By R. Rhobar. Montana Tech. 2019.
Your examination reveals no other neurologic signs but she has coffee- colored areas of discoloration on her abdomen and thorax purchase zestril now. Unilateral deafness may be because of local conditions 10mg zestril for sale, such as wax order zestril with amex, a foreign body generic zestril 10mg line, otitis media, or ruptured drum, or it may be because of neurologic conditions such as Ménière’s disease, acoustic neuroma, or multiple sclerosis. Bilateral deafness is more likely because of otosclerosis, acoustic trauma, presbycusis, or drug toxicity. It is very important to do a thorough examination of the ear as one may find wax, foreign body, otitis media, cholesteatoma, or ruptured drum. The presence of vertigo should make one think of Ménière’s disease or some neurologic condition such as acoustic neuroma, multiple sclerosis, or basilar artery insufficiency. In otosclerosis, the ratio approaches 1:1, but in sensory neural deafness the ratio is preserved at 2:1. This will lateralize to the affected ear if the problem is a conductive deafness, and it will lateralize to the good ear if the problem is a sensory neural deafness. If basilar artery insufficiency is suspected, four-vessel cerebral angiography should be done. Rather than performing these tests, the most cost-effective approach would be to refer the patient to a neurologist if other focal neurologic findings are evident. Significant weight loss would suggest anorexia nervosa, hyperthyroidism, celiac disease, cystic fibrosis, and uncontrolled diabetes, among other conditions. The presence of a short stature would suggest pituitary tumors, hypothalamic syndromes, gonadal dysgenesis, adrenal tumors, hyperplasia, hypothyroidism, and ovarian tumors. The presence of a normal or tall stature would suggest constitutional delayed puberty among other more rare conditions. Delirium with fever may simply indicate a self-limited infectious process, but it should bring to mind encephalitis and meningitis as well as cerebral abscess and cerebral hemorrhage. A history of head trauma would make one suspect a subdural or epidural hematoma and concussion. This is probably the most important single question to ask in the average case coming into the emergency room these days without a good history. Focal neurologic signs along with the delirium would make one think of subdural or epidural hematoma, cerebral abscess, or cerebral hemorrhage. If there is nuchal rigidity, the patient may have meningitis or subarachnoid hemorrhage. If the patient responds to intravenous thiamine, the diagnosis is usually Wernicke’s encephalopathy or Korsakoff’s syndrome. Intermittent delirium should suggest psychomotor epilepsy and transient global amnesia. Acute delirium may be an indication to administer intravenous glucose and thiamine. If there is fever, blood cultures and a spinal tap for analysis and culture need to be done. If there is impairment of memory, an organic psychosis should be suspected, such as senile and presenile dementia or general paresis. When there is no impairment of memory, the problem is probably a psychiatric disorder such as schizophrenia or manic-depressive psychosis. Following the algorithm, you ask about alcohol abuse and inquire about the medication he is taking. He has an occasional glass of wine and is on no medication other than an occasional aspirin for headache. Chronic barbiturate intoxication, ergotism, and other psychotropic or antidepressant drugs may cause dementia. Alcoholism may cause dementia in the form of Korsakoff’s psychosis or Wernicke’s encephalopathy. The most important condition to rule out in this category would be a space- occupying lesion, but normal pressure hydrocephalus, cerebral arteriosclerosis, acute cerebrovascular accident, and general paresis may present with focal neurologic signs. Response to these drugs would indicate that the patient has pellagra, Korsakoff’s psychosis, pernicious anemia, or myxedema. In patients with cerebral arteriosclerosis, the patient notices that his memory is slipping. Extrapyramidal tract signs should suggest Huntington’s chorea or Parkinson’s disease. Pyramidal tract signs are seen in general paresis and Jakob–Creutzfeldt syndrome, but myoclonus is also seen in Jakob–Creutzfeldt syndrome. Psychometric testing will help differentiate organic brain syndrome from other psychiatric disorders and malingering. A neurologist or psychiatrist should be consulted before ordering expensive diagnostic tests. In mild cognitive disturbances, consider a trial of antidepressants or hormone therapy, especially in postmenopausal women. A number of endocrinologic diseases may present with depression, including Cushing’s disease, myxedema, hyperthyroidism, and menopause. Endogenous depression, unipolar depression, and the depressive phase of manic– depressive psychosis may present with these findings. On the contrary, neurotic-depressive reaction usually is not associated with significant loss of appetite, weight, or libido. If Cushing’s syndrome is suspected, a 