what is secondary endo treatment

Treatment is intended to improve symptoms, manage acute attacks, deal with the damage to hearing and balance, and maintain quality of life. The treatment of secondary endolymphatic hydrops (SEH) is somewhat different.

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What is secondary treatment?

Treatment is intended to improve symptoms, manage acute attacks, deal with the damage to hearing and balance, and maintain quality of life. The treatment of secondary endolymphatic hydrops (SEH) is somewhat different.

What is endodontic treatment?

Secondary treatment is the removal of biodegradable organic matter from sewage or similar kinds of wastewater.: 11 The aim is to achieve a certain degree of effluent quality in a sewage …

How is type II endoleak treated?

Aug 06, 2017 · Type II endoleaks, can potentially enlarge and pressurize the aneurysm sac with a risk of rupture. However, many type II endoleaks spontaneously resolve or never lead to sac …

What is an example of an anaerobic secondary treatment system?

However, in secondary infertility you’re unable to conceive or carry a baby to full-term after having a previous successful pregnancy. Infertility can be caused by either the man or woman. …

What are the five phases of endodontic treatment?

What is the success rate of a second root canal?

How is a second root canal performed?

How many times can you have root canal on the same tooth?

Should I get a second root canal or extraction?

Is it common to have a root canal redone?

Can a root canal be done twice on same tooth?

Does a second root canal hurt?

Is a repeat root canal painful?

Can another dentist finish my root canal?

What are the symptoms of a failed root canal?

How do you know if root canal is infected?

What is endodontic material?

Endodontic materials are used in endodontic treatment, which is the procedure to save the tooth when the pulp and/or periradicular tissues are injured. These materials can be generally classified into two groups: materials used to maintain the vitality of the pulp (pulp capping materials), and materials used to disinfect (irrigants and intracanal medicaments) and fill the pulp in root canal therapy.

How successful is endodontic treatment?

The overall success of the endodontic treatment is based on the shaping, cleaning, disinfecting, and sealing of this root canal. The classical method for cleaning the root canal is based on endodontic mechanical instruments ( Fig. 20.4 ). It has been proved that before complex endodontic treatment only 80% of frontal teeth and 60% of lateral teeth were fully disinfected. Contamination may occur due to the fact that preparation of the root canal space mechanically creates a smear layer producing organic and mineral debris on the wall of the root canal. This smear layer can be beneficial in that it provides an obstruction of the tubules and decreases dentin permeability ( Brugnera et al., 2003 ).

What is endodontic treatment?

The term endodontic treatment covers all aspects of repair and treatment of a tooth in which the pulp has been either damaged or exposed as well as the treatment of peri-apical tissues. In the latter case, the pulp is at risk of further damage or destruction. Thus endodontic treatment includes pulp capping, both direct and indirect, as covered in Chapter 8, where the aim is to save the pulp in a viable state and to re-establish the tooth as a fully functioning entity. It also includes the treatment of a tooth whose pulp has become substantially damaged, either by trauma or infection, so that the pulp needs to be extirpated. When this is necessary, it must be followed by sealing of the tooth at the root. This enables the tooth to continue to function structurally, despite no longer being viable.

Why is endodontic treatment important?

It is carried out because preserving the natural teeth is important in maintaining full function of the dentition, with the associated health benefits that a fully functional set of teeth confers.

What is the treatment of root canals?

Endodontics deals with the treatment of root canals in teeth in which, due to the advanced decay, the tooth crown is destroyed. The modern lateral condensation method gives the possibility of hermetically closing the individual root canal by its filling. This approach prevents bacteria entering from the mouth into the canal. Laser radiation can reduce 99% of microbial pathogens during the endodontic treatment . It also leads to decontamination of the infected lateral canals. During laser irradiation, organic substances are completely removed, and coagulation of proteins in the dentinal tubules is achieved.

How to remove smear layer?

Laser radiation can remove the smear layer. Treatment continues either by application of a chemical sealant or by laser radiation which melts and disinfects the surface. The root canal wall, after cleaning with the mechanical instrument and then by Er:YAG or second harmonic of alexandrite laser radiation, is shown in Fig. 20.5. In both cases the smear layer has disappeared and the dentin tubules are partially sealed due to laser radiation spreading ( Fig. 20.6 ).

What is pulp capping?

