General objective

At the end of our case presentation we will be able to acquire more knowledge and determine the condition of the patient. Meet our goal in giving the appropriate nursing diagnosis and intervention through the information we had gathered.

Specific objectives
At the end of our case presentation, we will be able to: 1. Discuss about the patient condition and situation. 2. Evaluate the outcome of the case presentation.

3. Familiarized the drugs of the patient. 4. Formulate the nursing care plan prior to the patients condition. 5. Know the anatomy and physiology. 6. Observe signs and symptoms patient experience. 7. Know the psychopathophysiology . 8. Understand the existed mental disorder. 9. Discuss the prognosis. 10.Impart appropriate nursing considerations or teachings.

Posttraumatic stress disorder

Introduction

Post traumatic stress disorder (PTSD) -is a persistent and sometimes crippling condition precipitated by psychologically overwhelming experience. It develops in a significant proportion of individuals exposed to trauma, and untreated, can continue for years. Its symptoms can affect every life domain- physiological, psychological, occupational, and social. -post trauma stress reactions have been recognized throughout history. They are described in classical Greek literature and in modern times in the 1980 American Psychiatric Association Diagnostic and Statistical Manual. The surge of scientific and clinical interest in the condition over the past two decades has been largely due to awareness of problems associated with returning Vietnam combat veterans and advocacy by the feminist movement on behalf of rape victims. PTSD has not been documented in other groups including abuse children, victims of crimes, accidents and natural disasters. Not all trauma survivors develop PTSD. About 20% of crime victims, across type of crime, will meet diagnostic criteria. The rates are substantially higher for some crimes. For example, more than half of rape victims are afflicted. However, most crime victims do have initial PTSD symptoms that subside over time. PTSD is characterized by the symptoms that follow an extreme trauma. Diagnostic features, associated features, prevalence, course, differential diagnosis, and treatment considerations are discussed. PTSD involves symptoms that follow an extreme traumatic stressor. The response to the event needs to involve intense fear, helplessness, or horror persistent re experiencing of the trauma, and persistent symptoms of increased arousal. These symptoms must occur for more than one month and the distress must result in distress or impairment in social, occupational, or other functioning. Stimuli associated with the trauma are avoided, this may include thoughts, feelings, conversations, activities, situations, people or any reminders; this avoidance may also include amnesia for aspects of the trauma. Emotional numbing or diminished responsiveness to the external world may begin soon after the trauma. Feelings of detachment and loss of interest may occur. The future may feel shortened. Anxiety symptoms were not present prior to the trauma

and may include sleep disturbances with nightmares, hyper vigilance, exaggerated startle response, outburst of anger, and difficulty concentrating. Events that are threatening to life or bodily integrity will produce traumatic stress in its victim. This is normal, adaptive response of the mind and body to protect the individual by preparing him to respond to the threat by fighting or fleeing. If the fight or flight is successful, the traumatic stress will usually be released or dissipated allowing the victim to return to a normal level of functioning. PTSD develops: when fight or flight is not possible; the threat persists over a long period of time; and/or the threat is so extreme that the instinctive response of the victim is to freeze.

Definition of terms

1.) hippocampus is a major component of the brains of humans and other mammals. It belongs to the limbic system and plays important roles in the consolidation of information from short-term memory to long-term memory and spatial navigation. Like the cerebral cortex, with which it is closely associated, it is a paired structure, with mirror-image halves in the left and right sides of the brain. In Alzheimer's disease, the hippocampus is one of the first regions of the brain to suffer damage; memory problems and disorientation appear among the first symptoms. Damage to the hippocampus can also result from oxygen starvation (hypoxia), encephalitis, or medial temporal lobe epilepsy. People with extensive, bilateral hippocampal damage may experience anterograde amnesiathe inability to form or retain new memories. 2.) amygdalae ( /mdli/; singular: amygdala; also corpus amygdaloideum; Latin, from Greek , amygdal, 'almond', 'tonsil', listed in the Gray's Anatomy as the nucleus amygdal) are almond-shaped groups of nuclei located deep within the medial temporal lobes of the brain in complex vertebrates, including humans. Shown in research to perform a primary role in the processing and memory ofemotional reactions, the amygdalae are considered part of the limbic system.

