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In their research in India, Vijayan et al. Their study encompassed children between the ages of 10 to AN was diagnosed in A significantly high prevalence of insulin resistance was observed among the children with a waist circumference exceeding the 75th percentile, a BMI above the 85th percentile, or a diagnosis of AN. Vijayan et al. AN is not a disease, but a symptom of disease. A high prevalence has been observed recently, and there are a number of varieties. These include benign, obesity associated, syndromic, malignant, acral, unilateral, medication-induced, and mixed AN.

Different types of AN are listed in Table 1.

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It often appears gradually in the prediabetic state, but abruptly in malignancy. AN may be triggered by a plethora of medications, such as birth control pills, human growth hormones, thyroid medications, and even some bodybuilding supplements. All these medications may cause changes in insulin levels. Medications used to ease the side effects of chemotherapy have also been linked to AN. In most cases, the condition clears up when the medications are discontinued. When AN is present without any identifiable cause in middle-aged and older patients with extensive skin findings, internal malignancy needs to be ruled out.

AN has been reported in association with many kinds of cancer, by far the most common being an adenocarcinoma of gastrointestinal origin.

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In these patients it is a rapid-growing dermatological pigmentation disorder. The skin changes are typically more extensive and severe than those seen in benign AN. Pigmentary changes may be more pronounced than those observed in benign AN and they are not restricted to areas of hyperkeratosis.

Malignant AN is frequently associated with the mucous membranes and with distinctive abnormalities of the oral mouth region. Malignant AN is also commonly characterised by wart-like thickening around the eyes, unusual ridging or brittleness of the nails, thickening of the skin on the palms of the hands, hair loss, and sometimes other symptoms.

Investigators have reported that the development of malignant AN may occur as much as five years before the onset of other symptoms, although the time span before malignancy is typically of shorter duration. It is worth noting that certain types of AN may be genetically linked. It is a heterogenous disorder and there is a general consensus that diabetic comorbidities may be the outcome of genetic and environmental susceptibilities. It would be interesting to explore the possibility of a link between the diabetic genes and the AN gene.

DM type 2 may be potentiated by poor quality of insulin or decreased production of insulin, and the distinction between those manifestations is not well recognised. The controversy concerning the relative roles of insulin deficiency and insulin resistance in DM type 2 continues to be unresolved. The spiralling effect of hyperglycaemia adds to the malfunctioning of beta cells, and that results in impaired quantity and quality of insulin. Only a subset of diabetic patients shows AN, and other groups of obese diabetic patients do not develop AN.

AN is linked with higher insulin production and obesity, whereas AN may not be present in diabetes with a reduced quantity of insulin. The presence of AN may serve as one of the biological markers to determine subtypes of DM type 2. The incidence of AN varies in different races, which is evidence that AN may have a genetic contribution — indeed, it has been regarded by some as being strongly influenced by genetic factors.

It is thought to be autosomal in nature. DM type 2 is relatively common among people who have mental health issues. Increased risk for cardiovascular disease and other serious illnesses related to insulin resistance — for example, certain epithelial cell carcinomas, AN, and polycystic ovary syndrome — are long-term concerns associated with the cluster of metabolic abnormalities stemming from insulin resistance. These are often referred to as the metabolic syndrome.

The mechanisms underlying the relationship between schizophrenia and diabetes remain unexplained. The present author has argued in favour of the autoimmune hypothesis of a subset of schizophrenia. In other words, there may be a continuum of pathological process between AN and DM type 2.

It follows that schizophrenia sufferers may have a predisposition to develop DM type 2; schizophrenia may even be considered as a clinical surrogate of DM type 2. When AN occurs in a schizophrenic patient, they sometimes develop a delusional misinterpretation of the condition, such as that it is a result of skin cancer or even a manifestation of an external agency. Such situations may result in severe anxiety. Schizophrenia is frequently associated with poor lifestyle choices on the part of the patient, such as a diet high in fat, reduced levels of physical activity, and high rates of smoking-all of these may contribute to the development of a metabolic syndrome and insulin resistance.

It is now well recognised that patients treated with clozapine or olanzapine are more often classified as having DM type 2 or impaired glucose tolerance in comparison with patients treated with other second-generation antipsychotics. Clozapine increases the risk of diabetes if there is a history of pre-existing diabetes or a family history of diabetes. According to a US study, the risk is higher if the patient is African-American or of Hispanic origin.

Such patients may need close blood sugar monitoring during the initiation of clozapine treatment. I contend that if a patient already has AN, weight-increasing antipsychotics should be avoided. Even though aripiprazole is the most metabolic-sparing agent among the second-generation antipsychotics, Manu et al. That patient did have a family history of DM type 2, which adds to the interest of the case. There is no specific treatment for AN. Treatment is directed towards the specific symptoms that are apparent in each individual.

