By Z. Ben. Institute for Transpersonal Psychology.
A 60-year-old woman with a history of hypertension and mild chronic obstructive pulmonary disease (COPD) presents with a new complaint of progressive dyspnea purchase 50 mg lamictal overnight delivery treatment 02 binh. Grade IV to VI murmur at the apex that radiates to the axilla ❏ B lamictal 100mg online symptoms vaginal yeast infection. S4 gallop Key Concept/Objective: To understand the physical examination findings of left-sided systolic heart failure Mitral regurgitation resulting from annular dilatation is commonly audible in systolic heart failure. However, the regurgitant murmur is generally no louder than grade II to grade III in intensity and will wax and wane, depending on the extent of left ventricular dilatation. Murmurs of greater intensity should suggest intrinsic rather than functional valve disease. Paradoxical splitting of S2 can occur in systolic chronic heart failure as a result of either left bundle branch block or reversal of A2 and P2 caused by prolonged ejection of blood by the impaired left ventricle. Fixed splitting of S2 is associated with atrial septal defect or right ventricular failure. Patients with COPD also find it easier to breathe with the head of the bed and thorax elevated. A presystolic, or S4, gallop indi- cates reduced compliance of the left ventricle but not a failing left ventricle per se. Pulsus alternans, characterized by alternating weaker and stronger pulsations in the peripheral arteries, indicates a diseased left ventricle with poor systolic function. Pulsus alternans will usually be accompanied by an S3 gallop. A 60-year-old man presents with progressive symmetrical lower extremity edema. Pulsus paradoxus Key Concept/Objective: To understand the clinical findings of right-sided heart failure In right ventricular failure, constrictive pericarditis, or tricuspid stenosis, the compromised right ventricle cannot accommodate the normal increased venous return that occurs dur- ing inspiration. This causes a rise, rather than the normal fall, in jugular venous pressure during inspiration (a positive Kussmaul sign). This sign is a subtle indicator of right ven- tricular dysfunction and may be seen even in the presence of normal jugular venous pres- sure. In patients with severe and chronic systemic venous congestion, the prothrombin time can be prolonged. Thus, an abnormal international normalized ratio does not auto- matically indicate liver disease. Similarly, chronic congestion may produce mild elevations in bilirubin and alkaline phosphatase levels. An elevation of transaminase levels is more likely to be associated with acute liver congestion with hypoxia and hepatocellular dam- age. Splanchnic congestion in right heart failure can lead to nausea, diarrhea, and malab- sorption. Pulsus paradoxus consists of a greater than normal (10 mm Hg) inspiratory decline in systolic arterial pressure. It can occur in cases of cardiac tamponade, constric- tive pericarditis, hypovolemic shock, pulmonary embolus, and COPD. It would not be expected in isolated right-sided heart failure. A 54-year-old man presents to your clinic to establish primary care. He has a history of diabetes, CHF, and hypertension. His blood pressure is 160/90 mm Hg, 2+ edema is present, and mild crackles are heard in the bases of his lungs. Which of the following statements incorrectly characterizes attributes of the medications to be con- sidered for this patient? Hydrochlorothiazide may exacerbate hyperglycemia ❏ B. Without a loading dose, the blood level of digoxin will plateau in 7 days ❏ C. Oral bioavailability of loop diuretics varies little from drug to drug ❏ D.
