Steve L. Liao, MD

  • The James J. Peters Veteran Affairs Medical Center
  • Department of Medicine, Cardiovascular Division
  • Bronx, New York
  • The Zena and Michael A. Weiner Cardiovascular Institute
  • The Mount Sinai School of Medicine
  • New York, New York

Anxiety disorders are common and important in general medical practice as they often manifest with physical symptoms such as palpitations erectile dysfunction frequency order generic avana online, chest pain valsartan causes erectile dysfunction buy genuine avana on-line, and dizziness that can be misdiagnosed as medical conditions and lead to unnecessary investigation and treatment erectile dysfunction 18-25 buy discount avana 50mg on line. Anxiety disorder impotence your 20s cheap 100mg avana otc, especially phobic anxiety erectile dysfunction treatment in jamshedpur buy cheapest avana, can also lead to inability to adhere to medical treatments impotence natural remedies order 100 mg avana otc, for example, because of needle phobia interfering with blood tests and/or injected drugs treatment. For chronic anxiety, selective serotonin reuptake inhibitors are the drugs of choice, with benzodiazepines being reserved for short-term use. Words such as worry, nervousness, and apprehension all describe this everyday emotion. Normal worry can serve an adaptive function, motivating individuals to take action to avoid negative consequences. They experience more pervasive and persistent anxiety, as well as other psychological and physiological symptoms. Whereas normal worry can spur people to action, anxiety disorders can cripple them. Special circumstances Pregnancy Pregnancy and specifically the post-partum period is a high-risk period for women with bipolar disorder when as many as half relapse. There is a need to balance the risk of pharmacotherapy to the unborn fetus against the risk of recurrence of an affective episode in the mother. Appropriate diagnosis and treatment of anxiety disorders can reduce morbidity, minimize disability, and restore functionality. Aetiology Both genetic and psychosocial factors contribute to the aetiology of anxiety disorders. The brain regions most strongly implicated in the pathogenesis of anxiety disorders are the amygdala, the insular cortex, the cingulate cortex, and the prefrontal cortex. The neurotransmitters most strongly associated with anxiety disorders are -aminobutyric acid, serotonin, and norepinephrine. Panic disorder the most salient feature of panic attacks is their severity and short duration: they peak and typically resolve within minutes. Many patients have some familiarity with the concept of a panic attack and mistakenly describe other anxiety symptoms as panic attacks. Accurately eliciting a history of panic attacks is the crucial step in distinguishing panic disorder from other anxiety disorders. The hallmark of panic disorder is not simply the presence of panic attacks, but also a persistent worry about future attacks and/or the actions taken to avoid future attacks. Agoraphobia (fear/ avoidance of crowds, open spaces, or enclosed places) represents one such maladaptive response to the experience of panic attacks. Approximately one in five adults suffer from an anxiety disorder according to large population surveys performed in several international settings. Anxiety disorders disproportionately affect women and are associated with high rates of disability. Patients with anxiety disorders frequently seek treatment in primary and specialty medical care settings, often initially presenting with physical symptoms. Specific phobia Many individuals are afraid of some of the objects or situations. One category of phobias with particular relevance to clinicians is bloodinjection-injury phobia. This consists of specific aversions to blood, needles, or other invasive medical procedures. Specific phobias of this type may prevent patients from receiving other necessary medical care, and thus warrant prompt diagnosis and treatment. Clinical features the presenting complaints of patients with anxiety disorders can vary widely. The main psychological symptom of anxiety disorders is feeling anxious, tense, fearful, or agitated. The associated behaviours include avoidance of feared situations and compulsive behaviours that serve to reduce the anxiety (Table 26. These include fatigue, aches and pains, poor sleep, palpitations, breathlessness, dizziness, and chest pain. They are not however connected in a realistic way with what they are designed to prevent, or are clearly excessive. For instance, a person with normal shyness may keep to herself or himself at a large social gathering, but interact more openly with close friends, whereas a person with social anxiety disorder may avoid social functions altogether and consequently become socially isolated. Patients with social anxiety often self-medicate with alcohol, leading to an association with alcohol misuse disorders. The woman mentioned here spent 90 minutes every evening compulsively checking her food instead of going to her evening class, making the behaviour clearly abnormal. For example, seeing a physician to hear