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Y. Rufus, M.B. B.CH., M.B.B.Ch., Ph.D.

Professor, TCU and UNTHSC School of Medicine

Insulin resistance is a spectrum of metabolic derangements (type 2 diabetes is at one end), including hyperinsulinemia, that are related to obesity, inactivity, and advancing age and are associated with a greater risk of coronary artery atherosclerosis. This condition may represent an abnormality of the coronary microvascular bed and has been associated with insulin resistance. This is a risk factor for adult-manifest cardiovascular disease, and children with a strong family history of essential hypertension tend to "track" into adulthood with the highest blood pressures relative to their same-age peers. Some other risk factors, such as obesity and dyslipidemia, usually associate with essential hypertension, leading to speculation that a group of abnormal genes is responsible. Chronic and end-stage kidney disease is associated with early onset coronary artery disease, likely due to multiple mechanisms, including systemic hypertension, abnormal lipid and calcium metabolism, elevated homocysteine, and the effects of inflammation and uremia on endothelial function. Calcification of soft tissues, including coronary arteries, can develop in children with chronic renal disease, especially those on dialysis. High blood levels of this amino acid are associated with atherosclerosis and a hypercoagulable state. The observation was first made in homocystinuric children, rare individuals with an inborn metabolic error. For most individuals, adequate dietary intake of folate and other vitamins can decrease homocysteine levels. A diffuse form of coronary artery narrowing occurs in most children and adults following transplantation and may be due primarily to low-grade chronic rejection. In at least one-third of children it is a major factor in death or need for retransplantation. Although the pathology of transplant vasculopathy differs from that of atheroma, modifying traditional risk factors such as systemic hypertension and lipids has been proposed as a means to improve the outcome for these patients. In addition to tobacco, excessive alcohol consumption may adversely affect other risk factors, such as lipids, but it also has a direct toxic effect on the myocardium, which can result in a dilated cardiomyopathy. Cocaine and similar illicit drugs are associated with acute myocardial ischemia and sudden death. Dental disease and bacterial infection are speculative factors in the genesis of atheromas, presumably by direct (infection) or indirect (toxin or inflammatory) injury to the endothelium. Optimum care of the child with congenital cardiac disease entails attention to the effect of the disease on the behavioral, psychological, and intellectual growth of the child and on the family. Other considerations include the proper definition of the disease and medical and surgical management. In the current age of sophisticated diagnostic and surgical procedures, the common psychological factors of chronic disease are frequently overlooked. Some patients undergo expensive and extensive operative procedures to correct their cardiac malformations but suffer from the "crippling" effect of the severe emotional problems common to many children with chronic disease. Because of a murmur or cardiac disease, many potential problems can develop in the family. The physician must make the recognition of these problems of the utmost importance. On the initial visit, following the review of the clinical and laboratory findings with the parents, the parents should be given ample opportunity to express their feelings and to ask questions. Many parents are helped by the practitioner who, when explaining cardiac anomalies, points out that, except for rare cases, the medical community knows little of the etiology of the condition. Unless there are contraindications, the child should be treated in the same way as his or her siblings or peers in chores, responsibilities, and discipline. Grandparents in particular must be cautioned of the dangers of an overly sympathetic or solicitous approach. In summary, the child must be treated like other children to the greatest possible extent. In general, for women with well-repaired congenital malformations with normal or near-normal hemodynamics, the risk of pregnancy is similar to that in unaffected women. Disorders conferring the highest risk of maternal and fetal death include Marfan syndrome, severe dilated cardiomyopathy, pulmonary vascular obstructive disease or primary pulmonary hypertension, and severe unrepaired malformations. Reproductive issues and pregnancy Reproductive issues, including pregnancy, recurrence risk, and contraception, are issues of concern to young persons with congenital or acquired heart disease.