3.) prefrontal cortex (PFC) is the anterior part of the frontal lobes of the brain, lying in front of the motor and premotor areas.This brain region has been implicated in planning complex cognitive behaviors, personality expression, decision making and moderating correct social behavior. The basic activity of this brain region is considered to be orchestration of thoughts and actions in accordance with internal goals. The most typical psychological term for functions carried out by the prefrontal cortex area is executive function. Executive function relates to abilities to differentiate among conflicting thoughts, determine good and bad, better and best, same and different, future consequences of current activities, working toward a defined goal, prediction of outcomes, expectation based on actions, and social "control" (the ability to suppress urges that, if not suppressed, could lead to socially-unacceptable outcomes) 4.) defense mecahanism. Any of various usually unconscious mental processes, including denial, projection, rationalization, and repression, that protect the ego from shame, anxiety, conflict, loss of self-esteem, or other unacceptable feelings or thoughts. 5.) Denial. An unconscious defense mechanism characterized by refusal to acknowledge painful realities, thoughts, or feelings. 6.) Repression. The unconscious exclusion of painful impulses, desires, or fears from the conscious mind. 7.) Suppression. Conscious exclusion of unacceptable desires, thoughts, or memories from the mind. 8.) Dissociation. A psychological defense mechanism in which specific, anxietyprovoking thoughts, emotions, or physical sensations are separated from the rest of the psyche. 9.) Transference. The process by which emotions and desires originally associated with one person, such as a parent or sibling, are unconsciously shifted to another person, especially to the analyst. 10.) GABA-ergic antagonist. Are drugs which inhibit the action of GABA. In general these drugs produce stimulant andconvulsant effects, and are mainly used for counteracting overdose of sedative drugs. 11.) Nonadrenergic inhibitor. Is a class of psychiatric drugs used primarily as antidepressants. 12.) Beta-blocker. A drug, such as propanolol, that opposes the excitatory effects of norepinephrine released from sympathetic nerve endings at betareceptors and is used for the treatment of angina, hypertension, arrhythmia, and migraine. Also called beta-adrenergic blocking agent. 13.) SSRI. A reuptake inhibitor (RI), also known as a transporter blocker, is a drug which inhibits the plasmalemmal transporter-mediated reuptake of a neurotransmitter from the synapse into the pre-synaptic neuron, leading to

an increase in the extracellularconcentrations of the neurotransmitter and therefore an increase inneurotransmission. 14.) TCA. A drug used to prevent or treat clinical depression. 15.) MAOI. Any of a class of antidepressant drugs that block the action of monoamine oxidase in the brain, thereby allowing the accumulation of monoamines such as norepinephrine. 16.) Antipsychotics. Drug use in counteracting or diminishing the symptoms of psychotic disorders, such as schizophrenia, paranoia, and bipolar disorder.

PSYCHOPHATOPHYSIOLOGY
Precipitating Factor

-chronic abuse as a child or adult

-major personal losses -gender

Anxiety

Neurochemical s/sx: PR, BP, RR

Serotonin s/sx: Crying, horror, fear,helpessness Emotional Depression s/sx: blunted-flat affect, Fatigue Apathy, Sadness

Physiologic

Impairment in functioning

PTSD

neurotransmitters

The three major categories of substances that act as neurotransmitters are (1) amino acids (primarily glutamic acid, GABA, aspartic acid & glycine), (2) peptides (vasopressin, somatostatin, neurotensin, etc.) and (3) monoamines (norepinephrine, dopamine & serotonin) plus acetylcholine. The major "workhorse" neurotransmitters of the brain are glutamic acid (=glutamate) and GABA. The monoamines & acetylcholine perform specialized modulating functions, often confined to specific structures. The peptides perform specialized functions in the hypothalamus or act as co-factors elsewhere in the brain.

Although there are many neurotransmitters in the central nervous system, the peripheral nervous system has only two: acetylcholine and norepinephrine. Why are there so many brain neurotransmitters? Because the functions performed by brain neurotransmitters are not as uniform as they might superficially appear. Some (like glutamate) are excitatory, whereas others (like GABA) are primarily inhibitory. In many cases (as with dopamine) it is the receptor which determines whether the transmitter is excitatory or inhibitory. Receptors can also determine whether a transmitter acts rapidly by direct action on an ion channel (eg, nicotinic acetylcholine receptors) or slowly, by a second-messenger system that allows for synaptic plasticity (eg, muscarinic acetylcholine receptors). Speed & mechanism of transmitter inactivation after the signal has been sent is also a factor. There are probably also costs & benefits involved in synthesizing, transporting and recycling various neurotranmitters in the differing chemical mileus of the brain.

Neurotransmitters are the chemicals which allow the transmission of signals from one neuron to the next across synapses. They are also found at the axon endings of motor neurons, where they stimulate the muscle fibers. And they and their close relatives are produced by some glands such as the pituitary and the adrenal glands. In this chapter, we will review some of the most significant neurotransmitters. Acetylcholine Acetylcholine was the first neurotransmitter to be discovered. It was isolated in 1921 by a German biologist named Otto Loewi, who would later win the Nobel Prize for his work. Acetylcholine has many functions: It is responsible for much of the stimulation of muscles, including the muscles of the gastrointestinal system. It is also found in sensory neurons and in the autonomic nervous system, and has a part in scheduling REM (dream) sleep. The plant poisons curare and hemlock cause paralysis by blocking the acetylcholine receptor sites of muscle cells. The well-known poison botulin works by preventing the vesicles in the axon ending from releasing acetylcholine, causing paralysis. The botulin derivative botox is used by many people to temporarily eliminate wrinkles - a sad commentary on our times, I would say. On a more serious note, there is a link between acetylcholine and Alzheimer's disease: There is something on the order of a 90% loss of acetylcholine in the brains of people suffering from Alzheimer's, which is a major cause of senility. Norepinephrine In 1946, a Swedish biologist by the name of Ulf von Euler discovered norepinephrine (formerly called noradrenalin). He also won a Nobel Prize. Norepinephrine is strongly associated with bringing our nervous systems into "high alert." It is prevalent in the sympathetic nervous system, and it increases our heart rate and our blood pressure. Our adrenal glands release it