whether a serious disease such as cancer has progressed will cause many patients anxiety. Sometimes, however, the severity and persistence of anxiety means it is considered a psychiatric disorder as described here. Other psychiatric differentials to consider are alcohol or drug withdrawal, developing delirium or dementia, and occasionally anxiety secondary to the delusions and hallucinations of a psychotic disorder. There should be increased suspicion of these and other medical causes of anxiety if a patient is over 35 with no personal or family history of anxiety, has no history of using the substances and medications listed here, lacks significant stressors, and if standard pharmacological treatment of anxiety fails. Particular emphasis should be paid to screening for stimulant ingestion and withdrawal from ethanol or benzodiazepine use. Obsessive-compulsive disorder Most patients with obsessive-compulsive disorder experience both obsessions and compulsions. Compulsions similarly do not bring patients pleasure, merely temporary relief from the distress associated with the obsessions. They are also not realistically related to the obsessions that drive them, or are clearly excessive. For instance, in the aforementioned case, the woman could only relieve her anxiety by ritualistically checking and rechecking the expiration date on every food item in her kitchen. Awareness of this form of presentation reduces the risk of misdiagnosing anxiety as a medical disorder. Both drug and psychological treatment are effective and may be used in combination, especially for severe anxiety disorders. The most commonly used drugs are now the serotonin reuptake inhibitors, which while also used as antidepressants have proven to be even more effective for the treatment of anxiety. Benzodiazepines such as diazepam and lorazepam are highly effective in relieving anxiety, but these agents are now generally restricted to short-term use because of the risk of dependence. While many physicians are more comfortable prescribing medication than providing psychotherapy, it is important to ask the patient what their preference is. For mild to moderate anxiety, either modality may be effective as a first-line treatment. For patients with moderate to severe anxiety, pharmacotherapy on a short- or longterm basis is usually needed. Serotonin reuptake inhibitors the serotonin reuptake inhibitors are now first-line treatment for anxiety disorder. There is no clear difference in efficacy among these agents, but side effect profiles differ. Many anxious patients are highly sensitive to medications, so it is important to start slowly and provide education about the frequency of side effects and time course of response, in order to avoid premature discontinuation. Many patients will experience initial gastrointestinal discomfort including nausea, but it is important to reassure the patient that this side effect disappears for almost everyone within the first week of treatment. They should be told to take the medication with food, at least until the gastrointestinal side effects have remitted. For some patients, it may be beneficial to start at a lower than usual starting dosage and titrate up once the gastrointestinal side effects abate. Sexual side effects include decreased interest and anorgasmia for women and erectile or ejaculatory dysfunction for men. These side effects do not dissipate but are fully reversible upon discontinuation. If after four to six weeks of treatment there has not been substantial improvement, the dosage can be increased. If there is still no improvement, alternative agents or psychotherapy may be needed. Patients need to be educated not Withdrawal may cause anxiety missed medical diagnoses in patients with concurrent anxiety by highlighting those symptoms. It is important to note that anxiety commonly coexists with depression and that all anxiety patients should be assessed for depression. Diagnosis When a patient is anxious, it is important to first ask how persistent and severe the anxiety is. For patients whose level of functioning is poor, also asking about functional level prior to the onset of symptoms can help establish the extent to which anxiety is contributing to functional impairment. Treatment When a medical patient is anxious, the first step is to ask them why and see if information and addressing their fears, for example, about prognosis, is effective. Feeling nervous, anxious, or on edge Not at all = 0 Several days = 1 More than one-half of the days = 2 Nearly every day = 3 Not at all = 0 Several days = 1 More than one-half of the days = 2 Nearly every day = 3 2. Being unable to stop or control worrying Two-item total score of greater or equal to 3 represents a positive screen. Pharmacologic treatment for panic disorder should continue for at least six months after the symptoms have resolved. For patients with chronic or recurrent panic disorder, or years of generalized anxiety disorder, treatment may continue indefinitely. Some patients may be reluctant to taper off if there are ongoing severe psychosocial stressors. Other agents Benzodiazepines, while still widely