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Symptoms include vomiting quit smoking 2 buy 17.5 mg nicotinell, cramps quit smoking 3 months ago and still tired all the time cheap 35mg nicotinell visa, diarrhea quit smoking 15 months buy nicotinell 52.5 mg cheap, itching quit smoking 6 month benefits purchase nicotinell 35mg overnight delivery, wheezing quit smoking techniques generic 35 mg nicotinell fast delivery, and shortness of breath quit smoking encouragement generic nicotinell 35 mg without prescription, and death may occur within minutes. Complement-mediated cytotoxicity occurs when IgM or IgG binds to a cell surface antigen with complement activation and consequent cell membrane damage or lysis. Blood transfu sion reactions and autoimmune hemolytic anemia are examples of this form. Systemic anaphylaxis is a type I hypersensitivity reaction in which mast cells or basophils that are bound to IgE antibodies are reexposed to an allergen, which leads to a release of vasoactive amines that causes edema and broncho and vasoconstriction. This process is followed by chemotaxis and aggregation of neutrophils, which leads to release of lysosomal enzymes and eventual necrosis of tissue and cells. Interferon activates macrophages (epithelioid cells) and forms granulomas (caseating or non 130 Pathology caseating). A local area of erythema and induration peaks at about 48 h fol lowing intracutaneous injection of tuberculin. Granulomatous inflamma tion (with epithelioid cells), poison ivy reactions, and contact dermatitis are types of delayed type hypersensitivity. Contact dermatitis is often the result of sensitivity to nickel, which can be found in some watchbands. The latter may also reveal fibrinoid necrosis around blood vessels, while eosinophils in an allergic nasal polyp are an example of a type I hypersensitivity reaction. An autograft is a tissue graft taken from one site and placed in a different site in the same individual. A graft between individuals of two different species is a xenograft or heterograft. Hyperacute rejection, due to preformed host antibodies that are directed against antigens of the graft, occurs within minutes after transplantation. Histologically, neutrophils are found within the glomerulus and peritubu lar capillaries. These changes illustrate an antigen-antibody reaction at the vascular endothelium, similar to the Arthus reaction. Acute rejection can result from vasculitis or interstitial lymphocytic infiltration. The vasculitis is the result of humoral rejection (acute rejection vasculitis), while the interstitial mononuclear infiltrate is the result of cellular rejection (acute cellular rejection). Acute cellular rejection is responsive to immunosup General Pathology Answers 131 pressive therapy, but acute rejection vasculitis is not. Subacute rejection vasculitis occurs during the first few months after transplantation and is characterized by the proliferation of fibroblasts and macrophages in the tunica intima of arteries. In chronic rejection, tubular atrophy, mononu clear interstitial infiltration, and vascular changes are found. The vascular changes are probably the result of the proliferative arteritis seen in acute and subacute stages. The vascular obliteration leads to interstitial fibrosis and tubular atrophy, resulting in loss of renal function. Antimitochondrial antibodies are found in the majority of patients with primary biliary cirrhosis. Anti-smooth-muscle antibodies are charac teristic of lupoid autoimmune hepatitis. Antibodies to parietal cells of the stomach and intrinsic factor are seen in pernicious anemia, while antibodies to the microvascula ture of muscle are seen in dermatomyositis. Autoantibodies to IgG (called rheumatoid factor) are present in patients with rheumatoid arthritis. This type of antibody may also be seen in patients with other types of autoim mune diseases. Antibodies to antigens found in the intercellular space of the epidermis are seen with pemphigus vulgaris, while antibodies to antigens found in the epidermal basement membrane are seen with bullous pem phigoid. Histologic sections of affected areas reveal vascular lesions with fibrinoid deposits consisting of accumulations of pink-staining homoge neous masses of fibrin, immunoglobulins, and other plasma proteins. This leads to a polyclonal production of anti bodies to self and nonself antigens. Histologically there is liquefactive degeneration of the basal layer of the epidermis with a perivascular lym phoid infiltrate. Deposits of immunoglobulin and complement can be demonstrated at the dermoepidermal junction. The most common symptom is caused by involvement of the joints (arthritis), which produces a nonerosive synovi tis. Small vegetations may develop on the heart valves and are called Libman-Sacks endocarditis. These deposits are found within the mesangium as well as in subendothelial and subepithelial locations. The subendothelial deposits produce wire-loop lesions and are particularly important. Small arterioles in the aforementioned systems show obliteration caused by intimal hyperplasia accompanied by progressive interstitial fibrosis. Evi dence implicates a lymphocyte overdrive of fibroblasts to produce an excess of rather normal collagen. Eventually myocardial fibrosis, pul monary fibrosis, and terminal renal failure ensue. Over half of these patients have dysphagia with solid food caused by distal esophageal nar rowing. Eventually the amyloid deposits may strangle the cells, leading to 134 Pathology atrophy or cell death. The histologic diagnosis of amyloid is based solely on its special staining characteristics. It stains pink with the routine hema toxylin and eosin stain, but, with Congo red stain, amyloid stains dark red and has an apple-green birefringence when viewed under polarized light. There are many different types of proteins that stain as amyloid, and these are associated with a wide variety of diseases. These diseases may be either systemic, such as with immune dyscrasias, reactive diseases, or hemodial ysis, or they may be localized, such as with senile or endocrine disorders. This protein is a polypeptide derived from serum amyloid-associated protein, which is produced in the liver. Patients on chronic hemodialysis may develop amyloid deposits consisting of 2-microglobulin. Patients with medullary carcinoma of the