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STUDENT DIGITAL NEWSLETTER ALAGAPPA INSTITUTIONS |
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Anish K. Amin, MD
For people who have two disorders viruswin32virutce purchase 50mg minocin, treatment that targets both of them appears to be more effective than treatment that targets one or the other alone (Barrowclough et al bacteria worksheet middle school buy generic minocin 50 mg on-line. Targeting Social Factors in Treating Schizophrenia Treatments that target social factors address three of the four general treatment steps: They identify early warning signs of positive and negative symptoms through family education and therapy; when necessary sulfa antibiotics for sinus infection discount minocin 50 mg mastercard, such treatments involve hospitalizing people whose symptoms make them unable to care for themselves or whose symptoms put themselves or others at high risk of harm antimicrobial bath rug best 50mg minocin. These treatments also reduce certain negative symptoms through social skills training and improve overall functioning and quality of life through community-based interventions. Community-based interventions include work-related and residential programs (Tarrier & Bobes, 2000). Family Education and Therapy By the time a person is diagnosed with schizophrenia, family members typically have struggled for months-or even years-to understand and help their loved one. Psychoeducation for family members can provide practical information about the illness and its consequences, how to recognize early signs of relapse, how to recognize side effects of medications, and how to manage crises that may arise. Such education can decrease relapse rates (Pfammatter, Junghan, & Brenner, 2006; Pilling et al. In addition, family-based treatments may provide emotional support for family members (Dixon, Adams, & Luckstead, 2000). Moreover, family therapy, as noted in Chapter 4, can create more adaptive family interaction patterns: In 1989, my older sister and I joined Mom in her attempts to learn more about managing symptoms of her illness. Mom, who had never been able to admit she had an illness, now told us that she did not want to die a psychotic. In the first stage, we listed withdrawal, confusions, depression, and sleeping disorder. Fifteen years ago when mom reported her symptoms to me, I just told her everything would be okay. For 8 years she has maintained a low dosage of medications, with increases during times of stress. Social skills training teaches these skills by breaking down complex social behaviors into their components: maintaining eye contact when speaking to others, taking turns speaking, learning to adjust how loudly or softly to speak in different situations, and learning how to behave when meeting someone new. The leader and members of a group take turns role playing these different elements of social interaction. These social skills may be applied to interactions with mental health professionals, such as discussing with a psychiatrist the side effects a medication is causing. Research has shown that although social skills training does improve social skills and daily functioning that depends on social skills, it is less effective in preventing relapse or directly increasing employment (Bustillo et al. Apparently such training is not sufficient to remove enough stress or reduce other contributing factors that may trigger a relapse. Inpatient Treatment Short-term or long-term hospitalization is sometimes necessary for people with schizophrenia. A short-term hospital stay may be required when someone is having an acute schizophrenic episode (is actively psychotic, extremely disorganized, or otherwise unable to care for himself or herself) or is suicidal or violent. Inpatient treatment includes various therapy groups, such as a group to discuss medication side effects. Once the symptoms are reduced to the point where appropriate self-care is possible and the risk of harm is minimized, the patient will probably be discharged. Long-term hospitalization may occur only when other treatments have not significantly reduced symptoms and the patient needs full-time intensive care. Legal measures have made it difficult to hospitalize people against their will (Torrey, 2001). Although these tougher standards protect people from being hospitalized simply because they do not conform to common social conventions (see Chapter 1), they also mean that people who have a disorder that by its very nature limits their ability to comprehend that they have an illness may not receive appropriate help until their symptoms have become so severe that normal functioning is impossible. Early intervention for ill adults who do not want help but do not realize that they are ill is legally almost impossible today. Minimizing Hospitalizations: Community-Based Interventions In Chapter 1 we noted that asylums and other forms of 24-hour care, treatment, and containment for those with severe mental illness have met with mixed success over the past several hundred years. Traditionally, people with chronic schizophrenia were likely to end up in such institutions. However, beginning in the 1960s with the widespread use of antipsychotic medications and building into the 1970s, the U. Not everyone thinks that deinstitutionalization was a good idea, at least not in the way it has been implemented. The main problem is that the patients were sent out into communities without adequate social, medical, or financial support. The good news is that some communities have adequately funded programs to help people with chronic schizophrenia and other chronic and debilitating psychological disorders live outside of institutions. Community care (also known as assertive community treatment) programs allow mental health staff to visit patients in their homes at any time of the day or night (Mueser et al. Patients who receive such community care report greater satisfaction with their care; however, such treatment may not necessarily lead to better outcomes (Killaspy et al. Deinstitutionalization was mandated without adequate funding for communities to take care of people with schizophrenia and other serious mental illnesses. One result has been increased poverty and homelessness among those with such disorders. Residential Settings Some people with schizophrenia may be well enough not to need hospitalization but are still sufficiently impaired that they cannot live independently or with family members. At one extreme is highly supervised housing, in which a small number of people live with a staff member. They also have household chores and attend house meetings to work out the normal annoyances of group living. Those able to handle somewhat more responsibility may live in an apartment building filled with people of similar abilities, with a staff member available to supervise any difficulties that arise. In independent living, in contrast, a staff member provides periodic home visits to patients living on their own. Vocational Rehabilitation A variety of programs assist people with schizophrenia to acquire job skills; such programs are specifically aimed at helping patients who are relatively high-functioning but have residual symptoms that interfere with functioning at, or near, a normal level. Those who are more impaired may participate in sheltered employment, working in settings that are specifically designed for people with emotional or intellectual problems who cannot hold a regular job. Individuals in such programs may work in a hospital coffee shop or create craft items that are sold in shops. Those who are less impaired may be part of supported employment programs, which place individuals in regular work settings and provide an on-site job coach to help them adjust to the demands of the job itself and the social interactions involved in having a job (Bustillo et al. Examples of supported employment jobs might include work in a warehouse packaging items for shipment, or restocking items in an office or a store ("Project search," 2006). What predicts how well a patient with schizophrenia can live and work in the world Iris was less able to live independently and lived in the hospital, in supervised residential settings, or at home with Mrs. She lived with Nora in a supervised apartment until she died in 2003 (Mirsky & Quinn, 1988; Mirsky et al. Community care Programs that allow mental health care providers to visit patients in their homes at any time of the day or night; also known as assertive community treatment. When successful, medication (treatment targeting neurological factors) can reduce the positive and negative symptoms, and even help improve cognitive functioning. These changes in neurological and psychological factors, in turn, make it possible for social treatments, such as social skills training and vocational rehabilitation, to be more effective. If patients are not psychotic and have improved cognitive abilities, they can better learn social and vocational skills that allow them to function more effectively and independently. In turn, as psychotic symptoms become more manageable, stress levels-and cortisol production-should decrease and thereby have fewer effects on brain functioning. As family and social interactions become less stressful, cortisol levels should decrease. However, although medication can improve symptoms, it is not a panacea- in part because many patients stop taking it-which leaves an important role for psychosocial treatments. Community-based interventions include residential care and vocational rehabilitation. These symptoms must be present for a minimum of 6 months and must significantly impair functioning.
