By W. Hernando. State University of New York Institute of Technology at Canton. 2019.
In case of presence of associated prostatitis threads may be seen in the initial specimen generic prandin 0.5 mg online, so midstream urine specimen should be taken for culture and sensitivity test 1 mg prandin overnight delivery. X-ray is also required if the patient fails to respond to adequate antibiotic treatment for cystitis or the infection is recurrent and there is presence of obstruction purchase prandin line, vesicoureteral reflux, tuberculosis or calculus. But it should be done 10 days later when haematuria is continuing to exclude presence of vesical neoplasm or stone or foreign body. By raising the pH of the urine, it counteracts the burning sensation of acidic urine which normally accompanies infection. These are nalidixic acid 500 mg, nitrofurantoin 100 mg tablets, amoxycillin, trimethoprin and sulphamethoxazole, chloramphenicol, ampicillin etc. Rarely it may be secondary to tuberculosis of the prostate, seminal vesicles and epididy mis. This ulcer is round with ragged and overhanging edges and covered with grey shaggy floor. Though it covers a considerable area, it is seldom deep and perforation of the bladder is almost unknown. There is considerable submucous fibrosis which also prevents penetration of such ulcer. Fibrosis causes reduction in the capacity of the bladder which becomes smaller in size and is often called ‘thimble’ bladder. In majority of cases this treatment is enough to cure not only tuberculosis of the bladder but also tuberculosis of the kidney. In some intractable cases instillation of antitubercular agent into the bladder has been effective. B53 is a soap derived from a branched fatty acid which possesses a good antitubercular power. With removal of the offending kidney the bladder lesion starts recovering soon When the bladder has been considerably contracted with reduction of its capacity to a great extent, some sort of operation should be performed to increase the capacity of the contracted bladder The bladder should be first made free from ulcerations by medical treatment and even by nephroureterectomy. Once the bladder is free from ulceration, ileocystoplasty should be performed in which a portion of small intestine (ileum) is sutured to the dome of the contracted bladder. If the ureter is seen to be involved evidenced by dilatation on excretory urography, it should be implanted into the newly con structed pouch of intestine. The condition is characterised by presence of pus in the urine, but without any accompanying bacteria. Similarly an adenovirus has also been isolated from the urine of children suffering from this disease. Microscopically, the mucosa and submucosa are infiltrated with neutrophils, plasma cells and eosinophils Submucosal haemorrhages are common, similarly there are superficial ulceration of the mucosa. There is urethral discharge which at times clear and mucoid, but in majority of cases it is purulent. Suprapubic discomfort or pain is quite often complained of particularly when the bladder is full. Excretory urography is usually not diagnostic, but it may show dilatation of lower ureters and presence of vesicoureteral reflux. If it is performed due to inability to diagnose or in the suspicion of tuberculosis, one can see redness and oedema of the mucosa with superficial ulceration. But to shorten the period of discomfort the following treatment may be adopted :— A. General measuresBladder sedatives, analgesics and antispasmodic may be used with hot sitz baths. The main feature is a localised inflammatory thickening in the centre of which there is a minute exquisitely tender ulcer which comes and goes. The possibility is that an infective process starts in the paravesical tissues secondary to infection somewhere in the body. This leads to avascular atrophy of the mucous membrane and ultimately ulcer formation. Microscopically, there is oedema, congestion and round cell infiltration affecting all the coats of the bladder, particularly the submucosa. The disease is of long duration marked by periodic attacks of severe pain on distension of the bladder, frequency of micturition and great decrease of bladder capacity. Increased frequency seems to be the leading symptom Which is complained of in both day and night almost every hour. Pain is the next common complaint which is aggravated by distension of the bladder and is relieved to certain extent by voiding. In early cases the urine is clear and sterile, but in late cases it contains pyogenic bacteria in half the cases. There is an intense congested area, in the centre of which there is an ulcer, which bleeds easily. Local hydrocortisone irrigation of the bladder, though effective in few cases, is not a proven treatment. Intravesical instillation of dimethylsulphoxide has been proved to be effective in majority of cases. Ileocystoplasty after excision of the affected bladder wall (mostly dome of the bladder) is the second operation which has attained some success, though has failed to relieve permanently. This seems to be due to improved diet rich in protein and abolition of malnutrition. Primary vesical calculus, which develops in the sterile urine and mostly originates in the kidney which passes through the ureter into the bladder. In this group may be included another type of vesical calculus which occurs by deposition of urinary salts upon a foreign body in the bladder. Though calcium oxalate is white, yet this stone often looks dark brown or black due to incorporation of blood pigment on it. This is seen in alkaline infected urine when there are urea splitting organisms which split urea into ammonium compounds. The stone which grows by depositing urinary salts around foreign body is also made up of triple phosphate. Even desquamated epithelium and bacteria may form nidus for deposition of triple phosphate and formation of phosphate calculus. A vesical calculus usually remains free in the bladder and moves about according to the position of the patient. It gravitates to the most dependent part which is the neck of the bladder in erect posture and behind the interureteric ridge in recumbent posture. The most characteristic feature is that the patient does not feel satisfied after complete voiding and he feels to come back again for urination. Such pain is referred to the tip of the penis or to the labia majora at the end of micturition. This seems to be an extremely important symptom and almost diagnostic of vesical calculus. Such pain is due to the presence of vesical calculus on the trigone of the bladder. Pain or discomfort is also complained of in the suprapubic region and this is aggravated by running and jolting.
