med diagnosis pathophysiology

  1. hi all, I'm in the process of writing my care plan and the admitting dx of my pt was "altered consciousness: other"...not quite sure how to explain the pathophysiology on that one, what would you do?
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    About jesa

    Joined: Aug '06; Posts: 118; Likes: 28
    ED RN
    Specialty: ED


  3. by   PsychNurseWannaBe
    I would need more information...such as, what is causing the altered consciousness. Do you know?
  4. by   jesa
    pt has history of paranoid schizophrenia, he was brought in from an assisted living center with the thought that maybe he was being over-medicated - he was non-responsive, etc. pt also has parkinson's
  5. by   GingerSue
    not sure if this is an answer, but, as I sit here and read my mental health textbook (trying to understand the pathophysiology of schizophrenia)

    -sensory overload, hallucinations that may be triggered by anxiety or by functional changes in the central nervous system. Researchers found that the same brain area was activated when clients listened to audible speech as when they were experiencing audible hallucinations. The brain reacts as if unable to distinguish between its own internally generated speech and actual, audible speech. Auditory hallucinations occur in 50 to 80% of people with schizophrenia. Schizophrenia often disrupts the filtering process(filter out unnecessary and distracting information), causing sensory overload. When too many messages arrive at the cortex at the same time, thinking becomes disorganized and fragmented. Schizophrenics may be overly sensitiveto background noises and colors and shapes.

    It is thought that delusions represent dysfunctions in the information-processing circuits within and between the hemisphere.

    The basic flaw seems to be that certain nerve cells migrate to the wrong areas when the brain is first taking shape, leaving small regions of the brain permanently out of place or miswired. In some cases the neurons of the cortex may be deficient. A hypothesis is that exposure to nutritional deficiency during fetal life may be a risk factor for schizophrenia.

    Neurochemical factors - Glu, involved in learning and memory, may be responsible for some of the cognitive symptoms. Glu is necessary for the breakdown of dopamine and other transmitters, which affects the efficiency of prefontal information processing. Glu receptors may have a role in regulating the migration and pruning of neurons during brain development and may play a role in structural abnormalities seen in schizophrenia. Excessively high levels of norepinephrine are associated with positive symptoms, while paranoid symptoms have been related to increased dopamine activity.

    People with schizophrenia are depleted of both DHA (docosahexaenoic acid found in omega-3-type fish oil) and AA (arachidonia acid). These deficiencies may be related to the negative symptoms of schizophrenia.

    The areas most noted for abnormalities include the prefontal cortex, the temporal lobes, thehippocampus, the limbic system, the thalamus, and the ventricles. There could be decreased tissue volume in specific areas, in others there is disrupted cerebral blood flow, in some cases there is decreased utilization of glucose and oxygen, and in others there is increased ventricular size.

    One deviation is decreased blood flow to the thalamus that may affect the ability of the brain to filter sensory signals, causing the person to be flooded with sensory information. Changes in cerebral blood flow suggestabnormalities in the density, size, or configuration of blood vessels in the person with schizophrenia.

    For some people with schizophrenia, there is a deficiency of nicotinic receptors in the hippocampus, important area for attention to new sensory stimuli and memory function.
  6. by   Daytonite
    you can go to sites like medicine net and web md and look up the symptom of "unconsciousness" to get information on it. you may have to use alternative terms for it such as syncope, stupor or coma. you should also know what the various levels of consciousness are when you go looking for information about it (somnolence, confusion, lethargy, stupor, coma )
    just looking up the term "unconsciousness" in my copy of taber's cyclopedic medical dictionary netted some interesting information on the causes and gave some of the pathological process involved.

    since you probably don't have this book, i am printing the information from it for you. . .(from page 395-402, signs and symptoms: a 2-in-1 reference for nurses, published by lippincott williams & wilkins, 2005)
    "level of consciousness, decreased

    a decrease in level of consciousness (loc), which can range from lethargy to stupor to coma, usually results from a neurologic disorder and may signal a life-threatening complication, such as hemorrhage, trauma, or cerebral edema. however, this sign can also result from metabolic, gi, musculoskeletal, urologic, or cardiopulmonary disorders; severe nutritional deficiency; effects of toxins; or drug use. loc can deteriorate suddenly or gradually and can remain altered temporarily or permanently.