thyroid, a malignancy of the calcitonin-secreting parafollicular C cells of the thyroid, characteristically have amyloid deposits of procalcitonin within the tumor. These patients have severe abnormalities of immunologic function with lymphopenia. They are at risk for infection with all types of infectious agents, including bacteria, mycobacteria, fungi, viruses, and parasites. Patients have a skin rash at birth, possibly due to a graft-versus-host reac tion from maternal lymphocytes. Patients are particularly prone to chronic diarrhea, due to rotavirus and bacteria, and to oral candidiasis. This leads to General Pathology Answers 135 accumulation of adenosine triphosphate and deoxyadenosine triphos phate, both of which are toxic to lymphocytes. Levels of antibodies to gp120 are used to monitor the course of infection, while levels of p24 are used to measure virus load in the blood. An additional ligand that is a cytokine receptor is also necessary for entry into cells. In general, benign tumors are designated by using the suffix oma attached to a name describing either the cell of origin of the tumor or the gross or micro 136 Pathology scopic appearance of the tumor. Examples of benign tumors whose names are based on their microscopic appearance include adenomas, which have a uniform proliferation of glandular epithelial cells; papillo mas, which are tumors that form finger-like projections; fibromas, which are composed of a uniform proliferation of fibrous tissue; leiomyomas, which originate from smooth muscle cells and have elongated, spindle shaped nuclei; hemangiomas, which are formed from a uniform prolifer ation of endothelial cells; and lipomas, which originate from adipocytes. The suffix oma is unfortunately still applied to some tumors that are not benign. Carcinomas are malignant tumors of epithelial origin, while sarcomas are malignant tumors of mesenchymal tissue. Examples of malignant epithelial tumors (carcino mas) include adenocarcinomas, which consist of a disorganized mass of malignant cells that form glandular structures, and squamous cell carcino mas, which consist of a disorganized mass of malignant cells that produce keratin. Examples of malignant mesenchymal tumors include rhab domyosarcomas, leiomyosarcomas, fibrosarcomas, and liposarcomas. One clue that a tumor has developed from skeletal muscle, such as a rhab domyosarcoma, is the presence of cross-striations. The wall of the stomach consists of smooth muscle, and a tumor that originates from these smooth-muscle cells will consist of proliferating cells with elongated, spindle-shaped nuclei. If a tumor of this type is benign it is called a leiomyoma, while if it is malignant it is called a leiomyosarcoma. This distinction is based on the number of mitoses that are present and the degree of atypia displayed by the neoplastic cells. Benign neoplasms grow slowly with an expansile growth pattern that often forms a fibrous capsule. This histologic feature can also be useful in distinguishing a benign neoplastic lipoma from normal nonneoplastic adipose tissue. Histologically, benign neoplastic General Pathology Answers 137 cells tend to be uniform and well differentiated; that is, they appear similar to their tissue of origin. This histologic feature may not distinguish between benign neoplasms and normal tissue. In contrast to benign tumors, malignant neoplasms grow rapidly in a crablike pattern and are capable of metastasizing. Histologically, the malignant cells are pleomor phic because they differ from one another in size and shape. These cells have hyperchromatic nuclei and an increased nuclear-to-cytoplasmic ratio. These two features only indicate rapidly proliferating cells and can also be seen in reactive or reparative processes. The mitoses in malignancies, however, tend to be atypical, such as tripolar mitoses. Malignant tumors are graded by their degree of differentiation as well differentiated, moderately differ entiated, or poorly differentiated. This histologic feature is usually seen in poorly differentiated or undifferentiated malignancies. One example of this is the development of squamous cell car cinoma of the uterine cervix. The normal cervix is lined by a stratified layer of squamous epithelium, while the endocervix is composed of mucus secreting columnar epithelial cells. In response to chronic inflammation, the columnar epithelial cells change to stratified squamous epithelial cells. These dysplastic changes are character ized by disorganized stratified squamous epithelium with mitoses located above the basal layers of the epithelium. The intraepithelial dysplasia is divided into three types based on the degree of dysplasia present and the location of mitoses. In mild dysplasia there are mitoses in the basal one third of the epithelium; in moderate dysplasia mitoses occur in the middle one-third of the epithelium; and in severe dysplasia there are mitoses in the upper one-third of the epithelium. Next, the neoplastic cells start to invade the underlying tissue, form ing an invasive squamous cell carcinoma. For example, squamous cell carcinomas arise in organs that are normally lined by stratified squamous epithelium. That is, sites associated with the development of squamous cell carcinoma include the skin, lung, esophagus, and cervix. Adenocarcinomas arise from glandular epithelium, and therefore sites associated with the development of adenocarcinoma include the lung, colon, stomach, prostate, and endometrium. Sites for transitional cell carcinoma include the urinary bladder and kidney (renal pelvis). Two types of cancer associated with special sites include clear cell carcinoma and signet cell carcinoma. In this malignancy the cells infiltrate individually instead of forming recognizable glandular structures. Each individual cell is filled with a large drop of mucin, which pushes the nucleus to the side, giv ing it the appearance of a signet ring. The protein product of a proto-oncogene is often a growth factor, a growth factor receptor, or a protein kinase. A cel lular proto-oncogene may function as a cellular oncogene (c-onc) if it pro duces more of its protein product than it normally should. These normal cellular proto-oncogenes may become oncogenic (tumor-forming) by sev eral mechanisms, including gene mutations, translocations, amplification, or interaction with viruses.

