Joseph R. Hume PhD

• Emeritus Chairman of Pharmacology and Professor of Pharmacology & Physiology
• University of Nevada School of Medicine, Reno

https://med.unr.edu/directory/joseph-hume

Defaecography can also provide functional assessment; however diabetes symptoms uk buy actos online now, failure of relaxation of an acute anorectal angle is not reliably predictable and has high inter-observer variability blood glucose log buy discount actos 15mg. Solitary rectal ulcer syndrome is significantly associated with prolonged and incomplete evacuation (as well as internal and external rectal prolapse) diabetic feet purchase 30 mg actos amex. Much like any other assessment of pelvic floor function diabetes definition who 2010 buy actos once a day, there is a large crossover between findings in normal asymptomatic individuals and those with obstructed defaecation symptoms diabetes mellitus early symptoms buy generic actos on-line. The effectiveness of rectal emptying depends upon the paste consistency diabetes protocol program buy genuine actos, and so standardisation is difficult. Whilst some report poor inter-observer repeatability and question the impact upon treatment planning, when direct questions are asked of the requesting clinicians, it does increase diagnostic confidence, resolving diagnostic conflict and determining intended management,75,76 including selecting those most suitable for surgery. Examples include the assessment of the anal sphincters in patients with complex developmental abnormalities. The assessment of the anterior and middle compartments allows identification of coexisting bladder and vaginal prolapse, including visualisation of the anal sphincters, puborectalis and levator muscles. Variations of technique with the use of markers, tampons and catheters to identify pelvic structures and the use of contrast to opacify the vagina, bladder and small bowel also exist. Manometric equipment consists of four major components83: (1) an intraluminal pressure-sensing catheter, (2) pressure transducers, (3) a balloon for inflation within the rectum (integral to the catheter assembly) and (4) an amplification/recording/display system. The upper two rings have grooves which allow for mounting of a rectal balloon with thread ties. The resting tone provides assessment of (primarily) the internal anal sphincter, and the squeeze increment an evaluation of volitional external anal sphincter function. For all catheter types, proprietary software within dedicated manometry systems are available to amplify, interpolate, display (as either traditional line plots or contemporary colour-contour topographical plots) and analyse recorded pressure signals. The most distal sensor lies outside of the anal canal to provide a measure of atmospheric pressure. Manometric data undergo linear interpolation through dedicated software (Motility Visualization System; Medtronic), which displays 2D or 3D cylindrical topographical models of the anal canal; the latter can be rotated and viewed from all sides. To date, direct comparison of data collated from the different catheter types has not been obtained. Certain components of a manometric investigation may be considered more useful in the former. Consequently, a comprehensive manometric assessment incorporating all components should generally be performed. Anorectal manometry is also widely appreciated to be a useful tool to facilitate biofeedback training. The probe should then be positioned to ensure that sensors span the distal rectum to beyond the anal verge. Recent studies have illustrated a high degree of pressures asymmetry within the anal canal in health, with higher pressures in the posterior proximal and anterior distal regions of the sphincter. The length of the functional anal canal is usually shorter in incontinent patients,92 though the clinical significance of this measure remains unclear. Sphincter hypertonia (high anal resting pressure), with or without ultraslow anal pressure waves, may be a feature of anal fissure or constipation. In 2D images, the circular anal canal is split at the posterior midline to show a surface plot view of anal canal pressures. Tests of Anorectal and Pelvic Floor Motor Functions 291 from this normal manometric anatomy may be detected on either 3D or 2D pressure plots at rest and/or squeeze, and may be suggestive of pathology, though studies only demonstrate slight concordance with anal sphincter defects detected by endo-anal ultrasound. Additionally, it is well appreciated that study set-up and equipment, as well as patient position and compliance all have a significant impact on absolute values reported. Further, the test manoeuvres included within a standard manometric protocol may not appropriately test certain aspects of function. There is little evidence to support the long-standing assumption that individuals voluntarily squeeze their anal canal during normal deferral of defaecation, nor evidence to support that this behaviour is altered in incontinence. Even in healthy volunteers, a dyssynergic pattern of defaecation is found considerably more frequently in the left-lateral position compared to the sitting position. Intra-anal and intra-rectal pressures (from within the rectal balloon, which may or may not be distended)100 should be recorded simultaneously whilst the patient is asked to strain as if to defaecate. With a patient lying in the left lateral position with hips and knees flexed, a lubricated, preferably non-latex balloon attached to a plastic catheter with a stop-lock is inserted into the rectum and inflated with 50 mL of warm water. Pudendal Nerve Terminal Motor Latency the pudendal nerve is a mixed nerve providing efferent and afferent pathways to the external anal sphincter, urethral sphincter, perineal musculature, mucosa of the anal canal and perineal skin. The branches of the pudendal nerve, which course over the pelvic floor, are vulnerable to stretch injury, which leads to denervation of the external anal sphincter, and may result in muscle weakness and incontinence. A recent prospective study in 100 patients with functional constipation showed only fair agreement (kappa = 0. Standardisation of study protocol for wider applicability must be seen as a priority. Therefore, a prolonged latency indicates either demyelination or irreparable damage of a number of fast-firing fibres. Nevertheless, the clinical value and indeed the validity of pudendal nerve latency testing remains an area of great controversy. Diagnostic neurophysiological tests enable characterisation of nerve, muscle and neuromuscular junction integrity, help localise the nerve injury, and may also provide a measure of severity. Furthermore, technique and interpretation require specialised training and expertise which are not widely available. Performance of transcranial and translumbar/sacral magnetic stimulations in the same subject allows assessment of the whole descending pathway, the peripheral pathway and the central pathway (cortical minus root). The innervation of the rectum is more complex than that of the colon, as it is supplied by visceral afferents as well as somatic nerves arising from the pudendal nerve. This dual innervation appears confined to the lower third of the rectum (<7 cm from anal verge), as a pudendal nerve block has no effect on sensation to distension or thermal stimuli in the mid and upper rectum. Evaluation of rectal sensorimotor function is indicated in patients with disturbances