Moreover topical antibiotics for acne in pregnancy safe minocin 50mg, the right hemisphere was strongly activated in the control participants antimicrobial drugs antibiotics generic minocin 50mg with visa, but not in the patient infection vs virus cheap minocin 50 mg with visa. The right hemisphere is known to play a special role in the retrieval of autobiographical memories (Costello et al antibiotics given for tooth infection minocin 50mg lowest price. This patient performed poorly on neuropsychological tests that assess frontal lobe function (such as the ability to organize behavior and inhibit responses). In sharp contrast, when normal bilingual participants (who spoke German) were asked to pretend that they did not speak German when evaluating these words, they exhibited large amounts of activation in the frontal lobes-which shows that they worked hard to suppress their knowledge. The reduced activation in the frontal lobes of patients with dissociative fugue might be a result of high levels of stress-related hormones (Markowitsch, 1999), which could selectively affect processes that are involved in coordinating voluntary actions and mental events-including memory retrieval (Kopelman, 2002). People who have had dissociative fugue are often more hypnotizable than the general population and may have a greater ability to dissociate (American Psychiatric Association, 2000). Researchers have yet to begin to sort out the nature of this relationship, which is especially challenging because so few cases of the disorder are available to study. Social Factors: Combat Stress Dissociative fugue generally occurs in response to significant stressors that involve social factors, such as combat (American Psychiatric Association, 2000). That is, someone experiencing a dissociative fugue probably experienced a traumatic event beforehand. As with dissociative amnesia, the specific mechanism by which the traumatic event induces the fugue state is not clear. In sum, like dissociative amnesia, dissociative fugue is rare and poorly understood. Although there are clues as to possible factors that contribute to the disorder, the specific roles these factors may play and how they might influence each other are not known. Depersonalization Disorder Like many people, you may have experienced depersonalization. Although the primary symptom is depersonalization, people who have this disorder may also experience derealization. People afflicted with depersonalization disorder may feel "detached from my body" or "like a robot," but they do not believe that they are truly detached or actually a robot. Some researchers point out that symptoms of depersonalization have much in common with symptoms of certain anxiety disorders (see Chapter 7)-a sense of being numb or detached, dizziness or faintness, and a tendency to avoid stimuli associated with increased anxiety (Hunter et al. Moreover, panic attacks can include depersonalization and derealization, and people with depersonalization disorder often have a comorbid anxiety disorder, which can make accurate diagnosis difficult. Typically, it is the comorbid anxiety symptoms, rather than the dissociative symptoms themselves, that lead individuals with depersonalization disorder to seek help. Understanding Depersonalization Disorder Researchers are beginning to chart the neurological factors that contribute to depersonalization disorder. Unfortunately, less is known about possible psychological or social factors, perhaps because the disorder is relatively rare. The depersonalization causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. The depersonalization experience does not occur exclusively during the course of another mental disorder, such as Schizophrenia [discussed in Chapter 12], Panic Disorder [Chapter 7], Acute Stress Disorder [Chapter 7], or another Dissociative Disorder [discussed later in this chapter], and is not due to the direct physiological effects of a substance. In one sample of 204 people with depersonalization disorder, almost three quarters mal activity in parts of the temporal lobe that are involved had had an anxiety disorder (Baker et al. The findings may suggest that patients with depersonalization disorder regulate their emotions more strongly than normal-which may be why they have weaker than normal emotional reactions (Phillips et al. For the brain of a patient with depersonalization disorder example, when patients with this disorder viewed faces (right). Note the increased with highly emotional expressions, activity in the limbic activity in the parietal lobes system decreased-and this occurred in response to both of the patient; this part of the very happy and very sad expressions (Lemche et al. This is important, because if the frontal lobes can suppress emotional responses, the result might be the sense of emotional detachment that such patients report. Such an effect might also explain why brain areas involved in emotion are not activated when patients with depersonalization disorder try to remember words that name emotions, whereas these brain areas are activated when normal control participants perform this task (Medford et al. Neural Communication Patients with depersonalization disorder do not produce normal amounts of norepinephrine. In fact, the more strongly they exhibit symptoms of the disorder, the less norepinephrine they apparently produce (as measured in their urine; Simeon, Guralnick, et al. Norepinepherine is associated with activity of the autonomic nervous system, and thus this finding is consistent with the idea that these patients have blunted responses to emotion. This is consistent with neuroimaging studies that reveal decreased activity in parts of the brain that register input from the senses. However, it is not clear whether the attentional problems are a cause or an effect of the disorder: On one hand, if a person is feeling disconnected from the world, he or she would not pay normal attention to objects and events; on the other hand, if a person had such attentional problems, this could contribute to feeling disconnected from the world. Moreover, given that many patients with depersonalization disorder also have depression or an anxiety disorder (Baker et al. Social Factors: Childhood Emotional Abuse We noted earlier that stressful events (often social in nature) can trigger depersonalization disorder. Moreover, a