Diagnostic Work-up History and physical examination quit smoking health timeline buy cheap nicotinell line, including: Careful review of medical records and medications quit smoking and constipation buy genuine nicotinell on line. Investigations Full blood counts Urinalysis and urine culture and sensitivity Urea and electrolytes Serum creatinine Management Manage treatable causes quit smoking chantix purchase nicotinell 35 mg fast delivery. Replace fluid to a point of slight over hydration in patients who have vomiting quit smoking app for android buy 35mg nicotinell otc, diarrhoea quit smoking 26 months ago discount nicotinell 35mg otc, or burns quit smoking diarrhea discount nicotinell 17.5 mg with mastercard. Most important of all, transfer the patient to a centre with facilities for dialysis as soon as possible after the initial measures. These are sodium polystyrene sulphonate (kayexelate) 20g in 70% sorbitol solution 3 to 4 times a day. Carry out renal dialysis in patients whose fluid/electrolyte homeostasis and control of urea/creatinine levels are not being achieved rapidly with conservative manoeuvres. Causes include chronic glomerulopathies, hypertension, chronic interstitial nephritis, diabetes mellitus. Important Manifestations of Chronic Renal Failure Biochemical: Acidosis, hyperkalaemia. Do not transfuse blood or infuse fluids if the urine output is low or if there is evidence of fluid overload such as hypertension, heart failure, peripheral or pulmonary oedema. Carry out renal replacement therapy by hemodialysis and peritoneal diaslysis in selected centres if in end-stage renal disease. May also be secondary due to post acute glomerulonephritis, plasmodium malaria, allergy. The patient may be ill looking, not appreciating surroundings, not alert, not aware of time, place, or who they are. They may also be unable to remember, and may forget easily with poor attention and concentration. They may have visual/auditory hallucinations or delusions (grandiose or paranoid) or may be aggressive and excited. Investigations Blood sugar to exclude hypoglycaemia Full haemogram for evidence of macrocytosis Liver function test (especially liver enzymes) Management Admit patient. They are characterized by significant impairment in psychological, social and occupational functioning as observed over a 12-month period. Commonly abused substances in Kenya include tobacco, Cannabis sativa, khat (miraa), opioids (heroin), cocaine, and solvents (glue, petrol, wood varnish). Substance-related syndromes include intoxication, dependence, withdrawal, psychosis, mood disorders, anxiety, sleep disorders, sexual disorders. Tolerance develops rapidly and withdrawal features include agitation, lethargy, sweating, goose-flesh pimples, running nose, shivering, musculo-skeletal pains, diarrhoea, and abdominal cramps. Because of the highly addictive nature of the opioids, admission to hospital is necessary for effective management. Treatment of the psychiatric complication is the same as for the primary syndromes. Pathological anxiety includes panic disorder, which may be dramatic in presentation; phobias which are fears that are out of proportion; obsessive compulsive disorder, which is characterized by an irresistible urge to act; and generalized anxiety disorder. Clinical Features the patient presents with an empty feeling in the stomach, lightness in chest, pounding heart, perspiration, urge to void, non-exertion dyspnoea, blurred vision, hyper reflexia, dizziness, and light headedness. It is important to exclude physical causes like thyrotoxicosis, pheochromocytoma, hypoglycaemia, and temporal lobe epilepsy. Investigations Exclude organic causes like thyrotoxicosis and temporal lobe epilepsy. Psychological effects are those that affect different levels of functioning, including cognitive (perception and memory as a basis for thoughts and learning), affective (emotions), and behavioural. Clinical Features In the acute phase, these may include intrusive flashbacks, grief reaction, denial, disbelief, numbness, restlessness, anxiety, social withdrawal, and uncontrollable crying. Clinical Features May present as paralysis of a part of the body, tremors, blindness, deafness, seizures, aphonia. The severity of disability fluctuates and the patient fails to exhibit the seriousness the disability accords. Thorough physical examination; even though the patient often appears normal, this should be done. Clinical Features Dysphoric mood characterized by sadness, crying spells, irritability, or lowered ability to function socially. Negative views of self and the environment and the future, indicated by guilt, loss of interest, difficulties in concentrating or suicidal thoughts. A meticulous history is important as under-diagnosis is common and many patients suffering from depression are often missed and receive inadequate treatment. It is important for the care provider to maintain a positive and hopeful attitude towards the patient and to the extent possible involve the relatives in the management of the patient, especially to improve compliance. If medications are effective, they should be continued for 3 months and then reduced at 25mg/week. Patient Education Inform the patient that there will be a delay of 2 weeks before beneficial effects of treatment are experienced. Review the patient at least once every 2 weeks until maintenance dose is reached and then once a month until total drug withdrawal or as necessary. Clinical Features the clinical features include hyperactivity that is usually goal oriented, over generosity, extravagance, disinhibition (promiscuity and drug abuse), irritability, 125 Clinical Guidelines accelerated speech, infectious elated congruent mood, grandiose delusions, enhanced self-esteem, insomnia, and weight loss (no time for food). In severe forms patients appear disorganized and may be violent; legal involvement may be necessary in their management. History and physical examination are essential; it is necessary to establish if ever depressed in past. The normal association of ideas is lost and there is characteristic incongruence of affect. There are also delusions, hallucinations in any sensory modality, and disturbances in behaviour and motor function. If patient was diagnosed as a schizophrenic and missed the drugs, restart the drug as before. Caution: Aim to use lowest dose that is therapeutic in cases of long term use to minimize risk of side effects. Insomnia can be a symptom of most other psychiatric and physical disorders, which should be excluded. Management Forced naps at regular times of the day Methyl phenidate 30mg morning and 20mg midday until symptoms disappear, maximum dose 60mg daily. May occur in the following conditions: depression, schizophrenia, under influence of alcohol/drugs, under severe social problems or stress, or personality disorder. An empathetic approach is very important if you are to win the confidence of the patient so that he/she will be able to tell you the true story. Alternative treatment where side effect of psychotropic drugs are to be avoided. Fortunately this depends on a few clinical features that are easy to learn with practice. Parents/ care givers may have tried to treat the child at home or the child may have fallen sick quickly. They are advised to come to the health care facility as soon as possible if the child is weak, not able to drink, has severe diarrhoea, cold hands and feet, very high fever, or convulsion. In addition to the above, severe malnutrition is a common cause of death in young children. The figures shown below assist you to triage and manage these children as they arrive at the health facility. Carry out emergency investigation if you are able: Blood glucose, blood smear, haemoglobin. Make sure you write a comprehensive report of what you have done to the receiving hospital clinician. Continue oxygen After at least 2 good breaths Check the pulse for 10 seconds Pulse palpable and No or weak, slow pulse >60bpm Give 1 5 chest compressions then 1) Continue airway/breathing continue giving 15 chest support & oxygen compressions for each 2 breath s 2) Look for signs of dehydration/ for 1 minute. After resuscitation: Admit and look for the cause if not already obvious and treat. Ensure that the facilities and skills for intensive care management are available. Clinical Features these include extensive skin rash, pruritus, urticaria, respiratory distress that may be accompanied by a wheeze or a stridor (due to laryngeal oedema or bronchospasm), and hypotension. Management Parents and care givers are advised to take health care facility as soon as possible any child with extensive skin rash or difficulty in breathing. Inform parent/child the cause of reaction so as to know and to avoid the offending agent in future. Often they are playing with seeds, buttons or any small object that when put in the mouth easily goes the wrong way. All health care providers should learn how to dislodge the objects and it would be good if parents were taught the procedure. This is 137 Clinical Guidelines because the procedure may be required urgently: by the time the child arrives at the health facility they may have already choked to death. If obstruction persists, turn infant over and give 5 chest thrusts with 2 fingers a) Back slaps one on top of the other, one finger breadth below nipple level in midline ure 17. Diarrhoeal Diseases Causes of diarrhoea in children: Young children <5 years: rotavirus, E coli All ages except neonates: Shigella, cholera, salmonella spp. Others: Lactose intolerance, food poisoning Clinical Features Diarrhoea is defined as the occurrence of at least 3 loose or watery stools in a day. Diarrhoeal illness is classified for dehydration, presence of blood in the stool and duration. Definitions Acute watery diarrhoea: Watery stools lasting less than 14 days Dysentery: the presence of fresh blood in the diarrhoeal stool. The major cause of death from diarrhoea is dehydration, especially in infants and young children. Management of diarrhoea is aimed primarily at evaluation, prevention, and treatment of dehydration 18. Rehydration must be evaluated in terms of clinical signs, not in terms of volume of fluids given. Thereafter monitor other signs of dehydration: If signs of severe dehydration persists, repeat the rehydration in Plan C (Table 18. Evaluate preferably every hour until signs of dehydration disappear (usually within 4 hours). Continued feeding should be encouraged, for example: Under 6 months: Breastfeed on demand as soon as baby is able to feed. Give an extra meal per day and continue until 1 month after diarrhoea has stopped.

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Magnetic reso onset of oligohydramnios quit smoking ken guzzo order cheap nicotinell online, due to neonatal respiratory disease and nance imaging lung volume measurements may be helpful quit smoking 17 days buy nicotinell from india, espe longer-term renal dysfunction quit smoking virginia buy nicotinell online. The presence of oligohy Fetalurinaryelectrolyteshavebeenusedtoestimaterenalfunc dramniosisanimportantprognosticfeatureevenafteradjustment tion in lower urinary tract obstruction quit smoking online support best order nicotinell. Especiallyin There is insufficient evidence to make a recommendation on serial diseases where renal function may decline over the course of amnioinfusions for renal oligohydramnios (no grading) quit smoking using hypnosis discount nicotinell 52.5 mg with amex. Amnioinfusions into previously intact oligohydramnios quit smoking 28 days discount nicotinell 52.5mg with visa, parentsshouldbeofferedcounselingbyafetalmedi membranes are commonly complicated by iatrogenic premature cine specialist and a neonatologist; irrespective of the presence of rupture of membranes, premature labor, and miscarriage. The procedure should be considered only for pulmonary palliation Because of the broad spectrum of prognoses and diverse pos because it does not improve renal function. Because of the unknown balance of risks and parental anxiety is often encountered even in less severely af benefits, resultsofaplannedprospectivestudyshouldbeawaited. On nizations, which exist for several cystic nephropathies and genetic thecontrary, prematurityshouldbeavoidedbecauseitposesadditional renaldiseasesingeneralonanationalandinternationallevel, should perinatal risks, and lower body weight can complicate treatment of be offered. Oligohydramniosmaycausecordcompressionand Where termination of pregnancy is locally available, nondirec fetaldistressduringlabor, requiringobstetricmanagement. ThevisualanalogscaleshownintheeFigureinthe Delivery in Hospital With Specialized Neonatal Care Supplement may be helpful for this. Corticosteroids For fetuses with bilateral cystic renal disease without oligo Recommendation 3. Postnatal glucose levels should be monitored owing to the decisionsaboutofferingpalliativeorintensivecareorchoosingdialy significantlyhigherrateofneonatalhypoglycemia. Intheinitialneonatalphase, managementofpulmonarycompli been used routinely before delivery of fetuses with congenital dia cationsisusuallyparamount, butnephrologicalassessmentshouldnot phragmatic hernia, with supporting evidence from animal models bedelayedtoolongbecausetreatmentdecisionsmaytakesometime of diaphragmatic hernia. Involvementofageneticistmayalsobehelpful underlying disease and comorbidities, with poorest outcomes in (see the Genetic Testing section). In 6 single-center