of defaecatory function to assess for the presence of altered rectal sensation. During balloon inflation, subjects are instructed to volunteer three or four sensory thresholds: first sensation, desire to defaecate, urgency (optional) and maximum toleration. The distending volume (or pressure) at each of these sensory thresholds is then recorded. In healthy volunteers, biomechanical properties have been shown to differ significantly along the length of the anal canal, with the middle part being most resistant to distension. The first 30 seconds (x-axis) represent filling of the bag without distension of the anal canal. After 30 seconds, a change in diameter at the upper part is noticed (from dark blue to a lighter blue). The closed part of the anal canal (blue area) remains at a minimum diameter (around 5 mm) during distension with 20, 30 and 40 mL, but increases in diameter during distension with 50 mL. At 20 mL, the small impression made by the puborectalis muscle is seen at the upper end of the anal canal. When hyposensitivity is present, stool may leak before the external sphincter contracts. There are some significant limitations of the use of simple volumetric balloon distension. Abnormal sensory threshold volumes may not accurately reflect the function of visceral afferents in the presence of increased rectal diameter and/or compliance. Under such circumstances, greater volumes will be required to distend and thus 16. In its simplest form, this only requires a balloon tied to a Foley catheter and bladder syringe for inflation. Patients are examined in a semi-prone position to reduce pelvic hydrostatic pressure. During distension, intrabag (intrarectal) volumes and pressures are recorded concomitantly, allowing rectal compliance to be calculated from the derived pressure-volume curve. More specialised testing of rectal biomechanical function with a barostat is indicated in selected patients with alterations of rectal sensation on standard testing. With continued distension, the rectal wall becomes more resistant to stretch as its elastic limit is approached, and there are regular contractions of the rectal wall, causing intra-rectal pressure to rise. Increased rectal compliance has been reported in patients with gross dilatation of the rectum (megarectum)147 and in some patients with chronic constipation. The modalities of anal sensation can be precisely defined, with stimuli such as touch, pain and temperature being readily appreciated. Clinical assessment of anal sensation has most commonly been performed through evaluation of mucosal electrosensitivity, though thermosensitivity techniques have also been reported. Alternatively, anal sensation can be measured using thermal stimulation via specialised thermoprobes, which provide both hot and cold stimuli. The technique involves the brief presentation of a sensory stimulus, which is time and phase-locked to the recording of the electroencephalogram via surface electrodes placed on the scalp. However, though providing novel pathophysiological information, at the current time, the technique remains confined to the research setting. Rectal Mucosal Stimulation More direct assessment of the afferent pathway may be afforded by non-mechanical (distension) techniques that involve direct stimulation of the rectal mucosa. These have the advantage of not being influenced by rectal wall biomechanical properties, since they rely solely on mucosal contact. Both rectal electrostimulation (500 sec duration and 10 Hz frequency) and thermostimulation (to hot and cold) have both been used to assess rectal sensory function. Electrical stimulation results in the perception of discomfort, or a tingling or burning sensation, and has been shown to be safe and reproducible, and that the results correlate well with the findings of simple balloon distension. Having studied the long list of available techniques for assessing colonic and anorectal functions that have been covered in detail above, the non-expert reader might not be blamed for enquiring which tests they should adopt in practice. This question is addressed to a great extent by the chapters that consider patients with a main complaint of chronic constipation (Chapter 17) or faecal incontinence (Chapter 21). It has been noted that the division of patients into those with incontinence or those with constipation is, in part, artificial since many have symptoms of both. Nevertheless, some generalisations can be made based on current practice (see Table 16. In patients with a primary complaint of constipation, there is a need to assess transit and also evacuation ability. Importantly, the tests provide different information; for example, only defaecography can assess rectal structural abnormalities that may impede rectal emptying. Consequently, diagnosis may be test-dependent, and diagnostic agreement between the tests is acknowledged to be very poor. However, a test of evacuation should be performed in all patients who have any concomitant symptoms of obstructed defaecation to exclude a significant functional or dynamic structural impairment to evacuation that may alter therapeutic approach. In both groups of patients, basic rectal sensory testing is advised since this impacts on symptoms and also outcome to certain therapeutic strategies. However, those patients with intractable and sufficiently severe symptoms, in whom such measures have failed, warrant rigorous clinical evaluation incorporating a comprehensive assessment of colonic and anorectal structure and function. Several tests with proven clinical utility exist; technological advancement means others are on the cusp of progressing from research to the clinical field. Accurate and objective measurements can identify disease phenotypes, allowing definitive diagnoses that can have a direct impact on treatment decisions in clinical practice. Even when no specific treatment can be offered, a clear explanation of the causes of symptoms, based on the results of these tests, can be therapeutic in itself. Well-informed patients are more satisfied, cope with their condition better and seek medical attention less frequently than those that have not been fully informed. Pathophysiology as a basis for understanding symptom complexes and therapeutic targets. How useful are manometric tests of anorectal function in the management of defecation disorders Evaluation of gastrointestinal transit in clinical practice: Position paper of the American and European Neurogastroenterology and Motility Societies. Gastrointestinal and colonic segmental transit time evaluated by a single abdominal x-ray in healthy subjects and constipated patients. Regional gastrointestinal transit and pH studied in 215 healthy volunteers using the wireless motility capsule: Influence of age, gender, study country and testing protocol. Colonic transit studies: Normal values for adults and children with comparison of radiological and 15. Towards a relatively inexpensive, noninvasive, accurate test for colonic motility disorders. Whole gut transit scintigraphy in the clinical evaluation of patients with upper and lower gastrointestinal symptoms. Scintigraphic assessment of colonic transit in patients with slow transit constipation arising de novo (chronic idiopathic) and following pelvic surgery or childbirth. In patients with slow transit constipation, the pattern of colonic transit delay does not differentiate between those with and without impaired rectal evacuation.

