By X. Karrypto. Henry Cogswell College. 2019.
Vertigo This is the sensation of the environment spinning while stationary – like ‘stepping of a roundabout’ purchase remeron with paypal. Patients may not be familiar with this meaning of the word purchase 30mg remeron with amex, and so care should be taken to fully determine the nature of any dizziness cheap remeron express, faintness or unsteadiness that they report. Ataxia may be evident on walking, when a patient will tend to fall to the afected side of a unilateral lesion. Similar symptoms such as dysmetria (overshooting or undershooting a target) and impaired check (failure to stop a limb movement appropriately) also commonly occur in cerebellar lesions. As with many of the clinical abnormalities of cerebellar disease, it is thought to be due to poor co-ordination of agonist and antagonist muscles. There are distinct ‘cerebellar syndromes’ comprising a constellation of these symptoms that point to a particular anatomical location of the lesion. Syndrome Location of lesion Predominant clinical features Rostral vermis Anterior lobe/rostral Broad-based gait syndrome vermis Truncal ataxia Caudal vermis Posterior or Vertigo syndrome focculonodular lobe Staggering gait Truncal ataxia Nystagmus Hemispheric Cerebellar hemisphere Limb ataxia syndrome Intention tremor Dysmetria Dysarthria Dysdiodokokinesia Table 6. Lesions of the vermis tend to cause more truncal ataxia than limb ataxia, and fewer obvious limb signs. Lesions in the hemispheres cause a greater range of symptoms and include prominent limb signs ipsilateral to the lesion 132 Cerebellum Cerebellar disease has many underlying causes, both de- velopmental/hereditary and acquired. Developmental or hereditary Key causes include Arnold–Chiari and Dandy–Walker malforma- tions and the hereditary ataxias. The hereditary ataxias These include a large number of rare autosomal dominant and recessive conditions: • the most common autosomal dominant conditions are the spinocerebellar ataxias, which are chronic, progressive conditions. There is often arefexia of the ankles, cardiomyopathy and diabetes in up to one-quarter of cases Acquired There are a wide range of acquired causes of cerebellar disease, including vascular, toxic, neoplastic, infective and autoimmune pathologies. This causes headache in addition to cerebellar symptoms and commonly causes decreased consciousness and may lead to life-threateninghydrocephalus Toxins Alcohol is the most common toxic cause. Chronic overuse can lead to Wernicke’s (ataxia, acute confusion, eye movement disorder) or Korsakoff’s syndromes (a chronic amnesic state). Benzodiazepines, phenytoin, carbamazepine, chemo- therapeutic drugs and lithium are the more common drugs associated with dysarthria and ataxia. Tumours In children medulloblastomas, astrocytomas and ependy momasare relatively common primary tumours found in the cerebellum. Paraneoplastic syndromescausing cerebellar syn- dromes are well described and are usually the result of small cell lung carcinoma or breast cancer. Infective or immune There are many infective or immune causes, including: • encephalitis from any cause can result in an initial cerebellar syndrome but usually progresses to a more forid encephalitic picture • autoimmune diseases such as multiple sclerosisare a common cause in young people and are typically of a subacute nature • up to 10% of patients with coeliac diseasehave neurological involvement and this can include a slowly progressive cerebellar syndrome What happens next? Patients with cerebellar disease not readily explained by vascular causes or alcohol usually require careful and extensive investigation. Revisiting the family history is an ideal place to start and it may be helpful to actually see and examine family members. General observation Inspect body and feet Palpate pulse, auscultate carotids Palpate abdomen Vertigo Ataxia Sitting Standing Walking Nystagmus Primary gaze Gaze evoked Intention tremor Reassess with fnger–nose test Test for impaired check Speech Note any dysarthria or scanning speech Hypotonia Assess tone in limbs Dysdiodochokinesia Test alternating clapping Test heel–shin. Although it is less useful for fne localisation, it is very helpful in determining the impact of a disease process on a patient’s cognitive processes and for assessing its progression over time. This is often all that is needed in patients without significant cognitive impairment and provides an assessment of: • orientation Clinical insight • registration (immediate memory) Patients vary greatly in their background education and cultures. It is also more reliable at distinguishing between diferent subtypes or dementia, such as Alzheimer’s disease, frontotemporal dementia and supranuclear palsy. Bedside cognitive examinations are not designed to tease out precise anatomical regions; language function is the exception, and is discussed below. Language Language is such a defning feature of our human nature that the complexity of neural computations that it requires is easily overlooked. In recent years a ‘dual stream model’ of language processing has Anatomy and physiology review 137 emerged. This proposes that speech recognition depends on neural circuits in both: • the superior temporal lobes (the ventral stream) • the frontoparietal–temporal circuit in the left hemisphere in the majority of people (the dorsal stream). Wernicke’s area was historically considered to be a cortical area on the dominant superior temporal gyrus. In the dual stream model this area is part of the ventral stream and both hemispheres contribute to this aspect of speech (ure 7. Visuoperceptual function and calculation This includes functions such as spatial organisation, praxis (planning) and calculations. The underlying brain regions involved remain controversial, but the parietal lobesand theparietal-temporal junctionof the non-dominant hemisphere (usually the right) are important. There is a bilateral ventral stream underlying speech recognition and a dorsal stream involved with speech production. Again, the neuroanatomical regions involved in memory are legion; however, the hippocampus and other mesial temporal lobe structures are crucial for the formation of declarative memories and, in particular, working memory. Executive function This term refers to some of the ‘higher’ cortical functions such as abstraction, inhibition, planningand othersocial behaviours. Patients will be disorientated in time and place and unable to attend to stimuli or interact normally. This tends to fuctuate • dementia: attention and orientation are also markedly abnormal in the dementias. However, this tends not to be associated with the fuctuating level of consciousness seen in delirium • psychiatric disorders: depression can cause a so-called pseudo-dementia, largely due to reduced attention and concentration leading to poor functioning in other domains. Comprehension Language comprehension Clinical insight appears to be bilaterally localised along the superior Wernicke’s aphasia: damage to Wernicke’s area in the superior temporal temporal gyrus. Defcits in gyrus can cause a type of aphasia language comprehension are known as Wernicke’s or receptive particularly socially isolating. Speech Defcits in speech include: • dysphonia: patients with parkinsonism often display a slow, monotonous and quiet speech • dysarthria: this is a defcit in speech articulation. It may be caused by a lesion in the motor cortex, internal capsule, brainstem, cerebellum or cranial nerves • dysphasia:receptive dysphasiais the inability to understand speech; expressive dysphasia is also known as Broca’s or anterior aphasia and is impairment of the ability to generate 140 Higher cortical function speech not caused by a dysarthria. Speech Signifcant language def- comprehension is intact, but patients cits are found in some of the are unable to say what they want to say, dementias as well as in many resulting in non-fuent, broken speech. Stroke is a major cause of lan- A useful mnemonic for distinguishing guage problems in Western Broca’s from Wernicke’s aphasia is: Broca’s populations. In these popula- aphasia displays Broken (non-fuent) tions, a sudden onset expres- speech and anatomically is found Before sive or receptive dysphasia (anteriorly) Wernicke’s area. Visuoperceptual function and calculation Impaired visuoperceptual function and calculation manifests as: • poor spatial organisation • neglect • impaired praxis • problems with simple arithmetic and everyday tasks such as shopping These tasks require a baseline level of attention and concentration and so can be impaired when other cognitive domains are primarily afected. Testing this domain involves: • drawing tasks • copying multistep movements or procedures • arithmetic These can be impaired in most global encephalopathies, but in terms of dementias tend to be mildly impaired in Alzheimer’s disease and more severely afected incorticobasal degeneration and dementia with Lewy bodies. Bedside testing of cognitive domains 141 They are also commonly impaired in non-dominant hemisphere strokes, giving rise to the common features in these patients of neglect and dyspraxia. Alzheimer’s disease, dementia with Lewy bodies and frontal–temporal dementia all exhibit profound memory defcits. Progressive supranuclear palsy is typically associated with well preserved memory function, and can thereby be distinguished from other neurodegenerative processes.
