic Therapy for Acute Pain
RICHARD D. BLONDELL, MD; MOHAMMADREZA AZADFARD, MD; and ANGELA M. WISNIEWSKI, PharmD, State University of New York at Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York
Am Fam Physician. 2013 Jun 1;87(11):766-772.
http://www.aafp.org/afp/2013/0601/p766.pdf
When treating pain, using a pain scale helps determine the severity at baseline and the effectiveness of the treatment. The WHO's "pain relief ladder" can help with management. At any point during management, Adjuvant medications (antidepressants, anticonvulsants, and glucocorticoids) can be added.
The first step on the ladder are non-opioids such as acetaminophen and NSAIDs (celecoxib, aspirin, naproxen). These medications have similar effectiveness. Acetaminophen does not have any anti-inflammatory effects. There is a ceiling for the analgesic effects of NSAIDs, but not for its anti-inflammatory properties. NSAIDs better for treating osteoarthritis. Aspirin and the other NSAIDs can cause GI bleeding and ulcers. Aspirin is as effective as sumatriptan for acute migraines, with less adverse effects.
Celecoxib is a COX-2 selective inhibitor. It has anti-inflammatory properties without the GI problems seen in the COX-1 aspect. It can be used for bone pain, dental pain, dysmenorrhea, headache, osteoarthritis, RA, and AS. They are more expensive than other traditional NSAIDs with similar effectiveness. There is less incidence of GI bleeding with these as well. They will increase the risk of a cardiovascular event at high doses.
The next step on the ladder is opioid combinations with acetaminophen or NSAIDs. The combination is especially effective for postoperative pain. Concern over acetaminophen-induced liver injury has caused limitations in the dose of these medications. Patients should not used more than 4g of acetaminophen per day.
If the combinations are not effective for pain control, then full opioids can be considered. Morphine is more effective than codeine, due to the lower receptor affinity. Adverse effects include nausea, vomiting, constipation, pruritus, and respiratory depression. Opioid induced gastroparesis can be treated with metoclopramide, but extrapyramidal side effects can occur.
Dual action medications, (muopioid agonist and norepinephrine reuptake inhibitor) such as tapentadol, are as effective as oxycodone without as much nausea, vomiting and constipation. Tramadol is considered a second tier medication in this class.
Opioids have a high potential for abuse and most patients are first introduced to these meds as properly prescribed treatments. Doctors need to counsel their patients.
RICHARD D. BLONDELL, MD; MOHAMMADREZA AZADFARD, MD; and ANGELA M. WISNIEWSKI, PharmD, State University of New York at Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York
Am Fam Physician. 2013 Jun 1;87(11):766-772.
http://www.aafp.org/afp/2013/0601/p766.pdf
When treating pain, using a pain scale helps determine the severity at baseline and the effectiveness of the treatment. The WHO's "pain relief ladder" can help with management. At any point during management, Adjuvant medications (antidepressants, anticonvulsants, and glucocorticoids) can be added.
The first step on the ladder are non-opioids such as acetaminophen and NSAIDs (celecoxib, aspirin, naproxen). These medications have similar effectiveness. Acetaminophen does not have any anti-inflammatory effects. There is a ceiling for the analgesic effects of NSAIDs, but not for its anti-inflammatory properties. NSAIDs better for treating osteoarthritis. Aspirin and the other NSAIDs can cause GI bleeding and ulcers. Aspirin is as effective as sumatriptan for acute migraines, with less adverse effects.
Celecoxib is a COX-2 selective inhibitor. It has anti-inflammatory properties without the GI problems seen in the COX-1 aspect. It can be used for bone pain, dental pain, dysmenorrhea, headache, osteoarthritis, RA, and AS. They are more expensive than other traditional NSAIDs with similar effectiveness. There is less incidence of GI bleeding with these as well. They will increase the risk of a cardiovascular event at high doses.
The next step on the ladder is opioid combinations with acetaminophen or NSAIDs. The combination is especially effective for postoperative pain. Concern over acetaminophen-induced liver injury has caused limitations in the dose of these medications. Patients should not used more than 4g of acetaminophen per day.
If the combinations are not effective for pain control, then full opioids can be considered. Morphine is more effective than codeine, due to the lower receptor affinity. Adverse effects include nausea, vomiting, constipation, pruritus, and respiratory depression. Opioid induced gastroparesis can be treated with metoclopramide, but extrapyramidal side effects can occur.
Dual action medications, (muopioid agonist and norepinephrine reuptake inhibitor) such as tapentadol, are as effective as oxycodone without as much nausea, vomiting and constipation. Tramadol is considered a second tier medication in this class.
Opioids have a high potential for abuse and most patients are first introduced to these meds as properly prescribed treatments. Doctors need to counsel their patients.
Thursday, June 20, 2013
A Synopsis of AFPs "Gynecologic Procedures: Colposcopy, Treatment of Cervical Intraepithelial Neoplasia, and Endometrial Assessment"
Gynecologic Procedures: Colposcopy, Treatment of Cervical Intraepithelial Neoplasia, and Endometrial Assessment
BARBARA S. APGAR, MD; AMANDA J. KAUFMAN, MD; CATHERINE BETTCHER, MD; and EBONY PARKER-FEATHERSTONE, MD, University of Michigan Medical Center, Ann Arbor, Michigan
Am Fam Physician. 2013 Jun 15;87(12):836-843.
http://www.aafp.org/afp/2013/0615/p836.pdf
Women with abnormal pap smears need further testing. Colposcopy is typically done to determine where to biopsy the cervix, but this is not a reliable indicator. Some lesions (those that are small and those that are not HPV type 16) cannot be found with this procedure, and there is a high false negative rate. Taking multiple biopsies from the "white" area will increase the sensitivity of the procedure.
Depending on the result of the pap and colposcopy, and endocervical curettage may be needed. Recent thought has debated the necessity of the test, especially if the patient is going to require excision. It appears to be of limited benefit.
The treatment for CIN is ablation, excision (LEEP), or cold knife conation. The procedures have similar outcomes, but ablation destroys the tissue. Excision and conation allow histological evaluation. Cold knife conation is preferred when margin status must be preserved. There is a small risk of perinatal death with excision, but the benefits may outweigh this. Post LEEP margin status is not perfect, but those with positive margins should have repeat sampling 4-6 months later (rather than immediately). HPV DNA testing should be done at 1 and 2 years after excision. Positive testing will require additional sampling.