studies, 24 out of 42 neonates died, but Assessment in the Neonatal Period life-supporting therapy was not offered or was discontinued in at Recommendation 4. Owing to the small cohort sizes, it is difficult to distinguish nateswithaprenataldiagnosisofasolitarykidneycystshouldbeseen the effects of age at onset of renal oligohydramnios, presence of for ultrasound examination within the first 4 weeks of life. This will confirm the diagnosis or identify further cysts due to Also, respiratory support and dialysis techniques have improved the greater sensitivity of postnatal ultrasound in detecting smaller in recent years; therefore, outcome may now be better. In 5 epidemiological studies with a mean Despiteenormousadvancesinprenatalultrasound, thereisstill follow-up time of 5 years, portal hypertension occurred in 15% to a considerable proportion of children in whom the prenatal diagno 86% (mean, 36%), and liver transplantation was performed in 0% sis of unilateral cysts has to be revised postnatally, usually to severe to 50% (mean, 11%) of patients. While van Stralen et al67did not demonstrate differ Inadequate compensatory hypertrophy and other urogenital ing survival across 4 diagnosis groups, mortality was higher in abnormalitiesshouldbeexcludedbypostnatalultrasoundbecause children with polycystic kidney disease than in those with theyarethemainriskfactorsforrenaldamage(albuminuria, hyper obstructive nephropathy in an American cohort. Micturatingcystogramorscintigraphyisonlyindicatedifthere growth, and hospital admissions are summarized in eTable 7 in arecluestowardfurtherpathology, suchasuretericdilation, suspi the Supplement. Patients require long-term expenditure limits provision of specialized pediatric renal follow-up for repeated ultrasound scans and measurements of services. Inadditiontoconfirma tablished therapy even in neonates because available data show tory postnatal ultrasound, renal function should be assessed with marked improvement of survival in the last decades, with survival adequate time lag to allow clearance of maternal creatinine. Dialysismay and/or quality of life independent of kidney function should be need to be initiated after a few days or weeks of life depending on considered in the decision-making process. Learn about the 2 simple tests you can have to determine the health of your kidneys. Your two kidneys are under the lower ribs in the back of the body above the waist. The cleaned, filtered blood Tubes called ureters goes into the vein carry urine to the bladder. Healthy Kidneys From the artery, Blood Cells blood flows into aste the kidneys and passes Every 30 minutes through millions of tiny the kidneys filter all filtering units called the blood in the body! A kidney transplant replaces a failed kidney with a healthy kidney from someone else. A high sugar level in the blood damages the small filters (glomeruli) in the kidneys. They are more likely to filter out tiny amounts of albumin into the urine instead of keeping it in the blood. Did you know that more people with kidney disease How Is Kidney die of heart disease before their kidneys fail It is detected by low levels someone has diabetes, the blood glucose levels can be of hemoglobin. They can damage the kidneys when used Creatinine: A natural waste product that your body too often. Dialysis an inherited disease where the kidneys have many cysts, takes over for failing kidneys. It cleans wastes from which can replace the normal kidney tissue and reduce the blood using a machine or other special equipment. Chronic kidney disease can be detected and treated early, which may slow it from getting worse. Development of the human kidney begins at the end of the first month, and the kidney becomes functional in the course of the second month of antenatal life. In the last trimester, the fetal kidney already manifests first involutive changes. From then on to its adult maturity, the kidney is characterised by intensive processes of maturation, but also evident involutive changes. The antenatal period is characterised by intensive processes of nephrogenesis, realised in three successive phases of renal development: pronephros, mesonephros, and metanephros. The first two changes represent a temporary system, while the third stands for a permanent system of excretion, that is, a definitive kidney. The functioning of kidneys, though not necessary in the antenatal stadium, indicates their excretory, homeostatic and endocrine roles, and signifies the maturation process. After birth, there is a further process of structural and functional maturation of the kidneys. With a definitive number of nephrones at birth, renal mass increases at the expense of growth of certain nephrone structures and interstitium. The kidney reaches its full anatomical and functional maturity by the end of the third decade of life. From then on, the kidney is characterised by involutive changes of varying intensity. By the end of the sixth decade these changes are slow; afterwards, to the end of life, they show a trend of very rapid progression, and are a consequence primarily of the reduced renal perfusion. In spite of that, under normal conditions they do not show signs of renal insufficiency even in a well-advanced age. The involutive renal changes can be separate, but they can coincide with corresponding renal diseases. In some individuals this can result in a progressive failure of renal functions in an advanced age. Key words: Age, anatomy, function, human kidney Introduction netic theory of ageing which assumes that it is a result of a genetic programme determining the progressive One of the oldest definitions of ageing states that it manifestation of various age-related phenotype changes. Current research shows that the shortening Another definition states that "ageing represents an in of the telomere may be a phenomenon related to devel evitable process conditioned by natural laws, a process opment and not only ageing (3). There have been since various definitions of renal nephrones are lost by old age (4). It has been es ageing which, in their specific ways, contribute to the tablished that the processes of hialinosis and sclerosis of understanding of ageing as a complex phenomenon glomeruli in man begin as early as the seventh month of relevant to each living organism. Theories which con antenatal life with juxtamedullary nephrons, and in the ceive of ageing as of a global all-encompassing process ninth with cortical ones. Although these processes de have been recently replaced by the idea that the ageing velop very slowly, there is a clear correlation between of an organism represents a sum of its ageing individual the age and the number of affected glomeruli. It is supported by the