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EPPP disorders 3
| Term | Definition |
|---|---|
| Approaches to gender dysphoria | Dutch protocol and the gender-affirmative model are two approaches to the treatment of this disorder |
| Gender dysphoria kids | For children with this disorder, the diagnosis requires at least 6 of 8 symptoms that last for at least six months and cause significant distress or impaired functioning: , a strong desire to be the other gender, wearing clothes of the other gender, |
| Gender dysp teens and adults | adolescents and adults, the diagnosis requires at least 2/6 symptoms that last for at least six months and cause significant distress or impaired functioning: e.g., a strong desire to be rid of one’s primary and/or secondary sex characteristics, |
| The Dutch protocol | assumption “that gender dysphoria,transg identity, persists s teens in only a small minority ppl”.under 12 years of age, it recom“watchful waiting” accomp support 4child/fam. 1st signs of puberty, social transition/puberty-blockdrugs for child who persist |
| Dutch protocol part 2 | This gives children time to further explore their gender identity and decide if they want to start cross-sex hormone therapy when they’re 16 years of age and undergo gender-affirming surgeries after they’re 18 |
| Gender affirming model | has become the most widely accepted approach and is based on the assumption that “a child of any age may be cognizant of their authentic identity and will benefit from a social transition at any stage of development” |
| gender-affirmative model Details | Soc transition puberty blockers, sex hormones, gender issues address wyouth/families in a support non-judg way. gender variations not dis; gender diverse /vary. not always binary may be fluid. if”child’s psychprobs are neg interpersonalcultural reac |
| Gender surgery research | Research -outcomes of gender confirmation surgery (affirming surgery) has generally found :associated w a decrease in gender dysphoria, improved self-satisf low regret. evidence transgender male have somewhat more positive outcomes than trans female |
| Paraphillic disorder | persistent sexual interest /not genital stimulation-prep fondling w phenotyp normal, physically mature, consenting human partners. a paraphilia that “is causing distress or impairment to the individual or entailed personal harm, risk of harm,others” |
| Paraphillic treatment | combine cbt w other interventions including group therapy, marital therapy, and/or pharmacotherapy. orgasmic (masturbatory) reconditioning. Covert sensitization is a form of aversive counterconditioning that’s conducted in imag. Replace desire w fear CC |
| Drugs paraphillic treatment | used to treat severe forms of this disorder -gonadotropin-releasing hormones/antiandrogens. reduce sexual desire, they have serious side effec.high relapse when discontinued. SSRIsprescribed less serious disorders to reduce the depression/compulsions |
| Frotteurism diag | recurrent/intense sex arousal for at least 6 months from touching or rubbing against nonconsenting adult: manifested in fantasies, urges, and/or behaviors. the person must have acted on urges w/nonconsenting person or exper sig’distress or impaired funct |
| Transvestic disorder | cross-dressing for the purpose of sexual arousal. least 6 months as manifested in fantasies, urges, beha cause sign distress/impaired funct. men w this identify as heterosexual -may have had occasional sexual relations w men, especially cross-dres. |
| Pedophillic disorders | intense sex arousal at least 6 months -fant, urges, beh. involv. sexual activity w/a child13 years -under. person must have acted on these urges/must have exp sign distress,interpersonal probs bec of them,must be 16 yrs+ /at least 5yrolder than child. |
| Fetishistic Disorder | intense sexual arousal for at least six months in response to a nonliving object or specific non-genital body part with the arousal causing significant distress |
| Exhibitionistic Disorder | intense sexual arousal for at least six months from exposing one’s genitals to an unsuspecting person as manifested by fantasies, urges, or behaviors. Prepub child, adults, combo. Can apply s denial |
| Erectile Disorder | at least one of three symptoms on 75 to 100% of sexual activity: marked difficulty obtaining an erection during sexual activity, marked difficulty maintaining an erection until completion of sexual activity, marked decrease in erectile rigidity |
| Erectile Disorder Treatment | performance anxiety and increasing sexual stimulation. For example, sensate focus Drugs used to treat erectile disorder include sildenafil citrate (Viagra), tadalafil (Cialis), and vardenafil (Levitra), which increase blood flow to the penis |
| Premature Ejaculation | recurrent pattern of ejaculation during partnered sexual activity within approximately 1 min of vaginal penet/before person desires it. Sym for 6 months or more, occur during 75 to 100% of all occasions of sexual activity, and cause significant distress. |
| Premature ejact treatment | sensate focus 2 reduce performance anxiety, start-stop/pause-squeeze tech, used to learn to control ejaculation. evidence that a low level of 5ht contributes , research has confirmed an SSRI taken daily ( paroxetine) can delay ejaculation for some men |
