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G. Bogir, M.A., M.D.
Medical Instructor, Drexel University College of Medicine
The anemia of prematurity 2 Understand the pathophysiologic basis for the anemia of prematurity Understand the variable treatment modalities for the anemia of prematurity B symptoms xanax addiction cheap 75 mg prothiaden. Definitions and recognition of anemia Define normal ranges of hgb concentrations and erythrocyte indices at birth and throughout childhood and adolescence b treatment junctional tachycardia prothiaden 75mg on line. Classification of anemia: morphologic medications with dextromethorphan buy cheap prothiaden 75 mg online, kinetic Correlate erythrocyte morphology with clinical syndromes Know the origin of various erythroid inclusions seen on blood smears Know how to classify anemias according to altered erythrocyte production 2c19 medications order prothiaden 75mg on line, increased erythrocyte destruction, and blood loss Understand and interpret results of reticulocyte counts Know that classification of anemias based on cell size is also age-dependent Know the differential diagnosis of macrocytic anemia Know the differential diagnosis of microcytic anemia Know the differential diagnosis of normocytic anemia c. Pathogenesis Recognize the syndrome of milk-induced gastrointestinal bleeding and understand its laboratory evaluation Recognize the clinical and laboratory manifestations of pulmonary hemosiderosis and know the appropriate diagnostic approach Recognize the factors in medical history that predispose pediatric patients to iron deficiency 3 Recognize the association between occult blood loss and iron deficiency anemia (2). Clinical and laboratory features Know the effect of iron deficiency on erythrocyte morphology, serum iron concentration, total iron-binding capacity, ferritin, free erythrocyte protoporphyrin, and soluble transferrin receptor concentration Know the order of appearance of laboratory abnormalities as iron deficiency develops Know the association of pica and iron deficiency Know the effects on growth and development of iron deficiency (3). Diagnosis Know the laboratory studies that differentiate the anemia of lead poisoning from that of iron deficiency Understand the laboratory studies that distinguish iron deficiency anemia from other causes of microcytic anemia (4). Treatment Determine the proper place for dietary changes, oral iron, parenteral iron, and erythrocyte transfusion in the treatment of iron deficiency (5). Consequences Understand the relationship between chronic iron overload and clinical organ dysfunction (ie, cardiac, endocrine, liver, pancreas) (2). Diagnosis Be able to estimate the amount of iron in a volume of erythrocytes Understand laboratory tests and other studies, including imaging techniques, used to diagnose and monitor iron overload Know the genetics and appropriate biochemical and molecular testing for hereditary hemochromatosis (3). Treatment Know the principles for prevention and treatment, including treatment regimens 4 (eg, phlebotomy, iron chelators, erythrocytapheresis) of transfusional iron overload and hereditary hemochromatosis Know the toxicity of iron chelators and appropriate monitoring of therapy c. Anemia of chronic disease and secondary anemias Recognize the clinical and laboratory findings in the anemia associated with chronic disease and how this differs from iron deficiency Recognize the effect of acute infection on hgb concentration Know the indications for and appropriate use of recombinant human erythropoietin in the treatment of secondary anemia such as anemia of renal disease or anemia of chemotherapy Know the characteristics of anemia associated with hypothyroidism Know the mechanism of production of abnormal erythrocytes in liver disease Know the relationship between parvovirus B19 infection and anemia, including recognition of the clinical scenario and site of action of the infection and the potential impact of the immunocompromised state Understand the pathogenesis of anemia of chronic disease 4. Fanconi anemia Know the clinical and molecular features, laboratory findings, and chromosomal abnormalities in Fanconi anemia 5 Recognize the association between Fanconi anemia and acute leukemia and other malignancies Know the complications of androgen therapy, including peliosis hepatis, adenoma, and carcinoma, in Fanconi anemia Know the therapeutic options for Fanconi anemia, and their effectiveness c. Diamond-Blackfan syndrome Recognize the clinical, molecular, and laboratory manifestations of Diamond-Blackfan syndrome Know the clinical and laboratory parameters that differentiate transient erythroblastopenia of childhood from Diamond-Blackfan syndrome Know the clinical and laboratory features that distinguish an aplastic crisis of a hemolytic anemia from transient erythroblastopenia of childhood and Diamond-Blackfan syndrome Know the various treatment modalities and their effectiveness in Diamond-Blackfan syndrome d. Transient erythroblastopenia of childhood Recognize the clinical syndrome of transient erythroblastopenia of childhood and know how to treat it appropriately. Dyskeratosis congenita Know the clinical presentation, molecular biology, genetics, laboratory findings, and therapy in a patient with dyskeratosis congenita f. Pearson syndrome Know the clinical and laboratory features and underlying defects of Pearson syndrome 5. Hereditary hemolytic anemias Know that Rh null phenotype is