It should be borne in mind that such treatment may require the coordinated efforts of a team of medical professionals. Correcting the underlying disease improves the skin symptoms. Steps that may be taken, depending on what the disease is, include correcting hyperinsulinemia through diet and medication, encouraging the loss of weight in those with obesity-associated AN, removing or treating a tumour, and discontinuing a medication that causes AN.

The control of obesity contributes significantly to reversing the whole process, essentially by reducing both insulin resistance and compensatory hyperinsulinemia. However, the pigmentary changes may persist. In drug-induced AN, offending medicines should be stopped. For those with AN, the recommended treatment may include the use of certain synthetic, vitamin A-like compounds retinoids. For individuals with malignant AN, disease management requires treatment by oncologists.

Reports indicate that AN has improved with therapy used to treat underlying malignancies and has reappeared with tumour recurrences. Other treatment for this disorder is symptomatic and supportive. The treatments considered are used primarily to improve appearance, and include topical retinoids, dermabrasion, and laser therapy. The final outcome of AN varies depending on the cause of the condition. The prognosis for patients with malignant AN is often poor as the associated cancer is often advanced. AN may be diagnosed on the basis of thorough clinical evaluation, identification of characteristic physical findings, a complete patient history including medication history, a thorough family history, and various specialised tests.

For example, benign forms of AN often become evident during childhood or puberty. It is less common for benign AN to be apparent at birth or to develop in adulthood. The latter cases most typically involve AN in association with obesity. In individuals with skin changes that suggest AN, diagnostic assessment may include various laboratory tests. Examples are the glucose tolerance test and the glycated haemoglobin HbA1c test.

Additional laboratory studies or other specialised tests may also be utilised in diagnosis in order to help detect or rule out certain other underlying disorders — including a number of endocrine and autoimmune conditions — that may be associated with AN. In addition, in some instances, particularly where the patient presents with signs suggestive of malignant AN, testing may include biopsy and microscopic evaluation of small samples of skin tissue affected.

The onset of malignant AN usually occurs after the patient reaches 40 years of age. Various factors may be indicative of malignant AN in association with an underlying cancer. These include symptom onset in adulthood that is not associated with the use of particular medications, obesity, a positive family history, and certain underlying disorders known to be associated with AN. It is rare for malignant AN to develop during childhood.

In such instances, warning signs may include skin changes that progress rapidly and also involvement of the mucous membranes. AN may be metaphorically linked to the dark pigmentation that appears on the skin of the ripe Sharon fruit. Sharon fruit is the trade name for a variety of persimmon that is grown in Israel.

In the fruit the dark patches on the ripe and sugary fruits are the result of condensed tannins. Insulin-resistant AN may be referred to as the Sharon fruit sign in order to emphasise the diagnostic value of the condition. It has been suggested that the official terminology for AN is inappropriate for a significant warning of an increasingly common disease for which early diagnosis is imperative. Because the complex name may have a negative impact on its identification by both clinicians and patients, a less formal term is in use among some of those who are concerned with patient care. It must be borne in mind that AN, otherwise Sharon fruit sign, manifests only in those with the insulin-resistant condition and should not be considered a characteristic feature of DM Type 2.

Identification of the Sharon fruit sign may be helpful in the early diagnosis of DM type 2. Diabetes puts an enormous burden on patients, their families, and the health-care system. Detection of the disease at an early state using physical markers and instituting preventive measures will reduce the economic strain on society to a great extent. According to the latest global data from the World Health Organization , an estimated million adults are living with DM type 2 and diabetes prevalence is increasing rapidly.

Most often a diagnosis of DM type 2 is made only when such symptoms as loss of weight, polydipsia, and polyurea have become manifest. By that time the damage to the body may have already come about. Complications arising from diabetes cover the entire area of medical science, so early detection is crucial.

Intervention at the prediabetic stage helps to arrest the progress of this condition. AN may herald DM type 2, endocrinopathies, and malignancies. This cutaneous disorder is easily detectable and highly useful in the early detection of the disorders associated with it. Early screening for AN in preadolescent and adolescent people would provide a relatively simple, inexpensive, and non-invasive tool for identifying those young people who have hyperinsulinemia and could benefit from early intervention.

That would prevent the development of DM type 2. Young people tend to be reluctant to undergo traditional screening measures and definitive diagnostic tests as they find them invasive and unpleasant. A sedentary life style and unhealthy dietary habits — as well as the side effects of antipsychotics — make chronically ill psychotic patients more vulnerable to DM type 2 than the general population. Long-standing detained patients in particular are restricted in their mobility and may become more prone to obesity and insulin resistance.

It is not clear whether the pathogenesis of psychosis itself has a diabetogenic effect. It is evident that because of the high incidence of DM type 2 among mental health service users, psychiatrists need to become more alert in the diagnosis, management, and prevention of the complications of DM type 2. Despite being the most common mental disorder in older adults, depression is under- recognised.