used, should not usually be first line for an anxiety disorder as they can cause sedation and cognitive dysfunction, are addictive, and commonly abused. However, they are useful for short-term anxiety, such as that associated with a medical procedure. The serotonin and norepinephrine reuptake inhibitors venlafaxine and duloxetine are usually effective alternatives for anxiety. They may be preferentially indicated for patients with comorbid pain such as neuropathic pain or fibromyalgia. Psychological treatments Where available, psychotherapy is the treatment of choice for many patients with anxiety disorders. The physician can offer brief psychological interventions themselves that are often effective, particularly for those with mild to moderate anxiety. For example, they may encourage patients to question fearful thoughts, replacing undue fears with more realistic appraisals, and listing the worst possible scenarios in order to help the patient see that they can handle feared future events. Referral for specialized treatments Patients should be referred for consultation or treatment with a psychologist or psychiatrist for severe or refractory symptoms, patient preference, or selected disorders that are generally beyond the expertise of the primary care physician (Table 26. Specific phobias such as snake or bridge phobias rarely present in medical settings, but needle or pill-swallowing phobias may interfere with medical care. These trauma-related disorders are not only an important cause of suffering but may also complicate medical care, hence they require recognition and appropriate treatment. Introduction There is a group of psychiatric disorders specifically defined as being a response to severe psychological stress or trauma. Acute stress disorder is the immediate emotional and behaviour reaction to an acute stress, for example, being told that a family member has died unexpectedly. Adjustment disorders are longer-lasting emotional and behavioural reactions to ongoing stressors, such as a new diagnosis of cancer. Accidents and acute illness may be traumatic, as on occasion may treatment itself. These disorders are not only an important cause of suffering but may also significantly complicate medical care, for example, by leading to the avoidance of essential medical treatment. Overall, approximately half of patients with anxiety disorders respond fully to either drug or psychological treatment and the remainder respond to varying degrees, but the relapse rate is high. Consequently many hospitalized patients may be considered to have suffered trauma, but most people exposed to traumatic events do not go on to develop a mental disorder; they are surprisingly resilient in the face of adversity. However, many people who have suffered traumatic events become severely distressed and some go on to develop a mental disorder. Because trauma is so common in medical practice, in the form of accidents, severe illness, and sometimes medical and surgical treatments, these disorders are commonly seen by physicians. An initial severe reaction to a traumatic event such as severe accident is an acute stress disorder and is commonly characterized by dissociation. A more long-lasting emotional reaction to ongoing stress such as a new diagnosis of life-threatening illness is termed an adjustment disorder. An often longer-lasting and more severe psychological reaction Epidemiology the point prevalence of acute stress disorder following exposure to traumatic events is between 5 and 20%, depending on the type Box 26. The point prevalence of adjustment disorders in the general population is between 3 and 12%, with a much higher prevalence in medical populations. Avoidance Acute stress disorder this is an immediate response to a severe stressor. A person with acute stress disorder typically reports experiencing the world as unreal or dreamlike, feeling detached from their body, or that they are having increasing difficulty recalling specific details of the traumatic event (dissociative amnesia). The traumatic event may be persistently re-experienced as recurrent images, thoughts, or dreams. There may also be avoidance of stimuli that arouse recollections of the trauma. They may also suffer from anxiety or symptoms associated with increased arousal such as difficulty sleeping, irritability, and poor concentration. The symptoms of acute stress disorder must last for a minimum of three days and a maximum of four weeks, and must occur within four weeks of the traumatic event. The person may cope with their emotional reaction by misuse of drugs or alcohol, which complicates the clinical picture. Negative alterations in cognitions and mood Marked alterations in arousal and reactivity Adjustment disorders these disorders are a longer-term response to ongoing stressors of a range of severities. The symptoms of adjustment disorders are varied and often include low mood, anger, anxiety, and sleep disturbance. These symptoms must be out of proportion to the severity or intensity of the stressor and be associated with significant impairment in social, occupational, or other important areas of functioning.