It may also occur from paralysis of the intestinal muscle so that the peristalsis of the intestine is lost purchase prandin 0.5 mg fast delivery, so is the progression of the intestinal contents buy prandin 2mg low price. Adhesions may produce kinking or angulation of the intestine or create bands of tissue that compress the bowel cheap prandin 0.5 mg without prescription. Inguinal, femoral, umbilical and incisional hernia are important causes of bowel obstruction. Simple mechanical obstruction in which there is obstruction but blood supply to the intestine remains intact. Strangulated obstruction, in which the mesenteric vessels are occluded besides the usual mechanical obstruction. Closed loop obstruction when both limbs of the loop are obstructed so that there is neither progression nor regurgitation. Intestinal obstruction can be further classified into : (i) A cute obstruction, which is an obstruction to the small bowel and is characterised by central abdominal pain, early vomiting, central abdominal destension and constipation, (ii) Chronic obstruction, when obstruction is confined to the large bowel and is characterised by lower abdominal colic, absolute constipation and later on distension, (iii )Acute-on-chronJc obstruction, which starts in the large bowel but gradually involves the small intestine. The more distal is the obstruction, the more vigorous is the peristalsis and longer does it remain. If the obstruction is not relieved, increasing distension of the intestine ensues and a time comes when peristalsis ceases and the obstructed intestine remains flaccid and paralysed. For a few hours the intestine below the obstruction shows normal peristalsis and absorption. This will empty its contents and later on it becomes immobile, contracted and pale. Ingested fluid, digestive secretion and intestinal gas play the major role to form this distension. This phenomenon results in increased fluid accumulation in the bowel proximal to the obstruction. Accumulation of such huge amount of fluid alongwith repeated vomiting causes severe metabolic disturbances. Particularly in proximal obstruction there is relatively more vomiting and this leads to losses of water, sodium, chloride, hydrogen and potassium ions producing dehydration with hypochloraemia, hypokalaemia and metabolic alkalosis. Distal small bowel obstruction may cause loss of large quantities of fluid, but the abnormalities of serum electrolyte values are less dramatic, probably because of hydrochloric acid losses are less. If dehydration continues, there will be reduced cardiac output, low central venous pressure, hypotension and hypovolaemic shock. Distension of the abdomen will lead to elevation of the diaphragm to impair proper ventilation. This mainly consists of (i) gas swallowed from the atmospheric air, (ii) diffusion from blood into the bowel lumen (carbondioxide from neutralisation of bicarbonate) and (iii) organic gases (hydrogen sulph ide, ammonia, amines and hydrogen) from bacterial fermentation (10%). Swallowed air is the most important source of gas in causing intestinal distension. While the oxygen and carbondioxide are absorbed, nitrogen is not absorbed by intestinal mucosa. On the other hand carbondioxide diffuses very rapidly, as the partial pressure of carbondioxide is high in the intestine and intermediate in the plasma Thai is why though carbondioxide is produced in large amounts in the intestine, it contributes little to gaseous distension ofthe intestine due to its rapid diffusibility. Normally the small intestine contains very small quantity of bacteria and may be considered as almost sterile. Normal peristalsis with continued progression of luminal content minimises small intestinal bacterial flora. But during small intestinal obstruction, whatever may be the cause, bacteria proliferate rapidly. As the bacteria or bacterial toxins cannot cross normal intestinal mucosa the bacteria in the small intestine probably play no role in the ill effects of simple mechanical small intestinal obstruction. This frequently occurs secondary to (i) adhesive band obstruction, (ii) hemia, (iii) volvulus or (iv) intussusception. If the obstructed distending bowel is held by unyielding adhesive bands or hernial rings strangulation may occur. Similarly in volvulus or intussusception, the mesenteric vessels are occluded by twisting of the mesentery. In strangulated obstruction the patient suffers from all the ill effects of simple obstruction plus to the effects of strangulation. Unlike non-strangulated obstruction, early distension of the proximal intestine is absent. After this, vigorous peristalsis occurs in the proximal segment