Transvaginal ultrasound is a good test to look for endometrial problems. An endocervical thickness less than 3-4 mm in postmenopausal or 5 mm in premenopausal women can rule out endocervical cancer. Saline infusion ultrasound may give additional information regarding anatomical structure and differentiate consistent from focal changes in the endothelium. Hysteroscopy is a very sensitive and specific diagnostic procedure with little adverse risk
BARBARA S. APGAR, MD; AMANDA J. KAUFMAN, MD; CATHERINE BETTCHER, MD; and EBONY PARKER-FEATHERSTONE, MD, University of Michigan Medical Center, Ann Arbor, Michigan
Am Fam Physician. 2013 Jun 15;87(12):836-843.
http://www.aafp.org/afp/2013/0615/p836.pdf
Women with abnormal pap smears need further testing. Colposcopy is typically done to determine where to biopsy the cervix, but this is not a reliable indicator. Some lesions (those that are small and those that are not HPV type 16) cannot be found with this procedure, and there is a high false negative rate. Taking multiple biopsies from the "white" area will increase the sensitivity of the procedure.
Depending on the result of the pap and colposcopy, and endocervical curettage may be needed. Recent thought has debated the necessity of the test, especially if the patient is going to require excision. It appears to be of limited benefit.
The treatment for CIN is ablation, excision (LEEP), or cold knife conation. The procedures have similar outcomes, but ablation destroys the tissue. Excision and conation allow histological evaluation. Cold knife conation is preferred when margin status must be preserved. There is a small risk of perinatal death with excision, but the benefits may outweigh this. Post LEEP margin status is not perfect, but those with positive margins should have repeat sampling 4-6 months later (rather than immediately). HPV DNA testing should be done at 1 and 2 years after excision. Positive testing will require additional sampling.
Transvaginal ultrasound is a good test to look for endometrial problems. An endocervical thickness less than 3-4 mm in postmenopausal or 5 mm in premenopausal women can rule out endocervical cancer. Saline infusion ultrasound may give additional information regarding anatomical structure and differentiate consistent from focal changes in the endothelium. Hysteroscopy is a very sensitive and specific diagnostic procedure with little adverse risk
Tuesday, June 18, 2013
A Synopsis of AFP's "Pharmacologic Treatment of Hyperlipidemia "
Pharmacologic Treatment of Hyperlipidemia
ALLEN R. LAST, MD, MPH, University of Wisconsin Fox Valley Family Medicine Residency Program, Appleton, Wisconsin, JONATHAN D. FERENCE, PharmD, Wilkes University Nesbitt College of Pharmacy and Nursing, Wilkes-Barre, Pennsylvania, JULIANNE FALLERONI, DO, MPH, University of Wisconsin Fox Valley Family Medicine Residency Program, Appleton, Wisconsin
http://www.aafp.org/afp/2011/0901/p551.pdf
Am Fam Physician. 2011 Sep 1;84(5):551-558.
Hyperlipidemia is seen in over half of all patients with cardiovascular disease. Lowering cholesterol is an important part of primary and secondary prevention in CVD patients. LDL is the primary target of cholesterol lowering therapy. The "treat-to-target approach" (ATP III) uses the risk factors to determine the LDL goal. A "fixed-dose approach" uses risk factors to determine treatment with the same treatment goal. Neither approach was proven to be better, but the ATP III guidelines, which have a more aggressive strategy for higher risk patients, is more commonly followed.
Primary prevention is treating patients before the disease occurs (in this case, before an MI). Statins are the most widely used medication and the most commonly prescribed for hyperlipidemia. The results are conflicting and can be skewed (see the JUPITER study). Regardless, statins are the treatment of choice for primary prevention of cardiovascular events as well as in patients with a history of CVD and acute coronary syndrome.
Low HDL levels and high triglycerides are other lipid abnormalities. Fibrates have been shown to normalize these values. The have not, however, shown a mortality benefit, and may increase risk. Niacin can raise HDL levels, but has not shown to reduce mortality in primary prevention. Bile acid-binding resins may reduce LDL levels, but not all-cause mortality. Omega 3 fatty acids have poor results as well.
Secondary prevention is defined as treating patients to halt or slow disease progression. Statins are recommended in all patients with a history of CVD or CVD equivalent, regardless of of cholesterol levels. Lower doses of statins should be used in patients with CVD and higher doses reserved for patients with ACS. Fibrates reduced the risk of subsequent coronary events, but it does not reduce overall mortality. Niacin does not reduce overall mortality risk, but may improve disease-oriented outcomes when combined with a statin. Bile acid binders and omega 3's do not help either.
In cerebrovascular disease, statins can reduce the risk of recurrent strokes, but will not reduce all cause mortality. It will cause a small increase in hemorrhagic stroke. Statins will not reduce mortality in patients with peripheral arterial disease, but it will increase the patients maximal walking distance.
Monday, June 17, 2013
A Synopsis of AFPs "Causes and Evaluation of Mildly Elevated Liver Transaminase Levels"
Causes and Evaluation of Mildly Elevated Liver Transaminase Levels
ROBERT C. OH, LTC, MC, USA, and THOMAS R. HUSTEAD, LTC, MC, USA, Tripler Army Medical Center Family Medicine Residency Program, Honolulu, Hawaii
Am Fam Physician. 2011 Nov 1;84(9):1003-1008.
http://www.aafp.org/afp/2011/1101/p1003.pdf
LFTs are a commonly ordered lab in practice. Mildly elevated liver transaminase levels (less than 5x the upper limit of normal) require further workup. ALT is specific for the liver, whereas AST is seen in liver, muscle and red blood cells. Nonalcoholic fatty liver disease is the most common cause of mildly elevated LFTs. It can be broken down into two subtypes. Hepatic steatohepatitis is more benign and generally does not progress to severe disease. Nonalcoholic steatohepatitis has an increased risk of progression to severe disease. The ratio of AST/ALT will be less than 1. Nonalcoholic fatty liver disease is commonly associated with those patients who have diabetes, obesity, hypertriglyceridemia, and metabolic syndrome. Ultrasound and biopsy may be considered when diagnosing this disease. A biopsy will show inflammation and fibrosis. Alcoholic liver disease will have a AST/ALT ratio greater than 2, as well as an elevated y-glutamyl transpeptidase level.
There are many many medications that can cause a mild elevation of liver transaminases, including acetaminophen and statins. levels will spontaneously resolve in most patients taking statins. It is safe in patients with chronic liver disease. Statins may even lower transaminases in patients with nonalcoholic fatty liver disease.
Hepatitis B and C are also diseases to consider. Hepatitis B surface antigen and hepatitis C virus antibody can help identify infected patients. Hepatitis C may cause fluctuating transaminase levels, especially ALT. Hemochromatosis will have asymptomatic LFT elevations as well as transferrin saturation and ferritin. Less common causes consist of alpha antitrypsin deficiency, autoimmune hepatitis, wilson's disease, hemolysis, strenuous exercise, and celiac disease.