particular type of social stressor-severe and chronic emotional abuse experienced during childhood-seems to play a particularly important role in triggering depersonalization disorder (Simeon et al. Once the disorder develops, factors such as negative mood, stress, the perception of threatening social interactions, and new environments can exacerbate its symptoms (Simeon, Knuteska, et al. E] was a 29-year-old, single man, employed as a journalist, who reported a 12-year history of depersonalization disorder. He described feeling detached from the world as though he was living "inside a bubble" and found it difficult to concentrate since he felt as though his brain had been "switched off. The world appeared two-dimensional and he reported his sense of direction and spatial awareness to be impaired. He described himself as having lost his "sense of himself" and felt that he was acting on "auto-pilot. Prior to the onset of his [depersonalization disorder], he experienced transient [depersonalization] symptoms when intoxicated with cannabis. At the age of 17, he started at a new school and felt very anxious and experienced [depersonalization] symptoms when not under the influence of cannabis. He described the first time this happened as "terrifying" since he felt he had "gone into another world. He reports the symptoms as "enormously restricting" his life in that he felt frustrated since he has been "unable to express or enjoy myself. Following this, the disconnection between the intensity of the perceived stress and the lack of arousal may lead these patients to feel "unreal," which they may then attribute (a psychological factor) to being mentally ill (Baker et al. And, in turn, the incorrect and catastrophic attributions that the patients make about their symptoms can lead to further anxiety (as occurs with panic disorder). The attributions Dissociative and Somatoform Disorders 3 4 3 can also lead to further depersonalization or derealization symptoms. Patients then become extremely sensitive to and hypervigilant for possible symptoms of "unreality" and come to fear that the symptoms indicate that they are going "round the bend. Why might some people be more likely to interpret depersonalization symptoms as indicating that they are veering toward insanity Perhaps because they had a family member with a major mental illness (social factor) (Hunter et al. In the process of examining these factors, we delve into the controversy about the disorder. For example, a person with this disorder might have an "adult" alter that is very responsible, thoughtful and considerate and a "child" alter that is irresponsible, impulsive and obnoxious. Each alter can have its own name, mannerisms, speaking style, and vocal pitch that distinguish it from other alters. Some alters report being unaware of the existence of other alters, and thus they experience amnesia (because the memory gaps are Table 8. Perhaps the most compelling characteristic Dissociative Identity Disorder of alters is that, for a given patient, each alter can have unique medical problems and histories: One alter might A. Inability to recall important personal information that is too extensive to be becomes the dominant personality. The disturbance is not due to the direct physiological effects of a substance (American Psychiatric Association, 2000). The following excerpts present recollections from two of the alters, beginning with Robert: this is Robert speaking.
Anna was diagnosed with hysteria-a common diagnosis at the time-but this term is a vague label for a condition that includes a wide range of symptoms antibiotics for uti amoxicillin dosage buy minocin 50 mg with mastercard. The central feature of dissociative disorders is dissociation antibiotic resistance among bacteria buy 50mg minocin overnight delivery, the separation of mental processes-such as perception virus plushies buy 50mg minocin with amex, memory and self-awareness-that are normally integrated antibiotics early period minocin 50mg low cost. Generally, each 3 3 1 Somatoform Disorders Somatoform Disorders: An Overview Somatization Disorder Conversion Disorder Hypochondriasis Body Dysmorphic Disorder Is Somatoform Disorder a Useful Concept Dissociation the separation of mental processes- such as perception, memory, and selfawareness-that are normally integrated. In this chapter we explore dissociative and somatoform disorders-their diagnostic criteria, criticisms of those criteria, the causes of the disorders, and treatments for them. Mary Evans Picture Library/Alamy Dissociative Disorders Breuer reported that Anna O. She pursued this activity almost continuously while she was engaged in her household duties" (Breuer & Freud, 1895/1955, p. These dissociative states, or "absences," began in earnest when Anna became too weak to care for her father, and they became more prominent after his death in April 1881. Symptoms that were seen as part of hysteria are now generally considered to be symptoms of either dissociative disorders or somatoform disorders. Dissociative Disorders: An Overview Dissociation may arise suddenly or gradually, and it can be brief or chronic (Steinberg, 1994, 2001). Amnesia Memory loss, which is usually temporary but, in rare cases, may be permanent. Identity problem A dissociative symptom in which an individual is not sure who he or she is or may assume a new identity. After her father died, she recounted "that the walls of the room seemed to be falling over" (Breuer & Freud, 1895/1955, p. Normal Versus Abnormal Dissociation Before you start worrying about whether you might have a dissociative disorder, you may be relieved to learn that experiencing symptoms of dissociation is not necessarily abnormal; occasional dissociating is a part of everyday life (Seedat, Stein, & Forde, 2003). For instance, you may find yourself in a class, but not remember walking to the classroom. In some cases, periods of dissociation are part of religious or cultural rituals (Boddy, 1992). In some instances, dissociative experiences do indicate a disorder, but not necessarily a dissociative disorder; other psychiatric disorders can involve dissociative symptoms, such as when depersonalization or derealization occurs during a panic attack. Research findings suggest that pathological dissociation is qualitatively different, not simply quantitatively different, from everyday types of