24-hour urine-free cortisol and cortisol suppression test should be done. A trial of estrogen therapy may be warranted in women or a trial of testosterone therapy in men. Office tests to evaluate nonorganic depression include the Beck Depression Inventory and the Hamilton Depression Scale. A referral to a psychiatrist should also be considered early if the depression is severe or if there is suicidal ideation. Obviously, infectious disease is a very important cause of diaphoresis, particularly when the fever breaks. Look for tuberculosis, malaria, acute rheumatic fever, and bacterial endocarditis. Chest pain with diaphoresis would make one think of an acute myocardial infarction, but this combination is also found in coronary insufficiency. Weight loss and hypertension should make one think of hyperthyroidism and pheochromocytoma. Peripheral neuropathy is also associated with sweating because of involvement of the autonomic nervous system. The triad of obesity, diaphoresis, and increased appetite is typical of an insulinoma. A 24-hour urine collection for catecholamines can be done if a pheochromocytoma is suspected. A glucose tolerance test, a 36- to 72-hour fast, and insulin tolerance test may be done for an insulinoma. If infectious disease is strongly suspected, a workup for fever of unknown origin can be done (see page 198). From the algorithm, blood in the stool should indicate that there is Salmonella, Shigella, Campylobacter jejuni, ulcerative colitis, Crohn’s disease, and amebic dysentery. Without blood in the stool, it is more likely that the acute diarrhea is because of a staphylococcal toxin, giardiasis, traveler’s diarrhea, a virus, or contaminated food. Fever, especially with an elevated white count and blood in the stool, would suggest Salmonella, Shigella, C. The absence of fever would suggest amebic dysentery or giardiasis, although there may be fever in amebic dysentery in severe cases. Even traveler’s diarrhea and toxic staphylococcal gastroenteritis do not usually give more than a low- grade temperature at best. Pseudomembranous colitis may result in a significant elevation of the temperature once the patient becomes severely dehydrated. Traveler’s diarrhea and viral gastroenteritis may also cause severe vomiting, as may food that is contaminated. On the contrary, there is little or no vomiting in giardiasis and pseudomembranous colitis. This is a key question because it indicates whether there is a possibility of toxic staphylococcal gastroenteritis, botulism, or a contagious condition such as infection with Salmonella, Shigella, or Campylobacter. If only one member of the family was suffering from diarrhea and everyone is eating the same food, then it is less likely to be a contagious condition, and one must consider ulcerative colitis, pseudomembranous colitis, and conditions listed under chronic diarrhea. Recent foreign travel would suggest the possibility of traveler’s diarrhea, cholera, shigellosis, salmonellosis, and giardiasis.
In fact colchicine is presently used in the control of fibrous contractures in human beings cheap zestril 10 mg visa. Marginal basal cells lose their firm attachment to the underlying dermis generic 10 mg zestril with visa, enlarge and begin to migrate into the wound buy discount zestril 5 mg. The fixed basal cells in a zone near the wound edge undergo rapid mitotic divisions (proliferate) and the daughter cells migrate zestril 10 mg low cost. After bridging the wound defect, the migrating epithelial cells lose their flattened appearance and become more columnar in shape. Subsequent epithelial thickening and keratinization may produce marked foreign body reaction and formation of sterile abscess. In one sentence epithelialization of the wound mainly occurs by proliferation and migration of the marginal basal cells lying close to the wound margin. When there is skin loss, dermal pits which are left behind act as islands for regenerating epithelium. But there is no regeneration of hair follicles, sweat and sebaceous glands in the new epidermis. This formation of granulation is preceded by two phases — (i) phase of traumatic inflammation and (ii) phase of demolition. The mononuclear cells alongwith large phagocytic macrophages infiltrate and ingest particulate matters. It is in fact composed of in the first instance by capillary loops and fibroblasts with a variable number of inflammatory cells. So initially it is a highly vascular tissue, which gradually turns into an avascular scar tissue. The two stages are considered in this process — (a) stage of vascularization and (b) stage of devascularization. The ingrowth of capillary loops and fibroblasts which help to form living granulation tissue is known as organization. Solid buds of endothelial cells grow out of the existing damaged blood vessels at the surface of the wound. These undergo canalization and by anastomosis with their neighbours form a series of vascular arcades. Under the electron microscope gaps are seen between the endothelial cells and the basement membrane is poorly formed. These newly