In evaluating a patient with elevated transaminases, a proper history and exam should be performed. The patient should be asked about alcohol usage, medications, supplements, vitamins, and herbs. Hepatotoxic chemicals should be halted and labs should be retested in 3-4 weeks. Patients should also be assessed for metabolic syndrome by checking BMI, waist circumference, fasting lipids, glucose levels, and possibly ultrasound. If the LFTs remain elevated, then common causes should be ruled out. Testing for hepatitis B, hepatitis C, iron, ferritin, and TIBC should be done. Prothrombin time, albumin, platelet count, and CBC may be help tests to order. If the cause is still not found, the patient should be observed with instructions for lifestyle modifications and reassessed in 6 months. A liver biopsy or referral to a specialist may be needed.
ROBERT C. OH, LTC, MC, USA, and THOMAS R. HUSTEAD, LTC, MC, USA, Tripler Army Medical Center Family Medicine Residency Program, Honolulu, Hawaii
Am Fam Physician. 2011 Nov 1;84(9):1003-1008.
http://www.aafp.org/afp/2011/1101/p1003.pdf
LFTs are a commonly ordered lab in practice. Mildly elevated liver transaminase levels (less than 5x the upper limit of normal) require further workup. ALT is specific for the liver, whereas AST is seen in liver, muscle and red blood cells. Nonalcoholic fatty liver disease is the most common cause of mildly elevated LFTs. It can be broken down into two subtypes. Hepatic steatohepatitis is more benign and generally does not progress to severe disease. Nonalcoholic steatohepatitis has an increased risk of progression to severe disease. The ratio of AST/ALT will be less than 1. Nonalcoholic fatty liver disease is commonly associated with those patients who have diabetes, obesity, hypertriglyceridemia, and metabolic syndrome. Ultrasound and biopsy may be considered when diagnosing this disease. A biopsy will show inflammation and fibrosis. Alcoholic liver disease will have a AST/ALT ratio greater than 2, as well as an elevated y-glutamyl transpeptidase level.
There are many many medications that can cause a mild elevation of liver transaminases, including acetaminophen and statins. levels will spontaneously resolve in most patients taking statins. It is safe in patients with chronic liver disease. Statins may even lower transaminases in patients with nonalcoholic fatty liver disease.
Hepatitis B and C are also diseases to consider. Hepatitis B surface antigen and hepatitis C virus antibody can help identify infected patients. Hepatitis C may cause fluctuating transaminase levels, especially ALT. Hemochromatosis will have asymptomatic LFT elevations as well as transferrin saturation and ferritin. Less common causes consist of alpha antitrypsin deficiency, autoimmune hepatitis, wilson's disease, hemolysis, strenuous exercise, and celiac disease.
In evaluating a patient with elevated transaminases, a proper history and exam should be performed. The patient should be asked about alcohol usage, medications, supplements, vitamins, and herbs. Hepatotoxic chemicals should be halted and labs should be retested in 3-4 weeks. Patients should also be assessed for metabolic syndrome by checking BMI, waist circumference, fasting lipids, glucose levels, and possibly ultrasound. If the LFTs remain elevated, then common causes should be ruled out. Testing for hepatitis B, hepatitis C, iron, ferritin, and TIBC should be done. Prothrombin time, albumin, platelet count, and CBC may be help tests to order. If the cause is still not found, the patient should be observed with instructions for lifestyle modifications and reassessed in 6 months. A liver biopsy or referral to a specialist may be needed.
Friday, June 14, 2013
A Quick Review of AFPs "Inguinal Hernias: Diagnosis and Management"
Inguinal Hernias: Diagnosis and Management
KIM EDWARD LeBLANC, MD, PhD; LEANNE L. LeBLANC, MD; and KARL A. LeBLANC, MD, MBA ,Louisiana State University School of Medicine, New Orleans, Louisiana
Am Fam Physician. 2013 Jun 15;87(12):844-848
http://www.aafp.org/afp/2013/0615/p844.pdf
Inguinal hernia is a bulge of tissue through the inguinal canal in the groin. It is more common in men, and can occur in up to a quarter of all men. Symptoms can occur gradually or suddenly. It may present as burning, gurgling or achy pain. Pain will be located at the site of the hernia and will be increased with valsalva pressure (coughing, lifting, or straining). A bulge will be palpable when the patient is standing and may disappear while lying down. During the exam, the physician should palpate into the inguinal canal while having the patient cough for bear down. If no mass is palpated, another diagnosis, such as a sports hernia, osteitis pubis, or adductor tendinopathy, should be investigated. Imaging (ultrasound, MRI) is rarely needed, but may help in discovering causes other than hernia. Female patients may also have a palpable mass, but diagnostic testing or a surgical referral may be needed to determine if a hernia is present.
Small, minimally painful hernias can just be followed. Patients need to be educated on symptoms of strangulation and incarceration. If the hernia is large and painful, referral for open repair is recommended. Post op rest should range from 10 days to month, depending on activity level
KIM EDWARD LeBLANC, MD, PhD; LEANNE L. LeBLANC, MD; and KARL A. LeBLANC, MD, MBA ,Louisiana State University School of Medicine, New Orleans, Louisiana
Am Fam Physician. 2013 Jun 15;87(12):844-848
http://www.aafp.org/afp/2013/0615/p844.pdf
Inguinal hernia is a bulge of tissue through the inguinal canal in the groin. It is more common in men, and can occur in up to a quarter of all men. Symptoms can occur gradually or suddenly. It may present as burning, gurgling or achy pain. Pain will be located at the site of the hernia and will be increased with valsalva pressure (coughing, lifting, or straining). A bulge will be palpable when the patient is standing and may disappear while lying down. During the exam, the physician should palpate into the inguinal canal while having the patient cough for bear down. If no mass is palpated, another diagnosis, such as a sports hernia, osteitis pubis, or adductor tendinopathy, should be investigated. Imaging (ultrasound, MRI) is rarely needed, but may help in discovering causes other than hernia. Female patients may also have a palpable mass, but diagnostic testing or a surgical referral may be needed to determine if a hernia is present.