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It poses diagnostic difficulties in this population for several reasons; for example, symptomatic and phenomenological differences, age-related biological and psychological factors, and the presence of physical comorbidities. Depression in older adults is an important clinical topic because outcomes are worse in comparison to younger adults.

It is also associated with higher rates of morbidity and mortality, increased healthcare utilisation and economic costs. It is likely to become a more pressing issue in the future due to the projected increase in the older adult population. This article explores the topic of depression in older adults. Depression is a clinical syndrome. The International Classification of Diseases ICD diagnostic classification systems describe three core symptoms of depression; low mood, anhedonia and reduced energy levels 1.

Other symptoms include impaired concentration, loss of confidence, suicidal ideation, disturbances in sleep and changes in appetite. Symptoms must have been present for at least a period of two weeks for a diagnosis of depression to be made. Major depression refers to the presence of all three core symptoms and, in accordance with ICD criteria, at least the presence of a further five other symptoms 1. See Table 1 for severity criteria of a depressive episode according to ICD criteria.

Table 1: Severity criteria of a depressive episode according to ICD 1. Depressive symptoms, which can be clinically significant, can be present in the absence of a major depressive episode. Depressive symptoms are those that do not fulfil diagnostic criteria for a diagnosis of depression to be made. Depressive symptoms can be collectively referred to as sub-threshold depression, sub-syndromal depression or minor depression 2.

It has been proposed that there are two types of depression; early-onset and late-onset depression. Late-onset depression refers to a new diagnosis in individuals aged 65 years of age or older. Over half of all cases of depression in older adults are newly arising i. Late-onset type depression is associated more with structural brain changes, vascular risk factors and cognitive deficits.

It has been suggested that late-onset depression could be prodromal to dementia 3. This increase in population will consequently see the incidence and prevalence of depression rise. By it is estimated that depression will be the second leading cause of disability in the world regardless of age 5. Recognising, and so diagnosing, depression in older adults will become more important because of a greater demand on existing healthcare services and provisions, due to physical health consequences, impact upon healthcare utilisation and greater economic healthcare costs.

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The presentation of depression in older adults is markedly different to that in younger adults. The most significant and fundamental difference in presentation in older adults is that depression can be present with the absence of an affect component, i. It is common instead for older adults to report a lack of feeling or emotion when depressed Anhedonia is also less prevalent in this population.

However, reduced energy levels and fatigue are frequently reported Compared to younger adults, psychological symptoms of depression occur more frequently and are more prevalent in older adults Such psychological symptoms include feelings of guilt, poor motivation, low interest levels, anxiety related symptoms and suicidal ideation. The presence of irritability and agitation are key features as well 7. Hallucinations and delusions are also more common in older adults, particularly nihilistic delusions i.

Such deficits mainly concern executive function Pseudodementia is a phenomenon seen in older adults The term refers to cognitive impairment secondary to a psychiatric condition, most commonly depression Pseudodementia has become synonymous with depression. Pseudodementia can be mistaken for an organic dementia and so older adults who are depressed can present primarily to mental health services with memory problems.

It is associated with psychomotor retardation, which can be a core feature of depression in this population 7,14, Psychomotor retardation describes a slowing of movement and mental activity Like pure cognitive deficits, psychomotor retardation contributes significantly to functional impairment Both executive dysfunction and psychomotor retardation have been found to be related to underlying structural changes in the frontal lobes 14, Psychomotor retardation is further related to white matter changes in the motor system, which leads to impaired motor planning There is conflicting evidence of whether the presence of psychomotor retardation is related to depression severity Somatisation and hypochondriasis are associated with depression in older adults and increasing age in general Somatisation is often overlooked in older adults by healthcare professional who actively search to attribute such symptoms to a physical cause.

Somatisation is more common in those who have physical comorbidities. Somatisation in older adults is associated with structural brain changes and cognitive deficits Depression in older adults is associated with functional impairment cognitively, physically and socially 7,12, Such functional impairment is linked to loss of independent function and increased rates of disability Withdrawal from normal social and leisure activities can be marked 7, Social avoidance reduces interaction with others and is often a maintaining factor for depression Self-neglect is a classical feature of depression 7 , with the presence of depressive symptoms in older adults being predictive of it Behavioural disturbances can be a common mode of presentation, especially for older adults living in institutionalised care Behavioural disturbances include incontinence, food refusal, screaming, falling and violence towards others 7.

Depression in older adults has been a condition that has constantly been under-recognised. Several issues account for this. Firstly, phenomenological differences are present. Many have argued that phenomenological issues contribute heavily to diagnostic difficulties 28 ; both the DSM and ICD classification systems do not have specific diagnostic criteria for depression in older adults. Potentially invalid diagnostic criteria for depression in older adults could result in fundamental difficulties in understanding, with consequent impact on both clinical practice and research.