| Genito-Pelvic Pain/Penetration Disorder | 6 months prob wi at least 1 of following: vag penet intercourse; vulvovaginal /pelvic pain w intercourse or attempts; anxiety vulvovaginal or pelvic pain before, during, or as the result sex; tensing of pelvic floor muscles during attem vag penetration |
| Genito-Pelvic Pain/Penetration Disorder Research | This disorder has been linked to a history of sexual and/or physical abuse and, for some women, has an onset after a history of vaginal infections. |
| Treatment Genito-Pelvic Pain/Penetration Disorder | Interventions include relaxation training, sensate focus, a topical anesthetic, vaginal dilators, and Kegel exercises (which are useful for gaining control over pelvic floor muscles). |
| Female orgasmic disorder | delay in, infrequency of, or absence of orgasm or markedly reduced intensity of orgasmic sensations on all or almost all occasions of sexual activity for at least 6 months. Cbt w masturbation |
| Delirium | requires (a) a disturbance in attention/awareness .develops over a short period of time (often hours -few days), change from base att/awareness, an tends to fluctuate in severity over the day +1 disturb in cog (memory or lang).symptoms are due2 :sub/toxin |
| Causes of delirium | include a high fever, nutritional deficiency, electrolyte disturbance, renal or hepatic failure, head injury, and certain drugs and medications (e.g., alcohol, lithium, sedatives, anticholinergic drugs), and it’s most common in hospitalized older adults |
| Delirium treatment | Treatment addressing causal/contributing medical prob and reducing disorientation -environmental manipulation , providing lighting, reduce noise, minimizing number of visitors. haloperidol/ antipsychotic drug may help reduce agitation/psychotic sym. |
| Major neurocognitive disorder | decline from a previous level of fxn in 1or more cogn domains (e.g., executive function, learning and memory, social cognition) that does not occur only in the context of delirium and that interferes with the person’s independence in everyday activities |
| Minor neurocognitive disorder | a modest decline from a previous level of funct in 1 or more cognitive domains that does not occur only w/ delirium , does not interfere w the person’s independence in everyday activities but may require more effort or the use of compensatory strategies |
| Neurocognitive Disorder Due to Alzheimer’s Disease: 60 to 80% of all cases of NCD | when the person’s symptoms (a) meet the criteria for mild or major NCD, (b) an insidious onset ,gradual progresn of impairment in 1+ cogn domains -does not interf w daily activities for mild NCD . 2+ cogn domains /interfe w daily activities for major. |
| major NCD, the diagnosis of probable Alzheimer’s disease requires | evidence of causative genetic mutation frm genetic testing or family history and/or evidence of a decline in memory/learning. at least one other cognitive domain, a steadily progressive and gradual decline in cognition, and no evidence of a mixed etiology |
| mild NCD, the diagnosis of probable Alzheimer’s disease requires | assigned when there’s no evidence of a causative genetic mutation but there’s evidence of a decline in memory and learning, a steadily progressive and gradual decline in cognition, and no evidence of a mixed etiology. |
| Alzheimer’s prevalence facts | rate women is greater-men. not clear women higher rates men same age. 65 +,Blacks have highest rates -Hisp/White. onset 70 to 89 yrs. early ons ages 49-59 is often chromos. mut. young ppl survive full dis. older ppl tend2 hav med probs affects illness. |
| Alzheimer’s diagnosis | can be definitively confirmed only w brain biopsy or autopsy w death. brain biopsy is rarely done due2 discomfort/risks . Therefore, an in vivo clinical diagnosis requires the presence of characteristic symptoms as well as elimination of other explanati |
| Pseudo dementia depression | usually respond well to treatment, and they have an abrupt onset of symptoms, exaggerate their cognitive problems, have moderate memory loss and symptoms of melancholia and anxiety, and often say “I don’t know in response” to assessment questions |
| Pseudo dementia vs Alzheimer’s | with Alzheimer’s disease have an insidious onset of symptoms, minimize or deny their cognitive problems, have severe memory impairment, and symptoms of apathy and avolition, and often respond to assessment questions with wrong answers |
| Alzheimer’s and biology/brain | Neurotransmitter abnormalities include reduced acetylcholine (ACh) and excessive glutamate, which are both known to be involved in learning and memory. The hallmark brain abnormalities are amyloid plaques and neurofibrillary tangles, |
| Alzheimer’s link to other NCD biology | neuronal loss in the locus coeruleus has also been linked to neurocognitive disorder with Lewy bodies and neurocognitive disorder due to Parkinson’s disease |
| Olfaction and Alzheimer’s | rapid deterioration in the sense of smell during a period of normal cognition predicts the subsequent development of mild cognitive impairment or Alzheimer’s disease, with greater olfactory loss being associated with greater cognitive impairment |
| Down syndrome risk alz | Standard trisomy 21 common type of Down syndrome caused by an extra chromosome 21. have extra gene for amyloid precursor protein (APP) gene. amyloid begins to accumulate in the brains late teens to early 20s and increases risk for early-onset alz. |