Small, minimally painful hernias can just be followed. Patients need to be educated on symptoms of strangulation and incarceration. If the hernia is large and painful, referral for open repair is recommended. Post op rest should range from 10 days to month, depending on activity level
Wednesday, June 12, 2013
A Brief Synopsis of AFP's "Evaluation of the Patient with Chronic Cough"
A Brief Synopsis of:
Evaluation of the Patient with Chronic Cough
JOSEPH J. BENICH III, MD, and PETER J. CAREK, MD, MS, Medical University of South Carolina,
Charleston, South Carolina
Am Fam Physician. 2011 Oct 15;84(8):887-892
http://www.aafp.org/afp/2011/1015/p887.pdf
Cough is a protective reflex to clear the upper airways. If the cough has been going on for 3 weeks, then it is classified as acute. It is most often due to a viral infection, asthma, COPD, irritant exposure, or an underlying cardiopulmonary issue. Cough that last 3-8 weeks is considered subacute. It is usually due to a post infectious cause or asthma. Anything longer is considered chronic. Chronic cough is most likely from GERD, asthma, ACEIs, URI/LRI or upper airway cough syndrome (UACS). Often times there are multiple causes going on at the same time.
Evaluation of chronic cough starts with a history and exam. Patients who are smokers or on ACEIs should stop using them and see if the cough stops. The next step is to x ray the lungs to rule out bronchiectasis, pneumonia, sarcoidosis, and TB. Sputum tests, PFTs, CT, esophagography, bronchoscopy, and cardiac studies should also be done and results should be evaluated for treatment.
If at this point the cause of the cough is still a mystery, the patient should be evaluated for UACS, asthma, and GERD. UACS is the most common cause of chronic cough in nonsmokers with normal x rays. Patients will present with nasal discharge, drainage in the the posterior pharynx, cobblestoning of the oropharyngeal mucosa, and mucus in the oropharynx. Patients will respond to decongestants and H1 blockers. Resolution of cough after treatment reinforces a correct diagnosis. Patient who do not respond to treatment but are still thought to have USCS may undergo sinus imaging.
Asthma can present with cough (especially in "cough -variant asthma"!).Symptoms can be made worse with cold, exercise, or during the night. Asthma can be diagnosed with spirometry and methocholine challenge.
GERD can cause coughing when the acid reflux irritates the upper airway and stimulates the esophageal cough reflex. Diagnosis can be confirmed with resolution from a PPI. Esophageal pH monitoring can also be done.
ACEIs can cause cough in 5-20% of patients. It could occur after a week of using the medication, or it could take 6 months to show signs of cough. Resolution should occur after a few days to several weeks after discontinuation of the ACEI. ARBs can be used instead.
Some uncommon causes of cough include nonasthmatic eosinophilic bronchitis, postinfectious cough, and chemical irritants These causes would have a negative x ray result. Nonasthmatic eosinophilic bronchitis will have normal airway hyperresonance, eosinophilic sputum, normal spirometry, and a positive response from corticosteroids. Postinfectious cough should resolve on its own. Chemical irritants should be removed from the environment.
Bronchiectasis can cause cough and the x ray would show bronchial wall thickening. It can be associated with infection, CF, aspiration among others. Bronchogenic carcinoma, TB and sarcoidosis will have specific radiological and laboratory findings. In children, it is important to also consider aspiration, pertussis, and congenital abnormalities in the differential diagnosis.
Evaluation of the Patient with Chronic Cough
JOSEPH J. BENICH III, MD, and PETER J. CAREK, MD, MS, Medical University of South Carolina,
Charleston, South Carolina
Am Fam Physician. 2011 Oct 15;84(8):887-892
http://www.aafp.org/afp/2011/1015/p887.pdf
Cough is a protective reflex to clear the upper airways. If the cough has been going on for 3 weeks, then it is classified as acute. It is most often due to a viral infection, asthma, COPD, irritant exposure, or an underlying cardiopulmonary issue. Cough that last 3-8 weeks is considered subacute. It is usually due to a post infectious cause or asthma. Anything longer is considered chronic. Chronic cough is most likely from GERD, asthma, ACEIs, URI/LRI or upper airway cough syndrome (UACS). Often times there are multiple causes going on at the same time.
Evaluation of chronic cough starts with a history and exam. Patients who are smokers or on ACEIs should stop using them and see if the cough stops. The next step is to x ray the lungs to rule out bronchiectasis, pneumonia, sarcoidosis, and TB. Sputum tests, PFTs, CT, esophagography, bronchoscopy, and cardiac studies should also be done and results should be evaluated for treatment.
If at this point the cause of the cough is still a mystery, the patient should be evaluated for UACS, asthma, and GERD. UACS is the most common cause of chronic cough in nonsmokers with normal x rays. Patients will present with nasal discharge, drainage in the the posterior pharynx, cobblestoning of the oropharyngeal mucosa, and mucus in the oropharynx. Patients will respond to decongestants and H1 blockers. Resolution of cough after treatment reinforces a correct diagnosis. Patient who do not respond to treatment but are still thought to have USCS may undergo sinus imaging.
Asthma can present with cough (especially in "cough -variant asthma"!).Symptoms can be made worse with cold, exercise, or during the night. Asthma can be diagnosed with spirometry and methocholine challenge.
GERD can cause coughing when the acid reflux irritates the upper airway and stimulates the esophageal cough reflex. Diagnosis can be confirmed with resolution from a PPI. Esophageal pH monitoring can also be done.
ACEIs can cause cough in 5-20% of patients. It could occur after a week of using the medication, or it could take 6 months to show signs of cough. Resolution should occur after a few days to several weeks after discontinuation of the ACEI. ARBs can be used instead.
Some uncommon causes of cough include nonasthmatic eosinophilic bronchitis, postinfectious cough, and chemical irritants These causes would have a negative x ray result. Nonasthmatic eosinophilic bronchitis will have normal airway hyperresonance, eosinophilic sputum, normal spirometry, and a positive response from corticosteroids. Postinfectious cough should resolve on its own. Chemical irritants should be removed from the environment.
Bronchiectasis can cause cough and the x ray would show bronchial wall thickening. It can be associated with infection, CF, aspiration among others. Bronchogenic carcinoma, TB and sarcoidosis will have specific radiological and laboratory findings. In children, it is important to also consider aspiration, pertussis, and congenital abnormalities in the differential diagnosis.
Tuesday, June 11, 2013
A Synopsis of AFPs "Management of Common Arrhythmias: Part II.Ventricular Arrhythmias and Arrhythmias in Special Populations"
A synopsis of: Management of Common Arrhythmias: Part II.Ventricular Arrhythmias and Arrhythmias in Special Populations
A. KESH HEBBAR, M.D., and WILLIAM J. HUESTON, M.D., Medical University of South Carolina, Charleston, South Carolina
Am Fam Physician. 2002 Jun 15;65(12):2491-2497
http://www.aafp.org/afp/2002/0615/p2491.pdf
This is the second part of yesterday's article. PVCs are characterized by wide a QRS complex (more than 0.12 secs, three small boxes), no preceding P wave, and a large T wave in the opposite direction of the QRS complex. It is usually followed by a "full compensatory pause". Ventricular bigeminy is where the PVC alternates with a normal sinus contraction. In the absence of cardiac disease, there is no treatment needed for PVCs besides patient reassurance. If PVCs are causing severe, uncomfortable symptoms, beta blockers are a safe first line choice, with flecainide, amiodarone and radiofrequency ablation as alternatives. In patients with heart disease, cardiomyopathy, and CHF, treating the underlying cause is paramount. PVCs are considered dangerous when there are 10 or more seen per hour, or when there are 3-5 consecutive contractions seen.