Pulp capping materials should be able to induce hard-tissue formation in a superficial way, protect the pulp from further invasion of bacteria, and not have side effects so that the pulp can be alive. Hard-setting calcium hydroxide cements are the most commonly used pulp capping materials. This material causes the formation of a 1–1.5 mm thick necrosis layer in the superficial pulp. The layer will undergo calcification eventually and it is called a dentine-bridge.

How does BOD affect the ecosystem?

High BOD concentrations initially exceed the ability of the secondary treatment ecosystem to utilize available food. Ecosystem populations of aerobic organisms increase until oxygen transfer limitations of the secondary treatment bioreactor are reached. Secondary treatment ecosystem populations may shift toward species with lower oxygen requirements, but failure of those species to use some food sources may produce higher effluent BOD concentrations. More extreme increases in BOD concentrations may drop oxygen concentrations before the secondary treatment ecosystem population can adjust, and cause an abrupt population decrease among important species. Normal BOD removal efficiency will not be restored until populations of aerobic species recover after oxygen concentrations rise to normal.

How does an aerated lagoon work?

Aerated lagoons are a low technology suspended-growth method of secondary treatment using motor-driven aerators floating on the water surface to increase atmospheric oxygen transfer to the lagoon and to mix the lagoon contents. The floating surface aerators are typically rated to deliver the amount of air equivalent to 1.8 to 2.7 kg O 2 / kW·h. Aerated lagoons provide less effective mixing than conventional activated sludge systems and do not achieve the same performance level. The basins may range in depth from 1.5 to 5.0 metres. Surface-aerated basins achieve 80 to 90 percent removal of BOD with retention times of 1 to 10 days. Many small municipal sewage systems in the United States (1 million gal./day or less) use aerated lagoons.

How much BOD is in secondary treated sewage?

Secondary treated sewage is expected to produce effluent with a monthly average of less than 30 mg/l BOD and less than 30 mg/l suspended solids. Weekly averages may be up to 50 percent higher.

What is fixed film system?

Fixed-film systems are more able to cope with drastic changes in the amount of biological material and can provide higher removal rates for organic material and suspended solids than suspended growth systems . : 11–13 Most of the aerobic secondary treatment systems include a secondary clarifier to settle out and separate biological floc or filter material grown in the secondary treatment bioreactor.

Why does BOD drop in secondary bioreactors?

A similar problem occurs as BOD concentrations drop when low flow increases waste residence time within the secondary treatment bioreactor. Secondary treatment ecosystems of college communities acclimated to waste loading fluctuations from student work/sleep cycles may have difficulty surviving school vacations. Secondary treatment systems accustomed to routine production cycles of industrial facilities may have difficulty surviving industrial plant shutdown. Populations of species feeding on incoming waste initially decline as concentration of those food sources decrease. Population decline continues as ecosystem predator populations compete for a declining population of lower trophic level organisms.

How is primary clarifier effluent discharged?

Primary clarifier effluent was discharged directly to eutrophic natural wetlands for decades before environmental regulations discouraged the practice. Where adequate land is available, stabilization ponds with constructed wetland ecosystems can be built to perform secondary treatment separated from the natural wetlands receiving secondary treated sewage. Constructed wetlands resemble fixed-film systems more than suspended growth systems, because natural mixing is minimal. Constructed wetland design uses plug flow assumptions to compute the residence time required for treatment. Patterns of vegetation growth and solids deposition in wetland ecosystems, however, can create preferential flow pathways which may reduce average residence time. Measurement of wetland treatment efficiency is complicated because most traditional water quality measurements cannot differentiate between sewage pollutants and biological productivity of the wetland. Demonstration of treatment efficiency may require more expensive analyses.

What is primary treatment of sewage?

Primary treatment of sewage by quiescent settling allows separation of floating material and heavy solids from liquid waste. The remaining liquid usually contains less than half of the original solids content and approximately two-thirds of the BOD in the form of colloids and dissolved organic compounds.

What is the Nellix endograft?

The Nellix endograft (Endologix Inc., Irvine, USA), currently has an FDA Investigational Device Exemption, undergoing efficacy trials, and a European CE mark approval. The device is unique. The sac anchoring endovascular aneurysm sealing system is comprised of two balloon expandable stents that extend in parallel from the non-aneurysmal aorta proximally into the iliac arteries distally. Each balloon expandable stent is surrounded by a polymer filled endobag. The endobags obliterate the aneurysm flow lumen to achieve a seal to resist both lateral and longitudinal displacement forces. Given the filling of the aneurysm sac by the polymer-filled endobag, the device may decrease the incidence of type 2 endoleaks and reintervention rates (Figure 3). In a multicenter study with 171 patients treated with the Nellix device and observed for a median of 5 months (range, 0–14 months), technical success was 99% and type II endoleak rate was 2% (29). There were no aneurysm ruptures or need for open surgical conversion.