Diagnostic difficulties are also encountered because depression in older adults can present with vague symptoms, which do not correspond to the classical triad of low mood, low energy levels and anhedonia, which can all be cardinal symptoms in a younger population. Reports of fatigue, poor sleep and reduced appetite can be attributed to a host of causes other than depression and therefore it is no surprise that a diagnosis of depression is overlooked and goes undetected by healthcare professionals The absence of an affective component i.

Furthermore, symptoms of depression, especially somatic ones, are often attributed to physical illnesses. Depressive somatic symptoms — e. Further complicating diagnostic difficulties and under-recognition is the fact that older adults are less likely to report any symptoms associated with mental health problems and ask for help in the first place 7,10,32 ; explanations for this include older adults being less emotionally open, having a sense of being a burden or nuisance, and believing symptoms are a normal part of ageing or secondary to physical illness 7,10,29, Older adults also have a reluctance to report mental health problems due to their perception of associated stigma; many older adults hold the view the mental health problems are shameful, represents personal failure and leads to a loss of autonomy 7.

There is an overlap between symptoms of depression and symptoms of dementia. It is quite common for older adults with dementia to initially present with depressive symptoms. Depression has a high incidence in those with dementia, especially those with vascular dementia. Depression is particularly difficult to diagnose in dementia due to communication difficulties; diagnosis is often based on observed behaviours 8, In those with pre-existing physical health problems, depression is associated with deterioration, impaired recovery and overall worse outcomes For example, the relative risk of increased morbidity related to coronary heart disease is 3.

Mykletun et al. Several causative routes account for poor physical illness outcomes. Older adults with depression are less likely to report worsening health. Depressive symptomatology indirectly affects physical illness through reduced motivation often secondary to feelings of helplessness and hopelessness and engagement with management.

Poor compliance with management advice, notably adherence to medications is observed Feelings of hopelessness, helplessness and negativity will contribute to the failure to seek medical attention in the first place or report worsening health when seen by a healthcare professional.

Depression affects biological pathways directly, which impairs physical recovery. Such biological effects include pro-inflammatory factors, metabolic factors, impact upon the hypothalamic-pituitary axis and autonomic nervous system changes Older adults who are depressed are more likely to have existing physical health conditions and more likely to develop physical health conditions Depression is particularly associated with specific physical illnesses; cardiovascular disease and diabetes mellitus.

A study by Win et al. Higher incidents of cardiovascular disease and diabetes mellitus are seen in people with depression regardless of age. A study by Brown et al. The hypothalamic-pituitary axis dysfunction found in depression leads to increased levels of cortisol, which in turn, increases visceral fat. Increased visceral fat is associated with increased insulin resistance, promoting diabetes mellitus, and increased cardiovascular pathology Depression is a risk factor for the subsequent development of dementia; this is especially so if an older adult has no previous history of depression i.

Older adults are less likely to report depressive symptoms to healthcare professionals explaining the under-utilisation of mental health services for depression 32, Despite older adults under-utilising mental health services they over utilise other healthcare services 26, For example, those presenting with non-specific medical complaints or somatisation have been found to have an increase use of healthcare services.

Non-specific medical complaints and somatisation lead to an unnecessary use of resources, such as unnecessary consultations with healthcare professionals and investigations Increase in service utilisation means an increase in the associated economic cost of depression in older adults Healthcare costs of older adults with a comorbid physical illness and depression are far greater than those without depression — findings in diabetes mellitus are a good example The majority of the increased healthcare costs are associated with the chronic physical disease and not the care and treatment of the depression Poor compliance with physical illness management is associated with missed appointments and a greater number of hospital admissions, which both have financial implications.

Studies have found a significant higher rate and severity of white matter hyperintensities on MRI imaging in older adults with depression compared to those without depression 46,48, White matter hyperintensities represent damage to the nerve cells; such damage is a result of hypo-perfusion of the cells secondary to small blood vessel damage White hyperintensities are associated with vascular risk factors e.

In older adults with depression, white matter hyperintensities are associated with structural changes to corticostriatal circuits and subsequent executive functional deficits. Loss of motivation or interest and cognitive impairment in depression are hallmark features of structural brain changes associated with the frontal lobes, which in turn are associated with a vascular pathology A study by Hickie et al. It is not fully understood why vascular depression responds less well to antidepressants; poor response has been linked directly to vascular factors but has also been associated with deficits in executive function Baldwin et al.

Younger and older adults share a number of fundamental risk factors for depression; such as female gender, personal history and family history 7. Older adults have additional risk factors related to ageing, which are not just physiological in nature. Age related changes occurring in the endocrine, cardiovascular, neurological, inflammatory and immune systems have been directly linked to depression in older adults 3.