VT is defined as three continuous PVCs. The rate should be at least 100 BPM with a wide complex and no P waves. WPW or a bundle branch may mimic this ECG, and any wide complex tachycardia should be treated as a VT until it is ruled out. Management consists of amiodarone (or lidocaine) in asymptomatic, stable patients. Hemodynamically unstable patients should be treated with electrical cardioversion according to ACLs protocol. Patients with life threatening VT may eventually need an implantable defibrillator in situations such as: VT or VF which has lead to cardiac arrest; spontaneous, sustained VT; sustained VT with syncope; VT with CAD and LV dysfunction.
Pregnant women may have ectopic beats, it is usually benign. If there is a need for treatment, amiodarone and beta blockers should not be used during pregnancy. Amiodarone may cause fetal goiter, neonatal hypothyroidism, and fetal growth retardation. Beta blockers can cause IUGR and hypoglycemia.
It is common for athletes to have slow heart rates, even with an occasional pause. Patients with a history or syncope with exercise, or family history of a close relative with sudden cardiac death at a young age, should be checked for idiopathic hypertrophic cardiomyopathy. These patients may have an aortic murmur that gets louder with valsalva. Treatment includes a beta blocker or calcium channel blocker. They should also be instructed to avoid strenuous sports and exercise.
The most common arrhythmia in children is SVT. The treatment is the same as with adults (adenosine). Patients may also have extra atrial or ventricular beats. These children will need further evaluation because it is associated with structural disease and a higher risk of death.
Patients with acute MI can also develop rhythm abnormalities. Common abnormalities in this situation are sinus tachycardia, sinus bradycardia and PVCs. Accelerated idioventricular rhythm is basically when the beat originates in the ventricle, and at a faster rate (60-125 BPM) than what the SA node would do. It is a benign form of VT that occurs during the reperfusion portion of an MI. Treatment is not needed. PVCs do not require treatment as well. VT does not need to be treated unless it occurs after 48 hours in patients with LV dysfunction. Sustained VT for more than 30 seconds will need treatment with the ACLS protocol. Sinus bradycardia is common in inferior or posterior MI. Treatment can be done with atropine. If second degree type II or third degree heart block develops, pacing may be required.
A. KESH HEBBAR, M.D., and WILLIAM J. HUESTON, M.D., Medical University of South Carolina, Charleston, South Carolina
Am Fam Physician. 2002 Jun 15;65(12):2491-2497
http://www.aafp.org/afp/2002/0615/p2491.pdf
This is the second part of yesterday's article. PVCs are characterized by wide a QRS complex (more than 0.12 secs, three small boxes), no preceding P wave, and a large T wave in the opposite direction of the QRS complex. It is usually followed by a "full compensatory pause". Ventricular bigeminy is where the PVC alternates with a normal sinus contraction. In the absence of cardiac disease, there is no treatment needed for PVCs besides patient reassurance. If PVCs are causing severe, uncomfortable symptoms, beta blockers are a safe first line choice, with flecainide, amiodarone and radiofrequency ablation as alternatives. In patients with heart disease, cardiomyopathy, and CHF, treating the underlying cause is paramount. PVCs are considered dangerous when there are 10 or more seen per hour, or when there are 3-5 consecutive contractions seen.
VT is defined as three continuous PVCs. The rate should be at least 100 BPM with a wide complex and no P waves. WPW or a bundle branch may mimic this ECG, and any wide complex tachycardia should be treated as a VT until it is ruled out. Management consists of amiodarone (or lidocaine) in asymptomatic, stable patients. Hemodynamically unstable patients should be treated with electrical cardioversion according to ACLs protocol. Patients with life threatening VT may eventually need an implantable defibrillator in situations such as: VT or VF which has lead to cardiac arrest; spontaneous, sustained VT; sustained VT with syncope; VT with CAD and LV dysfunction.
Pregnant women may have ectopic beats, it is usually benign. If there is a need for treatment, amiodarone and beta blockers should not be used during pregnancy. Amiodarone may cause fetal goiter, neonatal hypothyroidism, and fetal growth retardation. Beta blockers can cause IUGR and hypoglycemia.
It is common for athletes to have slow heart rates, even with an occasional pause. Patients with a history or syncope with exercise, or family history of a close relative with sudden cardiac death at a young age, should be checked for idiopathic hypertrophic cardiomyopathy. These patients may have an aortic murmur that gets louder with valsalva. Treatment includes a beta blocker or calcium channel blocker. They should also be instructed to avoid strenuous sports and exercise.
The most common arrhythmia in children is SVT. The treatment is the same as with adults (adenosine). Patients may also have extra atrial or ventricular beats. These children will need further evaluation because it is associated with structural disease and a higher risk of death.
Patients with acute MI can also develop rhythm abnormalities. Common abnormalities in this situation are sinus tachycardia, sinus bradycardia and PVCs. Accelerated idioventricular rhythm is basically when the beat originates in the ventricle, and at a faster rate (60-125 BPM) than what the SA node would do. It is a benign form of VT that occurs during the reperfusion portion of an MI. Treatment is not needed. PVCs do not require treatment as well. VT does not need to be treated unless it occurs after 48 hours in patients with LV dysfunction. Sustained VT for more than 30 seconds will need treatment with the ACLS protocol. Sinus bradycardia is common in inferior or posterior MI. Treatment can be done with atropine. If second degree type II or third degree heart block develops, pacing may be required.