dissociation, such as "spacing out" (Seedat, Stein, & Forde, 2003). In one of these states she recognized her surroundings; she was melancholy and anxious, but relatively normal. In the other state she hallucinated and was "naughty"-that is to say, she was abusive, used to throw the cushions at people. At this stage of her illness if something had been moved in the room or someone had entered or left it [during her other state of consciousness] she would complain of having "lost" some time and would remark upon the gap in her train of conscious thoughts. These "absences" had already been observed before she took to her bed; she [would] stop in the middle of a sentence, repeat her last words and after a short pause go on talking. These interruptions gradually increased till they reached the dimensions that have just been described. At the moments when her mind was quite clear she would complain of the profound darkness in her head, of not being able to think. Cultural Variations in Pathological Dissociation People in different cultures may express dissociative symptoms differently. For example, latah, experienced by people-mostly women-in Indonesia and Malaysia (Bartholomew, 1994), involves fleeting episodes in which the individual uses profanity and experiences amnesia and trancelike states. Symptoms of hysteria were common among middle- and upper-class women of the Victorian era, the period in which Anna O. Women of that time and social class led severely limited lives: They were expected to marry, have children, and run the home; they were allowed to pursue only a restricted range of other activities. Some researchers hypothesize that the hysterical symptoms of Victorian women like Anna who wanted a different life were one of the few means of social protest they could employ (Kimball, 2000). Dissociative amnesia is a dissociative disorder in which the sufferer has significantly impaired memory for important experiences or personal information that cannot be explained by ordinary forgetfulness (see Table 8. The experiences or information typically involve traumatic or stressful events, such as occasions when the patient has been violent or tried to hurt herself or himself; the amnesia can come on suddenly. For example, soon after a bloody and dangerous battlefield situation, a soldier may not be able to remember what happened. To qualify as Soldiers with dissociative amnesia may forget dissociative amnesia, the memory problem cannot be explained better by another combat experiences that were particularly psychological disorder, a medical disorder, or substance use; as with all dissociative troubling or traumatic. This soldier is attending disorders, it must also significantly impair functioning or cause distress (American a memorial service in Iraq for three of his comrades who were killed in a convoy attack. The predominant disturbance is one or more episodes of inabilappear to be best explained as dissociative amnesia. The disturbance does not occur exclusively during the course of Dissociative Identity Disorder, Dissociative Fugue [both discussed later in this chapter], Posttraumatic Stress Disorder, Acute Stress Disorder [both in Chapter 7], or Somatization Disorder [discussed later in this chapter] and is not due to the direct physiological effects of a substance. Although common in television shows, this type of amnesia is, in fact, extremely rare. For instance, a soldier may forget about a particularly traumatic battlefield skirmish, but remember what he and another person spoke about between phases of this skirmish. She remembered what happened in the accident, and immediately preceding it, but suddenly had total loss of memory for the previous 12 years. She also had good autobiographical memory for her life events up to the age of 37. She was not only amnesic for these reputedly painful events, [but was unable] to recognize any of the friends she had made during that time. This included her present man friend, who was the passenger in her car at the time of the accident. Some people may spontaneously remember the forgotten experiences or information, particularly if their amnesia developed in response to a traumatic event and they leave the traumatic situation behind, as when a soldier with localized amnesia in response to combat leaves the battlefield. Understanding Dissociative Amnesia the following sections apply the neuropsychosocial approach as a framework for understanding the nature of dissociative amnesia. Unfortunately, because the disorder is so rare, not much is known about either the specific factors that give rise to it or how those factors might influence each other. Neurological factors are clearly involved in cases of amnesia that arise following brain injury, such as that suffered in a car accident (Piper & Merskey, 2004a). However, when amnesia follows brain injury, it is not considered to be dissociative amnesia. Brain Systems Some researchers have suggested that dissociative amnesia may result in part from damage to the hippocampus, which is critically involved in storing new information about events in memory. These researchers assume that periods of prolonged stress affect the hippocampus so that it does not operate well when the person is highly aroused (Joseph, 1999). The arousal-which typically accompanies a traumatic event-will impair the ability to store new information about that event. Later, this process would lead to the symptoms of dissociative amnesia for that event. However, the idea that damage to the hippocampus underlies dissociative amnesia cannot explain all cases of the disorder. Because such damage would prevent information from being stored in the first place, the subsequent amnesia would not be reversible: There would be no way to retrieve the memories later because the memories would not exist (Allen, Console, & Lewis, 1999). If damage to the hippocampus prevents new information from being stored, then such information is not available for later retrieval (even if the hippocampus itself recovers). Given that many cases of dissociative amnesia are characterized by "recovered" memories, it is not clear what brain systems would be involved. Neural Communication How might the hippocampus get damaged, which then could lead to some cases of dissociative amnesia As discussed in Chapter 2, our adrenal glands respond to stress by producing the hormone cortisol.