fact that age-induced dys gression curve drops from 95% of normal glomeruli at function of organs and tissues in man, such as brain or the age below 40 to 63% at the age of 90 (5). These subcutaneous fat tissue, is closely related to the reduc involutive kidney structural changes are also accompa tion of cell number (2). The same author quotes the ge nied by a progressive reduction of its function (6). Vlajkovic these data clearly illustrate how the kidney changes ised by the development of three successive, bilateral, from the moment of its budding in the embryonic period excretory systems: pronephros, mesonephros and to the well-advanced age of man. All of them develop from the so-called and dynamic changes from the emergence of pronephros nephrogenic cord, which take rise from intermediate to an aged kidney, and they are characterised by the proc mesoderm (. Pronephros and mesonephros are esses of maturation and involution, occasionally overlap temporary, while metanephros is a permanent excretory ping in certain ages of life. The development of pronephros begins at the end of the third week of preembryonic period, Kidney in an Embryo and Fetus from the first five cranial segments (nephrotomes) of the nephrogenic cord (. Pronephros in a human em Anatomical Characteristics bryo is first represented by seven to ten solid cell clus the antenatal life of man, including pre-embryonic, ters. Vesicles embryonic and fetal periods of development is character then elongate and form tubules. At their medial ends these tubules have holes represents the final developmental stage of mammal (nephrostomes) used for communication with the kidney, whose development begins in the fifth week of coelomic cavity. It develops from three sources: an entiated, they are short, the aorta does not branch into evagination of the mesonephric duct, the ureteric bud, them, so that glomeruli are not developed either. The and a local condensation of mesenchyme termed the regression of pronephric tubules begins very early, so metanephric blastema form the nephric structure, while that cranial tubules disappear before the caudal ones angiogenic mesenchyme migrates into the metanephric appear (7). On the disappearance of the pronephric tu blastema slightly later to produce the glomeruli and vasa bules, the pronephric duct made by them also disinte recta. By the end of the fourth week of the embryonic sary for metanephric kidney induction (11). Mesonephros appears starting with lower part of the mesonephric duct, in the close vicinity the fourth week of the embryonic life (9). It grows from the sixth cranial to the third lumbar segment of the dorsocranially and penetrates into the metanephric nephrogenic cord (. The vesicles then elongate and form spreads into the primary renal pelvis and then begins to tubules. The mesonephric tubule (in the S shape) con branch dichotomally and produces the next fifteen gen sists of the medial expanded and invaginated end erations of side-branches which will produce calyces (Bowman capsule) with which they enclose aortic cap and colleting ducts (12). Thus the whole excretory renal illaries and form Malpighi corpuscles; the proximal system is formed (. The contact between the segment which has a secretory function; and distal seg ureteric bud and the metanephric blastema is also the ment which through connection creates the mesonephric moment when the latter begins to differentiate into two duct (a continuation of the pronephric duct). The the mesonephric duct elongates caudally, and then first ones differentiate in the form of compact cell clus curves ventrally and opens into a cloaca. It is believed ters (metanephric caps) around the growing ends of that about 70 to 80 glomeruli and tubules develop in the ureteric bud side-branches (. They will develop mesonephros, but not all of them develop at the same into nephrones, the basic structural and functional renal time. During the process, the condensed mass first be units (nephrones) in each mesonephros amounts to 30 comes vesicular, then forms in the shape of a comma, and they are identified in the fifth and sixth weeks of and finally progressively extends and forms a tubular age (10). The proximal end of this is maximum length and represents a large, oval, bilateral S structure will along with the capillaries from the organ lying by the dorsal wall of the body cavity, on nearby blood vessels form the renal corpuscle, while the both sides of the middle line (11). The distal tubule connects with in its medial part, while the mesonephric (Wolffian) the collecting duct and establishes the connection be collecting duct are in the lateral one. The mesonephros, tween the secretory (nephrone) and the excretory renal unlike the pronephros, is not related to the body cavity, components. Stromagenic cells are not clearly defined and it is considerably longer with greater tubule curva and they will make the renal connective tissue. Various growth factors regulating cell proliferation, the mesonephros mainly disappears by the end of transformation, differentiation, morphogenesis and mo the eighth week of antenatal life. Degeneration of cra togenesis along with their surface receptors take part in nial tubules and glomeruli begins before the appearance the processes of induction as well as in the later phases of the caudal ones. In male foetuses, the remaining "formins", which has a critical role in the early proc mesophrenic tubules build up the efferent ductules of esses during the nephrogenesis. Renal agenesis and hy the testis, the rostral and caudal aberrant ductules, and poplasia are explained by the mutation of its genes (13). Vlajkovic Nephrones are being formed throughout the fetal the waste materials from the mother reach the blood of life. Out of 15 successive nephrone generations, each the fetus via the umbilical vessels through the placenta. The urine is excreted into the amniotic cav new nephrones is completed in the period between the ity surrounding the foetus and blends with the amniotic 28th and 36th week of gestation so that the number of liquid. The urine (filtrate) in fact represents the main nephrones is definite at birth (13, 14). The foetus by kidneys contains at birth about one million of nephrones, reflex swallows a few hundred millilitres of the amni at different stages of development. The greatest number otic liquid every day; it is absorbed from the intestines of mature nephrones is located close to the medulla, and and again transported through circulation back to the their maturity decreases in the direction of the outward kidneys where it is filtrated. Structural and functional maturation of the not necessary for the elimination of the waste materials nephrones continues after birth.