For cyclo- age discount remeron 30mg free shipping, which makes it more likely that patients with type 1 sporin levels in breast milk are usually greater than those diabetes mellitus have reached end‐stage renal failure in a simultaneously taken blood sample buy remeron online from canada. There be due to the presence of generalized cardiovascular is a view that mothers who want to breastfeed should be pathology generic remeron 15mg line, which is part of the metabolic risk factor syn- encouraged, so long as the baby is thriving [87,88] and drome. Successful pregnancies have been reported after monitoring fetal drug levels could be undertaken if there combined pancreas–kidney allografts . Preterm delivery is com- immunosuppressive agents, with eventual development mon (45–60%) because of intervention for obstetric rea- of malignant tumours in affected offspring, autoimmune sons and the common occurrence of preterm labour or complications and/or abnormalities in reproductive per- preterm rupture of membranes. Thus paediatric follow‐ monly associated with poor renal function, but in some it up is needed (Table 11. To date, information about has been postulated that long‐term immunosuppression general progress in early childhood has been good. Unless there are problems, spontaneous Preterm delivery and/or small for gestational age onset of labour can be awaited but most advise not Respiratory distress syndrome exceeding 38–39 weeks’ gestation. During labour careful Adrenocortical insufficiency monitoring of fluid balance, cardiovascular status and Septicaemia temperature is mandatory. Surgical induction of labour (by Depressed haematopoiesis amniotomy) and episiotomy warrant antibiotic cover. Reduced T lymphocyte and immunoglobulin levels Augmentation of steroids should not be overlooked. The ultimate measure of transplant success is the long‐ term survival of the patient and the graft. As it is only 40 Gynaecological problems years since this procedure became widely employed in There is a danger that symptoms secondary to genuine the management of end‐stage renal failure, few long‐ pelvic pathology may be erroneously attributed to the term data from sufficiently large series exist from which transplant because of its location near the pelvis . Furthermore, the long‐term results Transplant recipients receiving immunosuppressive for renal transplantation relate to a period when many therapy have a malignancy rate estimated to be 100 times aspects of management would be unacceptable by pre- greater than normal and the female genital tract is no sent‐day standards. This association is probably related to factors numbers of patients worldwide indicate that about 95% such as loss of immune surveillance, chronic immuno- of recipients of kidneys from related living donors are suppression allowing tumour proliferation (especially if alive 5 years after transplantation. With cadaver kidneys, virally driven) and/or prolonged antigenic stimulation of the figure is approximately 89%. Regular gynaecological mal 2 years after transplant, graft survival increases fur- assessment is therefore essential and any gynaecological ther. This is why women are counselled to wait about 2 management should be on conventional lines, with the years before considering a pregnancy even though a view outcome unlikely to be influenced by stopping or reduc- is now emerging that 1 year would be sufficient. Pregnancy occasionally and sometimes unpredictably causes irrevers- Kidney donors ible declines in renal function. However, the consensus is It has always been considered that living kidney donors that pregnancy, whilst often complicated, has little effect on are low risk for almost all medical conditions. However, long‐term graft function or survival providing function is recent data suggest that gestational hypertension and good at baseline, it is a first transplant and hypertension is pre‐eclampsia are about twice as common in those who not a major issue [72,87,89]. Contraception Oral contraception can cause or aggravate hypertension, Summary thromboembolism and/or subtle changes to the immune system. This does not necessarily contraindicate its use Women with kidney disease used to be discouraged from but careful surveillance is essential. It is now clear that with adequate containing contraceptives are not used due to the pre‐pregnancy planning, the vast majority can have safe increased risk of thrombosis. However, progesterone pregnancies with good outcomes for the mother and only methods – the mini-pill, an implant or progesterone baby. Women obscure symptoms and signs of early pregnancy abnor- should be followed up post partum to ensure stability of malities, such as threatened miscarriage or ectopic preg- renal disease, make the renal diagnosis if they have pre- nancy. Current data suggest that immunosuppressed sented for the first time during pregnancy, and to ensure women have no increased risk of pelvic inflammatory an appropriate long‐term care plan is in place. Prepregnancy care and counselling in chronic Consensus Conference on Reproductive Issues and renal patients. In: Macklon N, Greer I, Steegers E (eds) 144 Maternal Medicine Textbook of Periconceptional Medicine. Cambridge: Cambridge kidney disease: the Italian Study Group on Kidney and University Press, 2008. In: Creasy R, and pregnancy: obstetric outcome and long‐term renal Resnik R, Iams J (eds) Maternal–Fetal Medicine: prognosis. Epidemiology patients with primary and secondary glomerular of pregnancy‐related hypertension. An overview of pregnancy in women with Chesley’s Hypertensive Disorders in Pregnancy, 4th edn. Pregnancy of prediction equations for estimating glomerular in women with impaired renal function. J Am Soc converting enzyme inhibitors and the