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

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

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

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

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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