Blood pressure control is also an urgent consideration order 100 mg lamictal amex symptoms quitting smoking. An 84-year-old man comes to your office complaining of a severe left temporal headache discount lamictal 25 mg otc medications ending in pam, which he has had for the past 2 days. In addition, the patient states that over the past 2 days, he has had a low-grade fever, fatigue, and loss of appetite. Upon questioning, the patient admits to muscle weakness and jaw pain with mastication but has no visual complaint. The physical examination is within normal limits, with the exception of a tender, palpable left temporal artery. Laboratory evaluation reveals a slight ele- vation in the white blood cell count and a marked elevation in the erythrocyte sedimentation rate. Which of the following statements regarding giant cell arteritis is true? Giant cell arteritis often affects the branches of the proximal aorta ❏ B. Giant cell arteritis commonly occurs in patients 50 years of age or younger ❏ C. Giant cell arteritis never results in complete blindness despite the high frequency of visual complaints ❏ D. Standard therapy for this arteritis is prednisone, 5 to 15 mg/day Key Concept/Objective: To recognize that giant cell arteritis affects the branches of the proximal aorta Giant cell arteritis often affects the branches of the proximal aorta, particularly the branches supplying the head and neck, the extracranial structures (including the tempo- ral arteries), and the upper extremities. Aortic involvement often coexists with temporal arteritis and polymyalgia rheumatica. This illness is more commonly seen in patients older than 50 years (the mean age at onset of disease is 67 years). A serious complication of this syndrome is blindness, which results when arteritis affects the ophthalmic artery. Visual symptoms of some type occur in as many as 50% of patients. Standard therapy for giant cell arteritis is high-dose glucocorti- coid therapy (e. A 68-year-old man with a long history of cigarette smoking presents for routine evaluation. On physical examination, he has a pulsatile abdominal mass. He reports no symptoms of abdominal pain or back pain. Treatment with a beta blocker Key Concept/Objective: To understand the approach to the treatment of abdominal aortic aneurysms 34 BOARD REVIEW Studies have shown that the likelihood of rupture is highest in patients with symptomatic or large aneurysms. Aneurysms smaller than 4 cm in diameter have a low risk (< 2%) of rupture. Aneurysms exceeding 10 cm have a 25% risk of rupture over 2 years. Current man- agement strategies call for identification and observation of aneurysms that are asympto- matic and sufficiently small so as not to have a high risk of rupture. The median rate of expansion is slightly less than 0. Aneurysms that are expanding more rapidly are more likely to rupture than stable aneurysms. Patients with aneurysms larger than 6 cm are generally referred for surgery, whereas patients with aneurysms smaller than 4 cm generally undergo observation. Evidence of expansion, particularly if the aneurysm is larg- er than 5 or 5. It would be appropriate to assess its growth with ultrasonography over the next few years to see whether it is expanding more rapidly than expected. The rate of expansion is an important variable in assessing the risk of aneurys- mal rupture. If the patient becomes symptomatic at any time, urgent imaging is appro- priate. Aortography carries risk of contrast exposure and of atheromatous emboli, and it offers no advantages over ultrasonography for assessing the size of aneurysms.
Although HbS/HbC disease is less severe than HbSS disease quality lamictal 50 mg symptoms hiatal hernia, patients with HbS/HbC frequently tend to have avascular necrosis of the femoral head purchase lamictal 100 mg overnight delivery medications given im. Patients with α0-thalassemia have a very low concentration of HbA; in these patients, HbS consti- tutes more than 50% of the intracorpuscular hemoglobin. In extreme cases, the clinical picture of α0-thalassemia is identical to that of HbSS. As HbS decreases, the clinical picture comes to resemble that of patients with HbS/HbC disease. A 38-year-old African-American man is admitted to the hospital with congestive heart failure (CHF) of new onset. He is noted to have a blood pressure of 210/140 mm Hg. Therapy with intravenous furosemide, intravenous nitroglycerin, and oral angiotensin-converting enzymes controls his symptoms and blood pressure over the next 48 hours. On the third day, a 10% drop of his hematocrit is noted. Laboratory data show the following: Hb, 11 g/dl (admission Hb, 14. Which of the following tests is most likely to establish the diagnosis? Hemoglobin electrophoresis Key Concept/Objective: To understand hemolysis secondary to use of oxidating agents (furosemide and nitroglycerin) and the timing of the G6PD assay 14 BOARD REVIEW This patient experienced an episode of acute hemolysis after being hospitalized. It is like- ly that this is a case of drug-induced hemolysis. There are several mechanisms by which drugs can induce hemolysis; two well-recognized mechanisms are immunologic media- tion (e. Oxidative stress can occur as a result of hemoglobins becoming unsta- ble or through a decrease in reduction capacity (as would result from G6PD deficiency). Penicillins and cephalosporins produce immune hemolysis by acting as a hapten in the red cell membrane. The protein/drug complex elicits an immune response. An IgG anti- body is generated that acts against the drug-red cell complex. In such patients, the direct Coombs test is positive, but the indirect Coombs test is negative. Other drugs induce hemolysis by altering a membrane antigen. IgG autoantibodies that cross-react with the native antigen are produced. The direct Coombs test is also positive in this form of drug reaction. Methyldopa is the classic example of this form of interaction, although other drugs such as procainamide and diclofenac have been clearly implicated. Diclofenac can produce massive hemolysis with concomitant disseminated intravascular coagulation and shock. Sucrose lysis is still used to screen for membrane fragility. The most common dis- order associated with this abnormality is paroxysmal nocturnal hemoglobinuria (PNH). The lack of associated cytopenias, the acuteness of the onset of symptoms, and the lack of history of venous thrombosis (especially thrombosis at unusual sites such as the inferior vena cava or the portal mesenteric system or thrombosis that produces Budd-Chiari syn- drome) makes PNH an unlikely cause of this patient’s symptoms. Some unstable hemo- globins, such as HbE, are susceptible to hemolysis from oxidative stress. This patient was exposed to both furosemide (a drug with a sulfa moiety) and nitroglycerin. This hemoglo- binopathy is diagnosed by hemoglobin electrophoresis. However, this disease is seen almost exclusively in individuals from Southeast Asia (Cambodia, Thailand, and Vietnam). The most likely diagnosis in this case is G6PD deficiency.