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There are no dysmorphic facial features erectile dysfunction prevention generic 200mg avana mastercard, hepatosplenomegaly erectile dysfunction doctor memphis buy discount avana 100mg, or skeletal abnormalities impotence tumblr 200mg avana with visa. Neurologic examination typically reveals severe dysarthria or anarthria erectile dysfunction pumps buy avana 50mg generic, slow chewing erectile dysfunction prevalence age avana 100mg on line, slow eating and swallowing erectile dysfunction vitamin b12 cheap 100 mg avana otc, spasticity, and hyperactive tendon reflexes. Diagnosis may be based on electron microscopic examination of conjunctival and skin biopsies which show characteristic lysosomal inclusions as well as enlarged lysosomes in all cell types. However, molecular genetic analysis of common mutations is often used for diagnostic purposes. Eye care includes topical lubricating eye drops, artificial tears, gels, or ointments for ocular irritation. Pompe disease has a varied estimated frequency in different ethnicities of one in 40 000 in African-American to 146 000 in Australian populations. When the acid -glucosidase activity decreases below critical, lysosomal glycogen begins to accumulate. This threshold level of enzyme required to accumulate glycogen varies depending on the organ. Pathological changes in skeletal muscle, however, are prominent throughout the clinical spectrum. Pompe disease may present at any age, though the classic infantile form was first described by Pompe in 1932 and usually presents in patients within the first months of life with median age of onset between 1. Presenting symptoms are feeding difficulties, failure to thrive, respiratory infections, hypotonia, and diminished spontaneous movements. The heart is characteristically affected with hypertrophic cardiomyopathy, thickening of the ventricular walls and septum that may lead to outflow tract obstruction and cardiac failure. Motor development is delayed and major motor milestones such as rolling over, sitting, or standing are usually not achieved. Hearing deficit, osteoporosis and osteopenia are now noted as a features in children who survive longer following administration of enzyme replacement therapy. Symptoms of children and adults with a nonclassic presentation are predominantly related to skeletal muscle dysfunction, resulting usually in reduced mobility followed by respiratory problems. Presenting symptoms are difficulty running, climbing stairs, rising from an armchair, and walking. Early involvement of the diaphragm leads to low vital capacities in the supine position although pulmonary function in the upright position is still adequate. This leads to sleep disordered breathing and patients learn to sleep with their head elevated. Patients may report morning headache as a symptom of hypoventilation during sleep causing hypercarbia. Use of accessory muscles such as sternocleidomastoid may be evident during clinical examination. Patients progress slowly but relentlessly to loss of ambulation and wheel chair use along with ventilator support. Life expectancy is diminished in juvenile and adult patients with Pompe disease, usually related to pulmonary complications. Late-onset forms of Pompe closely mimic limb-girdle muscular dystrophy in presentation and often may be diagnosed in that category. The average diagnostic delay ranges from 7 to 10 years; although numerous cases are known where diagnosis is delayed for decades. Very high index of suspicion is necessary to ensure timely and appropriate diagnosis, given that enzyme replacement therapy is now available. Diagnosis is confirmed by enzyme estimation in peripheral leucocytes or isolated lymphocytes. Several new methods use assays of acid -glucosidase activity in dried bloodspots which offers a convenient and reliable method for screening. Infants with classic Pompe disease have less than 1% residual activity; children and adults have residual activity, but usually no more than 30% of average normal activity. Infusion associated reactions are common, which can be modified by slowing the rate of infusion or administration of antipyretics, antihistamines, or glucocorticoids. Affected individuals with high sustained IgG titers may have a poor clinical response to treatment. Treatment with alglucosidase alfa reduces the risk of mortality in late-onset patients to close to a fifth of that experienced in the natural course. Improvements in the six minute walk test occur quickly and are sustained over time. Diagnosis is established by demonstration of the respective enzyme deficiencies in peripheral leucocytes or cultured fibroblasts. Diagnosis is significantly aided by electron microscopy of