risk of congenital Nephrol 2015;26:2011–2022. A multicentre women with renal disease and moderate renal cohort study of histological findings and long‐term insufficiency. Pregnancy in chronic renal insufficiency: prolactin, sex hormones and thyroid function with single centre experience from North India. Intensive pregnancy outcomes in patients with lupus: a cohort hemodialysis associates with improved pregnancy study. Pregnancy in women on dialysis: is success systemic lupus erythematosus and lupus nephritis. Pregnancy in recommendations of pregnancies in lupus nephritis in dialysis patients: is the evidence strong enough to lead the 21st century. Transplantation of low blood urea nitrogen levels in pregnant patients 2006;82:1698–1702. The importance of increased dialysis and national transplantation pregnancy registry and anemia management for infant survival in pregnant experience. Therefore, patients should be managed is no need to repeat, but if abnormal a count should be within a multidisciplinary team including midwives, repeated at 3–5 days of age, when the neonatal spleen haematologists, anaesthetists and obstetricians. Unless contraindicated, 152 Maternal Medicine women should continue penicillin V for infection proph variety of genetic abnormalities exist. Blood tests and monitoring for asympto and those with thalassaemia major are transfusion matic urinary infections, pregnancy‐induced hyperten dependent and the main cause of morbidity and mortal sion and pre‐eclampsia should be carried out monthly, ity is organ dysfunction caused by iron loading. Blood transfusions are not required dia syndromes can be treated as ‘normal’ pregnancies, routinely but regular transfusion programmes may be except that pre‐conception counselling about a couple’s helpful in women with poor medical or obstetric histo risk of having a baby with a haemoglobinopathy should ries in order to suppress HbS production. Examples occur and women should have ferritin checked before include women previously on hydroxycarbamide, those starting on iron. Exchange transfusion severe intermedia syndromes are high risk and should be may be preferred in these cases, depending on Hb. Pre‐conception chest crisis, pre‐eclampsia or other emergencies may counselling should be offered, covering the risk of sub benefit from exchange Hb to allow more aggressive fertility due to hypogonadotrophic hypogonadism, fetal reduction in HbS levels. All patients should have an haemoglobinopathy and the risks pregnancy poses to life extended red cell phenotype; many will have red cell if patients have cardiac or hepatic dysfunction.
Modification of dialysis regimens for Immunosuppression in pregnancy: choices for pregnancy cheap 30 mg remeron free shipping. Diagnostic Long‐term functional recovery trusted remeron 15mg, quality of life cheap remeron 30 mg visa, and and predictive biomarkers for pre‐eclampsia in patients pregnancy after solid organ transplantation. Med Clin with established hypertension and chronic kidney North Am 2016;100:613–629. Breastfeeding and tacrolimus: serial Pregnancy outcomes in kidney transplant recipients: a monitoring in breast‐fed and bottle‐fed infants. There is usually an increase in circulat certain haematological complications, with thromboem ing immature neutrophils (left shift) and evidence of bolism and haemorrhage being leading causes of direct toxic granulation. This chapter covers the normal physi delivery but usually return to normal by 4 weeks post ological changes, haematological complications of preg partum. Lymphocyte counts are often reduced, particu nancy and common haematological diseases which may larly in the first and second trimesters, and monocyte impact on or be influenced by pregnancy. A reduction in platelet count, mainly secondary to hyperdestruction and shortened lifespan, is common Physiological changes to the blood and around 10% of pregnancies have a platelet count 9 in pregnancy below 150 × 10 /L in the third trimester. It is usually 9 mild, with 80% of counts remaining above 115×10 /L, To accommodate the developing uteroplacental circula and does not seem to have an adverse effect on platelet tion, plasma volume increases by approximately 1250 mL function, possibly due to increased fibrinogen levels in (45%) and red cell mass by approximately 250mL pregnancy. The natural anticoagulant protein Consequently, red cell count and haematocrit are lower S decreases with no change in protein C levels. There may also be a Non‐pregnant 20 30 40 link between iron deficiency, low birthweight and pre term delivery but this is, as yet, unproven. Plasma volume (mL) 2600 3150 3750 3850 the fetus is relatively spared, as preferential delivery of Red cell mass (mL) 1400 1450 1550 1650 iron is facilitated by upregulation of placental transfer Total blood volume (mL) 4000 4600 5300 5500 rin. However, infants born to iron‐deficient mothers Haematocrit 35 32 30 30 are more likely to develop iron deficiency in the first 3 months of life. Diagnosis Anaemia in pregnancy Initially, as iron stores are depleted, serum ferritin