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The antibody is called the Donath-Landsteiner antibody (previously associated with syphilis discount viagra plus 400mg on line erectile dysfunction pills names, but also with mycoplasma pneumonia measles cheap viagra plus express erectile dysfunction related to prostate, mumps cheap viagra plus 400 mg free shipping erectile dysfunction pills sold at gnc, and ill defned viral and “fu” syndromesQ. The endothelial layer of “helmet cells,” and “triangle small vessels is damaged with resulting fbrin deposition and platelet aggregation. It is identifed by the fnding of anemia and schistocytes, “burr cells,” “helmet cells,” and “triangle cells”on microscopy (should be > 3/5000 cells) and these should have 1-3 sharp spicules. Hemoglobinopathies HbA is a b (95-96%) • The normal hemoglobin is composed of heme (consisting of iron and protoporphyrin) 2 2 HbA2 is a b2 2 (3-3. HbF is a g2 2 (present in the • The adult hemoglobin (HbA) forms about 95-96% of total hemoglobin and is fetal life). Sickle cell anemia This is characterized by the presence of an abnormal type of hemoglobin called HbS. It results from a point mutation that causes the glutamic acid to be replaced by valine at the b6 position of the globin chain. Irreversible sickled cells get sequestrated in the spleen thereby contributing to extravascular hemolysis. The presence of relatively low concentration of HbS (25-40%) and the presence of HbA in heterozygotes prevents effcient HbS sickling thereby contributing to decreased severity of the disease in them. Other hemoglobins like fetal hemoglobin (HbF) and HbC (having a substitution of lysine for glutamic Sequestration crisis is the acid at β6 position) have inhibitory effect on the disease. HbF inhibits the polymerization of HbS, so, most dangerous crisis in sickle newborns do not manifest the disease till 5-6 months of age when their HbF levels fall. This fnding cell anemia because it can is utilized in the management of the disease with hydroxyurea which actually increases the HbF cause heart failure. Decrease in pH Acidosis decreases the affnity of hemoglobin for oxygen, so, there is more deoxygenated hemoglobin and increased chances of sickling. Clinical features • Severe anemia results in jaundice and pigment gallstone formation and is associated with reticulocytosis. Vaso-occlusive crisis clinically manifests as painful episodes in In most other causes of anemia, affected organs of the body. In the initial stages, there is splenomegaly due to congestion and trapping of red cells in the vascular sinusoids (Gamma gandy bodies; consisting of foci of fbrosis having iron or calcium salts deposited in connective tissue are seen). This also increases susceptibility to infection with capsulated anemia is done by ensuring that organisms like Hemophilus infuenzae, Pneumococcus, etc. Chronic anemia hydrated and with the help can cause hyperdynamic circulation resulting in cardiomegaly. However, this test cannot differentiate between sickle cell disease and sickle cell trait. HbS is slower moving as compared to normal HbA, so, heterozygotes show 2 bands of hemoglobin. Thalassemia Thalassemiais themostcommon It is a group of autosomal recessive inherited disorders characterized by decreased synthesis type of hemoglobinopathy in the of either α or β globin chain of HbA. The α globin chain is coded by a gene on chromosome 16 and the gene for β globin chain is located on chromosome 11. The clinical features therefore result from defciency of one chain and the relative excess of the other chain. Promoter region mutation: Causes reduced transcription of the β chains leading to β+ thalassemia. Chain terminator mutations: Either creation of a stop codon in exon or frameshift mutation inducing a downstream stop codon leads to premature chain termination resulting in β° thalassemia. Splicing mutation: They are the most common cause of thalassemia resulting in most common cause of b thalassemia. Thalassemia major (also called Cooley anemia): It is seen in individuals homo- Thalassemia major (also called zygous for the β thalassemia genes (β+/β+or β°/β°); these individuals have a severe Cooley anemia): is a severe transfusion dependent anemia in transfusion dependent anemia which manifests at usually 6 to 9 months after birth. Peripheral smear shows moderate to severe anemia, anisocytosis, microcytic hypochromic red cells, target cells, nucleated red cells, basophilic stippling, Howell Jolly bodies, etc. Since β chains are not produced but γ chains are synthesized normally, HbF is markedly increased and is the major constituent of red cells (90%). Bone marrow is hypercellular with erythroid hyperplasia