Monday, June 10, 2013
A Synopsis of AFP's "Management of Common Arrhythmias: Part I. Supraventricular Arrhythmias"
A synopsis of - Management of Common Arrhythmias: Part I. Supraventricular Arrhythmias
A. KESH HEBBAR, M.D., and WILLIAM J. HUESTON, M.D. Medical University of South Carolina, Charleston, South Carolina
Am Fam Physician. 2002 Jun 15;65(12):2479-2487.
http://www.aafp.org/afp/2002/0615/p2479.pdf
Most arrhythmias are usually benign, but those that are not, require treatment. The most common arrhythmia is atrial fibrillation. Most risk factors are associated with ischemic or structural heart disease, including hypertension, left ventricular hypertrophy, cardiomyopathies, COPD, and CAD. If the left atrium is not enlarged and the onset of the fibrillation is within the last year, then the patient has a better chance of maintaining sinus rhythm after treatment. Rhythm control through cardioversion can be done If the patient has been in atrial fibrillation for less than 48 hours and does not have any atrial thrombi on echocardiogram. Anticoagulation should be started before cardioversion. If thrombi are found on echocardiogram, anticoagulation may be needed for at least 3 weeks before cardioversion is considered. Synchronized electrical cardioversion is the treatment of choice. Medications such as amiodarone, and to a lesser extent quinidine, procainamide and disopyramide can be used for cardioversion as well. Radiofrequency ablation or a pacemaker are other options to consider. Rate control can be used in patients who do not qualify for rhythm control, or those with atrial fibrillation with rapid ventricular response. Calcium channel blockers (diltiazem and verapamil), beta blockers (propranolol and esmolol), or digoxin can be considered for rate control.
Paroxysmal supraventricular tachycardia is the most common type of SVT, and will be the focus of this part of the article. AV nodal reentry SVT occurs when there are two pathways that conduct the impulse at different rates. It is a narrow complex tachycardia without p waves. The rate is usually 160-190 BPMs. If there is a concomitant branch block, the tachycardia may have a wide complex. Wolff-Parkinson-White syndrome is a PSVT with an accessory pathway. There will be a shortened PR interval and the classic "delta wave on the QRS complex. If the cause of the SVT is due to increased automaticity, the atrium will be enlarged. The stretch atria will cause multiple premature beats and irregular p wave morphologies (also known as multifocal atrial tachycardia if three or more can be found). In most cases of PSVT, it is benign and self limited. If there is hemostatic instability, electrical cardioversion should be strongly considered. Symptomatic treatment can be done with vagal maneuvers, adenosine, calcium channel blockers, or beta blockers. Long term control for WPW or nodal reentry SVT may require radiofrequency ablation.
Sinus arrhythmia is normal in athletes and young adults. It is asymptomatic and can be resolved by holding ones breath. Occasionally it may be seen in patients with digoxin overdose and ICP. A wandering atrial pacemaker will present on an ECG as variable p waves and PR intervals. These are incidental findings and do not require treatment. Premature atrial complexes will have P waves of a different morphology because the impulse is from a different atrial focus. They do not require treatment, but a beta blocker may help if the patient is having symptoms.
A. KESH HEBBAR, M.D., and WILLIAM J. HUESTON, M.D. Medical University of South Carolina, Charleston, South Carolina
Am Fam Physician. 2002 Jun 15;65(12):2479-2487.
http://www.aafp.org/afp/2002/0615/p2479.pdf
Most arrhythmias are usually benign, but those that are not, require treatment. The most common arrhythmia is atrial fibrillation. Most risk factors are associated with ischemic or structural heart disease, including hypertension, left ventricular hypertrophy, cardiomyopathies, COPD, and CAD. If the left atrium is not enlarged and the onset of the fibrillation is within the last year, then the patient has a better chance of maintaining sinus rhythm after treatment. Rhythm control through cardioversion can be done If the patient has been in atrial fibrillation for less than 48 hours and does not have any atrial thrombi on echocardiogram. Anticoagulation should be started before cardioversion. If thrombi are found on echocardiogram, anticoagulation may be needed for at least 3 weeks before cardioversion is considered. Synchronized electrical cardioversion is the treatment of choice. Medications such as amiodarone, and to a lesser extent quinidine, procainamide and disopyramide can be used for cardioversion as well. Radiofrequency ablation or a pacemaker are other options to consider. Rate control can be used in patients who do not qualify for rhythm control, or those with atrial fibrillation with rapid ventricular response. Calcium channel blockers (diltiazem and verapamil), beta blockers (propranolol and esmolol), or digoxin can be considered for rate control.
Paroxysmal supraventricular tachycardia is the most common type of SVT, and will be the focus of this part of the article. AV nodal reentry SVT occurs when there are two pathways that conduct the impulse at different rates. It is a narrow complex tachycardia without p waves. The rate is usually 160-190 BPMs. If there is a concomitant branch block, the tachycardia may have a wide complex. Wolff-Parkinson-White syndrome is a PSVT with an accessory pathway. There will be a shortened PR interval and the classic "delta wave on the QRS complex. If the cause of the SVT is due to increased automaticity, the atrium will be enlarged. The stretch atria will cause multiple premature beats and irregular p wave morphologies (also known as multifocal atrial tachycardia if three or more can be found). In most cases of PSVT, it is benign and self limited. If there is hemostatic instability, electrical cardioversion should be strongly considered. Symptomatic treatment can be done with vagal maneuvers, adenosine, calcium channel blockers, or beta blockers. Long term control for WPW or nodal reentry SVT may require radiofrequency ablation.
Sinus arrhythmia is normal in athletes and young adults. It is asymptomatic and can be resolved by holding ones breath. Occasionally it may be seen in patients with digoxin overdose and ICP. A wandering atrial pacemaker will present on an ECG as variable p waves and PR intervals. These are incidental findings and do not require treatment. Premature atrial complexes will have P waves of a different morphology because the impulse is from a different atrial focus. They do not require treatment, but a beta blocker may help if the patient is having symptoms.
Wednesday, June 5, 2013
A Review of AFP's "Amenorrhea: An Approach to Diagnosis and Management"
A review of: Amenorrhea: An Approach to Diagnosis and Management
DAVID A. KLEIN, MD, MPH, San Antonio Military Medical Center, San Antonio, Texas, MERRILY A. POTH, MD, Uniformed Health Services University of the Health Sciences, Bethesda, Maryland
Am Fam Physician. 2013 Jun 1;87(11):781-788.
http://www.aafp.org/afp/2013/0601/p781.pdf
Amenorrhea can be primary or secondary. Primary is when the patient does not reach menarche. It should be considered if the patient is 15 years or age without having menses, does not have any pubertal development by the age of 13, or if the patient has not achieved menarche within five years of breast development. The most common causes are chromosomal or anatomical. Secondary amenorrhea is considered if the patient has irregular menses for six months or no menses for three months, after menarche. Causes in this case include PCOS, hypothalamic amenorrhea, hyperprolactinemia, or primary ovarian insufficiency.