levels fall. A low serum ferritin is diagnostic of iron deficiency Anaemia is defined as a haemoglobin (Hb) two standard but as it is an acute‐phase reactant, it can be elevated in deviations below the mean for a healthy age‐matched active inflammation or infection despite iron deficiency. However, consensus on what is normal in Levels of transferrin, the iron transporter protein, pregnancy is lacking. The British Society of Haematology increase as it attempts to deliver more iron to tissues. Western diets typically provide 15 mg/day, nopathy, who should have a serum ferritin before of which 10% is absorbed. During pregnancy, absorption starting iron, to confirm the diagnosis and exclude increases to around 30% by 30 weeks but this is often an iron loading state. Furthermore, many women – Anaemic women whose haemoglobinopathy status start pregnancy already iron depleted, due to poor diet, is unknown should commence a trial of iron therapy increased need, menstruation and previous pregnancies and simultaneous haemoglobinopathy screening. Iron deficiency anaemia is a significant prob ● In those women at high risk of iron deficiency but who lem worldwide, affecting 50% of pregnant women (56% are not yet anaemic, ferritin levels should be checked in developing and 18% in developed countries). The early stages of iron deficiency are often asympto matic or show non‐specific symptoms. As the anae the principles of treating iron deficiency are as follows: mia develops tiredness is common but patients also 1) establish cause; complain of headaches, palpitations, dizziness and 2) correct deficiency; shortness of breath. Specific signs, such as angular cheilitis, glossitis and koilonychia, the recommended daily iron intake for pregnant women can occur in severe cases. Cellular iron‐rich foods and factors that aid or inhibit absorption immunity and phagocytosis is impaired, rendering (Table 12. Intravenous iron preparations have no licence for use in the first trimester due to concerns that oxidative free Factors increasing iron absorption radicals could cause toxicity to placental membranes. The risk of anaphylaxis is exceedingly rare but other non‐allergic Factors reducing iron absorption Tannins in tea and coffee reactions occur in around 1 in 200 000. Foods rich in calcium the older intravenous preparations do not raise Hb Antacids levels quicker than correctly taken oral iron. However, newer preparations such as iron carboxymaltose, which is given as a single dose over 15min, produces a faster Table 12. Iron preparation size (mg) per tablet (mg) Intramuscular iron is rarely used as it is painful, has variable absorption and can cause permanent skin stain Ferrous sulfate 200 65 ing if not given correctly. Ferrous fumarate 200 65 With optimum care most women will no longer be Ferrous gluconate 300 35 anaemic at the point of delivery. However, women whose Hb is less than 100 g/L should deliver in hospital (<95 g/L in an obstetrician‐led unit), have intravenous access, a Iron deficiency in pregnancy cannot be corrected group and save available, and active management of the through diet alone so iron supplementation is necessary. For most women oral replacement is the best Megaloblastic anaemia option because it is effective, safe and inexpensive and can be started in primary care. Hb should rise by around 20g/L prevalence is less than 5% as many women take folate every 3–4 weeks and treatment should continue for at supplements to prevent neural tube defects. However, least 3 months after Hb has normalized and until at least women with haemolytic disorders, malabsorption 6 weeks post partum. Non‐anaemic women with low syndromes, myeloproliferative disorders and those on serum ferritin (<30µg/L) should be started on 65mg anticonvulsants are at high risk and should receive of elemental iron daily with a repeat Hb and ferritin in folate supplements. Around 10–20% of unaffected by recent folate intake but sensitivity and patients experience gastrointestinal side effects, which specificity during pregnancy are poor. Intravenous iron is reserved for patients who fail Vitamin B12 deficiency in pregnancy is extremely rare to respond to oral iron or who are truly intolerant. Its pathogenesis is unclear but likely reflects platelet consumption within the placental circulation, haemodi lution and hormonal inhibition of megakaryocytopoie Summary box 12. It usually causes a mild thrombocytopenia in the third trimester with no symptoms of bruising or bleeding ● Iron deficiency in pregnancy is common. It is therefore a ● Oral iron is best for the majority of women and should diagnosis of exclusion and may cause diagnostic diffi be taken on an empty stomach, to optimise absorption. It is extremely unu sual for gestational thrombocytopenia to produce plate 9 let counts below 70×10 /L so levels below this should Thrombocytopenia in pregnancy prompt consideration of alternative diagnoses. However, causes may be life‐threatening and via Fc receptors in the reticuloendothelial system (mainly thrombocytopenia has implications for mode of delivery