Flucytosine C Facial clefts and skeletal defects in rats; cleft palate in mice antibiotic resistance biofilm cheap 50mg minocin with mastercard, no defects in rabbits virus 4 year old trusted 50mg minocin. No reports of use in first trimester of human pregnancy; may be metabolized to 5-fluorouracil antibiotics for uti how long to take purchase minocin 50mg with amex, which is teratogenic in animals and possibly in humans virus 68 best minocin 50mg. Embryotoxic in rabbits and mice; teratogenic in rabbits (cleft palate, anophthalmia, aplastic kidney and pancreas, hydrocephalus). Not teratogenic in rats and rabbits; eight case reports of human use, only two in first trimester. Serious bacterial infections Because of limited experience, other treatment modalities such as cryotherapy or trichloroacetic acid recommended for wart treatment during pregnancy. All pregnant women should receive injectable influenza vaccine because of the increased risk of complications of influenza during pregnancy. Interferons Alfa, Beta, and Gamma C Abortifacient at high doses in monkeys, mice; not teratogenic in monkeys, mice, rats, or rabbits. Approximately 30 cases of use of interferon-alfa in pregnancy reported; 14 in first trimester without increase in anomalies; possible increased risk of intrauterine growth retardation. Case reports of craniofacial, skeletal abnormalities in humans with prolonged fluconazole exposure during pregnancy; no increase in defect rate noted among >300 infants born after first-trimester itraconazole exposure. Inhibits androgen and corticosteroid synthesis; may impact fetal male genital development; case reports of craniofacial, skeletal abnormalities in humans with prolonged fluconazole exposure during pregnancy. No evidence of teratogenicity with >3,700 first-trimester exposures reported to the Antiretroviral Pregnancy Registry. Ledipasvir/ Sofosbuvir Leucovorin (Folinic Acid) Linezolid B C Prevents birth defects of valproic acid, methotrexate, Use with pyrimethamine when phenytoin, aminopterin in animal models. Decreased fetal weight and Serious bacterial infections neonatal survival at expected human exposures, possibly related to maternal toxicity. No increase in birth defects among infants born to 89 women with first-trimester exposure in one study; another study suggests a possible increased risk of hypospadias with firsttrimester exposure, but confirmation required. Animal data and human data do not suggest an increased risk of birth defects, but miscarriage and stillbirth may be increased. Symptomatic treatment of diarrhea after the first trimester C Loperamide B Mefloquine C Second-line therapy of chloroquineresistant malaria in pregnancy, if quinine/clindamycin not available or not tolerated. Therapy of visceral leishmaniasis not responsive to amphotericin B or pentamidine Anaerobic bacterial infections, bacterial vaginosis, trichomoniasis, giardiasis, amebiasis Not recommended Not recommended Not indicated in chronic infection; seek expert consultation if acute infection or symptomatic reactivation of T. Severely symptomatic cryptosporidiosis after the first trimester Ribavirin, recommended to be used with this drug, is contraindicated in pregnancy so therapy in pregnancy not recommended. Studies on several hundred women with first-trimester exposure found no increase in birth defects. Possible increase in limb, ear anomalies in one study with 143 first-trimester exposures; no specific pattern of defects noted, several studies did not find increased risk. Vast experience with use in human pregnancy does not suggest teratogenicity, other adverse outcomes. Polysaccharide vaccines Initial or booster dose for prevention generally considered safe in pregnancy. Because alternative treatments for genital warts in pregnancy are available, use is not recommended; however, inadvertent use in early pregnancy is not indication for abortion. Dose-dependent increased risk of cleft palate in mice, rabbits, hamsters; dose-dependent increase in genital anomalies in mice. Risk of growth