| Big Five and Alzheimer’s | participants who obtained high scores on neuroticism and low scores on conscientiousness had more deposits of amyloid and tau (the hallmarks of Alzheimer’s disease) than did participants who Had opposite scores |
| Alzheimer’s onset to death | onset until death varies but is about 8 to 10 years. |
| Alzheimer’s Stage 1- early onset | about 2 to 4 years and involves short-term memory loss ( 1st symptom), anomia, personality changes (often indifference), anxiety or depression, impaired attention and concentration, poor judgment, and disorientation to time and space. |
| Alz stage 2-middle stage | 2 to 10 years and is characterized by increasing STM /LTM loss, labile mood, irritability, idisorientation, psychosis, wander/pacing, perseveration (repetitive speech), los impulse control, disrupted sleep , problems w normal daily activities, sundowning. |
| Alzheimer’s stage 3-late stage | 1to 3 years -severely deteriorated cognitive , severe disorientation, apathy, severely impaired comm, aggression, decreased appetite, urinary and fecal incontinence, loss of basic motor skills,all self-care, abnormal reflexes, seizures, freq infections. |
| Alzheimer’s treatment | Cholinesterase inhibitors include donepezil/rivastigmine and delay the breakdown of ACh, while memantine is an NMDA receptor antagonist and regulates glutamate activity. Treatment cognitive and behavioral interventions, SSRI or antipsychotic |
| Neurocognitive Disorder with Lewy Bodies: | fluctuating cognition w variations in attn/alertness, recurrent visual halluc, sym of parkinsonism that develop after the cognitive symptoms. Suggestive features are symptoms of REM sleep behavior disorder and severe neuroleptic sensitivity |
| NCD lewy bodies mild vs major | probable NCD, the person must have at least two core features or one core feature and one suggestive feature; for possible NCD, the person must have one core feature or one or both suggestive features. Visual hallucinations /Parkinsonism |
| difference between NCD with Lewy bodies and NCD due to Alzheimer’s disease | Lewy-the prominent early cognitive symptoms are deficits in complex attention and visuospatial and executive functions Alzheimer’s the prominent early cognitive symptoms are deficits in learning and memory |
| difference between NCD with Lewy bodies and NCD due to Parkinson’s disease | Motor symptoms precede cognitive symptoms in NCD due to Parkinson’s disease, cognitive symptoms precede (orare concurrent with) motor symptoms in NCD with Lewy bodies. |
| Vascular Neurocognitive Disorder | suggested by a temporal relationship between the onset of symptoms and a stroke or other cerebrovascular event or by a prominent decline in complex attention and executive functioning; and there’s evidence of cerebrovascular disease |
| Vascular neurocognitive prognosis | may involve an acute onset w partial recovery, a stepwise decline, or a prog course w fluct in sym severity/plateaus vary in duration. intervention efforts target risk /causa factors; hypert. heart dis, diabetes mell, obesity, high chol, heavy smoking. |
| Neurocognitive Disorder due to HIV Infection: | Symptoms are characteristic of those associated with damage to subcortical areas of the brain and include forgetfulness, impaired attention and concentration, cognitive slowing, psychomotor retardation, clumsiness, tremors, apathy, and social withdrawal |
| NCD due to prion | have an insidious onset followed (in most cases) by a very rapid progression of impairment, and symptoms include motor features associated with prion disease or there’s biomarker evidence of the disease (e.g., characteristic lesions on an MRI) |
| Creutzfeldt-Jakob disease (CJD) | The most common prion NCD. often meet major NCD in as few as 6 months. Symptoms; confusion/disorient, impaired memory and judgment,, other neurocognitive deficits; ataxia, myoclonus, chorea,. motor symp; and psychiatric sym; apathy, anxiety, mood sw |
| Frontotemporal Neurocognitive Disorder | most common cause of early NCD (onset prior to 65). symptoms (a) meet major/mild NCD; (b)insidious onset/gradual progression; (c) do not sign impact learning/memory/perceptual-motor fxn, esp early stages; and (d) is behavioral or language variant. |
| Frontotemporal Neurocognitive Disorder Most common variant | behavioral variant is most common and involves prominent declines in social cognition and/or executive abilities (socially inappropriate , deficits in organizing and planning) plus three or more of the following behavioral and personality symptoms |
| The Language variant of Frontotemporal NCD | a prominent decline in language - deficits in speech production, word finding, object naming, grammar, comprehension. [Note that the language variant is often referred to in the literature as primary progressive aphasia (PPA), which consists of 3 subtypes |
| NCD due to another medical condition | Some NCDs caused by a med condition are irreversible but, when the medical condition is treatable, may improve or not progress. For example, NCDs due to hypoxia, infections, endocrine dis, poisoning, or nutritional deficiencies are potentially reversible. |
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