spleen). It is often chronic and presents a particular prob and the bleeding risk of mother and neonate. Although rare, it is precipitated by pregnancy in thrombocytopenic purpura in pregnancy. Operative/instrumental delivery: >50 × 10 /L 9 Prompt plasma exchange can be life‐saving. For those that need treatment, the first line is usually oral corticos tions in which the sickle β gene is inherited with another teroids, starting with prednisolone 20mg daily and abnormal haemoglobin. Cells are inflexible in small blood vessels, con given immediately and platelet transfusion if birth is tributing to vaso‐occlusion and have a shorter lifespan, imminent or haemorrhage occurs. To minimize this or aplastic and many patients develop chronic organ risk, fetal scalp monitoring and blood sampling, ventouse damage.
For severe cases of radiation exposure to 5 to 10 Gy order remeron on line, early antiviral order remeron visa, antifungal remeron 30 mg discount, and antibiotics are started for anticipated significant immune suppression fluoroquinolones with or without amoxicillin/penicillin for streptococcal coverage, which is the preferred prophylactic regimen in these patients. Prophylactic antibacterials are continued until treatment failure or development of neutropenic fever or when the absolute neutrophil count 3 is greater than 500/mm. In such cases, fluoroquinolones are discontinued, and antibacterials with antipseudomonal coverage are introduced. The Infectious Diseases Society of America guidelines for neutropenic fever management are recommended for febrile neutropenic patients [13,30]. Transfusion requirements do not rise until 2 to 4 weeks after exposure unless the patient needs replacement of blood products for concurrent trauma. The purpose of blood transfusions for such patients is to provide erythrocytes for the improvement of oxygen-carrying capacity, blood volume to improve hemodynamic parameters, and platelets to help prevent bleeding. All cellular products in the blood to be transfused should be leukoreduced and irradiated to 25 Gy to prevent transfusion-related graft-versus-host reaction among immunocompromised patients . Allogeneic stem cell transplantation is indicated for individuals who have a radiation exposure dose of 7 to 10 Gy . The injuries from these blasts arise from the high pressures and wind, flash from the nuclear detonation, thermal pulses, and secondary fires. The management of combined radiation injuries and trauma presents special challenges to the physician. They are also very susceptible to operative and postoperative infections as a result of decreased neutrophil and lymphocyte counts and require 2 to 3 months for their bone marrow to recover from the acute radiation exposure. If surgery is not performed in this “window of opportunity” following acute radiation exposure, it may have to be postponed for up to 2 months until full hematopoietic recovery happens [13,30]. The symptoms and signs of acute radiation dermatitis typically appear several days after an acute radiation exposure. Although acute radiation dermatitis is essentially a radiation burn, it is different from the thermal burns that may occur immediately after exposure of the skin to a nuclear explosion. The Centers for Disease Control and Prevention has classified cutaneous radiation injury into three grades based on the extent of exposure to radiation. Exposure of the skin to radiation doses greater than 2 Gy causes epilation and typically occurs 14 to 21 days postexposure. On exposure to 6 Gy, erythema develops secondary to arteriolar constriction with capillary dilation and local edema. At 10 to 15 Gy radiation, dry desquamation occurs because of the involvement of the germinal layer of the epidermis. Wet desquamation occurs when the skin is exposed to 10 to 25 Gy of radiation to the development of intracellular edema progressing to macroscopic bullae. The two main approaches for managing acute radiation skin injury are operative and nonoperative treatment. Operative treatments include superficial debridement to prevent septic foci and skin grafting when this is required. Topical antibiotics with dressings are used for blistering phase, and silver sulfadiazine cream with nonadherent dressings is preferred for wet desquamation. Radiation-induced skin ulcers, nonhealing wounds, and skin ulcers with intractable pain need surgical interventions. Contamination enters via a variety of portals, such as the nose, the mouth, and a wound, or with a large enough dose, by the penetration of gamma rays or neutrons directly through intact skin. Internal organs commonly affected by internal radiation contamination are the thyroid, the lung, the liver, adipose tissue, and bone. Leukemia and various types of cancers can develop in these organs many years after an acute radiation exposure with internal contamination. Assessment of Potential Internal Radiation Contamination the patient history is crucial to determining whether they may have experienced internal contamination. Any history that suggests that a patient may have inhaled, ingested, or