associated with a hereditary hemolytic anemia Know the relationship between parvovirus infection and aplastic crisis in congenital hemolytic anemias Recognize the role of folate supplementation in patients with hemolytic anemia a. Genetics Recognize the differences in the phenotypes of the autosomal dominant and autosomal recessive variants of hereditary spherocytosis (b). Pathophysiology Know the cytoskeletal defects associated with hereditary spherocytosis (c). Evaluation Understand the clinical and laboratory diagnosis of hereditary spherocytosis Know the basis for and pattern of abnormal osmotic fragility in hereditary spherocytosis Distinguish between hereditary spherocytosis and autoimmune hemolytic anemia (d). Management Know the rationale for and hematologic sequelae of splenectomy in hereditary spherocytosis (e). Complications Understand the complications seen in hereditary spherocytosis before and after splenectomy (2). Genetics Know the mode of inheritance of hereditary elliptocytosis and pyropoikilocytosis (b). Pathophysiology Know the cytoskeletal defects associated with hereditary elliptocytosis and hereditary pyropoikilocytosis (c). Clinical features Recognize hemolytic and non-hemolytic variants of hereditary elliptocytosis Know the clinical features of elliptocytosis and pyropoikilocytosis and the clinical problems of distinguishing them in the neonatal period (d). Laboratory evaluation Recognize the morphologic characteristics and other laboratory features of hereditary elliptocytosis and hereditary pyropoikilocytosis (e). Management 7 Know the effects of splenectomy on hereditary elliptocytosis and pyropoikilocytosis (3). Clinical features Recognize the clinical and laboratory features associated with the inherited and acquired conditions characterized by acanthocytosis (4).
Supportive therapy with repeated red blood cell transfusions can lead to elevated levels of iron in the blood and other tissues symptoms ulcer discount prothiaden 75mg without a prescription. The very small amounts that are lost daily (1 to 2 milligrams) are balanced by absorption from the diet medicine for vertigo purchase prothiaden 75mg. Red blood cell transfusion and iron overload Each unit of packed red blood cells contains about 250 milligrams of iron treatment stye purchase 75mg prothiaden with amex. After approximately 20 transfusions symptoms 0f parkinson disease cheap prothiaden 75mg fast delivery, a patient will receive an additional 5 grams of iron, nearly doubling the amount of iron in their body. Normally, iron binds to plasma protein called transferrin, which circulates in the body, accumulating within cells in the form of ferritin. Iron overload occurs when transferrin becomes saturated, increasing the concentration of non-transferrinbound iron-a toxic substance to cells. As levels of non-transferrin-bound iron accumulate in the blood, they are absorbed into the surrounding tissues, leading to increased levels of unbound iron in the liver, heart, pancreas, pituitary gland, and other glands. As a general rule, iron overload occurs after you receive 20 units of red blood cell transfusions. However, iron overload may occur after as few as 10 units of transfused blood in some patients and may not be present in some patients who have received more than 60 units of blood. You may not know that excess iron is building up in your body because there may be no symptoms. Iron overload is a potentially dangerous condition because excess iron can damage tissues. Excess iron may accumulate in the heart, liver, lungs, brain, bone marrow, and endocrine organs, putting you at risk for a number of conditions. Many of these are not reversible and may be life-threatening, including heart failure, cirrhosis and fibrosis of the liver, gallbladder disorders, diabetes, arthritis, depression, impotence, infertility, and cancer. Much of the data on the damaging effects of iron overload are from other blood disorders such as sickle cell anemia and thalassemia which are also associated with transfusion-dependent anemia. This negative effect on survival depends on the number of red blood cell transfusions received per month. Although many tests are available to assess iron overload, the most commonly used one today is a simple blood test called a ferritin test. Ferritin is a protein in the serum that binds iron and helps to store iron in the body. Because it is a simple blood test, it is easy to perform repeatedly to obtain ferritin readings over time, and a trend can be observed and monitored. A serum ferritin value of 1,000 ng/mL may be reached after as few as 20 units of red blood cells have been transfused. One disadvantage to the ferritin test is that the results are affected by inflammation, infection, and ascorbic acid (vitamin C) deficiency. Therefore, the trends in the ferritin levels over a period of time are most useful in monitoring iron overload. High serum ferritin level May indicate hemolytic anemia, megaloblastic anemia, or iron overload. Fortunately, iron overload can be treated with chelation therapy using iron-chelating drugs. Even after organ toxicity has developed, chelation therapy can reverse some of the complications of iron overload. Phlebotomy involves removing a unit of blood-similar to donating blood- which, like iron-chelating agents, removes the iron carried in red blood cells, as well as unbound iron in the blood. Chelation therapy is continued until your serum ferritin level is less than 1,000 ng/mL.