formed capillary loops leak protein and thus the tissue fluid which is formed is a very suitable medium for fibroblastic growth. Gradually these capillary loops differentiate, a few acquire muscle coat and become arterioles, whereas others enlarge to form thin walled venules. The source of smooth muscle fibres to form arterioles is either cell migration or differentiation of existing primitive mesenchymal cells. The fibroblasts, which accompany the capillary loop, gradually become larger to become elongated fibrocytes. Collagen is an extracellular secretion from specialized fibroblasts and the basic molecules which fibroblasts synthesise are frequently called tropocollagen. This tropocollagen condenses in the mucopolysaccharide extracellular space to form fibrils. This collagen is not inert and it undergoes constant turnover under the influence of tissue collagenase. There are several types of collagen which differ in the aminoacid sequence of the constituent chains, though hydroxyproline, proline and glycin dominate. Other fibrous tissues such as elastin do not contain significant amount of hydroxyproline. Fibroblasts are also thought to be responsible for the production of mucopolysaccharide ground substance. So the granulation tissue looks pale at this stage, which is known as devascularization. The new lymphatics develop from existing lymphatics in the same way as do the capillary loops. Mast cells also make their appearance and their granules are derived from the ground substance. The gross appearance of remodelling scars suggests that collagen fibres are altered and rewoven into different architectural patterns with time. Approximately 12 hours after injury has occurred and when inflammation is established, epithelial migration, which is the first clear cut signs of rebuilding occurs. In a secondary healing wound migration of cells is rapid, as the line of cells from the wound margin become extended, but progress becomes slower, so that days or even weeks may elapse before epithelialization is complete. Later on granulation tissue appears as mentioned earlier but collagen synthesis which is the main feature of scar remodelling cannot be found before 4th to 6th day. On or about the 7th day wounds will show a delicate fine reticulum of young collagen fibres. As fibrogenesis proceeds, purposefully oriented fibres seem to become thicker presumably because there occurring more collagen particles. The overall effect appears to be one of lacing the wound edges together by a 3-dimensional weave. There is one of replacing granulation tissue, allowing the surface to become covered with epithelium and filling the remaining skin defect with scar tissue after contraction is complete. As far as the filling of the defect is concerned, contraction is the major influence. The central scar seems to remodel itself to fill the defect after contraction is over. Development of tensile strength (strength of per unit of scar tissue) and burst strength (strength of the entire wound) is the result initially of blood vessels growing across the wound, epithelialization and aggregation of globular protein. There is an almost imperceptable gain in tensile strength for 2 years subsequent to that. Collagen content of the wound tissue rises rapidly between the 6th and 17th days, but increases very little after 17 days. It must be remembered that secondary wounds contain slightly less collagen than primary wound of the same age. More effective cross-linking of better physical weave of collagen subunits is responsible for rapid gain in strength for secondary wounds. Experimentally it may be estimated by measuring the force necessary to disrupt the wound. In the first few days the strength of a wound is only that of the clot which cements the cut surfaces together. Later on various changes take place in the wound healing process as mentioned above and at the end the tensile strength of the wound corresponds to the increase in amount of collagen present. Tensile strength of the wound becomes more when this is parallel to the lines of Langer. That is why the transverse abdominal incisions produce stronger scar than the longitudinal ones. This effect is well accepted in the experimental animals, but corticosteroid in normal dosage may not influence wound healing in human beings. Healing of a clean incised wound, the edges of which are closed (closed wound) — takes place by a process known as healing by first intention. The following changes take place — (i) initial haemorrhage results in the formation of a fibrin-rich haematoma. In the first 24 hours basal cells mobilise from the undersurface of the epidermis. By 48 hours the advancing epithelial edge undergoes cellular hypertrophy and mitosis. Epithelial cells gradually line the wound deep to the fibrin clot and it also lines the suture tracks. The use of adhesive tapes instead of sutures for closing wounds avoids these marks and gives better cosmetic result. The main bulk of tissue which performs the healing process is the granulation tissue and that is why this type of healing is also called healing by granulation. But this does not mean that granulations are not formed in the simple incised wounds. The followings are the various important processes of this type of wound healing :— (i) Initial inflammatory phase affects the surrounding tissues and the wound is filled with coagulum. It must be remembered that the skin wound contracts by stretching the surrounding skin to close the defect and not by the production of new skin.