causing reversal of normal M:E ratio (it becomes 1:3 in thalassemia). Thalassemia minor or trait: It is seen in individuals heterozygous with one β thalassemia gene and one normal gene (β+/β or β /β). It is more common clinically0 Thalassemia minor (also called than the major variant and offers resistance against falciparum malaria. These Thalassemia trait): HbA2 is patients are usually asymptomatic with only mild anemia. Peripheral smear shows microcytic, hypochromic cells with basophilic stippling and presence of target cells. In this test 2 blood samples (1of a normal person serving as control and 1 of patient) Naked Eye Single Tube Red cell are added to 2 tubes with 0. The features of the disease are intermediate between the two other types of thalas- semia discussed above. The clinical picture in β-thalassemia trait is similar to that discussed in β-thalassemia minor which means there is presence of microcytosis, minimal or no anemia, and no abnormal physical signs. Hydrops fetalis is the most dangerous form of α-thalassemia and severe tissue anoxia leads to intrauterine fetal death. Complications of massive blood transfusion are: • Coagulopathy: Most common cause of bleeding after massive transfusion is dilutional thrombocytopenia. Clinically, signifcant hypocalcemia usually do not develop because citrate is metabolized by liver to bicarbonate. It results from conversion of citrate (present in stored blood) and lactate (accumulated due to hypoperfusion) to bicarbonate. Splenectomy • Indications of splenectomy include traumatic or iatrogenic splenic rupture (most common), symptom control in patient with massive splenomegaly, correction of cytopenias in patients with hypersplenism, staging of patients with Hodgkin’s disease, treatment of hairy cell leukemia and prolymphocytic leukemia. Acute manifestations of splenectomy include leukocytosis (up to 25000/µl) and thrombocytosis (up to 1 × 106/µl) but return back to normal levels within 2-3 weeks. Chronic Manifestations of splenectomy include: • Anisocytosis and poikilocytosis • Howell-Jolly bodies (nuclear remnants) • Heinz bodies (denatured hemoglobin) • Basophilic stippling • Target cells • Pappenheimer bodies (contain sideroblastic granules) • Irregular contracted red cells. When such erythrocyte abnormalities are seen without splenectomy, splenic infltration by tumor should be suspected. This condition is similar to endometriosis (presence of endometrial tissue at non- endometrial sites). Which of the following surface glycoproteins is most (b) Spherocytosis often expressed in human hematopoietic stem cell? Burr cell is seen in: (Jharkhand 2003) (d) Howell-Jolly bodies (a) Uremia (e) Cabot ring (b) Hepatocellular carcinoma (c) Gastric carcinoma 6. Which of the following surface glycoproteins is most (d) Ovarian carcinoma often expressed in human hematopoietic stem cell? A 74 year-old female Lajo Devi with renal failure (a) Renal cell carcinoma presents for hemodialysis.

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History must be sought for systemic disorders • Lower thrombopoietin levels in which can cause disseminated intravascular coagulation like thrombocytopenic neonates birth asphyxia and neonatal sepsis buy viagra plus 400 mg with visa impotence 20 years old. Hemophilia A and B are X­linked recessive disorders while von Willebrand factor • Increased von Willebrand factor defciency can be autosomal dominant Other coagulation factors • Decreased (by 50% as compared to or recessive cheap viagra plus 400 mg line erectile dysfunction even with cialis. Chromosomal protein C and protein S disorders like trisomy 13 purchase cheapest viagra plus impotence vacuum treatment, 18, or 21 can be associated with thrombocytopenia. Early onset (within 72 h of birth) • Vitamin K defciency • Pregnancy complications {{Early (within 24 h) Gestation at birth, age at onset of bleeding, and site (gestational hypertension, {{Classical (24 h to 7 days) of bleeding can indicate underlying cause. Subdural hemorrhage is more • Late­onset sepsis • Liver disease common with hemophilia while intraparenchymal bleed is • Necrotizing enterocolitis more common with thrombocytopenia (e. Systemic infections Clinical Pearl are most common underlying cause of late-onset thrombo- • Intracranial bleed in a term neonate should raise suspicion of cytopenia. History and physical Examination Maternal intake of antitubercular or antiepileptic drugs Detailed maternal history should be taken to rule out thrombo­ may be associated with development of early onset vitamin cytopenia due to immune causes. Neonates not receiving the recommended history of bleeding or thrombocytopenia in previous siblings. In case of