Full-thickness biopsy of the jejunum reveals inflammation and enteric neuropathy in irritable bowel syndrome diabetes ezy test wipes order actos with visa. A randomized diabetes diet menu in tamil buy cheapest actos, controlled diabetes mellitus type 2 epocrates order actos amex, crossover study of sacral nerve stimulation for irritable bowel syndrome type 1 diabetes questions and answers cheap actos master card. Sacral nerve stimulation enhances epithelial barrier of the rectum: Results from a porcine model diabetes mayo clinic actos 30mg on line. There is diabetes prevention jobs buy 45mg actos overnight delivery, however, recognition that this broad term encompasses several anatomical variants that may have a similar end presentation. These are classically attributed to single compartments that frequently dictate the surgeon selected to manage them, i. However, as outlined in the section preface, it is obvious that delineation of these compartments is artificial based on epidemiology (co-existence of more than one condition), shared pathophysiology (pelvic floor weakness) and management. A further question that may have some relevance to surgical management is whether there is a legitimate distinction between an intussusception whose take-off point is in the rectum but whose progression is beyond the anal verge versus a classic external prolapse where the eversion occurs at or around the level of the dentate line. Rectocele is covered in more detail in the Gynaecology for the Colorectal Surgeon section (Chapter 1). A sigmoidocele describes the same phenomenon except the main content of the sac is colon. These are also covered briefly in the Gynaecology for the Colorectal Surgeon section (Chapter 1). Many of these patients have complete rectal prolapse, whilst many more have a significant intussusception, perineal descent and impaired evacuation. At other times, this may have the appearance more in keeping with an erythematous area or polypoidal change. Part of the problem lies in the fact that the true incidence of external prolapse is almost certainly under reported. Elderly patients are often afraid to leave the house for fear of the prolapse occurring. Furthermore, they may also be too embarrassed to seek medical help for the condition. Interestingly, rectal prolapse is not restricted to the multiparous, and indeed in some studies of rectal prolapse, around one third of women are nulliparous. It is sometimes seen in habitual strainers, patients with a psychiatric background or occasionally those with voiding difficulties who have to strain to pass urine. In both women and men, rectal prolapse is sometimes seen in the malnourished and in those with eating disorders. The exact mechanism by which this causes prolapse is not understood, but the association is clear. Note the long rectovaginal pouch, the uterine and vaginal descent, the lax pelvic floor, the attenuated lateral ligaments, the obtuse anorectal angle and the weak external anal sphincter. Note this is a circumferential prolapse with a more prominent anterior component due to the rectovaginal pouch that descends with the prolapse. Internal rectal prolapse is a common condition and is being recognised more frequently with the greater availability of proctography. There is controversy over the phenomenon of intussusception, and its significance must be assessed on a background of symptoms, clinical examination findings, the degree of intussusception and other manifestations of pelvic floor dysfunction. As a consequence, there are few accurate data for the incidence of internal rectal prolapse in the general population. A solitary rectal ulcer is an uncommon condition, though with increasing awareness of the condition it is being seen more frequently. This same study reported a median age at diagnosis of 43 years, with one quarter having suffered misdiagnosis for an average of five years. Thus, both obesity and pregnancy contribute to the development of prolapse through an increased mass (downward force) on the pelvic floor. This seems to be true especially in the younger population, and in these patients there may be a relatively normal pelvic floor and frequently no symptoms of incontinence. Given that the constipation usually precedes the prolapse, it is generally assumed that constipation is the cause of the prolapse rather than the other way around. Sometimes, the disorder is seen in patients with severe diarrhoea secondary to a condition such as schistosomiasis or amoebiasis (this is a much more important factor in children: see later section). Increasing weakness of the pelvic floor and rectal supports may be seen with ageing (perhaps the main factor in development at least of external prolapse), and this is frequently accelerated around the time of the menopause. Weakness of the pelvic floor may also result from denervation atrophy secondary to prolonged labor during childbirth. In a significant minority, the predominant aetiology is that of some form of mental illness manifesting as a form of obsessional behaviour around bowel movements. Most nulliparous patients who develop rectal prolapse have a relatively normal pelvic floor. By contrast, those multiparous patients with a rectal prolapse tend to have a deficient pelvic floor. These differences translate to mechanical differences in the skin of patients with prolapse, which in turn suggests that the stretchiness of the pelvic tissues seen at surgery for prolapse is not a consequence of the prolapse but rather a cause. The terms recto-rectal intussusception and recto-anal intussusception give a more concise description of the fullest extent of descent of the apex of the prolapse. Internal rectal prolapse can be difficult to diagnose because patients will often have a relatively normal anal canal that remains closed and there may be very little perineal descent. With the advent of defaecating proctography, this has become easier to diagnose, and the investigation of rectal prolapse is covered in more detail in Chapter 16. A more formal method of classification of internal and external prolapse has been described (see Table 20. This and subsequent studies identified other abnormalities in prolapse that were secondary phenomena. The common features to these patients, however, are those of straining, tenesmus and incomplete evacuation. Most surgeons would agree that prolapse seems to be central to the pathophysiology of solitary rectal ulcer, though it is certainly not seen universally. Even in those patients with both prolapse and an ulcer, it is still not understood how the prolapse causes ulceration. One theory is that the ulcer is a result of trauma to the apex of the prolapse, either from it hitting a contracted anal sphincter, especially one which exhibits features of the diagnosis of defaecatory (pelvic floor) dyssynergia with