What materials are used for endoleak embolization?

Possible embolization materials include coils, EVOH, n-butyl-cyanoacrylate glue, and coils. Coils are the most widely used. The advantage of EVOH is that it can fill the endoleak nidus and the inflow and outflow vessels. It is also radiopaque, therefore, monitoring the injection and avoiding nontargeted embolization can be performed. Cyanoacrylate glue can be utilized in a similar manner such as after coiling when blood flow has slowed. Its viscosity can be adjusted by adjusting the quantity of ethiodol (27). A less typical approach is to utilize an MVP microvascular plug (Medtronic). The advantage of such a plug is that it leads to minimal artifact on imaging after intervention. Whereas EVOH, glue and coils make assessing for endoleak on post intervention CT scans difficult due to beam hardening artifact, the MVP plug has little associated artifact. Alternatively, MRI is an alternative to image for endoleak which minimizes artifact from the above embolic agents.

How to treat type II endoleak?

Treatment of type II endoleak by translumbar direct sac puncture and embolization with coils and onyx. (A) Direct sac puncture via a sheath needle to access type II endoleak under CT guidance; (B) contrast injection via sheath needle demonstrating endoleak cavity; (C) fluoroscopic image following placement of coils in the caudal aspect of the endoleak cavity; (D) image following embolization of the endoleak nidus with both coils and onyx. Note that the Onyx extends into several lumbar branches.

How long does an endoleak last after EVAR?

A type II endoleak may be early, occurring within 30 days of EVAR, persistent, lasting longer than 6 months, or late, occurring after 1 year (18). Imaging of type 2 endoleak. After EVAR has been completed, our follow-up protocol is a CT angiography (CTA) at 1, 6, and 12 months, and annually thereafter.

What is the best way to diagnose endoleaks?

A proper imaging protocol is necessary to ensure endoleaks are identified. A three-phase scan consisting of a non-contrast scan, an arterial phase, and delayed imaging is considered the standard of care, and review of previous studies is mandatory. There is newer data that suggests dual-source dual-energy multidetector CT may be as accurate as the standard triphasic protocol with a significant radiation dose reduction (21-23). The latter protocol is especially promising given the significant radiation exposure patients encounter during CT follow-up imaging after EVAR. Once an endoleak is identified, it is important to determine the endoleak type in order to direct urgency and management. Cross-sectional imaging may not always elucidate the type of endoleak present, making angiography the next step in management. Diagnostic angiography should include an aortogram, as well as selective angiography of the superior mesenteric artery (SMA) and bilateral hypogastric arteries. Power injection runs with adequate contrast volume and frame rate are required. Super-selective angiography of secondary and tertiary branches of the SMA and hypogastric arteries is often necessary to identify endoleaks which may not be well seen on nonselective angiograms. If a type III endoleak is suspected, angiography performed with a pigtail catheter tip within the endograft may be useful. Placement of an occlusion balloon above the pigtail catheter in the graft may increase the sensitivity for type III endoleak assessment. A type Ib endoleak can be uncovered in a similar fashion, wherein a compliant balloon can be deployed in the iliac limb as an angiogram is performed with the pigtail tip at the distal seal site. This may force contrast into the aneurysm sac from the distal seal site if a type Ib endoleak is present. Furthermore, filling of the IMA or lumbar arteries on cross-sectional imaging does not always represent a type II endoleak as we have seen many patients who have a subtle type Ia endoleak creating an inflow into the aneurysm sac, with resultant outflow in the IMA or lumbar vessels. This is best appreciated on aortography.

What is the Nellix device?

Utilization of a Nellix device (Endologix) to manage abdominal aortic aneurysm with goal of decreasing type II endoleak. (A) Aortogram demonstrates a 5.7 cm abdominal aortic aneurysm; (B) following placement of a Nellix device, there is no evidence of endoleak. This device may decrease the incidence of type II endoleaks because of filling of the aneurysm sac with polymer filled endobags.

What glue is used to embolize a nidus?

If there is difficulty addressing all inflow and outflow vessels, EVOH or cyanoacrylate glue may be utilized to embolize the nidus and vessels (Figure 2).

What causes low sperm production in men?