However quit smoking injection order line nicotinell, now it is known that all such viruses are not transmitted by arthropod vectors alone and hence now such haemorrhagic fevers are classifed according to the routes of transmission and other epidemiologic features into 4 groups: 1 quit smoking encouragement buy cheapest nicotinell and nicotinell. Of these quit smoking exhausted nicotinell 52.5 mg for sale, mosquito-borne viral haemorrhagic fevers in which Aedes aegypti mosquitoes are vectors quit smoking vapor cigarette nicotinell 17.5 mg online, are the most common problem the world over quit smoking coupons buy nicotinell 52.5 mg mastercard, especially in developing countries quit smoking zonix cheap nicotinell 35 mg without a prescription. Two important examples of Aedes mosquito-borne viral haemorrhagic fevers are yellow fever and dengue fever. Chikungunya virus infection is primarily a disease in nonhuman primates but the infection is transmitted to humans by A. The disease is endemic in parts of Africa and Asia and occurs sporadically elsewhere. Its general clinical features range from a mild afebrile illness similar to common cold by appearance of sudden fever, headache, myalgia, malaise, chills and respiratory tract manifestations such as cough, soar throat to a more severe form of acute respiratory illness and lymphadenopathy. Depending upon its antigenic characteristics of the nucleoprotein and matrix, 3 distinct types are known: A, B and C. Out of these, infuenza type A is responsible for most serious and severe forms of outbreaks in human beings while types B and C cause a milder form of illness. The virus is transmitted into the human body by the bite of infected carnivores. The organism enters a peripheral nerve and then travels to the spinal cord and brain. Parasites may cause disease due to their presence in the lumen of the intestine, due to infltration into the blood stream, or due to their presence 107 inside the cells. The condition is particularly more common in tropical and subtropical areas with poor sanitation. The parasite occurs in 2 forms: a trophozoite form which is active adult form seen in the tissues and diarrhoeal stools; and a cystic form seen in formed stools but not in the tissues. M/E the lesions of amoebiasis include amoebic colitis, amoeboma, amoebic liver abscess and spread of lesions to other sites. While Plasmodium falciparum causes malignant malaria, the other three species produce benign form of illness. The disease is endemic in several parts of the world, especially in tropical Africa, parts of South and Central America, India and South-East Asia. The main clinical features of malaria are cyclic peaks of high fever accompanied by chills, anaemia and splenomegaly. Major complications occur in severe falciparum malaria which may have manifestations of cerebral malaria (coma), hypoglycaemia, renal impairment, severe anaemia, haemoglobinuria, jaundice, pulmonary oedema, and acidosis followed by congestive heart failure and hypotensive shock. The lymphatic vessels inhabit the adult worm, especially in the lymph nodes, testis and epididymis. The eggs are passed in human faeces which are ingested by pigs or they infect vegetables. M/E the cysticercus may be single or there may be multiple cysticerci in the different tissues of the body. The cysts may occur virtually anywhere in body and accordingly produce symptoms; most common sites are the brain, skeletal muscle and skin. Cysticercus consists of a round to oval white cyst, about 1 cm in diameter, contains milky fuid and invaginated scolex with birefringent hooklets. The infection may be acquired by the foetus during intrauterine life, or perinatally and damage the foetus or infant. Dengue haemorrhagic fever is characterised by following laboratory fndings except: A. Granuloma inguinale and lymphogranuloma venereum are similar in following aspects, except: A. The tumours derive their nomenclature on the basis of the parenchymal component comprising them. Malignant tumours of epithelial origin are called carcinomas, while malignant mesenchymal tumours are named sarcomas (sarcos = feshy). However, some cancers are compo sed of highly undifferentiated cells and are referred to as undifferentiated malignant tumours. Although, this broad genera lisation regarding nomenclature of tumours usually holds true in majority of instances, some examples contrary to this concept are: melanoma for carcinoma of the melanocytes, hepatoma for carcinoma of the hepatocytes, lymphoma for malignant tumour of the lymphoid tissue, and seminoma for malignant tumour of the testis. Mixed tumours A few examples are as under: i) Adenosquamous carcinoma is the combination of adenocarcinoma and squamous cell carcinoma in the endometrium. But they occur at extra-gonadal sites as well, mainly in the midline of the body such as in the head and neck region, mediastinum, retroperitoneum, sacrococcygeal region etc. Blastomas (Embryomas) Blastomas or embryomas are a group of malignant tumours which arise from embryonal or partially differentiated cells which would normally form blastema of the organs and tissue during embryogenesis. These tumours occur more frequently in infants and children (under 5 years of age). Hamartoma Hamartoma is benign tumour which is made of mature but disorganised cells of tissues indigenous to the particular organ. Thus, choristoma is heterotopia but is not a true tumour, though it sounds like one. The regulation of tumour growth is under the control of growth factors secreted by the tumour cells. Cancer cells originate by clonal proliferation of a single progeny of a cell (monoclonality). Cancer cells arise from stem cells normally present in the tissues in small number and are not readily identifable. On the other hand, malignant tumours grow rapidly, may ulcerate on the surface, invade locally into deeper tissues, may spread to distant sites (metastasis), and also produce systemic features such as weight loss, anorexia and anaemia. In fact, three cardinal clinical features of malignant tumours are: anaplasia, invasiveness and metastasis (discussed later). Gross appearance of benign and malignant tumours may be quite variable and the features may not be diagnostic on the basis of gross appearance alone. They are encapsulated or well-circumscribed, freely movable, more often frm and uniform, unless secondary changes like haemorrhage or infarction supervene. Secondary changes like haemor rhage, infarction and ulceration are seen more often. Sarcomas typically have fsh-fesh like consistency while carcinomas are generally frm. Depending upon the degree of differentiation, the extent of anaplasia is also variable i. As a result of anaplasia, noticeable morphological and functional 113 alterations in the