active bleeding, platelet widespread derangement of the laboratory markers indicates transfusion can be given if platelet count is below 50,000/µL. If these are not available without delay, random donor platelets can be Clinical Pearl transfused. Platelet counts need to count, prothrombin time, activated partial thromboplastin be monitored for frst 10–14 days after birth. Due to lack of demonstrable efcacy in preventing serious hemorrhages, threshold platelet count below which platelet Specifc factor assay can be done on clinical suspicion. However, results need to be interpreted carefully in view of Most of neonates with platelet count above 20,000/µL will not altered levels in neonates. T erefore, classical hemophilia can be diagnosed in otherwise healthy neonates with thrombocytopenia. In case of active major Additional laboratory investigations may be warranted bleeding, platelet count may be maintained above 50,000/µL. A dose of 10 mL/kg is usually sufcient to increase the platelet count above therapeutic threshold. It involves factors related to maternal causes and intrapartum insults Clinical Pearl ){Laboratory values of coagulation factors are diferent than • Platelet count should be maintained above 50,000/µL in adults a neonate with active bleeding and above 30,000/µL in a ){Platelet and component therapy should be used very neonate without active bleeding. Current approaches to the evaluation and management of the fetus and neonate with immune thrombocytopenia. Dose of cryoprecipitate is the clinical evidence for their use in the neonatal intensive care unit? Platelets in the neonatal period: developmental differences in platelet production, function, and hemostasis and the potential impact of of other coagulation factors are rare and can be managed by therapies. Incidence is reported as 60% in term and around • Appears at >24 h and • Appears within 24 h of life 80% in preterm neonates. However, neurotoxic is seen at 3–5 day of life • Peak level crosses 95th centile potential of the unconjugated bilirubin which can result in in term and 5–7 day in for age in hours/in intervention permanent neurodevelopmental sequelae in some neonates is preterm zone well known. Hence, it is necessary that all those neonates who • Usually, needs no • Persists >14 days in term are at high risk are identifed and managed appropriately. Instead, various nomograms are available to • Needs intervention evaluate risk and decide intervention for a particular neonate. Table 1 lists • Extraneous blood source: cephalohematoma, bruising some important diferentiating points for various categories. However, absolute total serum bilirubin • Isoimmune hemolytic disease value tends to be higher than that expected for physiological • Glucose­6­phosphate dehydrogenase defciency jaundice. These guidelines do not address treatment of newborns born less than 35 weeks of gestation. There are graphs available for each phototherapy gestation outlining phototherapy and exchange thresholds • Blood group of the baby and the mother from birth itself. Evidence Based Clinical Practice Guidelines by National Neonatology Forum, Excellence charts, following conversion needs to be applied: India, October 2010. Hyperbilirubinemia in the newborn infant ≥35 weeks’ gestation: an update with clarifcations. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Glucose oxidase and factor like birthweight, gestational age, body store, feeding glucose electrode method are two most commonly used status, as well as the presence or absence of the disease. If it stays greater • Mother receiving drugs like, b­blocker, oral hypoglycemic, than 50 mg/dL then decrease frequency of monitoring from every hour to 4–6 hourly and received intrapartum glucose infusion. Unanimous opinion does not exist for the need then it’s considered to be refractory hypoglycemia. Management of Important causes asymptomatic hypoglycemia is summarized in table 2. Subsequently Other secondary investigations can be done according to <20 mg/dL manage as symptomatic hypoglycemia the etiology suspected. Incidence of neonatal seizures is inversely • Meningitis/sepsis proportional to the birthweight with incidence of approxi­ • Subdural/subarachnoid/interventricular mately 60 per 1,000 at less than 1,500 g and 3 per 1,000 at more hemorrhage intrauterine infection than 2,500 g at birth. Metabolic: hypocalcemia, hypomagnesemia, hypo­ • Half of the seizures in newborns are subclinical and one-third glycemia, hypo­ or hypernatremia of seizures do not have an electroencephalogram correlate. It is important to fnd out the cause as the transporter deficiency, biotinidase deficiency, Leigh prognosis is dependent on the etiology of