The normal ageing process sees changes to sleep architecture and circadian rhythms with resultant changes to sleep patterns Thus sleep disturbances are common in older adults and positively correlated to advancing age 52 ; over a quarter of adults over the age of 80 years report insomnia, and research has well-established that this is a risk factor for depression A meta-analysis by Cole et al. Sensory impairments, whether secondary to the ageing or a disease process, are risk factors 53, Research has found that hearing and vision impairments are linked to depression A sensory impairment can lead to social isolation and withdrawal, which, in turn, are further risk factors for depression.

Physical illness, regardless of age, is a risk factor for depression. Older adults are more likely to have physical illnesses and so in turn are more at risk of depression. See Table 2. Physical illness is associated with sensory impairments, reduced mobility, impairment in activities of daily living and impaired social function, all of which can lead to depression. Physical illnesses associated with chronicity, pain and disability pose the greatest risk for the subsequent development of depression 7,53, Physical illness affecting particular systems of the body, such as the cardiovascular, cerebrovascular and neurological, are more likely to cause depression 3.

Essentially, however, any serious or chronic illness can lead to the development of depression. It should be noted that a large proportion of older adults have physical illness but do not experience depression symptoms, therefore other factors must be at play 5, Treatments of physical illness are directly linked to aetiology in depression, for example, certain medications are known to cause depression; cardiovascular drugs e. Propranolol, thiazide diuretics , anti-Parkinson drugs e. NSAIDs , antibiotics e. Penicillin, Nitrofurantoin , stimulants e. Haloperidol , anti-anxiolytics e.

Phenytoin, Carbamazepine 7, Polypharmacy is present in many older adults further increasing the risk of depression. Pharmacokinetic and pharmacodynamic age related changes also contribute to an increased risk of medication induced depression in older adults. Dementia is common in old age and those with dementia are at higher risk of developing depression compared to those who do not have it Depression is a risk factor for the subsequent onset of dementia.

When compared to younger adults, older adults are at a greater risk of developing depression due to the increased likelihood of experiencing particular psychosocial stressors, in particular adverse life events. Stressors include lack of social support, social isolation, loneliness and financial hardship. Financial hardship and functional impairment often sees older adults downsizing in property. Deteriorating physical health often sees older adults no longer being able to manage living independently at home necessitating a move into institutional living.

Bereavement, especially spousal, and the associated role change that follows this are risk factors for depression 3. The prevalence of depression in older adults in England and Wales was found to be 8. A meta-analysis by Luppa et al. Sub-threshold depression is times more prevalent than major depression in older adults 26, These depressive symptoms are often clinically relevant 26, Incidence and prevalence are greater in women; Older women are more likely to experience recurrent episodes of depression compared to older men The gender gap in incidence and prevalence becomes narrower with increasing age 3.

It should be acknowledged however that women are more likely to present to healthcare services and seek help in comparison to men The prevalence of major depression in older adults varies by setting Highest rates are seen in long-term institutional care and inpatient hospital settings Table 3 summaries prevalence rates of major depression by setting. Depression in older adults is associated with a slower rate of recovery 9 , worse clinical outcomes compared to younger adults 3 and is associated with higher relapse rates Worse prognosis in older adults correlates with advancing age, physical comorbidities and functional impairment The structural brain changes associated with depression in older adults are linked, as discussed, to poorer treatment response.

Morbidity and mortality associated with depression can be described as primary or secondary; primary morbidity and mortality arises directly from the depressive illness; whereas secondary morbidity and mortality arises from physical health problems, which are secondary to depression. Outcomes from sub-threshold depression are on par with those of major depression; however sub-threshold depression which develops into major depression is associated with worse outcomes 2. Proportionally more people over the age of 65 years commit suicide compared to younger people This further supports and suggests the fact the depression is under-detected.

Unlike younger adults, older adults are less likely to report suicidal ideation and can experience suicidal ideation without feeling low in mood 3,7. Older adults have few suicide attempts, compared to younger adults, because their suicide methods are more lethal Hypertensive emergencies involve a series of clinical presentations where uncontrolled blood pressure BP leads to progressive end-organ dysfunction affecting the neurological, cardiovascular, renal, or other organ systems.

In these situations, the BP should be controlled over minutes to hours. Many causes are involved in severe elevation of blood pressure; inadequate treatment of hypertension, renal diseases, head trauma and pre-eclampsia. Intraoperative hypertension is also common and has many causes. It is usually successfully controlled by anaesthetists. However, there is a lack of agreement concerning treatment plans and appropriate therapeutic goals, making common management protocols difficult.