The presence of mycoplasma, which is a type of bacteria. Anesthesia. Testicular varicocele. This is an enlargement of veins in the scrotum, or the sack of skin encasing the testicles. This condition is a common cause of low sperm production and infertility in men. About 30% of infertile men have testicular varicocele.

What does a doctor ask about menstrual cycle?

The doctor will ask if you’ve experienced irregular menstrual cycles and will want to find out if you’re ovulating and producing eggs normally. For men, a medical history will show if thyroid disease, cancer or age-related conditions might have affected sperm count or quality.

How long does it take for secondary infertility to be diagnosed?

Secondary infertility typically is diagnosed after trying unsuccessfully to conceive for six months to a year. A related condition is recurrent pregnancy loss where patients and couples are able to conceive but are unable to carry to term. Cleveland Clinic is a non-profit academic medical center.

Why do women have secondary infertility?

Causes of secondary infertility in women include: Problems in the quantity or quality of eggs: Women are born with a limited supply of eggs and are unable to create new eggs after birth. As women approach their 40s and beyond, the numbers of eggs left in their ovaries decrease, and the remaining eggs have a higher chance ...

Why do fallopian tubes block eggs?

Problems with the fallopian tubes: The fallopian tubes, which carry eggs from the ovaries to the uterus, can become blocked due to pelvic infections such as chlamydia or gonorrhea. Problems with the uterus: There are many conditions related to the uterus that can cause secondary infertility.

What happens if a woman feeds her baby only by breastfeeding?

Breastfeeding: If a woman feeds her baby only by breastfeeding, her body stops ovulating or releasing eggs for potential fertilization. Weight gain or other lifestyle changes: Weight gain can lead to ovary dysfunction in some patients. Certain diets may effect fertility. Medications may also effect fertility.

What are the emotional effects of secondary infertility?

If treatments for secondary infertility fail, couples might suffer from a range of emotions, including anger, sadness, grief, guilt and loneliness.

What is AIMS in medical terms?

AIMS (I): To investigate the effects of study characteristics on the reported success rates of secondary root canal treatment (2 degrees RCT or root canal retreatment ); and (ii) to investigate the effects of clinical factors on the success of 2 degrees RCT.

What is the success rate of a secondary root canal?

The pooled estimated success rate of secondary root canal treatment was 77%. The presence of pre-operative periapical lesion, apical extent of root filling and quality of coronal restoration proved significant prognostic factors with concurrence between all three strands of evidence whilst the effec …

What to look for in a tooth with a discolored crown?

The most important factor in the treatment is a correct diagnosis which is achieved by careful history taking, examination and the use of special tests.16Specific things to look for in the history include past disease, trauma and pain. The teeth are examined for abnormalities such as caries, defective restorations, erosions, abrasions, cracks, fractures, and discolorations. A discolored permanent tooth may often be associated with a necrotic pulp. A “pink spot” detected in the tooth crown may indicate an active internal resorption process. A conclusive diagnosis for pulpal disease cannot be achieved by visual examination alone. It therefore must always be accompanied by additional tests. Visual examination is dramatically improved by the use of enhanced magnification and illumination. Vitality testing should be carried out on relevant teeth as well as radiographic examination, paying close attention to shape, location and extension of any lesion, crestal and furcation involvement and signs of fracture or perforation.65Diagnosis of primary endodontic disease and primary periodontal disease usually presents no clinical difficulty. In primary endodontic disease, the pulp is infected and non-vital. On the other hand, in a tooth with primary periodontal disease, the pulp is vital and responsive to testing. However, primary endodontic disease with secondary periodontal involvement, primary periodontal disease with secondary endodontic involvement, or true combined diseases are clinically and radiographically very similar. If a lesion is diagnosed and treated as a primarily endodontic disease due to lack of evidence of marginal periodontitis, and there is soft-tissue healing on clinical probing and bone healing on a recall radiogragh, a valid retrospective diagnosis can then be made. The degree of healing that has taken place following root canal treatment will determine the retrospective classification. Radiographs are essential for detection of anatomic landmarks and a variety of pathological conditions. In addition, radiographs are of utmost importance for documentation and legal purposes. Radiographic examination will aid in detection of carious lesions, extensive or defective restorations, pulp caps, pulpotomies, previous root canal treatment and possible mishaps, stages of root formation, canal obliteration, root resorption, root fractures, periradicular radiolucencies, thickened periodontal ligament, and alveolar bone loss. Advanced lesions and true-combined lesions are difficult to differentiate between and therefore, where doubt exists they should be considered as an endodontic lesion in origin.65

What causes root canal leakage?