neoplastic cells are obser ved which are best appreciated under higher magnifcation of the microscope. This is due to cell-mediated immunologic response by the host in an attempt to destroy the tumour. But characteristically, they are distinguished from benign tumours by invasion, infltration and destruction of the surrounding tissue, besides spread to distant sites or metastasis. Besides anaplasia, invasiveness and metastasis are the two other most important features to distinguish malignant from benign tumours. The involvement of lymph nodes by malignant cells may be of two forms: i) Lymphatic permeation ii) Lymphatic emboli Generally, regional lymph nodes draining the tumour are invariably involved producing regional nodal metastasis However, all regional nodal enlargements are not due to nodal metastasis because necrotic products of tumour and antigens may also incite regional lymphadenitis of sinus histiocytosis. The sites where blood-borne metastasis commonly occurs are: the liver, lungs, brain, bones, kidney and adrenals. However, a few organs such as the spleen, heart, and skeletal muscle generally do not allow tumour metastasis to grow. Blood in the pulmonary veins carrying cancer cells from the lungs reaches left side of the heart and then into systemic circulation and thus may form secondary masses elsewhere in the body. Important examples are vertebral metastases in cancers of the thyroid and prostate. Peritoneal cavity is involved most often, but occasionally 115 pleural and peri cardial cavities are also affected. Aggressive clonal proliferation and angiogenesis the frst step in the spread of cancer cells is the development of rapidly proliferating clone of cancer cells. Entry of tumour cells into capillary lumen the tumour cells after degrading the basement membrane are ready to migrate into lumen of capillaries or venules. Thrombus formation the tumour cells protruding in the lumen of the capillary are now covered with constituents of the circulating blood and form the thrombus. Extravasation of tumour cells Tumour cells in the circulation (capillaries, venules, lymphatics) may mechanically block these vascular channels and attach to vascular endothelium and then extravasate to the extravascular space. Survival and growth of metastatic deposit the extra vasated malignant cells on lodgement in the right environment grow further under the infuence of growth factors produced by host tissues, tumour cells and by cleavage products of matrix components. Grading is defned as the gross appearance and microscopic degree of differentiation of the tumour, while staging means extent of spread of the tumour within the patient. Gross features like exophytic or fungating appearance are indicative of less malignant 116 growth than diffusely infltrating tumours. However, grading is largely based on 2 important histologic features: the degree of anaplasia, and the rate of growth. Lymphoma Lymphoma Soft tissue sarcoma Due to varying etiologic factors, cancers of the cervix and oral cavity are more common in India while cancers of the breast and lung are commoner in the Western populations. In general, most common cancers in the developed and developing countries are as under: Developed countries: lung, breast, prostate and colorectal. About one-third of all cancers worldwide are attributed to 9 modifable life-style factors: tobacco use, alcohol consumption, obesity, physical inactivity, low fber diet, unprotected sex, polluted air, indoor household smoke, and contaminated injections. In general, the risk of developing cancer in relatives of a known cancer patient is almost three times higher as compared to control subjects. Some of the cancers with familial occurrence are colon, breast, ovary, brain and melanoma. Familial cancers occur at a relatively early age, appear at multiple sites and occur in 2 or more frst-degree blood relatives. The overall estimates suggest that genetic cancers comprise about 5% of all cancers. Mutations in these genes appear in about 3% cases and these patients have about 85% risk of development of breast cancer. A few examples are: i) Cigarette smoking ii) Alcohol abuse iii) Synergistic interaction of alcohol and tobacco iv) Cancer of the cervix v) Penile cancer vi) Betel nut cancer vii) Industrial and environmental substances viii) Overweight indi viduals, defciency of vitamin A and people consuming diet rich in animal fats. Generally, cancers occur in older individuals past 5th decade of life (two-third of all cancers occur above 65 years of age), though there are variations in age incidence in different forms of cancers. Miscellaneous conditions Certain infammatory (both infectious and non-infectious) and hyperplastic conditions are prone to development of cancer. Hormone-sensitive tissues developing tumours are the breast, endo metrium, myomet rium, vagina, thyroid, liver, prostate and testis. Adenocarcinoma of the vagina is seen with increased frequency in adolescent daughters of mothers who had received oestrogen therapy during pregnancy. Other tumours showing a slightly increased frequency in women receiving contra ceptive pills for long durations are benign tumours of the liver. Monoclonality of tumours There is strong evidence to support that most human cancers arise from a single clone of cells by genetic transformation or mutation. For example: i) In a case of multiple myeloma (a malignant disorder of plasma cells), there is production of a single type of immunoglobulin. Field theory of cancer In an organ developing cancer, in the backdrop of normal cells, limited number of cells only grow in to cancer after undergoing sequence of changes under the infuence of etiologic agents. Multi-step process of cancer growth and progression Carcino genesis is a gradual multi-step process involving many generations of cells. Genetic theory of cancer Cell growth of normal as well as abnormal types is under genetic control. In cancer, there are either genetic abnormalities in the cell, or there are normal genes with abnormal expression. Thus the abnormalities in genetic composition may be from inherited or induced mutations (induced by etiologic carcinogenic agents namely: chemicals, viruses, radiation). Eventually, the mutated cells trans mit their characters to the next progeny of cells and result in cancer. Genetic regulators of normal and abnormal mitosis In normal cell growth, regulatory genes control mitosis as well as cell ageing, terminating in cell death by apoptosis. Thus, corresponding abnor malities in these 4 cell regulatory genes are as under: i) Activation of growth-promoting oncogenes causing transformation of cell (mutant form of normal proto-oncogene in cancer is termed oncogene).

References

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