paradoxical anal contraction. A further alternative theory has been that the repeated straining results in congestion of the apex of the prolapse that in turn leads to ischaemia. In the former, the anus and thus the internal sphincter remain in the pelvis, whereas in the latter they can be readily accessed extracorporeally by some perineal procedures. Indeed, a classic Delorme procedure cannot be performed for a transanal rectal intussusception, since if mucosectomy and muscle plication of the evident external prolapse proceed in such patients, then the subsequent repaired area (donut) will (once reduced) lie above the anus in the rectum. Of these patients, 79 had intussusception on the first proctogram, and of these, 38 patients had not had any surgery between first and second proctograms. Amongst these 38 patients, one patient had an external prolapse at the second proctogram and one other patient developed an external prolapse after the second proctogram. Furthermore, when a prolapse emerges after straining, it is circumferential in appearance. If it were a sliding hernia, then the anterior part of the prolapse would be longer. The sliding hernia theory was thought to account for the deep rectovaginal septum that allowed the rectum to prolapse through the pelvic floor, but in fact it seems that it is simply a secondary phenomenon from intussusception. There is probably an important distinction between patients who have an advanced intussusception arising from a high take-off point, i. Indeed, a study from Edinburgh found that of 50 patients with rectal prolapse, eight had uterine prolapse, 20 had had a hysterectomy and 12 had some form of colporrhaphy. A similar study from Cleveland found that genital prolapse was seen in 14% of patients with rectal prolapse compared to 12% in an age-matched population. Furthermore, coexistent urinary incontinence was seen in 65% of those patients with rectal prolapse compared with 30% of controls. A short anal canal is also commonly seen, with descent of the perineum and pelvic floor at rest. However, when patients with external prolapse were considered, relative to those with internal prolapse, there is a significant reduction in both resting and squeeze pressure. In all the incontinent patients, there was histological evidence of denervation, most prominent in the external anal sphincter and least prominent in the levator ani muscles. This led them to postulate that incontinence in these patients occurred as a result of entrapment or stretching of the pudendal nerves. There has also been a suggestion that it is persistent stimulation of the rectoanal inhibitory reflex that is responsible for incontinence with rectal prolapse. He demonstrated the presence, in patients with rectal prolapse only, of high pressure rectal waves associated with inhibition of the internal anal sphincter. Furthermore, these waves were abolished by resection rectopexy and a concomitant improvement in continence was also seen. Finally, Ihre23 postulated that the cause of pelvic floor weakness was more of a mechanical phenomenon from repeated dilatation of the pelvic floor by the prolapse. This may reduce spontaneously or may be reduced by the patient, either by pushing it in manually or by sitting upon it. In many patients, this is the most troublesome of symptoms, and though other symptoms may co-exist, any surgical procedure that gets rid of the lump is considered a success by many patients. The bleeding may result from trauma to the prolapsing mucosa or from venous engorgement of the prolapse. Many patients report incomplete evacuation, and some but not all have symptoms of faecal incontinence. The longer the existence of a prolapse, the greater the risk of faecal incontinence. Many elderly patients accept wearing a increasing prevalence of enterocoele with worsening grade of prolapse. Historically, it was thought that a weak pelvic floor might be the primary aetiology. First, there are patients with external prolapse who have relatively normal pelvic floor function. On the other hand, pelvic floor weakness 384 Chapter 20 Rectal Prolapse and Associated Pelvic Organ Prolapse Syndromes pad after surgery for prolapse without complaint. The usual measures can be undertaken for persistent incontinence after prolapse repair. Without doubt, the most important intervention for patients with incontinence on a background of prolapse is to fix the prolapse. Temporary test stimulation was successful in 86% of those without prolapse but in only 69% with prolapse. The message from the authors was that in patients with faecal incontinence and rectal prolapse, the algorithm for treatment involves correction of the prolapse first. This is supported by recent consensus (Japan, 2016) published by the international continence society (see Chapter 21 on faecal incontinence). It is unusual to see a patient with a symptomatic, isolated internal rectal prolapse. Repeated toilet visiting can be very disruptive and have a significant impact on quality of life. The degree of symptoms can be assessed using the Cleveland Clinic Constipation Score28 or the more specific Obstructed Defaecation Syndrome Score. The classical presentation of solitary rectal ulcer syndrome includes rectal bleeding, mucous discharge, rectal pain and obstructed defaecation. Note: Each domain has four to five possible answers scoring from zero (symptom free) to four (more severe symptom). Studies summarising the prevalence of symptoms in solitary rectal ulcer syndrome are shown in Table 20. Signs External Rectal Prolapse the diagnosis of rectal prolapse may be obvious when the patient strains in the left lateral position. If this is inconclusive, the patient should be asked to sit on a commode or toilet and evacuate in an effort to demonstrate the prolapse. It is also important to differentiate between mucosal prolapse and full thickness prolapse. When the prolapse is seen, it should be palpated between the gloved index finger and thumb. The anus is often patulous, and indeed anal tone should be assessed by rectal examination. The rectovaginal septum should also be examined to look for a rectocoele and to assess the integrity of the perineal body. The vagina can be inspected and examined to look for evidence of gynaecological prolapse. Reduction is usually possible with gentle pressure on the prolapse to reduce the oedema before pushing the prolapse back in. The patulous anus that co-exists with most cases of external prolapse tends to facilitate this. Helpful adjuncts to facilitate reduction might include application of sugar or honey to the prolapsed bowel, reducing the tissue oedema. Initial inspection of the perineum may reveal evidence of faecal leakage that in turn might reflect faecal impaction. There may be an overt prolapse, haemorrhoids or a sentinel pile from an anal fissure.