The overfilling of root canals produces a lesion in exactly the same way as the lesion originating adjacent to the apical foramen rather than the lateral wall or pulpal floor. Coronal leakage is the leakage of bacterial elements from the oral environment along the restoration's margin to the endodontic filling. Studies have indicated that this factor may be an important cause of endodontic treatment failure.43–46Root canals may become recontaminated by microorganisms due to delay in placement of a coronal restoration and fracture of the coronal restoration and/or the tooth.43Madison and Wilcox44found that exposure of root canals to the oral environment allowed coronal leakage to occur, and in some cases along the entire length of the root canal. Ray and Trope45reported that defective restorations and adequate root canal fillings had a higher incidence of failures than teeth with inadequate root canal fillings and adequate restorations. Nevertheless, even popular permanent restorative materials may not always prevent coronal leakage.47Cemented full crowns48–49, as well as dentin-bonded crowns50also leaked. Dental injuries or trauma may take on many shapes but generally can be classified as enamel fractures, crown fractures without pulp involvement, crown fractures with pulp involvement, crown-root fracture, root fracture, luxation, and avulsion.51Treatment of traumatic dental injuries varies depending on the type of injury and it will determine pulpal and periodontal ligament healing prognosis.52–57The most common cause of vertical root fracture in endodontically treated teeth is the excessive force used during lateral condensation of gutta-percha. Widening of the periodontal ligament along one or both sides of the root, or bone loss in solitary tooth are the major radiographic findings. Mild pain or discomfort and swelling are the major clinical symptoms, and solitary pocket around one aspect of the suspected tooth is the major clinical sign. Certain chemicals used in dentistry have the potential to cause root resorption. Clinical reports58–63have shown that intracoronal bleaching with highly concentrated oxidizing agents, such as 30-35% hydrogen peroxide, can induce root resorption. The irritating chemical may diffuse through the dentinal tubules and when combined with heat, they are likely to cause necrosis of the cementum, inflammation of the periodontal ligament, and subsequently root resorption.62,64Replacement resorption or ankylosis occurs following extensive necrosis of the periodontal ligament with formation of bone onto a denuded area of the root surface. This condition is most often seen as a complication of luxation injuries, especially in avulsed teeth that have been out of their sockets in dry conditions for several hours. Certain periodontal procedures have been reported to induce replacement root resorption. The potential for replacement resorption was also associated with periodontal wound healing. Granulation tissue derived from bone or gingival connective tissue may induce root resorption and ankylosis. Vertical root fractures are most often caused when a tooth, often weakened due to undermining by caries, previous restorative treatment or a non-vital pulp becomes traumatised.39Leaching of the root canal contents or bacterial contamination of the fracture line may cause an inflammatory lesion in periodontal tissues.36The continuing lesion mimics those due to root perforation or over-filling of root canals.

What are the complications of root canal perforation?

These include root perforations, overfilling of root canals, coronal leakage, trauma, chemical induced root resorption, intra-canal medicaments and vertical root fractures.39Root perforations are undesirable clinical complications that may lead to periodontal lesions. When root perforation occurs, communications between the root canal system and either peri-radicular tissues or the oral cavity may often reduce the prognosis of treatment. Root perforations may result from extensive carious lesions, resorption, or from operator error occurring during root canal instrumentation or post preparation.41,42At the site of perforation, an inflammatory reaction in periodontal ligament produces a degradation of surrounding tissues and formation of a lesion which can progress as a conventional primary endodontic lesion.36

What causes pulpal necrosis?

Primary periodontal lesions with secondary endodontic involvement; periodontal disease causes a resultant pulpal necrosis as it progresses apically.

What is a true combined lesion?

True-combined lesions: both an endodontic and periodontal lesion developing independently and progressing concurrently which meet and merge at a point along the root surface.

What is an endodontic lesions?

Endodontic lesions: an inflammatory process in the periodontal tissues resulting from noxious agents present in the root canal system of the tooth.

How does periodontal inflammation affect the pulp?

