Development and Psychobiology NUR 250 PDF

Development and Psychobiology NUR 250: Pathophysiology Cerebral Palsy Definition: Brain damage before, during, or after birth that affects movement, walk, and posture Risk Factors: cerebral hypoxia, hemorrhage, infection, genetic abnormalities, or low birth weight Types: 1. Pyramidal/spastic: i...

Development and Psychobiology NUR 250: Pathophysiology Cerebral Palsy Definition: Brain damage before, during, or after birth that affects movement, walk, and posture Risk Factors: cerebral hypoxia, hemorrhage, infection, genetic abnormalities, or low birth weight Types: 1. Pyramidal/spastic: increased muscle tone, reflexes, hyperactive reflexes, rigidity of the extremities, contractures 2. Extrapyramidal/non-spastic: damage to cells in the basal ganglia, thalamus, or cerebellum a. Dystonic: difficulty in fine motor coordination and purposeful movements b. Ataxic: damage to the cerebellum ADD/ADHD Attention Deficit Disorder: trouble paying attention, difficulty finishing tasks, distracted Attention Deficit Hyperactivity Disorder: ADD but also overly active Risk factors: No one knows… genetics, maternal alcohol/tobacco use, preemies? Types: 1. Predominantly inattentive: difficulty finishing tasks, easily distracted, and forgets routines 2. Predominantly hyperactive-impulse: fidgets or talks a lot, jumps/runs constantly, restless, impulsive, risk-taking 3. Combined: both symptom types Behavioral therapy is first line treatment! Down Syndrome (Trisomy 21) Most common chromosomal condition Smaller total intracranial volume, difference in cerebellum, brainstem and frontal lobes Signs and symptoms: Intellectual disability, low nasal bridge, protruding tongue, poor muscle tone, hearing problems Risk factors: Rising maternal age Treatments: speech therapy, physical therapy, communication techniques Adults with Down Syndrome are at higher risk of sensory loss, hypothyroidism, and Alzheimer’s Autism Spectrum Disorder Risk factors: Unknown… may be due to genetics, paternal age, maternal health, inflammatory process in brain Vaccines do not cause autism! Signs and symptoms: Deficits in communication/social interaction, restricted and repetitive patterns or behavior, weak executive function Psychobiology: Diathesis-Stress Paradigm A theory that says a combination of predisposition and external stressors cause mental health conditions Components: 1. Genetics 2. Life stressors 3. Personality/coping 4. Environmental influences Basically… environmental stressors can make what’s already there worse Symptom Categories Cognitive symptoms: anything that affects thinking, learning, judgement Problems with memory, mood, anxiety, aggression Physical symptoms: fatigue, insomnia, restlessness Perceptual/Positive symptoms: what the disease adds (not necessarily good…) Ex: Hallucinations in schizophrenia Negative symptoms: what the disease takes away (a loss of functioning) Ex: Flat affect in schizophrenia More Parts of the Brain!! Prefrontal Cortex: receives info, plans appropriate reaction to stimuli Hippocampus: storing information into long term memory, emotional responses to memories Amygdala: primitive impulses such as aggression and sexuality, dysfunction can cause suicidality Hypothalamus: controls many functions key for survival such as temperature, feeding, sleep-wake cycles Thalamus: relays sensory information to CNS and filters unnecessary stimuli Brainstem: cardiac/respiratory control center Basal ganglia: Muscle tone, coordination, activity, posture Neuroplasticity vs Kindling Neuroplasticity: Brain can structurally and functionally reorganize itself and make new connections to compensate for loss of function (age dependant) Ex: People who lose their vision gaining enhanced senses over time Kindling: Repeated stimulation to a neuron will sensitize it Ex: PTSD, panic disorder “triggers” How Can NT Communication Go Wrong? No neurotransmitter Too much or too little neurotransmitter Pumps don’t work Receptor sites don’t work Degrading enzymes don’t work Anxiety Sense of dread without stimulus Signs and symptoms: palpitations, rapid breathing, rapid breathing Risk factors: trauma, stress, genetics NTTs: Less GABA (less calm), less serotonin (less happy), too much norepinephrine (fight or flight) Brain: Caudate nucleus only recalls negative, amygdala does TOO MUCH! Consolidation-reconsolidation abnormalities Generalized Anxiety Disorder Excessive worrying that interferes with daily function Signs and symptoms: worry centered anxiety, “free floating” Risk factors: trauma, stress, genetics NTTs: Less GABA (less calm), too much norepinephrine (fight or flight) Brain: Limbic system, midbrain OCD Obsessions that drive compulsions NTTs: Less serotonin (less happy), more cortisol (more stressed) Brain: Prefrontal cortex is overactive, frontal lobe causes too much guilt and worry, basal ganglia abnormalities PTSD Trauma “beyond the realm of normal human experience” Signs and symptoms: flashbacks, intrusive thoughts, impaired memory, hypervigilance, sleep disturbances, high suicide rate NTTs: Less GABA (less calm) Brain: Amygdala is hyperresponsive (suicidality), hippocampus causes flashbacks Also has consolidation-reconsolidation abnormalities Panic Disorder Sudden episodes of intense fear Signs and symptoms: “fear centered” anxiety, impending doom feeling, palpitations, sweating, numbness, paresthesia NTTs: Too much norepinephrine (fight or flight), less GABA (less calm), too much glutamate (too much excitement) Brain: Hippocampus, limbic system, prefrontal cortex Depression The big sad Major depressive disorder: 5 or more symptoms lasting 2 weeks or longer Risk factors: chronic illness, chronic stress, genetics, anxiety NTTs: more cortisol/CRF (more stressed), less serotonin (less happy), less norepinephrine (apathy/fatigue), less dopamine (less reward) Brain: Amygdala contributes to suicidality, neurons filter to only see the negative, negative feedback receptors are desensitized Bipolar Bipolar I: Manic and major depressive Bipolar II: Major depressive and hypomania Cyclothymic: alternating hypomanic and depressive symptoms not enough to meet criteria Risk factors: genetics, stress NTTs: more norepinephrine in mania and less in depression (fight or flight), serotonin and dopamine are all over the place, too much glutamate (can cause excitotoxicity over time) Brain: smaller/dysfunctional prefrontal cortex Schizophrenia Faulty perceptions, disconnection from reality, delusions, hallucinations First hit/Second hit theory: genetic susceptibility is triggered by stressful event(s) during adolescence Risk factors: genetics, other mental illnesses NTTs: norepinephrine, GABA, serotonin are all dysregulated, dopamine (causes language issues) Brain: Enlarged ventricles, widened sulci and fissures, decreased cerebral cortical volume in temporal and frontal lobes, volume reductions in hippocampus, amygdala, basal ganglia and thalamus, reduction in left-right temporal lobe asymmetry Addictions Compulsive drug use despite desire to stop and harm it’s causing to daily life Binge and intoxication: increased release of dopamine; activation of brain’s reward system. The nucleus accumbens and amygdala are pathologically altered over time so no happy without drug Preoccupation: decreased function of prefrontal cortex Tolerance: repeated use doesn’t cause same effect Withdrawal: physical dependance Treatments include support groups, CBT, meds Alcohol High risk for cancer, liver disease, cognitive dysfunction Alcohol is a CNS depressant NTTs: more GABA (more calm), less glutamate (less excitatory), more dopamine (reward) Rebound overstimulation and nervousness without alcohol ETOH withdrawal can cause delirium tremens, hallucinations, seizures Really bad alcohol withdrawal: Wernicke's encephalopathy Tobacco Nicotine addiction NTTs: binds to nicotinic cholinergic receptors, links to dopaminergic reward center, releases epinephrine Causes vasoconstriction which increases stress on the heart Half of all smokers will die from tobacco-related disease if they do not quit! Withdrawal causes irritability, difficulty concentrating, insomnia Opioids Fentanyl, oxy, morphine, heroin Interact at opioid receptors (don’t worry… you’ll learn these soon in pharm) Opioids are CNS depressants Overdose: sedation, respiratory depression, coma, death All done!!! :)