a skin biopsy and observation of nerve endings that show the typical inclusions. It is recommended that skin biopsy be obtained from sensitive skin areas such as the axilla where the density of nerve endings may be higher. Palmitoylation plays a critical role in neuronal vesicular transport and intracellular signalling. Most patients have infantile onset between 8 and 18 months of age with irritability, deceleration of head growth, muscular hypotonia, ataxia, motor clumsiness, irritability, sleep disturbance, and visual failure after a period of normal development during the first year. Rapid developmental deterioration occurs during the second year of life with loss of all motor abilities and social interest, blindness, and increasing spasticity, seizures, and myoclonus. Some patients may have late-infantile, juvenile, and even adult-onset as late as 40 years of age. Onset is between second and fourth year of life with unexpected delay of psychomotor development or epilepsy of sudden onset. Seizures are generalized tonic-clonic or partial, frequently of a severe myoclonic type, which may soon become resistant to drug treatment. Gross and fine motor abilities, cognitive functions, and, later, vision are rapidly lost within 3 years of onset. Clinical features of the juvenile form include developmental delay and growth retardation, seen in early childhood with mild coarsening of the facial features, hepatomegaly, and psychomotor retardation. Increased amounts of free sialic acid are found in the serum and urine, as well as in cultured skin fibroblasts and several tissues, including the brain. The form that predominates in a particular patient correlates with the particular mutated gene. They share common clinical features that include epileptic seizures, progressive psychomotor decline, visual failure, and premature death. There are an increasing number of examples of different mutations in a single gene giving rise to quite different diseases. Ocular pathology is initially a pigmentary retinopathy often misdiagnosed as retinitis pigmentosa or cone dystrophy. In adolescence, speech, mobility, and cognitive skills deteriorate and seizures set in. Children have behavioural problems such as aggressiveness, psychosis, mood disturbance, and anxiety. As the disease progresses, myoclonic jerks and parkinsonian features and gait develop. Lipopigments are distributed in the central nervous system and extracerebrally, and include fingerprint bodies, curvilinear profiles, lamellar inclusions, and occasionally condensed fingerprint figures associated with lipid droplets. Early features include gait and speech disturbance, seizures, and developmental delay. Milder form with missense mutations in one patient is described with childhood-onset neurodegenerative disease with ataxia, retinopathy, severe cognitive decline, and no seizures at age 17. It begins with the insidious onset of loss of recent memory, increasing forgetfulness, disorientation, decreased abstraction ability, and word-finding difficulty. Behavioural problems arise including agitation, restlessness, insomnia, paranoia, and sometimes delusions or hallucinations. As the disease progresses the patient becomes increasingly immobile, incontinent, and mute with death occurring one to two decades after symptom onset. Pathological hallmarks, in both familial and sporadic cases, are extracellular plaques of amyloid- (A) and intraneuronal inclusions of hyperphosphorylated tau within the cortex and subcortical nuclei. The neuritic plaques containing extracellular deposits of amyloid -protein (A) are intimately associated with dystrophic neurites, activated microglia within the amyloid deposit, and reactive fibrillary astocytes surrounding the lesion. In the 1990s it was confirmed that the disease could be caused by autosomal dominantly inherited genetic mutations. Over 200 changes, including mutations, polymorphisms, and variants of unknown significance have now been described in these genes. A peptides, particularly A42, may have toxic effects on neuronal and synaptic function intracellularly, and seed extracellularly to precipitate in the form of amyloid plaques. Mutations beyond codon 200 tend to have type-2 pathology, which is more severe leptomeningeal and intraparenchymal amyloid angiopathy with large diffuse plaques concentrated around amyloidotic arteries. Individuals with type 1 pathology have a younger age at onset (on average 5 years earlier) and shorter disease duration (c. It has been suggested that in addition to increasing the production and deposition of A42 some mutations affect Notch signalling, inducing breakdown of the vascular epithelium causing leakage of A into brain tissue. Families with mutations at these sites were