After you remove it from your skin treatment 4 water order prothiaden 75 mg with mastercard, the transparent tip will lock over the needle 97140 treatment code 75 mg prothiaden free shipping. Go to Step 4 Step 4: After the Injection Care of injection site: There may be a little bleeding at the injection site medications not to take during pregnancy 75 mg prothiaden otc. Do not throw away (dispose of) loose needles and prefilled syringes in your household trash symptoms 5th week of pregnancy order prothiaden 75mg fast delivery. If your injection is administered by a caregiver, this person must also handle the Autoinjector carefully to prevent accidental needle stick injury and possibly spreading infection. Why do I need to allow the Autoinjector to warm up at room temperature for 30 minutes prior to injecting Never try to speed the warming process in any way, like using the microwave or placing the Autoinjector in warm water. While you prepare for the injection, carefully place the Autoinjector on its side on a clean, flat surface. To unlock, firmly push the Autoinjector down on the skin without touching the button. Once the stop-point is felt, the device is unlocked and can be triggered by pushing the button. If you experience any side effects, including pain, swelling, or discoloration near the injection site, contact your healthcare provider or pharmacist immediately. Before lifting the Autoinjector from the injection site, check to ensure that the blue indicator has stopped moving. Then, before disposing of the Autoinjector, check the bottom of the transparent viewing window to make sure there is no liquid left inside. If the medicine has not been completely injected, consult your healthcare provider or pharmacist. If you do not have one, you may use a household container that is: made of a heavy-duty plastic, can be closed with a tight-fitting, puncture-resistant lid, without sharps being able to come out, upright and stable during use, leak-resistant, and properly labeled to warn of hazardous waste inside the container. There may be state or local laws about how you should throw away used needles and Autoinjectors. Your healthcare provider or pharmacist may be familiar with special carrying cases for injectable medicines. Be sure to pack your Autoinjector in your carry-on, and do not put it in your checked luggage. Prior to flying, get a letter from your healthcare provider to explain that you are traveling with prescription medicine that uses a device with a needle; if you are carrying a sharps container in your carry-on baggage, notify the screener at the airport. If you have questions or concerns about your Autoinjector, please contact a healthcare provider or call our toll-free help line at 1-800-673-6242. The drug offers a distinct mechanism of action and convenient oral route of administration beyond the current treatment armamentarium. This potential first-in-class treatment formulated as a desirable cream would provide a novel topical option for physicians and patients. Currently, corticosteroids and vitamin D derivatives are the preferred topical agents in psoriasis, however, long-term use of topical steroids is limited by the risk of skin atrophy. Interviewed Key Opinion Leaders in the gastroenterology space have voiced their enthusiasm towards Rinvoq and would like to prescribe it to more patients than Xeljanz as well as earlier in the treatment paradigm. Further to this, AbbVie has extensive commercial resources and marketing experience with Humira (adalimumab). In that condition, the thickened and stiff walls of the heart lead to obstruction of outflow, and paradoxically, the degree of obstruction can depend on the contractile force. On safety, a few patients did have reduced ejection fractions below 50%, which required temporary discontinuation of therapy, but this was also seen in the placebo group. While standard-of-care includes generic drugs with negative inotropic properties (betablockers, calcium channel blockers, and for combination therapy, disopyramide), a number of patients are still symptomatic or may require surgical intervention. However, chances for the drugs are mixed, and there is limited outcomes data in this segment. The numbers of patients in these subgroups were small and they were not separately randomized, so the data are fairly tentative. We have not included Zynquista as a highlighted drug, as it is so late to the market and likely to lag these other treatments.