Shunt operation is usually done as an elective operation after one bout of haemorrhage discount 2.5 mg zestril fast delivery. There is no place of prophylactic shunt operation order line zestril, as being far from beneficial safe zestril 10 mg, it is sometimes deleterious cheap 5 mg zestril. This operation is contraindicated in cases of (i) elderly patients, (ii) with severe encephalopathy, (iii) with marked liver failure i. The patients who remain in the contraindication group of the shunt operation should be treated by one of the emergency operations. But these do not decrease the portal vein pressure or prevent subsequent haemorrhages. The periosteum of the rib is elevated from its outer as well as the inner surface. The whole rib is then resected and an incision is made on the periosteum as well as the parietal pleura. The parietal pleura lying over the oesophagus is incised very carefully to expose the lower end of the oesophagus. The oesophagus is now transected transversely and resutured with continuous catgut so that all the bleeding vessels are held and occluded by the catgut suture. Nowadays circular stapling device is being used which can be quickly applied and the result is also similar to this operation. This operation gradually lost its popularity as the oesophagus is not a good gut to anastomose because of its low vascularity. For this reason Boerema-Crile and Milnes-Walker introduced the operation where the oesophageal musculature was incised longitudinally so that the anasto motic leakage did not follow. Similarly Tanner introduced subcardiac gastric transection due to high vascularity of the stomach and anastomosis in this organ is not followed by leakage. The patient is laid in the right lateral position and a nasogastric tube is pushed into the stomach. The steps of this operation are more or less similar to those of the previous one till the exposure of the lower end of the oesophagus. The muscles of the oesophagus are incised longitudinally and the edges are held apart by stay sutures. The columns of varices, usually 3 in number, are under-run with continuous catgut sutures. Recently sophisticated staplers are being used for oesophageal transection and reanastomosis. The technique is as follows : For transection of the oesophagus, the peritoneal cavity is entered and the oesophagogastric junction is exposed. The lower 3 cm of the oesophagus is mobilised and particular care is taken to avoid vagus nerve injury. The mucous and the submucous coats of the oesophagus are taken out off the musculature as a single tube and completely divided across. This operation may be performed when the bleeding varices are mostly in the stomach, otherwise this operation does not prove to be useful. In this technique portal hyperten sion is maintained which ensures portal venous perfusion and maintenance of liver function, but stops bleeding from varices and Fig. Note that the injec tion is made by the side of the varices, so that surrounding sclerosis causes constriction of varices. Injection is made inside the varices, so that intravariceal thrombosis occurs leading to cure of the condition. Left thoracotomy is performed for oesophageal transection and paraoesophageal devascularisation. Laparotomy is then performed for splenectomy, gastric devascularisation, selective vagotomy and pyloroplasty. But at the hands of other surgeons applying the same technique the mortality rate was higher (20% to 40%) and 5 years survival was 40% to 70% and rebleeding rate was 20% to 50%. Predominantly poor risk cirrhotics who are not even fit for emergency operations, may be given the advantage of this method. The benefits of sclerotherapy lie in the preservation of portal perfusion (portal blood flow is maintained) and maintenance of hepatic function. The poor risk patients who will not tolerate major surgery will mostly be benefited. Moreover morbidity and mortality of these operations in the acute man agement of variceal haemorrhage is quite high. However surgical shunts are quite effective in preventing rebleeding from oesophageal and gastric varices as they reduce the pressure in the portal circulation by diverting the blood into low-pressure systemic circulation. Surgical shunts may be divided into 2 groups — (i) selective — which includes splenorenal as it preserves blood flow to the liver while decompressing the left side of the portal circulation which is responsible for giving rise to the oesophageal and gastric varices. Similarly the selective shunts are asso ciated with a lower incidence of postsurgical encephalopathy. There are principally three types