Natural infection (other than transplacental transmission) takes place only through the bite of an infected female Anopheles mosquito diabetes in dogs and urination 15 mg actos sale. A successful malaria vaccine used in conjunction with other interventions will greatly reduce the burden of disease and offers hope for eventual interruption and elimination in defined areas blood glucose graph order actos 15mg line. Babesiosis in these individuals may resemble falciparum malaria blood glucose flow chart actos 30mg on line, with high fever diabetes signs of pregnancy purchase 45 mg actos overnight delivery, hemolytic anemia diabetes urine test strips boots discount actos 15mg otc, hemoglobinuria diabetes type 1 reason order actos with a mastercard, jaundice, and renal failure; infections are sometimes fatal. These are the only hosts in which the oocyst-producing sexual stage of Toxoplasma can develop. After sexual fusion of the gametes, oocysts develop, exit from the host cell into the gut lumen of the cat, and pass out via the feces. When oocysts are ingested by the cat, the parasites repeat their asexual and sexual cycle. If oocysts are ingested by intermediate hosts such as certain birds, rodents, or mammals, including humans, the parasites can establish an infection but reproduce only asexually. These rapidly multiplying crescentic cells (tachyzoites) initiate the acute stage of disease. Subsequently, they penetrate nerve cells, especially of the brain and eye, where they multiply slowly (as bradyzoites) to form quiescent tissue cysts, initiating the chronic stage of disease. The tissue cysts (zoitocysts or pseudocysts) are infective when ingested by cats (resulting in the intestinal sexual stage and oocyst production); when they are eaten by other animals, more tissue cysts are produced (asexually). Varying degrees of disease may occur in immunosuppressed individuals, resulting in retinitis or chorioretinitis, encephalitis, pneumonitis, or various other conditions. The tachyzoite directly destroys cells and has a predilection for parenchymal cells and those of the reticuloendothelial system. Humans are relatively resistant, but a low-grade lymph node infection resembling infectious mononucleosis may occur. When a tissue cyst ruptures, releasing numerous bradyzoites, a local hypersensitivity reaction may cause inflammation, blockage of blood vessels, and cell death near the damaged cyst. Congenital infection leads to stillbirths, chorioretinitis, intracerebral calcifications, psychomotor disturbances, and hydrocephaly or microcephaly. Prenatal toxoplasmosis is a major cause of blindness and other congenital defects. Second- and third-trimester infections induce less severe neurologic damage, though they are far more common. Clinical manifestations of these infections may be delayed until long after birth, even beyond childhood. Neurologic problems or learning difficulties may be caused by the long-delayed effects of late prenatal toxoplasmosis. Epidemiology Avoidance of human contact with cat feces is clearly important in control, particularly for pregnant women with negative serologic tests. Since oocysts usually take from 1 to 5 days to become infective, changing cat litter daily (and its safe disposal) can prevent transmission. An equally important source of human exposure is raw or undercooked meat, in which infective tissue cysts are frequently found. Humans (and other mammals) can become infected either from oocysts in cat feces or from tissue cysts in raw or undercooked meat. Kitchen cleanliness, handwashing after touching raw meat, thoroughly washing fruits and vegetables, and avoidance of cats and cat litter are essential during pregnancy. Serologic screening for immunoglobulin IgG and IgM antibodies to Toxoplasma is available (Guerrant et al, 2006; Montoya and Remmington, 2008). Pathology and Pathogenesis the organism in humans produces either congenital or postnatal toxoplasmosis. Congenital infection, which develops only when nonimmune mothers are infected during pregnancy, is usually of great severity; postnatal toxoplasmosis is usually much less severe. A modified trichrome-blue stain may detect microsporidia in urine, stool, and nasopharyngeal specimens. All classes of vertebrates (especially fish) and many invertebrate groups (especially insects) are infected in essentially all tissues. They are widespread, abundant, and nonpathogenic in immunologically intact persons but are a continuing threat to immunocompromised individuals. Ocular infections: Encephalitozoon hellem, Vittaforma corneae (Nosema corneum), and Nosema ocularum. Most infections are acquired by ingestion of the egg or larval stage, with the exception of the hookworms, human threadworms, and schistosomes, whose larvae penetrate the skin, and the filarids, which are vectorborne. Generally speaking, most intestinal nematode and cestode infections involve the adult stages and are not very pathogenic, except when there are large numbers of worms. Most of the pathology is associated with the larval stages (eg, microfilariae and trichinae in the case of nematodes; and cysticerci and hydatid cysts in the case of cestodes). In trematode infections, the pathology is generally associated with the adult stage, because the adult worms are found in human tissues, eg, liver fluke and lung fluke (larval stages occur in animal hosts or on other sources). The exception to this is the blood fluke (schistosomes) whose adult stages reside in the blood vessels and main pathology is associated with the eggs in tissues. The pathologic features of the tissue-infecting nematodes are closely tied to the host response. Elephantiasis, a morbid gross enlargement of limbs, breasts, and genitalia, is an immunopathologic response to long-continued filarial infection by Wuchereria or Brugia. Most helminths do not multiply by asexual multiplication in the human host: one egg or one larva yields one worm. The exception is Echinococcus granulosus, which multiplies asexually within hydatid cysts. The only intracellular helminth is Trichinella, whose larval stage is intracellular within a muscle cell (known as a nurse cell). Most worms that inhabit the intestinal lumen are easily treatable, whereas worms inhabiting tissues are more difficult to treat with drugs. The severity of disease and symptoms caused by helminthic infections are generally associated with heavy worm burdens (eg, hookworm disease and anemia). Larva migrans is a term used when the larval stage of a nematode that normally infects an animal host migrates throughout human tissues (eg, skin, viscera, and central nervous system). A strong host immune response is elicited to the migrating worm and induces the pathology. Larva migrans is associated with zoonotic infections in which animals are the normal hosts and humans are accidentally infected. The combination of poor sanitation, human behaviors, and tropical climates leads to a high prevalence of infection by the "soilborne" nematodes (Ascaris, whipworm, and