A wide range of pharmacological alternatives are available to control blood pressure and reduce the risk of complications in these patients. This article reviews the perioperative hypertensive crisis and the common strategies used in management. Perioperative hypertension commonly occurs in patients undergoing surgery. Hypertension is the most common risk factor for perioperative cardiovascular emergencies. Many surgical events may induce sympathetic activity, leading to sudden elevations in BP 2.

The long term end-organ effects add to patient morbidity and mortality. Ensuring cardiovascular stability and pre-optimization of BP allows safe manipulation of physiology and pharmacology during anaesthesia 2. Different medications are available for the management of hypertensive emergencies.

The greatest challenge is the acute care setting where the need for proper and sustained control of BP exists. Acute severe elevations in BP have several terms. The international blood pressure control guidelines removed this term and replaced it with hypertensive emergency or crisis 4. Criteria for hypertensive emergencies crises include: dissecting aortic aneurysm, acute left ventricular failure with pulmonary oedema, acute myocardial ischemia, eclampsia, acute renal failure, symptomatic microangiopathic haemolytic anemia and hypertensive encephalopathy 5.

While they suggest 'hypertensive urgency' for patients with severe hypertension without acute end-organ damage 3. The difference between hypertensive emergencies and urgencies depends on the existence of acute organ damage, rather than the absolute level of blood pressure 5. Cessation of antihypertensive medications is one of the main causes.

Other common causes are autonomic hyperactivity, collagen-vascular diseases, drug use stimulants, e. Signs and symptoms of hypertensive crisisinclude severe chest pain, severe headache accompanied by confusion and blurred vision, nausea and vomiting, severe anxiety, shortness of breath, seizures and unresponsiveness.

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Endothelial injury accompanies severe elevations of BP resulting in fibrinoid necrosis of the arterioles with the deposition of platelets and fibrin, and a breakdown of the normal autoregulatory function. Previous history of diastolic hypertension greater than mmHg is a common predictor of perioperative hypertension.

The level of risk depends on the severity of hypertension 9. Sympathetic activation during the induction of anaesthesia increases the BP by 20 to 30 mmHg and the heart rate by 15 to 20 beats per minute in normotensive individuals 8. These responses may be more obvious in patients with untreated hypertension in whom the systolic BP can increase by 90 mmHg and heart rate by 40 beats per minute.

Intraoperative hypertension is associated with acute pain induced sympathetic stimulation besides certain types of surgical procedures like carotid surgery, intrathoracic surgery and abdominal aortic surgery. In the early postanaesthesia period, hypertension often starts within 10 to 20 minutes after surgery and may persist for 4 hours.

Besides pain induced sympathetic stimulation, hypoxia, intravascular volume overload from excessive intraoperative fluid therapy and hypothermia can promote postoperative hypertension. If untreated, patients are at high risk for myocardial ischemia, cerebrovascular accidents and bleeding Hypertension might happen 24 to 48 hours postoperative due to fluid mobilisation from the extravascular space, besides cessation of antihypertensive medication in the early postoperative period During preoperative assessment we have to review associated medical problems such as ischaemic heart disease, cerebrovascular disease and renal failure.

This can assess the risk for anaesthesia and so the hypertensive end-organ damage. Some patients with hypertension are asymptomatic and accidentally discovered during preoperative assessment. Incidental hypertension may suggest long standing hypertensive disease 1.

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Idiopathic hypertension comprises about ninety percent of hypertensive patients 6. The treatment plan of perioperative hypertension differs from treatment of chronic hypertension. Hypertensive patients undergoing elective surgery are at risk for increased perioperative hypertensive attacks.

The most appropriate medication for management of hypertensive emergency should have a rapid onset of action, a short duration of action, be rapidly titratable, allow for dosage adjustment, have a low incidence of toxicity, be well tolerated and have few contraindications 2, A parenteral antihypertensive agent is preferred due to rapid onset of action and ease of titration 5. The goal of therapy is to halt the vascular damage and reverse the pathological process, not to normalise the BP.

Postoperative hypertension is best managed by correction of precipitating factors pain, hypothermia, hypervolemia, hypoxia and hypercarbia Unintentional hypotension and associated organ hypoperfusion happens with aggressive attempts to lower BP since the homeostatic mechanisms depend on higher blood pressure for adequate organ perfusion. While inadequate lowering of BP may result in increased morbidity and mortality.

Since chronic hypertension shifts cerebral and renal perfusion autoregulation to a higher level, the brain and kidneys are prone to hypoperfusion with rapid decrease in blood pressure.

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  4. So control of blood pressure to baseline levels should take 24 to 48 hours 5. In cases of aortic dissection, the systolic BP should be reduced to less than mmHg within twenty minutes. Gentle volume expansion with intravenous saline solution will maintain organ perfusion and prevent sudden drop in BP with using antihypertensive medications 5. Preoperative hypertension is a hypertensive urgency, not an emergency, as it rarely involves end-organ damage with adequate time to reduce the BP Longer acting oral medications such as Labetalol and Clonidine may be more suitable Common antihypertensive medications used in hypertensive crises.