The second conformational change in gp41 results in insertion of a fusion peptide into the cell membrane of the target T-cells or macrophages. Fusions of infected & uninfected cells with formation of syncythia (giant cells) develop ballooning and these cells usually die in few hours. Similar to cells majority infected cells are found in tissues not in peripheral blood. A relatively high productive infection of macrophages (10 to 15%) is detected in certain tissues such as Brain and lungs. I) Monocytes and macrophages represent a veritable virus factory and reservouir whose output remains largely protected from host defences. B-lymphocyte dysfunctions Hypergamaglobinemia and circulating immune complexes Inability to mount do novo antibody response to a new antigen Decreased immunoglobuline production in response to new antigen 4. Impaired humeral immunity renders these patients prey to disseminate infections caused by encapsulated bacteria such as S. In addition, nitric oxides also induce neuronal damage (according to most investigators). Early acute phase High level of viral production, viremia and widespread seeding of lymphoid tissues. The level of viral load in early acute phase of the disease is called the set point and anti retroviral therapy can reduce this set point thus, early detection especially in cases of needle stick injuries, rape and other known risky exercises can benefit from it. The middle chronic phase Relative containment of the viruses with a period of clinical latency (not viral latency). The final, crisis phase Characterized by breakdown of host defences with increased plasmal viral load and clinical disease. Discuss the pathogenic mechanisms of each type of hypersensitivity reaction with examples. Learning objectives: At the end of this chapter, the student is expected to: Explain the etiology, pathogenesis, morphologic, & some clinical features of typhoid fever, tuberculosis, leprosy, syphilis, malaria, leishmaniasis, schistosomiasis, & selected fungal. Typhoid Fever Definition: Typoid fever is an acute enteric disease caused by an obligate intracellular bacillus called Salmonella Typhi and this bacillus resides within mononuclear phagocytic cells of lymphoid tissues. The disease is unique humans and it is characterized by fever, splenomegaly and neutropenia. Pathogenesis: Infection is by ingestion of the organism, (>10 to the power of 7) in 50% of cases penetrate the small intestine mucosa and reach the circulation with transient bactremia the bacilli are taken by the lymphatic to lymph nodes and they are engulfed by mononuclear phagocytic cells. After a period of multiplication in these phagocytic cells, the organisms rupture the cells and invade the blood stream via the thoracic duct. The liver, gallbladder, spleen, kidney and bone marrow become infected during this second bactermic phase, characterizing the clinical features of the diseases. Others include pseudomonas, Klebsiella, Salmonella in sickle cell anemic patients. Sites: Any bone may be affected but the metaphysics of long bones (distal femur, proximal tibia and humorus) adjacent to actively growing epiphyses and the vertebral column are most often involved. Pathogenesis: the location of the lesions within specific bones is influenced by the vascular circulation, which varies with age. In the neonate, the metaphysical vessels penetrate the growth plate resulting in frequent infection of the metaphysis, epiphysis or both. In adults, the epiphyscal growth plate is closed and the metaphysical vessels reunite with their epiphyses counterparts, which provide a route for bacteria to seed in the epiphysis and subchondral regions. The susceptibility of the metaphysis to acute osteomylitis is in part, explained by the dilated vascularature of the marrow spaces where sluggish blood flow provides an ideal site for multiplication of bacteria.

The aim of this study is to evaluate the incidence of acute neonatal respiratory disorders and the main related complications. The results are described of a 1-year single centre study,which focused on the following points: the incidence of respiratory diseases in newborns and related mortality; the relationship between acute neonatal respiratory disorders rates and gestational age, birth weight, gender, Apgar score, maternal age, mode of delivery; and the incidence of complications associated with respiratory disturbances. Patients and Methods 16 494 live births was born in Zekai Tahir Burak Hospital, of these patients 2546 (15. Other disorders were sepsis, congenital airway and cardiac malformations,chromosal disorders, perinatal asphyxia, pulmonary hypoplasia and hydrops fetalis. Our study has a different epidemiological point of view in terms of evaluating the etiology of respiratory distress and complications in the neonatal period. With the completion of our study we are expecting to reach more reliable and updated results. Due to clinical instability and skin immaturity, early surgical intervention carries additional risk to the infant. In these patients fetal patch coverage of the lesion obviates the need for early postnatal surgery. He was noted to have an open low lumbar myelomeningocele with marked lower limb muscular hypotrophy. He was placed in a plastic bag and given surfactant following intubation at 5 minutes of age. During the initial few weeks he developed a left sided intraventricular haemorrhage with parietal parenchymal infarction. The lesion was left to allow granulation healing and dressed with moist sterile gauze and tegaderm. It prevents a "secondary hit" from intervention related complications due to skin immaturity and an unstable clinical condition. Picture Pulmonology / Mechanical ventilation Is it beneficial to treat ureaplasma urealyticum in ventilated preterm infants The rationale in treating the infection/colonisation in preterm infants is to facilitate extubation or weaning the ventilator requirement. Aim: To evaluate the efficacy of treating ureaplasma infection or colonisation with erythromycin in ventilated preterm infants. Patients and Methods Retrospective observational study of 4 years (from Feb 2011 to Jan 2015) in a busy non-surgical neonatal intensive care unit of all the positive ureaplasma cases in preterm infants. Conclusions In 22% of the ventilated preterm infants with ureaplasma infection/colonisation, erythrmocyin treatment may have facilitated extubation. Large randomised control trials are needed to evaluate the true effect of erythromycin treatment on ventilated preterm infants in facilitation of extubation. Vitamin D is known for its role in bone metabolism, but physiology suggests it influences lung fibroproliferation, remodelling and function by various cytokines, cellular elements, oxidative stress and protease/antiprotease levels. An animal study speculates that decreased vitamin D levels may contribute to the pathogenesis of bronchopulmonary dysplasia. The definition of chronic lung disease used is the requirement of oxygen at 36 weeks (corrected gestation) in <32 weeks gestation at birth. Larger randomised control trials are needed to establish the role of Vitamin D deficiency and chronic lung disease. Table Early supplementation group (n=13) Gestation mean Weight mean 26,69 841,77 Late supplementation group (n=11) 25,73 722,55 52,58 Unpaired ttest p value 0,318 0,214 <0. All of them but one shared a universal symptom of passing stool mixed with fresh blood. However, they developed the infection at a corrected gestation of 38 and 44 weeks respectively. The other two babies were term well babies who were reported to pass fresh blood mixed with their stool shortly after birth while on the postnatal ward. Interestingly, with one of these two babies, there was a history of confirmed neonatal amoebiasis with his older sibling. He developed small bowel perforation as a complication of Necrotising Enterocolitis. His infection has manifested by sudden increase in his ileostomy output associated with raised C-reactive protein.