retardation, low birth weight may be increased with chronic use; monitor for hyperglycemia with use in third trimester. Teratogenic in mice, rats, hamsters (cleft palate, neural tube defects, and limb anomalies). Limited human data have not suggested an increased risk of birth defects; because folate antagonist, use with leucovorin. Therapeutic doses have not been associated with an increased risk of defects in humans or animals. Reports of treatment during second half of pregnancy in nine women without incident; first 49 cases in registry did not suggest increased risk, but limited data. Teratogenic at high doses in mice (cleft palate) and rats (spina bifida) but not in rabbits. Embryofetal toxicity with increased rate of malformations and fetal loss noted in rats and rabbits. Decreased fetal weights and increased skeletal variants in mice at 4 times human exposure. Increased deaths and decreased fetal and neonatal growth and developmental delay after in utero exposure in rats. No evidence of teratogenicity in rats and rabbits after oral or intravaginal dosing. Recommended Use During Pregnancy Contraindicated in early pregnancy; no clear indications in pregnancy. Report exposures during pregnancy to the Ribavirin Pregnancy Registry (1-800-593-2214). Simeprevir C Sinecatechin Ointment Sofosbuvir C Not recommended based on lack of data. Could be used if benefits felt to outweigh unknown risks in patients not needing ribavirin. Ribavirin is contraindicated in pregnancy, so not recommended for patients needing ribavirin based on subtype or resistance. No clear teratogenicity in humans; potential for increased jaundice, kernicterus if used near delivery. No evidence of increased birth defects in nearly 2,000 first-trimester exposures in women. Possible increase in congenital cardiac defects, facial clefts, neural tube and urinary defects with first-trimester use. Experience with valacyclovir in pregnancy limited; prodrug of acyclovir, which is considered safe for use in pregnancy. Administer a HepA-containing vaccine series to adults and adolescents at risk which includes chronic liver disease, receive clotting factor concentrates, men who have sex with men, inject illicit drugs, and travel in countries with endemic hepatitis A. Hepatitis B vaccination Administer a 3-dose series of single-antigen hepatitis B vaccine (HepB) or combined hepatitis A and hepatitis B vaccine (HepA-HepB) at 0, 1, and 6 months. Administer Hib to those with asplenia, hematopoeitic stem cell transplant, and other indications. Tetanus, diphtheria, and pertussis vaccination Administer 1 dose of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine (Tdap) to adults and adolescents who were not previously vaccinated with Tdap, followed by a tetanus and diphtheria toxoids (Td) booster every 10 years. Information on the use of Tdap or Td as tetanus prophylaxis in wound management is available at For exposed persons who have received a complete HepB vaccine series without documentation of antibody response, administer a single dose of HepB vaccine. Ideally the series should be initiated at age 11 or 12 years, but may be started as early as age 9 years. Annual epidemics of seasonal influenza typically occur in the United States between October and April. Although booster doses can make the influenza vaccine more effective, that benefit is limited to specific groups such as solid organ transplant recipients. Many licensed injectable influenza vaccine options are available, with no recommendation favoring one product over another. Information on currently available influenza vaccines is available at. Adults aged 65 years can receive standard inactivated influenza vaccine, high-dose inactivated influenza vaccine,24 adjuvanted inactivated influenza vaccine,25 or recombinant influenza vaccine,26 each of which has been studied in this age group. Inactivated influenza vaccine can be administered to persons receiving influenza antiviral drugs for treatment or chemoprophylaxis.
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