    Sodium Nitroprusside is a combined venous and arterial vasodilator which decreases both afterload and preload. The onset of action is within seconds and duration of action lasts for one to two minutes, so continuous BP measurement is recommended. If the infusion is stopped, the BP rises immediately and returns to the pretreatment level within one to ten minutes. Labetalol, an alpha- and beta-blocking agent has proven to be beneficial to treat patients with hypertensive emergencies. Labetalol is preferred in patients with acute dissection and patients with end-stage renal disease.

    The onset of action is five minutes and lasts for four to six hours. The rapid fall in BP results from a decrease in peripheral vascular resistance and a slight fall in cardiac output A reasonable administration protocol is to give an initial intravenous bolus of Labetalol 0. Once an adequate BP level is achieved, we can start oral therapy with gradual weaning from parenteral agents Fenoldopam, a peripheral dopaminereceptor agonist, induces peripheral vasodilation; administered by intravenous infusion.

    Duration of action from 30 to 60 minutes. Gradual decrease in blood pressure to pretreatment values occurs without rebound once the infusion is stopped because of short elimination half-life. A starting dose of 0. Fenoldopam provides rapid decline in blood pressure with reflex tachycardia so beware in patients at risk of myocardial ischemia Clevidipine, a dihydropyridine calcium channel blocker, produces rapid and precise BP reduction. It has a short half-life of about one to two minutes with potent arterial vasodilation without affecting venous capacitance, myocardial contractility or causing reflex tachycardia Clevidipine is an ideal agent to manage acute severe hypertension moreover safe for patients with hepatic and renal dysfunction 2.

    Subarachnoid haemorrhage, acute intracerebral haemorrhage, hypertensive encephalopathy, and acute ischemic stroke require rapid BP reduction. For acute ischemic stroke, the preferred medications are Labetalol and Nicardipine. Early intensive BP control is recommended to reduce hematoma growth 26, In subarachnoid haemorrhage, Nicardipine, Labetalol and Esmolol are also the preferred agents; while Nitroprusside and Hydralazine should be avoided. Rapid BP reduction is also indicated in cardiovascular emergencies such as aortic dissection, acute heart failure, and acute coronary syndrome.

    Beta-blockers should be avoided if there is aortic valvular regurgitation or suspected cardiac tamponade. Give vasodilators besides diuretics when SBP is mm Hg In cocaine toxicity, tachycardia and hypertension rarely require specific treatment. Phentolamine is proper for cocaine-associated acute coronary syndromes. In pheochromocytoma, beta blockers can be added after alpha blockade for BP control Nitroprusside, Nitroglycerin and Esmolol are used.

    Perioperative beta blockers are best to use in patients undergoing vascular procedures or at risk of cardiac complications Bed bugs belong to the family Cimicidae and there are two species involved in the modern resurgence; the Common bed bug, Cimex lectularius and the Tropical bed bug, Cimex hemipterus. They are wingless insects with an oval-flat shape that allows them to hide in narrow cracks and crevices.

    The adults are dark brown, mm long, becoming to around 10mm when fully blood-engorged. There are five smaller juvenile stages nymphs that are similar in appearance, although lighter in colour. All nymphs require a blood meal to moult to the next stage, and both adults also bloodfeed for nutrition, and egg development in the case of the female. Bed bugs are solely haematophagous ectoparasites. After feeding they return to a harbourage and do not remain on the host. The main hosts are humans, but pets, bats, and birds may act as secondary hosts. In the past, bed bugs were particularly an affliction of the poor.

    However, in the early part of the modern resurgence it was the tourist areas and the hospitality sector that were initially impacted. Most commonly, bed bugs travel in comfort as stowaways in luggage, although they can be transferred via furnishing and other belongings, as well by spreading to adjoining properties. Unfortunately, exact figures on the occurrence of bed bugs are unknown, as there are no mandatory reporting requirements. Additionally, due to the stigma associated with bed bugs, many infestations are simply not reported. During the day, the largely nocturnal bed bugs will crawl deep into crevices of bed frames and mattresses Fig.

    Here they tend to lay their eggs, often several hundred during the female lifetime. Live bed bugs, shed nymphal skins, and dark excrement spots indicate an active infestation. At night they are attracted by carbon dioxide, heat and other host odours to a victim, from which they may take a blood meal every days. The adult bugs can survive long periods of starvation, up to five months at 22 o C or even longer at cooler temperatures.

    When a host is found, they insert their mouthparts into the skin, blood feeding for minutes. When bed bugs are in large numbers, often lines of bites occur on the unfortunate victim and this sign is almost a sure indication of the presence of the insect. The bites tend to occur along the arms and legs, down the back and across the shoulders. There has been long speculation whether bed bugs can transmit diseases, and in fact more than 40 different pathogens have been implicated.