found to have, in addition to early impairment of episodic memory, dyscalculia, lack of insight, and prominent myoclonus and seizures. Pathologically, although diffuse parenchymal deposits of A are present, neuritic plaques and neurofibrillary tangles are absent. However, clinically patients presented with progressive cognitive impairment and not recurrent cerebrovascular events. Comparing the Arctic and Dutch mutations, which occur at exactly the same position (amino acid 693) but give rise to totally different phenotypes suggests that the polarity of the substituted amino acid influences the pathology. The Dutch mutation replaces glutamic acid with polar and hydrophilic glutamine, which may have a greater affinity for, and propensity to disrupt, the vessel wall than the Artic mutation involves replacement with nonpolar and hydrophobic glycine. Pathologically prominent amyloid angiopathy and clinically high frequency of seizures are characteristic. The size of the duplication does not appear to influence the clinical presentation. The receptor is normally involved in phagocytosis of neural debris in the brain and profoundly down-regulates proinflammatory cytokine production. However, patients ultimately progress to more global impairment in frontal and temporal lobe functions. Mutations that disturb alternative splicing regulation lead to an increase in the four repeat (4R, sticky) form over three repeat (3R, nonsticky) form of tau, and along with missense mutations in exon 10 are associated with a tauopathy composed of 4R tau. Missense or splice-site mutations affecting exon 10 cause neuronal and glial inclusions while mutations outside of exon 10 cause neuronal inclusions only comprised of all six isoforms. Neuronal inclusions in these cases did not show tau-positive staining, but did stain for ubiquitin. Males are more frequently affected and this group has the shortest life expectancy at just over five years on average. The protein has several conserved domains, a transcriptional activation domain, multiple nucleic acid binding domains and a nuclear localization signal. Normal copy number ranges from zero-30 copies to an excess of four thousand in mutation carriers. These inclusions, evident particularly in dopaminergic neurons, are mainly made up of filamentous -synuclein and ubiquitin proteins. The disease is mostly sporadic; however, there are rare cases of familial aggregation. Prion disorders Prion diseases, or transmissible spongiform encephalopathies, are fatal neurodegenerative disorders that affect humans and animals. Prion diseases have in common the accumulation of an abnormal isoform of the normal human protein PrP. Prion diseases cause a spongiform change within brains associated with astrogliosis and neuronal loss. Most cases are sporadic but 15% have a familial basis and 1% are acquired iatrogenic. It presents with psychiatric symptoms, painful dysaesthesias, ataxia, dementia, and a movement disorder. There are extensive PrP-amyloid plaques and in some cases also neurofibrillary tangles. Other signs are ataxia, pyramidal and extrapyramidal dysfunction, and dysautonomia. Pathological examination reveals almost no vacuolization but neuronal loss and gliosis are found in the thalamus, inferior olives, and to a lesser degree in the cerebellum. Nonsyndromic genetic epilepsies Consideration of nonsyndromic genetic epilepsies can pragmatically be based on age of onset of seizures. Neonatal epileptic encephalopathies these are severe neonatal and early infantile epilepsy syndromes in which recurrent clinical seizures are associated with impairment of cognitive, sensory and motor development (see Table 24. Mutations are often found in genes involved in a wide range of elements required for nerve function. Epilepsies of infantile onset Benign familial infantile seizures Benign familial infantile seizures is an autosomal dominant epilepsy with onset between 4 and 8 months of age. Dravet syndrome Dravet syndrome, also known as severe myoclonic epilepsy of infancy, was described first by Charlotte Dravet in 1978. Clinically infants present at the age of 6 months, typically with prolonged generalized febrile seizures with subsequent evolution into other seizure types such as myoclonic, complex partial seizures, atypical absence seizures. Genetic testing should be considered in any patient with epilepsy in whom there is a positive family history, or there are features such 24. Some benefit may be seen with the use of stiripentol, topiramate, valproate, clobazam, clonazepam, and levetiracetam, as well as a ketogenic diet. Certain anticonvulsants including lamotrigine and carbamazepine may exacerbate seizures in these patients.

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