of shunt operations : (i) Portacaval, (ii) Lieno-renal and (iii) Mesenterico-caval. The duodenum and the head of the pancreas are mobilised to the left by Kocher’s manoeuvre to expose the inferior vena cava. Now the portal vein is exposed in the posterior part of the free border of the lesser omentum and is mobilised as far as possible. The spleen is removed as usual leaving behind as great length of the vein as possible. The vein is now separated from the body of the pancreas by ligating and dividing its tributaries. The left renal vein is dissected out and the peritoneum over it is carefully incised. A special clamp is applied to renal vein to partially occlude it and the splenic vein is anastomosed to the renal vein in an end-to-side fashion (Fig. The lower cut end is ligated and the proximal cut end is joined to the side of the superior mesenteric vein at the root of mesentery. Sometimes a dacron graft may be used to connect the superior mesenteric vein and the inferior vena cava. Occlusion of anastomosis by thrombosis, which makes the shunt operation a failure. Nor mally the toxic products of protein break down, mainly ammonia, enter the liver where they are detoxicated. After shunt operation these toxic products get direct access into the systemic circulation and reach the central nervous system particularly the brain causing encephalopathy. The clinical features are disorientation, rigidity of the limbs, flapping tremor of the outstretched hand and deep coma. In electroencephalogram there is marked slowing of the frequency upto the delta range. Treatment is restriction of protein diet, removal of blood from bowel with enemas or purgation with magnesium sulphate. Oral lactulose in the dose of 20 to 30 ml 3 to 4 times daily help in clearing protein or blood in the intestine. The right anterior and the right posterior segmental ducts join to form the right hepatic duct. The right hepatic duct joins with the left hepatic duct to form the common hepatic duct. The right hepatic duct joins with the left with a sharp curve, this is why calculi are less commonly found in the right hepatic duct. The common hepatic dud— The length of the common hepatic duct is extremely variable. Common bile duct— The common bile duct is approximately 8 to 10 cm in length and 6 to 10 mm in diameter. The retroduodenal portion, which curves to the right behind the first part of the duodenum and here it moves away from the hepatic artery and the portal vein; 3. The infraduodenalportion, curves more to the right lying in a groove in the posterior surface of the head of the pancreas. The right edge of the inferior vena cava lies quite near to this part of the common bile duct; 4.
Two commonest sites which are involved zestril 2.5 mg without prescription, are the terminal ileum and the anal canal cheap zestril 2.5 mg otc. The particular predisposing factors at these sites are not known with certainty buy discount zestril line, but could be related to the distribution of excessive lymphoid tissue at these sites or to relative stasis of the bowel contents that could occur in these sites zestril 2.5mg with amex. Cell-mediated immune function seems to be defective in patients with Crohn’s disease. Presence of granulomas and systemic manifestations such as elevation of gamma globulin, erythema nodosum, iritis, eczema etc. Moreover favourable response to corticosteroids and azathioprine also supports this theory. Above all, Crohn’s statement that ‘the actual aetiology is completely unknown’ is still very much true even today. Remainders are seen with ileal disease alone or more proximal small bowel involvement. It must be remembered that though Crohn’s disease is uncommon in oesophagus, stomach and duodenum, anal lesions are quite common. Diseased segments are dull purple-red thickened two or three times normal diameter and covered with strands and patches of thick greyish white exudate. The lumen becomes narrow and the diseased portion of the bowel is thickened by fibrosis, oedema and cellular infiltration. Mesenteric fat tends to grow over the serosa so that it nearly encompasses the bowel. The thick mesentery nursing and draining the diseased bowel contains numerous enlarged lymph nodes. Due to this intense serosal reaction affected loops adhere to the neighbouring structures. Abscesses develop in between the loops and fistulas may originate with the diseased bowei to penetrate into any organ within the abdominal cavity (internal fistula) or may open outside on the abdominal wall (external fistula). The most characteristic feature is that the segments of diseased bowel are separated by apparently normal bowel to form characteristic ‘skip lesions’. The mucosal surface may vary from grossly normal to slightly oedematous and hyperaemic. Long ‘snail-track’ ulcers may be produced from coalescence of the previous ulcers. These transverse ulcers intensify ‘cobblestone’ appearance of the mucosa as these ulcers intervene between the elevated mucosa caused by submucosal thickening. These ulcers penetrate deep into the muscle layers of