ANA 442 Exam 3 (Answered) 2022 Graded A+

ANA 442 Exam 3 (Answered) 2022 Graded A+ PD as not just a disease of DA neurons Midbrain/brainstem and some peripheral DA neurons of SN and VTA 5-HT neurons of brainstem, descending projections NE neurons of LC Substance P, ACh, Vagal nerves ALL SEEM TO BE LIGHTLY MYELINATED Clinical PD Bradykinesia Rigidity resting tremor gait changes Biochemistry of PD 80% loss of DA in caudate/putamen Pathology of PD 50% loss of DA neurons in Pars Compacta (SN) Premotor Phase of PD constipation- gut alpha synuclein, smell, cardiac, sleep disturbances Anticholinergics for PD treat the resting tremor, avoid in older patients MAO-B inhibitors prevents metabolism of DA, fairly well-tolerated but with little efficacy PD Non-motor manifestations and their associated neurobiology PNS: pain, constipation Spine: orthostatic hypotension Brainstem: anxiety, depression, sleep dist. Cortical: cognitive deficits, psych disorders, anosmia Ideal animal model of PD 1. human brain anatomy (both caudate and putamen) 2. clinical symptoms (motor and non-motor) 3. neuropathology: lose DA neurons + Lewy bodies 4. Neurochemistry: striatal DA depletion 5. behavioral response to L-DOPA Invertebrate models of PD fruit fly: molecular and cellular roundworm: genetic and molecular Zebrafish PD MPTP elucidates genetic pathways, is responsive to DA mimetics Mice and rats PD model unilateral: 6-OHDA bilateral: systemic MPTP or Rotenone Toxicity mechanisms for PD 6-OHDA: taken up by DA transporter, generates free radicals rotenone: C1 inhibitor MPTP: turned into MPP+, taken up into mitochondria, leading to C1 inhibition and free radical formation 6-OHDA animal model behavior d-amphetamine: DA released, ipsilateral turning APO (apomorphine): DA receptor agonist, contralateral turning 6-OHDA weaknesses and benefits benefits: cheap, DA cell loss, motor deficits, reponds to DA mimetics weakness: 6-OHDA doesn't cross BBB, rat basal ganglia different than human, rapid and non-progressive, young animals, no Lewy bodies MPTP rodents adv. and weaknesses advantages: cheap, BBB, DA cell loss Disadvantages: not all strains of mice are susceptible to MPTP, sometimes spontaneous recovery MPTP monkey model adv: similar basal ganglia, motor and cognitive deficits disadvantages: expensive, non-progressive, spontaneous recovery, no lewy bodies, non-motor deficits PTSD core features emotional numbing, hyper-arousal, re-experiencing, avoidance re experiencing in PTSD recurrent and intrusive recollection, dreams, feeling event is happening, distress at symbolism avoidance features of PTSD don't want to think of incident, literally forget, avoid hoomans and stuff arousal features of PTSD sleepless, irritability, anxiety, hypervigilence, poor concentration, startle response DSMV PTSD 2 of the following: intrusion, avoidance, negative alterations in cognition, alterations in arousal Risk events for PTSD rape, assault, shoot/stab, death of family, witness killing, natural disaster Fight or flight neurobiology NE and epi release, locus coerulus firing, amygdala HPA neurobiolgy hypothalamus releases corticotropin releasing hormone pituitary releases adrenocorticotrophic hormone this all increases cortisol levels physiological markers of PTSD autonomic increase increased baseline HR and BP increased resting HR in traumatized children Neurobiology/ neurochemistry for PTSD increased DA NE and E, increased affinity for adrenergic Endocrinology studies PTSD decreased level of cortisol, but increased corticol response PTSD and therapy group therapy effective- a social aspect implied? very high suicide rates, as with MDD Hippocampus and PTSD decreased hippocampal volume Medications for PTSD SSRIs, NE antagonist PTSD after TBI brain injury causing impaired consciousness no memory- how PTSD?? learning, stress hormones, HPA is primed TBI increases chance of PD, ALS, AD PTSD General idea network-disorder maybe neurodegenerative used to seem psychiatric, but now looks to be more neurodegenerative and chronic none of these are ever really a "single illness" at all Suicide in military very high in army most vulnerable to TBI DSMV for Schizophrenia 2+ of the following: delusions hallucinations disorganized speech grossly disorganized OR catatonic behavior negative symptoms (like mundane expressions) Cognition in schizophrenia may be a bit cognitively impaired change into phenotype in late adolescence Current schizophrenia treatment biopsychosocial model group therapy watch for one person in their unit/family that cna cause relapse meds for psychoses biological basis of schizophrenia genetic load structural brain changes- PFC antrophy, enlarged ventricles, hippocampal and thalamic atrophy neurochemial abnormalities MAY BE NEURODEGENERATIVE Dopamine hypothesis of schizophrenia