hookworm). Most intestinal helminthic infections are fairly benign, except when worm burdens are high and numbers of adult worms in the intestine reach the hundreds. In these worm infections, the intestine usually harbors the adult stage of the parasite, except for Strongyloides, Trichinella, and T. In the case of the three most common intestinal infections (whipworm, hookworm, and ascariasis), the eggs require incubation in the soil for several days or weeks in warm, tropical climates. Dietary habits of eating raw or lightly cooked food dishes contribute to most trematode and cestode infections. These infections can be acquired by eating improperly cooked intermediate hosts, including vegetables, fish, beef, and pork. Thorough cooking and freezing kill the parasites, thus preventing foodborne infections. Human behaviors and close associations with pets also are contributing factors for infection by Dipylidium caninum and E. Pinworms are found worldwide but more commonly in temperate than tropical climates. They are the most common helminthic infection in the United States and infect mostly children. Pathology and Pathogenesis the main symptom associated with pinworm infections is perianal pruritus, especially at night, caused by a hypersensitivity reaction to the eggs that are laid around the perianal region by female worms, which migrate down from the colon at night. Scratching the anal region promotes transmission, as the eggs are highly infectious within hours of being laid (hand-to-mouth transmission). Irritability and fatigue from loss of sleep occur, but the infection is relatively benign. Eggs are recovered using the "Scotch Tape" technique in the morning before a bowel movement. Transparent Scotch Tape is applied directly to the perianal area, and then placed on a microscope slide for examination. Because the eggs are lightweight and highly infectious, it is important for bed linens, towels, and clothing to be washed in hot water to prevent reinfection. The anterior end of the worms is slender, and the posterior end is thicker, giving it a "buggy whip" appearance, hence the name whipworm. Once eggs are swallowed, the larvae hatch in the small intestine, where they mature and migrate to the colon. Pathology and Pathogenesis the anterior ends of the worms lodge within the mucosa of the intestine, leading to small hemorrhages with mucosal cell destruction and infiltration of inflammatory cells. Severe infection may lead to profuse bloody diarrhea, cramps, tenesmus, urgency, and rectal prolapse. Humans acquire the infection after eggs are ingested; larvae hatch in the duodenum, penetrate through the mucosa, migrate in the circulatory system, lodge in lung capillaries, penetrate the alveoli, and migrate from the bronchioles to the trachea and pharynx; larvae are swallowed and return to the intestine and mature into adults. After mating, females can release 200,000 eggs per day, which are passed in the feces. Pathology and Pathogenesis If present in high numbers, adult worms may cause mechanical obstruction of the bowel and bile and pancreatic ducts. A: Adult females are larger than the adult male worms (length of ruler = 16 centimeters). Larvae can survive in moist soil for several weeks, waiting for an unsuspecting barefooted host to walk by. These larvae penetrate host skin and migrate throughout the host similarly to Ascaris and end up in the small intestine where they mature into adult worms. A few dozen worms in the intestine, or even fewer, can cause hookworm disease, which is characterized by severe anemia and iron deficiency. Feet and ankles are common sites of infection due to exposure from walking barefoot. They lay eggs within the intestine; larvae hatch from the eggs and are passed into the feces. These larvae can either develop into parasitic forms or develop into free-living male and female worms that mate and produce several generations of worms in the soil, a great example of an evolutionary adaptation to sustain a population. The larvae of these free-living forms, under certain environmental conditions such as temperature, can develop into parasitic forms. In disseminated infections, clinical signs and symptoms primarily involve the gastrointestinal tract (severe diarrhea, abdominal pain, gastrointestinal bleeding, nausea, vomiting), lungs (coughing, wheezing, hemoptysis), and skin (rash, pruritus, larva currens). Larvae migrating from the intestine carrying enteric bacteria can cause local infections or sepsis, resulting in death. In the small intestine, the larvae molt into adult worms, and, after mating with male worms, the female worms release live larvae. The larvae penetrate the intestine, circulate in the blood, and eventually encyst in muscle tissue. Adult female worms live for several weeks and after the first week of infection may cause diarrhea, abdominal pain, and nausea. Pathology and Pathogenesis Of medical significance, Strongyloides can produce an internal reinfection or autoreinfection if newly hatched larvae never exit the host but, instead, undergo their molts within the intestine. The tissue migration phase lasts for about 1 month, with high fever, cough, and eosinophilia. As larvae encyst, edema occurs, and inflammatory cells (polymorphonuclear cells and eosinophils) infiltrate the tissue. Highly active muscle tissue, such as the diaphragm, tongue, Strongyloides stercoralis larvae from a bronchiolar lavage. This condition in humans is known as cysticercosis, and symptoms are associated with the involved tissues (eg, diminution of visual acuity with ophthalmocysticercosis; in neurocysticercosis, symptoms include headache, nausea, vomiting, mental disturbances, and seizures caused by encysted cysticerci in the brain). Individuals may suffer from myalgia and weakness, and eosinophilia may be increased for the first 6 months and then decreases. Trichinellosis is a zoonotic disease; humans acquire the infection by eating raw or undercooked meat (eg, pork, bear meat, or homemade sausages) but are a dead-end host for this infection. The life cycle is maintained in wild animals such as boars and bears or in domestic animals, where pig-to-pig transmission occurs. The larval metacercarial stage encysts on vegetation, such as water chestnuts or red caltrops. They are ingested with uncooked vegetation and then excyst and mature in the intestine. Most infections are light and asymptomatic, but heavy worm burdens cause ulceration, abscess of the intestinal wall, diarrhea, abdominal pain, and intestinal obstruction. The cysticerci, which are about the size of peas, develop into adult worms that can reach lengths of several meters in the intestine. Adult worms generally cause few problems, and most infections are asymptomatic; mild intestinal symptoms include diarrhea and abdominal pain. In the intestine, egg-filled terminal segments break off from the adult worm and pass out with human feces. Humans become infected when they eat raw or undercooked meats containing the cysticerci.