into the blood stream, along with its close relative epinephrine (aka adrenalin). It is also important for forming memories. Stress tends to deplete our store of adrenalin, while exercise tends to increase it. Amphetamines ("speed") work by causing the release of norepinephrine, as well as other neurotransmitters called dopamine and seratonin.. Dopamine Another relative of norepinephrine and epinephrine is dopamine, discovered to be a neurotransmitter in the 1950s by another Swede, Arvid Carlsson. It is an inhibitory neurotransmitter, meaning that when it finds its way to its receptor sites, it blocks the tendency of that neuron to fire. Dopamine is strongly associated with reward mechanisms in the brain. Drugs like cocaine, opium, heroin, and alcohol increase the levels of dopamine, as does nicotine. If it feels good, dopamine neurons are probably involved! The severe mental illness schizophrenia has been shown to involve excessive amounts of dopamine in the frontal lobes, and drugs that block dopamine are used to help schizophrenics. On the other hand, too little dopamine in the motor areas of the brain are responsible for Parkinson's disease, which involves uncontrollable muscle tremors. It was the same Arvid Carlsson mentioned above who figured out that the precursor to dopamine (called Ldopa) could eleviate some of the symptoms of Parkinson's. He was awarded the Nobel Prize in 2000. Recently, it has been noted that low dopamine may related not only to the unsociability of schizophrenics, but also to social anxiety. On the other hand, dopamine has been found to have relatively little to do with the pleasures of eating. That seems to involve chemicals such as endorphin (see below). GABA In 1950, Eugene Roberts and J. Awapara discovered GABA (gamma aminobutyric acid), which is also usually an inhibitory neurotransmitter. GABA acts like a brake to the excitatory neurotransmitters that lead to anxiety. People with too little GABA tend to suffer from anxiety disorders, and drugs like Valium work by enhancing the effects of GABA. Lots of other drugs influence GABA receptors, including alcohol and barbituates. If GABA is lacking in certain parts of the brain, epilepsy results. Glutamate Glutamate is an excitatory relative of GABA. It is the most common neurotransmitter in the central nervous system - as much as half of all neurons in the brain - and is especially important in regards to memory. Curiously, glutamate is actually toxic to neurons, and an excess will kill them. Sometimes brain damage or a stroke will lead to an excess and end with many more brain cells dying than from the original trauma. ALS, more commonly known as Lou Gehrig's disease, results from excessive glutamate production. Many believe it may also be responsible for quite a variety of diseases of the nervous system, and are looking for ways to minimize its effects Glutamate was discovered by Kikunae Ikeda of Tokay Imperial Univ. in 1907, while looking for the flavor common to things like cheese, meat, and

mushrooms. He was able to extract an acid from seaweed - glutamate. He went on to invent the well known seasoning MSG - monosodium glutamate. It took decades for Peter Usherwood to identify glutamate as a neurotransmitter (in locusts) in 1994. Serotonin Serotonin is an inhibitory neurotransmitter that has been found to be intimately involved in emotion and mood. Too little serotonin has been shown to lead to depression, problems with anger control, obsessive-compulsive disorder, and suicide. Too little also leads to an increased appetite for carbohydrates (starchy foods) and trouble sleeping, which are also associated with depression and other emotional disorders. It has also been tied to migraines, irritable bowel syndrome, and fibromyalgia. Vittorio Erspamer first discovered what we now call seratonin in the 1930s. It was found in blood serum in 1948 by Irvine Page, who named it serotonin (from serum-tonic). Another researcher in Pages lab - Maurice Rapport proved that it was an amine (a group of chemicals that include the neurotransmitters). John Welsh found that it was a neurotransmitter in molluscs in 1954, and Betty Twarog (also at Page's lab) found it in vertebrates in 1952. All this gives you a sense of the cooperative nature of most of scientific discovery! Prozac and other recent drugs help people with depression by preventing the neurons from "vacuuming" up excess seratonin, so that there is more left floating around in the synapses. It is interesting that a little warm milk before bedtime also increases the levels of seratonin. As mom may have told you, it helps you to sleep. Serotonin is a derivative of tryptophan, which is found in milk. The "warm" part is just for comfort! On the other hand, serotonin also plays a role in perception. Hallucinogens such as LSD, mescaline, psilocybin, and ecstasy work by attaching to seratonin receptor sites and thereby blocking transmissions in perceptual pathways. Endorphin In 1973, Solomon Snyder and Candace Pert of Johns Hopkins discovered endorphin. Endorphin is short for "endogenous morphine." It is structurally very similar to the opioids (opium, morphine, heroin, etc.) and has similar functions: Inhibitory, it is involved in pain reduction and pleasure, and the opioid drugs work by attaching to endorphin's receptor sites. It is also the neurotransmitter that allows bears and other animals to hibernate. Consider: Heroin slows heart-rate, respiration, and metabolism in general - exactly what you would need to hibernate. Of course, sometimes heroin slows it all down to nothing: Permanent hibernation.