seizure. Jitteriness • Rhythmic character with equal forward and backward movement • Can be restrained and is stimulus sensitive Clinical Pearl • No eye movements • Sixty percent of the causes of seizures are due to hypoxic Benign sleep • Myoclonic activity confned to sleep ischemic encephalopathy and 20% are related to stroke. However, all these variables Treatment for neonatal seizures ultimately are related to the degree of brain injury at the time of seizure occurrence, and, in turn, the seizure etiology. Summary proceedings from the neurology group on neonatal ))Neonatal period is the most common time in one’s life to get seizures. It can be divided into Maternal factors • Neonatal intensive two categories based on the onset. If mother is positive for group • Chest X-ray if respiratory distress B streptococcus then double dose of ampicillin should be • Lumber puncture: should be performed when index of used. Clinical Pearl Clinical Pearls • Consideration of fungal sepsis should be given for very • Blood culture should always be obtained before starting low birthweight babies, especially with central lines who antibiotic therapy, but inability to obtain blood culture should deteriorate on antibiotics. Asymptomatic neonate with minor risk factors should be <29 weeks 0–28 days 12 h observed, pending blood culture and septic screen and >28 days 8 h treatment should be started if baby becomes symptomatic or 30–36 weeks 0–14 days 12 h screening results are positive, whereas neonates with major >14 days 8 h risk factors should be started on antibiotics pending the sepsis screen results. All symptomatic neonates where alternative >37 weeks 0–7 days 12 h diagnosis is not possible should be started on antibiotics. Clinically evaluate and consider other Management of Late Onset Sepsis clinical diagnosis in the absence of positive laboratory 56 Management of late onset sepsis is represented in algorithm 2. Babies with minor modulator) symptoms should be started on treatment based on the sepsis • Colony-stimulating factor screen results. Instead, these neonates should be the neonatal period directly started on antibiotics pending blood culture ){We should have a high index of suspicion for diagnosis, and • Lumbar puncture should be done in all cases of late onset antibiotics must be used judiciously where required along sepsis. Duration of antibiotics depends upon clinical levels in the diagnosis of neonatal infection. Fanaroff and Martin’s Neonatal- and blood culture is negative and baby is asymptomatic or Perinatal Medicine: Diseases of the Fetus and Infant.

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Retention of water and electrolytes restores the blood volume order viagra plus 400 mg visa johns hopkins erectile dysfunction treatment, but the concomitant dilution of the blood causes a further decrease in the red cell count viagra plus 400mg with mastercard erectile dysfunction pump images, hemoglobin concentration cheap viagra plus 400 mg without prescription erectile dysfunction over 75, and hematocrit. Chronic bleeding is compensated by erythroid hyperplasia, which eventually depletes iron stores. The last category, increased rate of red cell destruction, includes the Rh factor and sickle cell anemia. The Rhesus (Rh) blood group antigens are involved in maintaining erythrocyte structure. Sickle cell anemia, associated with the abnormal hemoglobin HbS gene, is common in Africa, India, and among African Americans but is rare in the Caucasian and Asian populations. In the sickle cell trait, which occurs in about 9% of African Americans, one abnormal gene is present. A single point mutation occurs in the hemoglobin molecule, causing the normal glutamic acid at position 6 of the beta chain to be replaced with valine, resulting in HbS. The amino acid substitution is on the surface, resulting in a tendency for the hemoglobin molecule to crystallize with anoxia. However, heterozygous people have no symptoms, and oxygen transport by fetal (HbF) and adult hemoglobin (HbA) is normal. Sickle cell disease represents the homozygous condition (S/S) and occurs in about 0. The onset of sickle cell anemia occurs in infancy as HbS replaces HbF; death often occurs early in adult life. Patients with sickle cell anemia have >80% HbS in their blood with a decrease or an absence of normal HbA. Symptoms include pallor of the lips and skin, weakness, fatigue, lethargy, dizziness, and fainting. This situation can arise from a chronic obstructive pulmonary disorder (such as emphysema) or depressed respiration (as a result of a head injury or a drug overdose, for example). If a patient has a low PaO and a normal A–aO gradient, the2 2 cause of hypoxemia is