The mean onset for BSMA is 30 years (range buy generic lamictal 200 mg line 2d6 medications, 15–60 years) generic 100mg lamictal medicine pill identification. Patients exhibit Symptoms symmetrical weakness that progresses slowly over many years, and typically do not need canes or walkers until they are in their fifties or sixties. Facial, tongue, and proximal weakness are typical at presentation. Dysphagia, dysarthria, and masseter weakness are commonly observed. As BSMA only affects lower motor neurons, there are no upper motor neuron Signs signs. Vibratory sensation may be reduced, and patients often show a mild postural tremor. BSMA is an X-linked recessive disorder, caused by a tri-nucleotide repeat Pathogenesis expansion in the first exon of the androgen receptor gene on chromosome Xq11–12. It is unknown how disruption of the androgen receptor in this way leads to specific loss of lower motor neurons, as there are other mutations in 452 this gene that cause testicular feminization but have no affects on motor neurons. Diagnosis Genetic: Patients with appropriate signs and symptoms are diagnosed by positive genetic testing. Laboratory: As muscles are chronically denervated, creatine kinase levels are elevated (up to 10-fold). A muscle biopsy is frequently performed and shows evidence of denervation. EMG: Chronic denervation is also demonstrated by EMG. Differential diagnosis ALS: BSMA has no upper motor neuron signs, distinguishing it from ALS. Therapy Currently, the only treatment is supportive care when the muscle weakness becomes problematic. Prognosis The number of CAG repeats present in the gene directly correlates with the age of onset and severity of the disease (i. Saunders, London, pp 325–369 Wang CH, Carter TA, Gilliam TC (1997) Molecular and genetic basis of the spinal muscular atrophies. In: Rosenberg RN, Pruisner SB, DiMauro S, Barchi RL (eds) The molecular and genetic basis of neurological disease, 2nd edn. Mantak Chia was born in Thailand to Chinese parents in 1944. When he was six years old, Buddhist monks taught him how to sit and “still the mind. He was then taught Tai Chi Chuan by Mas- ter Lu, who soon introduced him to Aikido, Yoga and broader levels of Tai Chi. Years later, when he was a student in Hong Kong excelling in track and field events, a senior classmate named Cheng Sue-Sue introduced him to his first esoteric teacher and Taoist Master, Mas- ter Yi Eng (I Yun). At this point, Master Chia began his studies of the Taoist way of life in earnest. He learned how to circulate energy through the Microcosmic Orbit and, through the practice of Fusion of the Five Elements, how to open the other Six Special Channels. As he studied Inner Alchemy further, he learned the Enlightenment of the Kan and Li, Sealing of the Five Senses, Congress of Heaven and Earth and Reunion of Heaven and Man. It was Master Yi Eng who authorized Master Chia to teach and heal. When Mantak Chia was in his early twenties he studied with Master Meugi in Singapore, who taught him Kundalini, Taoist Yoga and the Buddha Palm. He was soon able to clear blockages to the flow of energy within his own body. He learned to pass the life force energy through his hands also, so that he could heal Master Meugi’s patients. A while later, he studied with Master Cheng Yao-Lun who taught him the Shao-Lin Method of Internal Power.
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