without any distension. When gangrene is imminent, retrograde thrombosis of the related tributaries of the mesenteric vein will cause distension of both the proximal and distal segments of the strangulated intestine. The greatest distension occurs when the venous return is completely impaired and the arterial supply continues uninterrupted. Now the serous coat loses its glistening appearance, the mucous membrane becomes ulcerated and thus wet gangrene develops. This loss of blood and plasma will cause shock particularly if the patient is already dehydrated. The amount of loss of blood volume will depend upon the length of the strangulated segment. As mentioned above, the bacteria proliferate and produce toxic meterial within the strangulated segment. When the intestinal mucous membrane is normal this toxic material is not absorbed, but when the wall of the intestine becomes partly devitalised, both bacterial toxin and the products of tissue autolysis pass through the wall of intestine into the peritoneal cavity, whence these are absorbed into the circulation. So if the strangulation is external, it is far less dangerous than intraperitoneal strangulation. It is dangerous as this type of obstruction very rapidly becomes strangulated even before the usual manifestations of intestinal obstruction. Obstruction to blood supply occurs either from the same mechanism which produces such obstruction or by the twist of the bowel on the mesentery. Development of distension and onset of gangrene are almost same as strangulated obstruction described above. If the ileocaecal valve is competent colon obstruction will lead to closed-loop obstruction (described above). In this case pressure within the caecum becomes quite high to compress blood vessels within its wall. If the ileocaecal valve is incompetent, signs of small bowel distension may accompany colon obstruction. Otherwise colon obstruction is less dangerous as it produces less fluid and electrolyte imbalance than small bowel obstruction. The pain is represented by severe cramps with intervals of 4 to 5 minutes in proximal intestinal obstruction and with more intervals (15 to 20 minutes) in distal obstruction. The pain is diffuse, poorly localised and is felt across the upper abdomen in high obstruction, at the level of the umbilicus in low ileal obstruction, in the lower abdomen in colon obstruction and in the perineum in case of rectosigmoid obstruction.
The valves are destroyed by transurethral route by fulguration through panendoscopy or by fragmentation by the passage of sounds buy prandin on line amex. Diagnosis can be made by cystoscopy through which hypertrophied interureteric ridge can be seen buy prandin 0.5mg low cost. When the aetiology is congenital muscular hypertrophy buy cheap prandin on-line, patients are usually young children. Dysuria is the main symptom with ultimate development of hydroureter and hydronephrosis. When the condition presents after the age of 50 years, it is difficult to differentiate from benign enlargement of the prostate from symptoms point of view. That straining helps to increase the flow of urine and that there is no prostatic enlargement are the findings in favour of this condition. The condition may recur in a few cases due to inadequate division of the fibres at the bladder neck. The apex between two limbs of the Y is brought down to the end of the vertical limb of the Y to make the incision a V-shaped one. Such calculus may be formed behind a urethral stricture or in an urethral diverticulum. Calculus may secondarily come to the urethra from above and become arrested in the prostatic (rarest), bulbous or in penile part of the urethra. Such migratory calculi are usually seen in children due to the comparatively large neck of the bladder which allows these calculi to pass through. The varieties of neoplasms which can be seen in the urethra are—polyp, papilloma, angioma and carcinoma Polyp. Occasionally multiple papillomas of the posterior urethra have been detected which are usually associated with papilloma of the bladder. Treatment of all benign neoplasms is diathermy coagulation through a urethroscope. When carcinoma is situated in the posterior urethra, more extensive operation in the form of radical prostatectomy should be considered. This thickened epithelium continues to proliferate displacing the mesonephros in a dorsilateral direction and forming a projection into the coelomic cavity, which is termed the genital ridge. The proliferating epithelium on the surface sends a number of cellular cords inwards which are known as testis cords. At the 7th week a mesenchyme cuts off the testis cords from the surface