internalized radioactive material through open wounds should prompt further evaluation for internal contamination. This assessment should attempt to identify both the radiation dose received and, if possible, the specific isotopes that caused the internal contamination. An initial survey of the patient should be performed with a radiac meter, especially around the mouth, nose, and wounds, to give some idea of the extent of any possible internal exposure. The diction of radioactive isotopes on nasal swabs can be very helpful to determine whether a patient has been exposed internally. If it is suspected that a person has inhaled a significant amount of radioactive material, bronchoalveolar lavage can be considered for identifying inhaled radioactive isotopes as well as for removing residual contaminated materials from the lungs. Bronchoalveolar lavage has been shown to be effective for removing inhaled material contaminated with radioactive isotopes from the lungs of animals. The collection and analysis of stool and urine samples can be very helpful for determining both the type and the amount of internal radiation that an individual might have received. Chest and whole body radiation counts can also be helpful for determining the extent of internal radiation contamination. Unfortunately, however, most medical institutions do not have the capability to do either chest or whole body radiation counts. The analysis of nasal swabs, stool samples, and urine samples is the most practical method for determining the type and extent of internal radiation contamination that is used by hospital-based physicians . Treatment of Internal Radiation Contamination Patients who have experienced internal radiation contamination should be promptly treated to reduce the absorbed radiation dose and prevent the development of future health problems. The goals of treatment are to reduce absorption and enhance elimination of the internal radionuclide contaminant. There are three main categories of agents that are used to treat internal radiation contamination: purgative agents, blocking agents, and chelation agents. Gastric lavage can be used to empty the stomach completely after the potential ingestion of radionuclides. When promptly performed, it can decrease the concentration of radionuclides in the gastrointestinal tract. In deciding whether to treat a patient for internal radiation contamination, the physician should treat potentially exposed individuals empirically based on the information that is available [1,13,26,30]. The most common purgatives are laxatives and enemas, which are helpful for reducing the residence time of radionuclides in the colon. Prussian blue (ferric ferrocyanide) is an ion exchange resin that binds cesium-137 in the gastrointestinal tract and facilitates its secretion. Patients who have experienced internal cesium-137 should be treated with oral Prussian blue (3 g, three times daily) for at least 3 weeks. A single, 100 mL oral dose of aluminum phosphate gel will reduce the gastrointestinal absorption of strontium-90 by 85%. Oral aluminum phosphate should be used if internal contamination with strontium-90 is expected [1,13,26-30]. Blocking Agents Blocking agents block both the uptake and bioavailability of internal radionuclide contaminants.
Cardiac arrest Epinephrine may be used to restore cardiac rhythm in patients with cardiac arrest order discount remeron on line. Local anesthesia Local anesthetic solutions may contain low concentrations (for example buy generic remeron from india, 1:100 cheap 30mg remeron visa,000 parts) of epinephrine. Epinephrine greatly increases the duration of local anesthesia by producing vasoconstriction at the site of injection. Epinephrine also reduces systemic absorption of the local anesthetic and promotes local hemostasis. Intraocular surgery Epinephrine is used in the induction and maintenance of mydriasis during intraocular surgery. Pharmacokinetics Epinephrine has a rapid onset but a brief duration of action (due to rapid degradation). The preferred route for anaphylaxis in the outpatient setting is intramuscular (anterior thigh) due to rapid absorption. It may also be given subcutaneously, by endotracheal tube, or by inhalation (ure 6. It can trigger cardiac arrhythmias, particularly if the patient is receiving digoxin. Epinephrine can also induce pulmonary edema due to increased afterload caused by vasoconstrictive properties of the drug. Patients with hyperthyroidism may have an increased production of adrenergic receptors in the vasculature, leading to an enhanced response to epinephrine, and the dose must be reduced in these individuals. Inhalation anesthetics also sensitize the heart to the effects of epinephrine, which may lead to tachycardia. Nonselective β-blockers prevent vasodilatory effects of epinephrine on β receptors, leaving α receptor stimulation unopposed. However, when administered in therapeutic doses, the α- adrenergic receptor is most affected. Vasoconstriction Norepinephrine causes a rise in peripheral resistance due to intense vasoconstriction