entirely a result of generalized hypoventilation. The best corrective measure for generalized hypoventilation is to place the patient on a mechanical ventilator, breathing room air. Administering supplemental oxygen to a2 2 patient with generalized hypoventilation will correct hypoxemia but not hypercapnia because ventilation is still depressed. This condition occurs when the diffusion distance across the alveolar–capillary membrane is increased or the permeability of the alveolar– capillary membrane is decreased. If the PaO is low and the A–aO gradient is high, then the cause can be a shunt, a2 2 regional low ratio, or a diffusion block. Diffusion impairment is the least likely cause and can be deduced if the other three causes have been eliminated. She went to the university hospital with progressive shortness of breath and generalized lethargy. She stated that she lost 15 lb over the last 3 months and had a total loss of energy, which was devastating because she was so active. She was transferred to the intensive care unit for further observation and monitoring. The patient was married, was a nonsmoker, and had no history of intravenous drug use. She had no prior history of pulmonary or cardiac conditions and was not taking any prescription or herbal medications. The clinical examination revealed oxygen saturation of 87% breathing ambient air, tachypnea, tachycardia, bilateral pulmonary rales in basal fields, and a low-intensity systolic murmur. The patient received packed red blood cell transfusions to correct for her low O saturation2 and her low red cell count. However, her symptoms did not improve and was readmitted to the university hospital. The echocardiogram revealed an enlarged heart, tricuspid regurgitation, and moderate-to-severe pulmonary hypertension. Antiviral therapy was initiated in addition to presumptive antibiotics for possible Pneumocystis (carinii) jiroveci infection. This case is a common presentation of pulmonary hypertension: a previously health young woman develops a life-threatening disease with no outward manifestation. Because these individuals look normal at rest, family, friends, and coworkers have a difficult time accepting they are sick or have a serious disease. Whatever the initial cause, this devastating disease involves the narrowing of pulmonary blood vessels that increase pulmonary vascular resistance, which makes it harder for the heart to pump blood through the lungs. Over time, the affected blood vessels become stiffer and thicker known as fibrosis. This further increases the blood pressure within the lungs and impairs blood flow. Under normal conditions, in the presence of oxygen, the nitric oxide synthase produces nitric oxide from L-arginine. These include phoshoidesterase-5 inhibitors, such as sildenafil; prostanoids, such as epoprostenol; endothelin receptor antagonists, such as bosentan; calcium channel blocker, such as diltiazem; diuretics to reduce swelling in ankles and feet (e. Under normal conditions, oxygen uptake in the pulmonary capillaries is limited primarily by blood flow. Under resting conditions, ~250 mL of oxygen per minute is transferred to the pulmonary circulation. Oxygen is transported by the blood in two forms: oxyhemoglobin and dissolved O in the plasma. When Hb-binding affinity to O increases, the P2 50 changes in the opposite direction. A normal alveolar–arterial oxygen gradient is present because alveolar ventilation and capillary blood flow are not evenly matched in regions of the lung and because bronchial circulation mixes with oxygenated blood. Regional hypoventilation (low ventilation/perfusion ratio) is the major cause of hypoxemia. The A–aO gradient in a healthy person is due to both a low 2 ratio at the base of the lungs and a small shunt from the bronchial circulation. Which of the following parameters would best reflect adequate oxygenation to the tissues? Arterial oxygen tension and arterial oxygen saturation can be normal in situations like anemia. Arterial–venous oxygen tension difference can also be unchanged in anemic patients. The P50 reflects the ability of the hemoglobin-binding affinity for oxygen and provides little information about tissue oxygenation. A 40-year-old patient had normal blood gas values with an arterial oxygen tension (PaO ) = 952 mm Hg, O content = 19 mL/dL, O capacity = 20 mL/dL, and arterial oxygen saturation (SaO ) =2 2 2 95%. Which of the following would best describe her blood gases following anemia compared to her normal values? Which of the following gas tensions would most likely be predicted in a2 lung unit with a ratio of 2? A lung unit with a high results in that region being overventilated with respect to blood flow.