This requirement for a source of lipid for growth and development explains the concordance of neonatal systemic disease with the infusion of intravenous lipid emulsions medicine 7253 discount prothiaden 75 mg line. Skin colonization with Malassezia species is nearly universal among adults medicine cabinets surface mount proven 75mg prothiaden, and direct transmission from caregivers to infants is the most common route of acquisition in the neonate [565 treatment algorithm order 75 mg prothiaden fast delivery,566] medicine 2016 order prothiaden 75mg with amex. These organisms persist on the hands of caregivers, despite appropriate hand hygiene, and on many hospital surfaces [561,567]. Malassezia organisms can be recovered from contaminated plastic surfaces for up to 3 months, and this persistence may facilitate nursery transmission [568]. Catheter-associated infections typically occur in infants older than 7 days of age, with the peak incidence in the third week of life [562,573,574]. Neonatal pustulosis typically develops between 5 days and 3 weeks of age [575,576]. Sebum on the skin, especially that of the face, provides the required source of fat in the case of neonatal pustulosis [561]. Catheter-related infections are always associated with the administration of intravenous lipid emulsions, whether Broviac central intravenous or percutaneously placed Silastic catheters are used [566]. Intravascular catheters used only for hyperalimentation (without intralipids) or medication administration and other types of indwelling catheters do not become infected because the infusate they deliver does not provide the lipid nutritional support necessary for Malassezia organisms to proliferate. Intravascular catheters frequently develop thrombi or fibrin sheaths that become adherent to the vascular wall, which then may become infected [564,576,577]. The infected thrombus then serves as a source for ongoing fungemia or dissemination to visceral organs through microembolism [576,578,579]. Persistent fungemia is common with neonatal Malassezia infections, yet disseminated disease rarely occurs. Rare cases of meningitis, renal infection, liver abscess, and severe pulmonary or cardiac involvement have been reported [573]. Additional predisposing conditions for the development of neonatal systemic Malassezia infections include short-gut syndrome, gastroschisis, necrotizing enterocolitis, and complex congenital heart disease [560,570,580,581]. The need for prolonged parenteral, rather than enteral, nutrition is the common denominator in all of these predisposing conditions. Although less common than infections due to spread of the skin-colonizing organisms, infections due to direct nosocomial transmission of Malassezia species are documented [561,582]. Lesions are not irritating to the infant, do not disseminate, and typically resolve over time without therapy-yet the appearance of neonatal pustulosis often is disturbing to parents. Infants with catheter-related Malassezia fungemia typically have any combination of the following nonspecific findings: lethargy, poor feeding, temperature instability, hepatosplenomegaly, hemodynamic instability, and worsening or new respiratory distress [565]. Fever occurs in 53% of cases, and thrombocytopenia, which may be severe, is observed in 48% of cases. Most infants do not become critically ill but have the clinical picture of an ongoing indolent infection. Infants also may have a malfunctioning catheter following occlusion by a Malassezia-infected thrombus [561]. When Malassezia infection is suspected, the laboratory should be notified because these yeasts are not recovered from routine culture media, and special lipid supplementation is required for their growth and identification [583]. Echocardiography is indicated in infants who have persistent fungemia, so that an infected thrombus on the catheter tip can be excluded [586]. Although dissemination is rare, antifungal therapy usually is provided to ensure clearance of the organism from the bloodstream. Amphotericin B is the most frequently used agent, although in vitro testing suggests only moderate susceptibility of Malassezia species to this agent [580]. With removal of the catheter, and thereby the high concentration of lipid, the organism will no longer survive. Vascular catheter complications, including retained catheters and catheter breakage, have been reported with Malassezia infections, with one series suggesting M. Thrombolytic therapy with urokinase and tissue plasminogen activator has been used to facilitate the removal of adherent M.