The effect of periodontal inflammation on dental pulp is controversial and conflicting studies abound.2–10It has been suggested that periodontal disease has no effect on the pulp before it involves the apex.5On the other hand, several studies suggested that the effect of periodontal disease on the pulp is degenerative in nature including an increase in calcifications, fibrosis, and collagen resorption, in addition to the direct inflammatory sequelae.11,12Dental pulp and periodontium have embryonic, anatomic and functional inter-relationships.13They are ectomesenchymal in origin, the cells from which proliferate to form dental papilla and follicle, which are the precursors of the pulp and periodontium, respectively. They are separated by the formation and development of tooth bud from the overlaying ectoderm into enamel and dentine.14The embryonic development gives rise to anatomical connections which remain throughout the life of the tooth. The apical foramen decreases in size as the proliferation of the Sheath of Hertwig continues. It remains patent and serves as the communication on which the pulpal tissues rely for nutrition and nervous innervation. As the root develops, ectomesenchymal channels get incorporated, either due to dentine formation around existing blood vessels or breaks in the continuity of the Sheath of Hertwig, to become accessory or lateral canals.15The majority of accessory canals are found in the apical part of the root and lateral canals in the molar furcation regions.16Tubular communication between the pulp and periodontium may occur when dentinal tubules become exposed to the periodontium by the absence of overlying cementum. These are the pathways that may provide a means by which pathological agents pass between the pulp and periodontium, thereby creating the perioendo lesion.15Blomlof et al.17created defects on root surfaces of intentionally extracted monkey teeth with either open or mature apices. The root canals were either infected or filled with calcium hydroxide and replanted back in their sockets. After 20 weeks, marginal epithelial downgrowth was found on the denuded dentin surface of the infected teeth. Noxious elements of pulpal origin including inflammatory mediators and bacterial byproducts may leach out through the apex, lateral and accessory canals, and dentinal tubules to trigger an inflammatory response in the periodontium including an early expression of antigen presentation.18Released products are from living bacterial strains including spirochetes as well as of non-living pathogen.19–23Fungi and viruses are also implicated.24–27In certain cases, epithelial growth is stimulated and affects the integrity of periradicular tissues.28–33Jansson et al.34assessed the effect of endodontic pathogens on marginal periodontal wound healing of denuded dentinal surfaces surrounded by healthy periodontal ligament. Their results showed that in infected teeth, the defects were covered by 20% more epithelium while the noninfected teeth showed only 10% more connective tissue coverage. They concluded that pathogens in necrotic root canals may stimulate epithelial downgrowth along denuded dentin surfaces with marginal communication and thus augment periodontal disease. The organisms most often in volved are probably bacteroides, fusobacteria, eubacteria, spirochetes, wolinellas, selenomonas, campylobacter, and peptostreptococci. Important qualities of cross-infecting organisms may be the ability to survive in highly reduced environments and motility. Precautions should be taken to prevent in vivo seeding of such micro-organisms, particularly in compromised teeth and hosts.21

What is secondary adrenal insufficiency?

Secondary Adrenal Insufficiency. Secondary adrenal insufficiency is adrenal hypofunction due to lack of adrenocorticotropic hormone (ACTH). Most of the symptoms and signs of this condition are similar to those of Addison disease.

What causes inadequate acth?

Inadequate ACTH can also result from failure of the hypothalamus to stimulate pituitary ACTH production, which is sometimes called tertiary adrenal insufficiency. Panhypopituitarism may occur secondary to pituitary tumors, various other tumors, granulomas, and, rarely, infection or trauma that destroys pituitary tissue.

What test is used to differentiate primary and secondary adrenal insufficiency?

Tests to differentiate primary and secondary adrenal insufficiency are discussed under Addison disease. Patients with confirmed secondary adrenal insufficiency (see table Confirmatory Serum Testing for Secondary Adrenal Insufficiency) should have CT or MRI of the brain to rule out a pituitary tumor or pituitary atrophy.

What is the normal response to corticotropin releasing hormone?

After administration of CRH 100 mcg (or 1 mcg/kg) IV, the normal response is a rise of plasma ACTH of 30 to 40 pg/mL (6.6 to 8.8 pmol/L); patients with pituitary failure do not respond, whereas those with hypothalamic disease usually do.

Why is fludrocortisone not required?

Fludrocortisone is not required because the intact adrenals produce aldosterone.

What is the name of the disease that causes hyperpigmentation and hypotension?

Addison Disease Addison disease is an insidious, usually progressive hypofunctioning of the adrenal cortex. It causes various symptoms, including hypotension and hyperpigmentation, and can lead to adrenal crisis... read more

How long does ACTH last after corticosteroids?

These problems may persist for up to 1 year after corticosteroid treatment is stopped.