    Recently, research has indicated that bed bugs are capable of transmitting the agent of Chagas Disease, Trypanosoma cruzi ,in the laboratory. However, to date there is not one piece of evidence that bed bugs have transmitted any pathogen to humans. During the act of feeding, saliva is injected which contains a variety of anticoagulants as well as other proteins whose function has yet to be determined.

    Contrary to popular belief, there is no evidence that bed bugs inject an anaesthetic. One protein, Nitrophorin, is involved in the transport of nitric oxide into the wound. This results in local vasodilation that increases blood supply to the feeding insect. The same protein can also induce a sensitivity to the bite. The diagnosis of Cimicosis is via the clinical appearance of the bite reaction and confirmation of an actual bed bug infestation Table 1. In young children, the face and even the eyelids can be bitten.

    Rarely, however, armpits are bitten, which are often preferred by other insects and ticks Table 2. Figure 1: Typical appearance of bed bugs. Figure 2: Bites on the back, note the lines of bites common in moderate to large infestations. Figure 3: Bed bug bites on the arm, typical formation.

    Figure 4: Bed bug bites on the torso and arm. Figure 5: Bullae due to bed bug bites. Figure 6: Bed bugs, their droppings and eggs underneath a mattress. The degree of the bite reaction often depends on the level of prior exposure. With low level sensitization, individuals may develop a cm wheal, with a small central haemorrhagic point. This haemorrhagic point can be recognized easily by diascopy. In contrast, a highly sensitized person will react immediately and may develop a wheal up to 15cm across 6 inches. If many bed bugs are present, an urticarial rash may develop as a result of the large number of bites and subsequent trauma to the area from scratching.

    On rare occasions, vesicles and bullae Fig. In the course of Cimicosis, papules that are extremely itchy may develop and can persist for several days to weeks. Due to the strong pruritus eczematous lesions, bacterial infections may occur, although this is extremely rare. There are case reports of systemic reactions such as anaphylaxis and asthma, although these are uncommon.

    Through repeated exposure, some individuals may develop a tolerance to the bites. The clinical symptoms are then largely inapparent with small punctures at the bite site. Small blood spots are then the only clues that an infestation may be present. Since reactions to stings and bites of various arthropods are non-specific, bed bug bites are commonly misdiagnosed.

    Single bites, notably that of other insects such as mosquitoes, fleas and biting midges may appear very similar morphologically Table 2. Consideration of where the bites are on the body can assist in the differential diagnosis. For bed bugs, lines of bites are very common in moderate to large infestations and this clinical picture is virtually unique amongst blood sucking arthropods.

    For the most part, the identification of the actual pest is required to confirm the diagnosis. Skin cancer rates in this country are rising—rapidly—to the point where approximately 3. But what most of us fail to realize and, perhaps the most fundamental reason why skin cancer rates in this country continue to climb, is that none of us are immune to it.

    To get all the facts straight, we talked to three derms to uncover what they really want us to know about our increasing risk of skin cancer, and how we can protect ourselves the best way possible. This is why so many people end up with serious sunburns after spending a not-so-sunny day outdoors sans sunscreen. That means, in order to keep skin looking its youngest and healthiest, you should be applying sunscreen or this year days a year.

    Bottom line: cover up no matter what. Also be wary of sunscreens that come with a 'natural' label. And a higher SPF number doesn't necessarily mean you're more protected. Also, try to avoid direct sun exposure during peak sun hours when UV rays are the strongest and most likely to cause sunburns and skin damage. Though people with naturally darker skin shades have a lower risk of skin cancer than those with fair skin, they still need to protect themselves with sunscreen and see a dermatologist for annual skin checks.

    In fact, the overall average five-year melanoma survival rates for African Americans is only 70 percent versus 93 percent for Caucasians, according to Shainhouse. Play it safe: Check your skin monthly and be alert to changes in the number, size, shape or color of spots on your skin or sores that do not heal. Did you know that melanoma is the most common form of cancer in young adults ages 25 to 29? Tanning booths are one of the top reasons younger people develop melanoma and other skin cancers.

    skin health

    The American Academy of Dermatology AAD and its policy group, Skin Pac, have lobbied the federal government for years to restrict minors from tanning salons and reduce access to tanning booths on school campuses. And studies have already demonstrated the effectiveness of these regulations.

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    Experts recommend examining your skin from head to toe at least once a month to look for changes in your skin. A is for asymmetry, B is for borders with irregular edges, C is for color varied from one area to another, D is for diameter larger than a pencil erase, and E is for evolving over time or changing in shape, size or color. Sign up for our Newsletter and join us on the path to wellness.