of most vascular beds, including the kidney (α effect). The weak β activity of2 2 norepinephrine also explains why it is not useful in the treatment of bronchospasm or anaphylaxis. Baroreceptor reflex Norepinephrine increases blood pressure, and this stimulates the baroreceptors, inducing a rise in vagal activity. The increased vagal activity produces a reflex bradycardia, which is sufficient to counteract the local actions of norepinephrine on the heart, although the reflex compensation does not affect the positive inotropic effects of the drug (ure 6. When atropine, which blocks the transmission of vagal effects, is given before norepinephrine, stimulation of the heart by norepinephrine is evident as tachycardia. Therapeutic uses Norepinephrine is used to treat shock (for example, septic shock), because it increases vascular resistance and, therefore, increases blood pressure. In addition, norepinephrine is a potent vasoconstrictor and may cause blanching and sloughing of skin along an injected vein. If extravasation (leakage of drug from the vessel into tissues surrounding the injection site) occurs, it can cause tissue necrosis. Impaired circulation from norepinephrine may be treated with the α receptor antagonist phentolamine. Alternatives to phentolamine include intradermal terbutaline and topical nitroglycerin. Its nonselectivity is a disadvantage and the reason why it is rarely used therapeutically. Isoproterenol produces intense stimulation of the heart (β effect), increasing1 heart rate, contractility, and cardiac output (ure 6. Isoproterenol also dilates the arterioles of skeletal muscle (β effect), resulting in decreased peripheral resistance. Because of its2 cardiac stimulatory action, it may increase systolic blood pressure slightly, but it greatly reduces mean arterial and diastolic blood pressures (ure 6. The adverse effects2 of isoproterenol are similar to the β receptor–related side effects of epinephrine. For example, at higher doses, it causes vasoconstriction by activating α receptors,1 whereas at lower doses, it stimulates β cardiac receptors. In addition, D and D dopaminergic receptors, distinct1 1 2 from the α- and β-adrenergic receptors, occur in the peripheral mesenteric and renal vascular beds, where binding of dopamine produces vasodilation. D receptors are also found on presynaptic adrenergic neurons, where their2 activation interferes with norepinephrine release. Cardiovascular Dopamine exerts a stimulatory effect on the β receptors of the heart, having both positive inotropic and1 chronotropic effects (ure 6. At very high doses, dopamine activates α receptors on the vasculature, resulting1 in vasoconstriction. Renal and visceral Dopamine dilates renal and splanchnic arterioles by activating dopaminergic receptors, thereby increasing blood flow to the kidneys and other viscera (ure 6. These receptors are not affected by α- or β-blocking drugs, and in the past, low-dose (“renal-dose”) dopamine was often used in the prevention or treatment of acute renal failure. However, more recent data suggest there is limited clinical utility in the renal protective effects of dopamine. Therapeutic uses Dopamine can be used for cardiogenic and septic shock and is given by continuous infusion. It raises blood pressure by stimulating the β receptors on the heart to increase cardiac output, and α receptors on blood vessels to increase1 1 total peripheral resistance. Increased blood flow to the kidney enhances the glomerular filtration rate and causes diuresis. By contrast, norepinephrine can diminish blood supply to the kidney and may reduce renal function. Dopamine is also used to treat hypotension, severe heart failure, and bradycardia unresponsive to other treatments. Adverse effects An overdose of dopamine produces the same effects as sympathetic stimulation. It is used as a rapid-acting1 vasodilator to treat severe hypertension in hospitalized patients, acting on coronary arteries, kidney arterioles, and mesenteric arteries. Headache, flushing, dizziness, nausea, vomiting, and tachycardia (due to vasodilation) may occur with this agent. The drug increases cardiac output and does not elevate oxygen demands of the myocardium as much as other sympathomimetic drugs. Oxymetazoline directly stimulates α receptors on blood vessels supplying the nasal mucosa and conjunctiva, thereby producing vasoconstriction and decreasing congestion. It is absorbed in the systemic circulation regardless of the route of administration and may produce nervousness, headaches, and trouble sleeping. Use for greater than 3 days is not recommended, as rebound congestion and dependence may occur. It has no effect on the heart itself but, rather, induces reflex bradycardia when given parenterally, making it useful in the treatment of paroxysmal supraventricular tachycardia. The drug is used to treat hypotension in hospitalized or surgical patients (especially those with a rapid heart rate). Phenylephrine acts as a nasal decongestant when applied topically or taken orally.
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