and forms the tunica albuginea. At this stage one can differentiate between testis (where tunica albuginea is prominently present) and ovary (where tunica albuginea is absent). The testis cords encroach on the medulla where they unite with the network derived from the mesenchyme and become rete testis. The premordial germ cells are incorporated in the cords (testis cords), which later become enlarged and canalised to form the seminiferous tubules. The cells derived from the surface of the gonad form the supporting cells of Sertoli. The interstitial cells of the testis are derived from the mesenchyme which do not become incorporated into the tubules. The cords of the rete testis canalise at a later stage and become connected to the mesonephric duct by 5 to 12 most cephalic of the persisting tubules and these become exceedingly convoluted and form the lobules of the head ofthe epididymis. The mesonephric duct becomes the canal of the epididymis and the ductus deferens of the testis. Mesenchymal cells form a cord which extends from that part of the skin which later forms the scrotum, through the inguinal fold to the lower pole of the testis. This cord later becomes a fibromuscular bundle and is termed the gubemaculum testis. It traverses the site of the future inguinal canal, which is formed around it by the muscles of the abdominal wall as they become differentiated The testis descends along the path of the gubemaculum whether or not due to pull of it. A fold peritoneum protrudes down the inguinal canal along with the testis forming the processus vaginalis. The lower pole ofthe testis is kept in apposition with the deep inguinal ring by the gubemaculum until the 7th month Suddenly the testis passes through the inguinal canal and gains the scrotum As it descends, it is necessarily accom panied by its peritoneal covering and by a fold of peritoneum from the adj oin- ing peritoneum from the iliac fossa which is drawn down as the processus vaginalis as also its blood vessels and nerve supply. The peritoneal covering of the testis which represents the distal end of the processus vaginalis and into which the testis projects, is termed the tunica vaginalis testis. The part of the processus vaginalis which is associated with the spermatic cord in the scrotum and in the inguinal canal normally be Fig. The fascial covering of the testis and spermatic cord includ ing the Cremaster are developed from the surrounding structures as the testis descends. At the superficial inguinal ring — at the later part of the 7th month or 8th month. When both the testes are absent in the scrotum, the condition is called cryptorchidism (Hidden testes). As the right testis descends later than the left testis, undescended testis is more common on the right side Pathology of undescended testis. Proper development of spermatogenic tubules cannot take place in abdominal cavity As a result the spermatogenic tubules are of diminished size and fewer spermatogonia have been detected in undescended testis in boys at about 6 years of age. After puberty, the difference is obvious and the undescended testis is much smaller and flabby than the normal intrascrotal testis. So secondary sex characters appear and endocrinologic cause of impotence is rare in this group. However in bilateral cryptorchidism, androgen level is diminished to certain extent. In a series, about 90% of cases of undescended testis were associated with patent processus vaginalis. The chance is more if the undescended testis remains in a patient of 10 years of age or older and many surgeons recommended orchidectomy for unilateral undescended testis at this age group rather than orchidopexy. It is often a retractile testis due to contraction of overactive cremaster muscle. In fact the child or the parents first notice that the scrotum is not developed, rather than absence of testis within it. An incompletely descended testis should lie anywhere on the line of normal descent i. It must be remembered that when a testis is palpable in front of the inguinal canal it is an ectopic testis lying in the superficial inguinal pouch, a space lined by loose areolar tissue superficial to the external oblique aponeurosis and it is not an undescended testis. Such testis is often retractile testis and attains that position by the strong contraction of the cremaster muscle which is very well developed in childhood. But two points should be borne in mind to differentiate this condition from incomplete descended testis — (a) In this case the scrotum is normally developed, whereas scrotum is under-developed in case of incompletely descended testis, (b) Such testis can be milked into the scrotum.