It is easily absorbed by the body and accumulates primarily in the liver and kidneys. In high-selenium areas of China, peripheral anesthesia and pain in the limbs have been reported. Exaggerated tendon reflexes, convulsions, paralysis, and hemiplegia were estimated to occur at a minimum chronic exposure of 0. Mice appear to be more sensitive to selenium with regard to lung toxicity than rats. Hematological effects have been observed in multiple acute and chronic animal studies. Endocrine effects have been observed in animals fed seleniferous wheat at doses of 0. Depression of the immune system was observed in rats exposed subchronically to sodium selenite at 0. In animals, selenium has caused growth retardation, decreased fertility, embryotoxicity, fetotoxicity, and teratogenic effects. Chronic exposure studies in animals have identified multiple adverse effects on the reproductive ability of animals and on offspring viability. Decreased sperm counts have been observed in male rats exposed subchronically to 0. Inorganic selenium compounds appear to have genotoxic effects at relatively high doses and antigenotoxic effects at lower doses. Most forms of selenium interact with arsenic to reduce the toxicity of both elements. This compound and other tributyltin compounds have high bioconcentration factors in aquatic organisms and are acutely and chronically toxic to these organisms at low concentrations. The tributyltin compounds registered for use as antifoulants are: tributyltin oxide, tributyltin adipate, tributyltin dodecenyl succinate, tributyltin sulfide, tributyltin acetate, tributyltin acrylate, tributyltin fluoride, tributyltin methacrylate, and tributyltin resinate (U. This toxicological profile discusses only tributyltin oxide, since this is the only tributyltin compound with risk assessment information (an RfD) and there is more toxicological information on this compound than any other. One study specific to tributyltin oxide found the highest levels of tin in the liver and kidneys, with levels in the brain and adipose tissue at 10 to 20 percent of the liver and kidney levels. The metabolism of organotin compounds appears to involve dealkylation, with the liver as the active site. This was based on a chronic rat feeding study in which immunotoxicity was observed. This is based on the fact that the principal study was a well-designed and well-conducted chronic toxicity assay. In a two-generation reproductive study in rats, there were no effects on mating, pregnancy, fertility, litter size, or pup survival in either generation. Compound-related developmental effects were limited to decreased pup body weight during lactation in both generations at the high dose. When pregnant rats were exposed to high doses of tributyltin oxide (>10 mg/kg-d), decreased numbers of live births and decreased growth and viability of 5-30 5. A developmental study in mice reported dose-related decreases in fetal weights, some skeletal abnormalities, such as fused ribs and cleft palates, at all dose levels and also in the controls. Tributyltin oxide was negative in a variety of studies with Salmonella typhimurium and Chinese hamster cells; the only positive results were with metabolic activation. In vivo studies were also mainly negative; the compound was negative in Drosophila melanogaster and in the micronucleus test (at cytotoxic doses) in mice. The study in rats noted an increased incidence of some benign tumors at the highest dose level. However, this study is inconclusive because of increased mortality at the high dose and variable background rates for the tumors observed. For example, preweanling rats were shown to be more sensitive than adult rats to the immunotoxic effects of tributyltin oxide. Because the RfD is based on the effects observed when weanlings were dosed for the remainder of their lives, any potential childhood sensitivity is already accounted for. Animal toxicity studies showed no evidence of gender differences in the toxic responses to tributyltin oxide (U. These data adequately characterize the noncancer toxicity from oral exposure to tributyltin oxide. In addition, there is a two-generation reproduction study and several developmental studies in rats and mice.