the gut distinguishing Crohn’s disease from other inflammatory diseases of the bowel such as ulcerative colitis or ischaemic colitis. Infection gains access to the muscle layers through these ulcers and transmural inflammatory reaction sets in. This gives rise to characteristic thickening of the wall of the gut and later fibrotic stenosis. It is the ulceration penetrating through the muscle to the serosal layer of the gut that is responsible for the complications of perforation, abscess and fistula. Fissures may develop from the mucosal ulcers and extend a variable distance into the bowel wall. The anal lesions consist of fissures, fistulas, perianal abscesses and/or spreading superficial ulcerations. Mucosa is essentially normal except for an increase in the proportion of goblet cells. In the intermediate p/iasethickening of the bowel is more attributable to fibrosis of submucosa and subserosa. Small focal ulcers that rarely penetrate the muscularis mucosa develop numerous in the mucosa. The lamina propria is infiltrated with lymphocytes, plasma cells and variable number of eosinophils. In the later stage, in the submucosa, the extensive fibrosis is accompanied by diffuse infiltration of mononuclear cells and prominent hypertrophy and hyperplasia of lymphoid follicles. They resemble the epithelioid giant cell granulomas of tuberculosis but do not caseate and do not contain tubercle bacilli. There is midabdominal or right lower quadrant pain, low grade fever, leucocytosis, often nausea and vomiting and occasionally diarrhoea. Diagnosis is extremely difficult, but probably diarrhoea from the very beginning of the disease gives a clue to distinguish this condition from acute appendicitis where constipation is more common in the early stage. Very rarely there can be free perforation of the small intestine resulting in a local or diffuse peritonitis. Similarly in colon there may be toxic megacolon, but is much less common than in ulcerative colitis. This is due to partial obstruction of the lumen and increase in motility proximal to the site of obstruction. The frequency of stool is not so great as compared to ulcerative colitis and the stools rarely contain mucus, pus or blood as in ulcerative colitis. Frothy and foul smelling stools characteristic of steatorrhoea represent an advance stage of illness. Fever can reflect the development of intramural or abdominal abscesses or may be a systemic sign produced by unknown toxins. Malnutrition manifested by weight loss, anaemia, hypoproteinaemia and vitamins and mineral deficiencies is quite common. Extra-intestinal manifestations in the form of (i) skin (erythema nodosum, pyoderma gangrenosum), (ii) eye (uveitis, iritis), (iii) joint (arthritis, ankylosing spondylitis), (iv) mouth (aphthous stomatitis), (v) kidney (nephrolithiasis, hydronephrosis, amyloidosis), and (vi)hepatobiliary (cholelithiasis, sclerosing cholangitis) etc. Though anal lesions invariably present when the large bowel is involved, yet these lesions may be seen less frequently with disease of the small bowel. It is a broad, shallow ulcer rather than a crack and it may occur anteriorly and laterally as often as posteriorly. Fistula-in-ano, ischiorectal abscess and a simple fissure are also common anal lesions. The anal pathology may be considered as a form of ‘skip lesion’ because the proximal rectal mucosa is usually normal. Fistula may be internal, with pelvic colon (enterocolic) or urinary bladder (enterovesical). It must be remembered that any patient who presents with a history of the triad of colicky abdominal pain, diarrhoea and weight loss, the patient should be suspected to be suffering from Crohn’s disease. The clinical manifestations are so variable that diagnosis is often made quite late. The diagnosis rests on clinical evaluations supported by endoscopy, biopsy and radiology. Involvement of the colon and rectum becomes more evident in barium enema examination. The earliest mucosal changes and aphthous ulceration are visualised by meticulous attention with double contrast barium technique. After submucosal infiltration and oedema develop, barium study demonstrates thickening and distortion of the mucosa. Both longitudinal and transverse mucosal ulcers or fissures present as ‘spicules’ in profile views. Ulceration tends to take the form of sharp ‘fissures’ passing from the lumen into the bowel wall shown as ‘spikes’ (‘Raspberry thorns’ or ‘Rose thorns’). Filling defects may also be due to hyperplastic lymph follicles, which may be the first indication of a ‘neoplastic’ consequence of a chronic disorder. At times the mucosa may be completely denuded, giving the radiologic appearance of a nonpliable, nondistensible, rigid, cast like tube. It is usually due to acute transmural inflammation and oedema with spasm, but it could be the end result of fibrosis leading to stricture formation. Direct visualisation of the pathology of Crohn’s disease is very helpful in diagnosis of this condition. It must be remembered that in Crohn’s disease there will be areas of normal colon or rectum.