Evaluation of primary amenorrhea starts with a history and physical exam. Some important points include galactorrhea, hirsutism, acne, sexual activity, vasomotor symptoms, BMI, thyroid exam, dysmorphic features, tanner staging, and pelvic exam. Lab work includes a pregnancy test, FSH, TSH, prolactin, as well as a pelvic ultrasound. If there is no uterus present on ultrasound, karyotyping and testosterone levels can be done to determine if the patient has mullerian agenesis (46,XX) or androgen insensitivity syndrome (46,XY). Mullerian agenesis may present in a patient with normal breast development, who has not reached menarche. It may be caused by a malformed genital or urinary tract, imperforate hymen, or transverse vaginal septum. Patients with androgen insensitivity may have little or no pubic hair, a blind vaginal pouch, and normal breasts. If the uterus is present, the FSH and LH levels should be checked. Low levels suggest a functional amenorrhea, constitutional delay of puberty, or a gonadotropin releasing hormone deficiency. Functional amenorrhea can be associated with the "female athlete triad" of deficient calorie intake, amenorrhea, and low bone density. If the levels are normal, an outflow tract obstruction should be considered. If the levels are elevated, the cause may be primary ovarian insufficiency or Turner syndrome. Patients with primary ovarian insufficiency may need hormone therapy until the age of menopause. It will decrease ischemic heart disease, vasomotor symptoms, and bone health. In Turner syndrome (45,XO) patients will have the short stature, a webbed neck and a low hairline.
Evaluation of secondary amenorrhea is also done with a history, exam and lab work. If the FSH and LH are high, they should be repeated in one month. Causes include primary ovarian insufficiency or the onset of menopause. When the levels of FSH and LH are low or normal, further investigation must be completed. Functional amenorrhea will be associated with an eating disorder, excessive exercise, or poor nutrition. An MRI can be done to rule out neoplasia if the patient has evidence of increased ICP. Asherman syndrome is due to uterine instrumentation during OB/GYN procedures. It the patient has evidence of hyperandrogenism, the clinician should order a serum testosterone, DHEA-5 and a 17-hydroxyprogesterone level. Elevated 17-OH progesterone can be due to congential adrenal hyperplasia. Elevated androgen levels may be seen in an adrenal or ovarian tumors. PCOS will be hyperandrogenistc, with polycystic ovaries on ultrasound. There will also be insulin resistance, ovulatory dysfunction, hirsutism and acne. Metformin, low-dose combined OCP's, weight loss, and exercise will improve symptoms.
DAVID A. KLEIN, MD, MPH, San Antonio Military Medical Center, San Antonio, Texas, MERRILY A. POTH, MD, Uniformed Health Services University of the Health Sciences, Bethesda, Maryland
Am Fam Physician. 2013 Jun 1;87(11):781-788.
http://www.aafp.org/afp/2013/0601/p781.pdf
Amenorrhea can be primary or secondary. Primary is when the patient does not reach menarche. It should be considered if the patient is 15 years or age without having menses, does not have any pubertal development by the age of 13, or if the patient has not achieved menarche within five years of breast development. The most common causes are chromosomal or anatomical. Secondary amenorrhea is considered if the patient has irregular menses for six months or no menses for three months, after menarche. Causes in this case include PCOS, hypothalamic amenorrhea, hyperprolactinemia, or primary ovarian insufficiency.
Evaluation of primary amenorrhea starts with a history and physical exam. Some important points include galactorrhea, hirsutism, acne, sexual activity, vasomotor symptoms, BMI, thyroid exam, dysmorphic features, tanner staging, and pelvic exam. Lab work includes a pregnancy test, FSH, TSH, prolactin, as well as a pelvic ultrasound. If there is no uterus present on ultrasound, karyotyping and testosterone levels can be done to determine if the patient has mullerian agenesis (46,XX) or androgen insensitivity syndrome (46,XY). Mullerian agenesis may present in a patient with normal breast development, who has not reached menarche. It may be caused by a malformed genital or urinary tract, imperforate hymen, or transverse vaginal septum. Patients with androgen insensitivity may have little or no pubic hair, a blind vaginal pouch, and normal breasts. If the uterus is present, the FSH and LH levels should be checked. Low levels suggest a functional amenorrhea, constitutional delay of puberty, or a gonadotropin releasing hormone deficiency. Functional amenorrhea can be associated with the "female athlete triad" of deficient calorie intake, amenorrhea, and low bone density. If the levels are normal, an outflow tract obstruction should be considered. If the levels are elevated, the cause may be primary ovarian insufficiency or Turner syndrome. Patients with primary ovarian insufficiency may need hormone therapy until the age of menopause. It will decrease ischemic heart disease, vasomotor symptoms, and bone health. In Turner syndrome (45,XO) patients will have the short stature, a webbed neck and a low hairline.
Evaluation of secondary amenorrhea is also done with a history, exam and lab work. If the FSH and LH are high, they should be repeated in one month. Causes include primary ovarian insufficiency or the onset of menopause. When the levels of FSH and LH are low or normal, further investigation must be completed. Functional amenorrhea will be associated with an eating disorder, excessive exercise, or poor nutrition. An MRI can be done to rule out neoplasia if the patient has evidence of increased ICP. Asherman syndrome is due to uterine instrumentation during OB/GYN procedures. It the patient has evidence of hyperandrogenism, the clinician should order a serum testosterone, DHEA-5 and a 17-hydroxyprogesterone level. Elevated 17-OH progesterone can be due to congential adrenal hyperplasia. Elevated androgen levels may be seen in an adrenal or ovarian tumors. PCOS will be hyperandrogenistc, with polycystic ovaries on ultrasound. There will also be insulin resistance, ovulatory dysfunction, hirsutism and acne. Metformin, low-dose combined OCP's, weight loss, and exercise will improve symptoms.
Tuesday, June 4, 2013
A synopsis of AFP's "Management of Hypertriglyceridemia"
A synopsis of: Management of Hypertriglyceridemia
ROBERT C. OH, MPH, MAJ, MC, USA, Tripler Army Medical Center, Honolulu, Hawaii, J. BRIAN LANIER, CPT, MC, USA, Martin Army Community Hospital, Fort Benning, Georgia
Am Fam Physician. 2007 May 1;75(9):1365-1371.
http://www.aafp.org/afp/2007/0501/p1365.pdf
I was listening to a podcast on hypertriglyceridemia on the way to work today, so I thought it would be a good idea to review it. The article I am writing about is from 2007 and I believe much has changed on this topic, such as the usage of fish oils. Regardless, we will truck ahead.
Triglycerides are the red-headed stepchild of cholesterol. Physicians do not focus on the level unless it is really high. Levels above 500-1000 mg/dL are associated with pancreatitis and metabolic syndrome. Although high triglyceride levels are an independent risk factor of cardiovascular risk, it is unclear whether reduction will modify such risk.
Statins are a first line agent in patients with elevated LDL's. It can also lower triglyceride levels by 20-40%. Fibrates can lower triglycerides 40-60% and can raise HDL's. Unfortunately, fibrate therapy has not shown to decrease all-cause mortality. Combination therapy with statins may increase the risk of rhabdomyolysis by inhibiting statin metabolism.