Tesfaye is married to an unrelated woman called Tenagne, & has a 2 year old daughter, Mimi. Hypersensitivity Reactions the purpose of the immune response is to protect against invasion by foreign organisms, but they often lead to host tissue damage. An exaggerated immune response that results in tissue injury is broadly referred to as a hypersensitivity reaction. This bridging of IgE molecules activates signal transduction pathways from cytoplasmic portion of IgE fc receptors. One leading to mast cell degranulation with discharge of preformed (primary) mediators and the other involving denovo synthesis and release of secondary mediators. Initial phase (response): Characterized by vasodilatation, vascular leakage, and depending on the location, smooth muscle spasm or glandular secretions. Mast cells are bone marrow driven cells widely distributed in tissues around blood vessels, and sub epithelial sites where type I reaction occurs. Morphology: Histamine and leukotriens are released rapidly from sensitized mast cells and are responsible for intense immediate reaction characterized by edema, mucous secretions and smooth muscles spasms. Three different antibody-dependent mechanisms are involved in this type of reaction these cells secrete other waves of 141 (i) Complement-dependent reaction i. This membrane attack complex then disrupts cell membrane integrity by drilling a hole. In anucleated cells once and in nucleated cells many attacks of the complex are needed for cell lysis, because the latter ones have abilities to repair cell membrane injuries rapidly. Examples include red blood cells, leukocytes and platelets disorders: Transfusion reaction; haemolytic anemia; Agranuloytosis; Thrombocytopenia; Certain drug reaction ii. The target cells coated with IgG antibodies are killed by a variety of nonsensitized cells that have Fc receptors. Antibody-mediated cellular dysfunction In some cases, antibodies directed against cell surface receptors impair or dysregulated function without causing cell injury or inflammation. For example: In Myasthenia Gravis, antibodies reactive with acetylcholine receptors in the motor end plates of skeletal muscles impair neuromuscular transmission and cause muscle weakness. The converse is noted in Graves disease where antibodies against the thyroidstimulating hormone receptor on thyroid epithelial cells stimulate the cells to produce more thyroid hormones. Endogeneous origin Nuclear components (systemic lupus erythematosis) Immunoglobulins (rheumatoid arthritis) Tumour antigen (glomerulonephritis) Therefore, autoimmune diseases are hypersensitivity diseases in which the exaggerated immune response is directed against the self antigens as exemplified by the above three diseases. Formation of Ag-Ab complex Introduction of an antigen into the circulation, then Production of specific antibodies by immuno-competent cells and subsequent antigen antibody formation b. Deposition of immune complexes the mere formation of antigen-antibody complex in the circulation does not imply presence of disease. Other factors for immune deposition include charge of immune complexes, valence of antigen, avidity of the antibody, affinity of the antigen to various tissue components, three-dimenstional /lattice/ structure of the complex, hemodynamic factors, etc. Sites of immune complex deposition include: Renal glomeruli, joints, skin, heart, serosal surfaces, & small blood vessels 143 c. Inflammatory reaction After immune complexes are deposited in tissues acute inflammatory reactions ensues and the damage is similar despite the nature and location of tissues. Due to this inflammatory phase two mechanisms operate i) Activation of complement cascades: - C-3b, the opsonizing, and -C-5 fragments, the chemotaxins are characterized by neutrophlic aggregation, phagocytosis of complexes and release of lysosomal enzymes that result in necrosis. Neutorphiles and macrophages can be activates by immune complexes even in absence of complements. With either scenario, phagocytosis of immune complexes is effected with subsequent release of chemical mediators at site of immune deposition and subsequent tissue necrosis. Morphology of immune complex-mediated hypersensitivity reaction the morphologic consequences are dominated by acute necrotizing vasculitis with intense neutrophilic exudation permiting the entire arterial wall. Affected glomeruli are hyper cellular with proliferation of endothelial and mesengial cells accompanied by neutrophillic and mononuclear infiltration. Classification of immune complex-mediated diseases: Immune complex-mediated diseases can be categorized into systemic immune complexes diseases. Systemic immune-complex diseases: Acute forms: If the disease results from a single large exposure of antigen / ex: acute post-streptococal glomerulonephritis and acute serum sickness/ all lesion then tend to resolve owing to catabolism of the immune complexes. Arthus reaction: the Arthur reaction is defined as a localized area of tissue necrosis resulting from an immune complex vasculitis usually elicited in the skin. Arthus reaction occurs at site of inoculation of an antigen and depends on the presence of precipitating antibody in the 144 circulation / with antibody excess/ that resulted in immune complex deposition.