These are three condensations of the outer diabetes mellitus in zimbabwe buy actos overnight, longitudinal diabetes test online 45mg actos visa, muscle coat of the bowel diabetes gestacional proven 15mg actos. Because the taeniae are shorter than the bowel to which they are attached blood sugar tester cheap 45mg actos fast delivery, the colon adopts its typical sacculated shape diabetes insipidus def discount actos, as may be noted in a plain X-ray of the abdomen as haustrations when the large bowel is distended diabetes type 2 low blood sugar order actos without a prescription. This is in contrast to the radiological appearance of a distended small bowel, which demonstrates complete transverse lines due to the transverse mucosal folds of the small intestinal known as the valvulae conniventes. The colon, but not the appendix, caecum or rectum, bears characteristic fatty peritoneal-covered tags referred to as appendices epiploicae. Caecum the caecum is the widest part of the large bowel and lies in the right iliac fossa just above the lateral half of the inguinal ligament on the iliacus muscle. It represents an outpouching of the large bowel below the level of the ileocaecal junction, where the terminal ileum enters the large intestine via the ileocaecal valve. The caecum is completely covered with visceral peritoneum and can be considerably mobile though it does not possess a mesentery. Its mobility puts it at risk of becoming involved by 4 Chapter 1 Anatomy Spleen Gallbladder Stomach Taenia coli Transverse colon Ascending colon Terminal ileum Caecum Appendix Sigmoid colon Rectum Levator ani Sphincter ani externus Pelvic arch Appendices epiploicae Peritoneum Extraperitoneal rectum Sphincter ani internus Omentum Descending colon 1. The longitudinal muscle of the caecal wall is restricted to three taeniae coli, which converge on the base of the appendix, providing for the latter a complete longitudinal muscle coat. The ileocaecal valve is a rudimentary structure consisting of two horizontal folds of mucous membrane that project around the orifice of the terminal ileum. Lymphatic drainage is to local paracolic nodes and ultimately to the superior mesenteric lymph node basin. Autonomic nerve supply is provided by the superior mesenteric plexus via sympathetic and parasympathetic nerve fibres. Appendix the appendix is a narrow muscular tube containing a large amount of lymphoid tissue that can vary markedly Middle colic artery Right colic artery Superior mesenteric artery Jejunal branches Ileolocolic artery Caecal branch Ileal branches Ileal artery Appendicular branch 1. The appendiceal base is attached to the posteromedial aspect of the caecum, but the tip is free and is subject to considerable positional variation as a result. This variability in anatomical location can lead to a variable clinical picture as a consequence of acute appendicitis. Consequently, patients with pelvic appendicitis or retrocaecal appendicitis may not develop right iliac fossa peritoneal irritation. The appendix is completely covered with visceral peritoneum that is attached to the mesentery of the distal ileum by a short meso-appendix, within which resides the appendicular artery, a branch of the posterior caecal artery. Lymph drainage is via mesoappendix nodes and eventually into the superior mesenteric lymph node chain. The appendix is autonomically innervated via sympathetic and parasympathetic nerves from the superior mesenteric plexus. Visceral pain in appendicitis is triggered by the distension of the appendiceal lumen or a longitudinal muscle spasm. The afferent nerve fibres enter the spinal cord at the level of the tenth thoracic vertebra leading to a dull para-umbilical pain. Once the inflamed appendix irritates the parietal peritoneum, the pain migrates to the right iliac fossa, where it is felt as a precise localised pain. As described earlier, the outer longitudinal layer of bowel muscle is completely formed around the appendix, but then diverges to form the taeniae coli. Tracing the taeniae on the caecum downward is thus a helpful manoeuvre in trying to identify the base of the appendix in complicated cases of acute appendicitis. Lymphatic drainage is via the superior mesenteric lymphatic drainage basin, and the sympathetic and parasympathetic nerve supply arises via the superior mesenteric plexus. It begins at the hepatic flexure and hangs downward suspended by the transverse mesocolon from the antero-inferior surface of the pancreas. It terminates at the splenic flexure in the left upper quadrant, becoming continuous with the descending colon. The splenic flexure lies higher than the hepatic flexure and is suspended from the diaphragm by the phrenico-colic ligament. The greater omentum, arising from the greater curvature of the stomach, covers the transverse colon. The inferior peritoneal coat of the omentum is adherent to the anterior surface of the transverse colon and the transverse mesocolon containing the middle colic vessels and lymphatics. These peritoneal layers can be divided so that the transverse colon and mesocolon can be freed from the omentum. The proximal two-thirds of the transverse colon are supplied by the superior mesenteric artery via the middle colic arterial arcades. The distal third is supplied by the left ascending colic branch of the inferior mesenteric artery. Veins drain correspondingly into the superior and inferior mesenteric veins (the latter draining into the splenic vein). Nerve supply to the proximal two-thirds of the transverse colon is via sympathetic and vagal nerves via the superior mesenteric plexus. The distal third is innervated by sympathetic and parasympathetic pelvic splanchnic nerves via the inferior mesenteric plexus. Ascending Colon the ascending colon extends from the caecum to the inferior surface of the right hepatic lobe, where it turns sharply to the left at the hepatic flexure, becoming continuous with the transverse colon. The lower part of the ascending colon lies on the iliopsoas muscle with the genital branch of the genitofemoral nerve. The upper part of the right colon lies on the quadratus lumborum muscle and the origin of the transversus abdominis. The hepatic flexure lies over the lower pole of the right kidney, medial to which are the second and third parts of the duodenum. The arterial blood supply is derived from the ileo-colic artery and right colic artery (which is present as a distinct artery arising from the superior mesenteric artery in approximately 20% of individuals). At the hepatic flexure, numerous veins lie immediately underneath the peritoneum, and these may have to be cauterised when dividing the peritoneum during the mobilisation of the hepatic flexure. These veins enlarge considerably in portal Descending Colon the descending colon commences at the splenic flexure and down towards the pelvic brim where it becomes continuous with the sigmoid colon. The anterior aspect and sides of the descending colon are peritonealised, thereby making it retroperitoneal. The left colic and sigmoid branches of the inferior mesenteric artery provide blood supply, with corresponding venous drainage into the interior mesenteric vein. Sigmoid Colon the sigmoid colon commences as a direct continuation of the descending colon in front of the pelvic brim. It is completely peritonealised, and below it becomes continuous with the rectum near the pelvic