Niacin can lower triglyceride levels by 30-50% as well as raising HDL and lowering LDL. Studies are mixed on the effects of all-cause mortality and glycemic control. Vasomotor side effects and liver enzyme elevation has limited its use as well.
"According to this article", fish oil (omega 3 fatty acids) has shown a modest decrease in all cause mortality when used in conjunction with ACEIs, BBLs, antiplatelet meds, and other lipid medications. Fish oil and statin combos have showed a decrease in triglycerides as well. New studies question the benefits of fish oil supplements on cholesterol control and heir pro inflammatory effects may cause more harm than good.
The initial management of high triglyceride level is initiating therapeutic lifestyle changes, glucose control, and screening for metabolic syndrome and secondary causes, such as hypothyroidism, CKD, nephrotic syndrome and diabetis. After that, the focus becomes centered on LDL control, with statins. A cardiac risk profile should be determined and stratified. Patients with triglycerides above 1000 mg/dL need aggressive control of diet and weight reduction. Fibrates or niacin may be an appropriate first line choice in this case.
Monday, June 3, 2013
A Brief Synopsis of AFP's "Update on the Management of Chronic Kidney Disease"
A brief synopsis of:
Update on the Management of Chronic Kidney Disease
JOSETTE A. RIVERA, MD, University of California, San Francisco, California, ANN M. O’HARE, MD, University of Washington, Seattle, Washington, G. MICHAEL HARPER, MD, University of California, San Francisco, California
Am Fam Physician. 2012 Oct 15;86(8):749-754
http://www.aafp.org/afp/2012/1015/p749.pdf
Chronic kidney disease (CKD) is defined by a GFR less than 60ml/min/1.73 m2, or three or more months of kidney damage regardless of GFR. Staging is based mostly on GFR. Patients with CKD more often die from cardiovascular disease (CVD) than require dialysis. For this reason, cardiovascular disease management is an important aspect in treating patients with CKD.
Diabetes is the leading cause of CKD, as well as a risk factor for CVD. Current recommendations suggest an A1C level of less than 7% in patients without proteinuria. This may be too aggressive because of a higher rate of complications such as hypoglycemia, without any proven reduction in mortality, need for dialysis or cardiovascular events.
Proteinuria is a risk factor for all-cause and cardiovascular mortality. Patients with diabetic kidney disease, or nondiabetic kidney disease with a protein-to-creatinine ratio greater than 200 mg/g, should be started on an ACEI or ARB. Patients without proteinuria may not benefit from the medication. Combinations of ACEI and ARBs have not shown any outcome benefit, but have shown increased adverse effects, including decreasing renal function.
The JNC 7 has recommended a BP of less than 130/80 in patients with CKD. Studies show no benefit compared to a BP of 140-160/90-100. It may have benefit in patients with proteinuria over 300 mg/day.
Raising hemoglobin can adversely affect patients with CKD. Target levels above 13.3 g/dL can cause a higher risk of all-cause mortality, stroke, and cardiovascular death. Target levels should stay at 11-12 g/dL. Treatment can be administered at levels less than 10 g/dL, or during an acute drop in hemoglobin triggering the need for a transfusion.
Imaging contrast can affect patients with CKD. Patients with a GFR less than 60 mL/min are at an increased risk of contrast induced nephropathy. It is seen as a rise in creatinine greater than 25% above normal or an increase of 0.5 mg/dL. This will occur within a few days after the contrast is used. Patients can minimize the risk of nephropathy with adequate hydration and avoiding NSAIDs. IV hydration with sodium bicarb or NS can reduce the risk as well. N-ac has had inconsistent results as a preventative tool for contrast induced nephropathy. It is a relatively cheap and safe medication with little risk to use as an adjunct. Gadolinium-based contrast in MRI has been associated with kidney injury and fibrosis. It should not be used in patients with a GFR less than 30 ml/min/1.73m2.
Update on the Management of Chronic Kidney Disease
JOSETTE A. RIVERA, MD, University of California, San Francisco, California, ANN M. O’HARE, MD, University of Washington, Seattle, Washington, G. MICHAEL HARPER, MD, University of California, San Francisco, California
Am Fam Physician. 2012 Oct 15;86(8):749-754
http://www.aafp.org/afp/2012/1015/p749.pdf
Chronic kidney disease (CKD) is defined by a GFR less than 60ml/min/1.73 m2, or three or more months of kidney damage regardless of GFR. Staging is based mostly on GFR. Patients with CKD more often die from cardiovascular disease (CVD) than require dialysis. For this reason, cardiovascular disease management is an important aspect in treating patients with CKD.
Diabetes is the leading cause of CKD, as well as a risk factor for CVD. Current recommendations suggest an A1C level of less than 7% in patients without proteinuria. This may be too aggressive because of a higher rate of complications such as hypoglycemia, without any proven reduction in mortality, need for dialysis or cardiovascular events.
Proteinuria is a risk factor for all-cause and cardiovascular mortality. Patients with diabetic kidney disease, or nondiabetic kidney disease with a protein-to-creatinine ratio greater than 200 mg/g, should be started on an ACEI or ARB. Patients without proteinuria may not benefit from the medication. Combinations of ACEI and ARBs have not shown any outcome benefit, but have shown increased adverse effects, including decreasing renal function.
The JNC 7 has recommended a BP of less than 130/80 in patients with CKD. Studies show no benefit compared to a BP of 140-160/90-100. It may have benefit in patients with proteinuria over 300 mg/day.
Raising hemoglobin can adversely affect patients with CKD. Target levels above 13.3 g/dL can cause a higher risk of all-cause mortality, stroke, and cardiovascular death. Target levels should stay at 11-12 g/dL. Treatment can be administered at levels less than 10 g/dL, or during an acute drop in hemoglobin triggering the need for a transfusion.
Imaging contrast can affect patients with CKD. Patients with a GFR less than 60 mL/min are at an increased risk of contrast induced nephropathy. It is seen as a rise in creatinine greater than 25% above normal or an increase of 0.5 mg/dL. This will occur within a few days after the contrast is used. Patients can minimize the risk of nephropathy with adequate hydration and avoiding NSAIDs. IV hydration with sodium bicarb or NS can reduce the risk as well. N-ac has had inconsistent results as a preventative tool for contrast induced nephropathy. It is a relatively cheap and safe medication with little risk to use as an adjunct. Gadolinium-based contrast in MRI has been associated with kidney injury and fibrosis. It should not be used in patients with a GFR less than 30 ml/min/1.73m2.
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