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Hypotension due to cardiogenic shock hemoglobinemia and antibodies (Myocardial infarction buy discount viagra plus online impotence lipitor, constrictive peri- against red cells purchase viagra plus amex impotence quotes the sun also rises. Renal causes: (intrinsic renal failure) multiple factors are involved ing over a period of hours to days resulting i discount viagra plus 400mg amex erectile dysfunction treatment in tampa. Loss of fuid and salt drome in which there is severe arterial thrombosis, emboli or stenosis, a. From the gut in severe vomiting, contusion of the muscles of the bilateral renal vein thrombosis. Section 12  Urology by stones and tumor, or bladder outfow pyelography may help in assessing the vi. Antibiotics may be needed to avert infec- obstruction due to prostatic hypertrophy nature and site of the obstruction. Improved urine output may be obtained lesions by the appropriate means may gives information about excretion and by infusion of dopamine (2–5 µg/kg/min) result in rapid resolution of the acute renal diferential function between the two and frusemide (10–15 mg/kg/hour) and failure. Almost 80 percent of acute renal failure is cially in the early phase despite azotemia. Clinical Microscopically, there is mitochondrial cal drainage either endoscopically or by open 1. The recovery phase may last (postdiuretic patient alive till recovery of the renal lesion Peritoneal Dialysis Versus phase) from 3 to 12 months during which takes place. Fluid replacement - Intake of fuid is Peritoneal dialysis is the simplest form of lar function gradually improve to nearly restricted to replacing the lost volumes treatment, although hemodialysis may be baseline levels. Preexisting Dialysis Acute renal failure usually comes to the atten- over hydration should be taken note of. Both forms of dialysis are efective when tion of the physician either because of a raised Fluid is best given orally. A low protein diet with additional calo- who cannot tolerate hypotensive episodes ries (daily intake of 3000kcal) is generally or the heparinization required to perform Clinical Evaluation recommended and should be ordered in hemodialysis. Hemodialysis, on the other hand, achieves to make the diagnosis of acute renal failure. Nephrotoxic drugs should be discontin- more rapid clearance of the plasma and is The background factors and the etiology ued or avoided. Hypertension (Nephrosclerosis) • Metabolic acidosis results as the hydro- fold and can be of biological origin, e. Diabetic nephropathy gen ion excretion (40 – 60 mcg/day) is arterial and heart valve grafs or syn- 3. Interstitial nephritis ing the arterial pH to nearly normal Preparation of the Recipient 6. Active tuberculosis or other systemic disease is progressive, leading to end stage infection. Extremes of age (Elderly people > 65 years Conservative treatment-In case of estab- or very young children). Coagulopathy-due to decreased platelet transplantation are used when conservative Donor Selection adhesiveness. The majority of donated kidneys come from efective treatment of platelet dysfunction. Electrolyte disturbance – The most serious transplants are taken from live related donors. Renal trans- fcial ventilation but have no evidence of magnesium levels may accompany plantation means transplantation of a kidney malignant disease. Preoperative Management Chronic hypocalcemia will lead to • Heterotopic graf is a graf placed at a site 1. Tissue typing hyperparathyroidism with resulting diferent from that where the organ is nor- i. The behavior of organs and tissues bone decalcifcation, development of mally located. Infection due to immunosuppression Antibodies and cellular immune mech- similar to a nephrectomy for other rea- 2. Acute rejection - Tis occurs between The most important transplanta- length of the artery, vein and ureter as 1 and 8 weeks afer transplantation. Chronic rejection - Tis may occur face of most cells of the body, they able a cadaveric kidney is used as men- at any time afer transplantation. Surgical complications which are expressed by a group of genes • The kidney is transplanted in the retro- a. Vascular complications on the short arm of chromosome 6 peritoneal tissues of the right iliac fossa. Tere are other minor histocompat- renal vein with external iliac vein end to in approximately 5 percent of cases. Tis is evidenced by the fact The ureter is implanted into the bladder afer transplantation with sudden that even when grafs are matched for through the submucosal tunnel. The diagnosis is confrmed by sion may still be required to prevent Postoperative Management Doppler ultrasonography. Hence it is vital for all types of organ agents are azathioprine, cyclosporine – A When angioplasty fails or is not allograf to ensure that the recipients and corticosteroids. Urinary leak giving rise to urinoma It Test Done Before given in relatively low nontoxic doses so usually results from technical error at Transplantation that bone marrow depression for azathio- the ureteric anastomosis or ureteric 1. The urethra consists of the prostatic, mem- develops from the prolonged urogenital On either side of the orifce of the prostatic branous and spongy parts. Posterior wall is developed from the vesi- cells does not canalize and there is accom- It is the shortest portion of the urethra and courethral part of endodermal cloaca panying failure of complete fusion of the runs from the prostate to the bulb of the incorporated with the caudal parts of the genital folds the result is hypospadias - a penis. The Spongy Part the colliculus, corresponds in develop- The cause of epispadius is obscure. Part below the colliculus - All walls are Surgical Anatomy upwards and forwards to lie below the pubic developed from the endoderm of pelvic symphysis and then in its faccid state bends part of urogenital sinus. Membranous Part (2cm) The prostatic urethra as the name implies, The Female Urethra It is the part lying within the deep perineal traverses the prostate. Its posterior wall con- The female urethra is about 4cm in length and pouch and developed from the endoderm of tains a longitudinal elevation called the ure- lies embedded in the anterior wall of vagina. Penile part-Upto the base of glans penis At about the middle of the crest is an 84. In this condition the exter- • Chordee -Many of the cases are associ- urethroplasty. Hence circumcision should nal urethral meatus is situated at some point ated with bending of the penis on erection. The chordee is the fbrous cord distal to the One stage procedure: Nowadays one ectopic meatus.