brim. The sigmoid colon is relatively mobile and is attached by the sigmoid mesocolon to the posterior abdomino-pelvic wall. The sigmoid mesocolon is V-shaped, running upward and medially over the psoas muscle, the genital vessels and the ureter to the aortic bifurcation. The sigmoid is subject to considerable variation in length, and its mobility predisposes it to the risk of rotation about its mesentery, 6 Chapter 1 Anatomy known as the sigmoid volvulus. Although this can autocorrect, the rotation can continue leading to a compromise to the arterial inflow and venous drainage and large bowel obstruction. Sigmoidal branches of the inferior mesenteric artery provide arterial blood supply with corresponding venous drainage. This chain lies behind the inferior vena cava on the right and to the side of the aorta on the left. The parasympathetic nerve supply to the right colon is probably from the posterior vagus, the fibres of which join the superior mesenteric plexus. The outflow for the left colon takes its origin from the first three lumbar segments of the cord. Fibres leave the ganglionated sympathetic trunks to form a plexus around the superior and inferior mesenteric arteries. It is only in the perivascular ganglia that synapses form, from which nerves follow the arteries to supply the gut. The marginal artery is almost always present and runs in the colonic mesentery close to the bowel wall. This does not follow the artery, however, instead passing to the left of the duodeno-jejunal flexure (where it may be located during surgery), before passing beneath the pancreas to drain into the splenic vein. The Rectum Splenic vein 7 1 Portal vein Inferior mesenteric vein Superior mesenteric vein Superior haemorrhoidal vein Inferior haemorrhoidal vein 1. Posterior vagus nerve Anterior vagus nerve Superior mesenteric artery and plexus Sympathetic chain Preaortic plexus (mixed) Inferior mesenteric artery and plexus Hypogastric plexus Presacral plexus Presacral nerve Lumber nerve Sacral plexus = Parasympathetic = Sympathetic = Mixed 1. The upper and lower curves are directed to the right and the middle curve to the left. Corresponding to each curve there is, on the luminal aspect of the rectal tube, a transverse, sickle-shaped fold. These folds are referred to as rectal shelves, or the valves of Houston, and are produced by the condensed muscle of the rectal wall projecting inwards covered with overlying mucosa. The middle rectal shelf is the most prominent and is readily visualised during rigid and flexible sigmoidoscopy. The rectum is further divided from a surgical perspective into three portions: upper third, middle third and lower third. With respect to peritoneal coverings, the upper third of the rectum is covered by peritoneum on its anterior and lateral surfaces, and the middle third is covered by peritoneum only on its anterior surface. The lower third of the rectum lies below the peritoneal reflexion and thus possesses no peritoneal covering on any aspect. Arterial Supply and Venous Drainage the principal artery supplying the rectum is the superior rectal artery (the name given to the inferior mesenteric artery at the point where the latter crosses the pelvic brim to enter the pelvic cavity). The superior rectal artery runs with the pelvic attachment of the sigmoid mesocolon to enter the perirectal fat behind the rectum. Here it breaks into two, sometimes three longitudinal vessels that travel on either side of the rectum before sinking into the rectal wall. Supplementary arteries that make a contribution to the blood supply of the rectum are the middle rectal arteries and the inferior rectal artery. The longitudinal orientation of the rectum conforms to the ventral concavity of the sacrum and coccyx. Thus, the rectum passes downward and backward initially, and then downward and forward to reach the pelvic diaphragm. In addition to ventral curvature, the rectum possesses a series of three laterally orientated External sphincter Internal sphincter 1. The middle rectal arteries are inconstant in size both between different individuals and from side to side in the same individual. They are usually not prominent vessels but can be large enough to require separate ligation at times. Each inferior rectal artery (also known as the inferior haemorrhoidal artery) is a branch of the internal pudendal artery and is given off as soon as the latter enters the perineum. The inferior rectal artery crosses the ischioanal fossa (ischio-rectal) from lateral to medial to enter the anal wall. However, through the anal wall it is capable of supplying the distal third of the rectum. From a rich and valveless intramural venous plexus, blood enters the perirectal venous plexus, from where rectal blood is carried mainly in the superior rectal vein. The superior rectal vein, running alongside the artery, crosses the pelvic brim from below upward to become the inferior mesenteric vein. Thereafter, the inferior mesenteric vein drains the sigmoid, descending colon and splenic flexure before emptying into the splenic vein and thereby into the portal vein. Some venous blood from the intramural and perirectal venous plexuses travels bilaterally in the middle rectal veins and drains into the internal iliac veins. These veins are usually multiple and small, but can occasionally be large and require ligation. Venous blood from these rectal plexuses also finds its way through the anal wall into the inferior rectal veins which drain into the internal iliac veins via the internal pudendal veins. The anal mucosa and submucosa thus represent sites of natural porta-systemic venous anastomoses. Rarely they can give rise to life-threatening rectal bleeding in patients with portal hypertension. Thereafter, the lymph passes successively through three tiers of mesorectal lymph nodes (equivalent to epicolic, paracolic and intermediate nodes) before reaching the so-called principal nodes. The principal lymph nodes that receive most of the lymph from the upper two-thirds of the rectum are the mesorectal nodes and inferior mesenteric lymph nodes that are situated along the path of the inferior mesenteric artery. Although a point of controversy in the past, there is an increasing recognition that lymph from the lower third of the rectum may also drain into two additional sets of lymph nodes: the internal iliac lymph nodes bilaterally (also called the pelvic side wall nodes) and inguinal nodes (similar to drainage of the anal canal). At present, the involved pelvic sidewall and inguinal nodes are classified (perhaps erroneously) as not representing regional nodal spread, and hence involvement of these is recorded as representing M1 disease. If resection is performed in this area, one needs to be wary of aberrant venous anatomy. Fibres from the hypogastric plexus travel with the arteries to supply the urethra, prostate, seminal vesicles, penis, vagina and base of the bladder as well as the rectum and anal canal. The parasympathetic supply to the left colon, rectum and anal canal, as well as the pelvic viscera, is from the second, third and fourth sacral nerve roots as they emerge on the piriformis from the sacral foramina. The parasympathetic fibres continue laterally as the nervi erigentes to join the presacral nerves, which, with the sympathetics, supply the genital organs, bladder and anorectum.

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