    consciousness is affected by the reticular activating system (ras), an intricate network of neurons with axons extending from the brain stem, thalamus, and hypothalamus to the cerebral cortex. a disturbance in any part of this integrated system prevents the intercommunication that makes consciousness possible. loss of consciousness can result from a bilateral cerebral disturbance, an ras disturbance, or both. cerebral dysfunction characteristically produces the least dramatic decrease in a patient's loc. in contrast, dysfunction of the ras produces the most dramatic decrease in loc--coma.

    the most sensitive indicator of decreased loc is a change in the patient's mental status. the glasgow coma scale, which measures a patient's ability to respond to verbal, sensory, and motor stimulation, can be used to quickly evaluate a patient's loc.
    try to obtain history information from the patient, if he's lucid, and from his family. did the patient complain of headache, dizziness, nausea, visual or hearing disturbances, weakness, fatigue, or any other problems before his loc decreased? has his family noticed any changes in the patient's behavior, personality, memory, or temperament? also ask about a history of neurologic disease or cancer; recent trauma or infection; drug and alcohol use; and the development of other signs and symptoms.
    physical assessment
    decreased loc can result from a disorder affecting virtually any body system. after performing a complete neurologic examination, let the results of your history guide the rest of your physical assessment.
    medical causes
    [i am just listing the information that was highlighted at the edges of the pages for each condition]
    adrenal crisis - decreased loc, ranging from lethargy to coma, may develop within 12 hours of onset.
    brain abscess - decreased loc varies from drowsiness to deep stupor; intractable headache, nausea, vomiting, and seizures occur.
    brain tumor - loc decreases slowly, from lethargy to coma; apathy, behavior changes, memory loss, decreased attention span, morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances may occur
    cerebral aneurysm (ruptured) - somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding
    cerebral contusion - unconscious patients may have dilated, nonreactive pupils and decorticate or decerebrate posture; conscious patients may be drowsy, confused, disoriented, agitated, or violent
    diabetic ketoacidosis - decrease in loc is rapid and ranges from lethargy to coma; polydipsia, polyphagia, and polyuria precede decreased loc
    encephalitis - decreased loc may range from lethargy to coma within 24 to 48 hours of onset
    encephalopathy - with hepatic encephalopathy, decreased loc ranges from slight personality changes to coma depending on the stage; with hypertensive encephalopathy, loc progressively decreases from lethargy to stupor to coma; with hypoglycemic encephalopathy, loc rapidly deteriorates from lethargy to coma; hypoxic encephalopathy produces a sudden or gradual decrease in loc, leading to coma and brain death; with uremic encephalopathy, loc decreases gradually from lethargy to coma
    epidural hemorrhage (acute) - patient has momentary loss of consciousness; rapid deterioration in consciousness follows, possibly leading to coma
    heatstroke - as body temperature increases, loc gradually decreases from lethargy to coma
    hypernatremia - loc deteriorates from lethargy to coma; patient is irritable and exhibits twitches that progress to seizures
    hyperosmolar hyperglycemic nonketotic syndrome (hhns) - loc decreases rapidly from lethargy to coma; early findings include polyuria, polydipsia, weight loss, and weakness
    hypokalemia - loc gradually decreases to lethargy
    hyponatremia - decreased loc occurs in late stages
    hypothermia - when severe, loc decreases from lethargy to coma; mild to moderate cases produce memory loss, slurred speech, shivering, weakness, fatigue, and apathy
    intracerebral hemorrhage - a rapid, steady loss of consciousness occurs within hours and is accompanied by severe headache, dizziness, nausea, and vomiting
    meningitis - confusion and irritability occur; stupor, coma, and seizures may occur in severe cases
    myxedema crisis - decline n loc may be swift
    pontine hemorrhage - a sudden, rapid decrease in loc to the point of coma occurs within minutes; death occurs within hours
    seizure disorders - a complex partial seizure causes decreased loc, manifested as a blank stare, purposeless behavior, and unintelligible speech; an absence seizure involves a brief change in loc, indicated by blinking or eye rolling, blank stare, and slight mouth movements; a generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness but consciousness returns after the seizure; an atonic seizure produces sudden unconsciousness for a few seconds; status epilepticus involves rapidly recurring seizures
    shock - decreased loc occurs late
    stroke - loc changes vary in degree and onset; loc changes may be abrupt or take several minutes, hours, or days
    subdural hematoma (chronic) - loc deteriorates slowly
    subdural hemorrhage (acute) - agitation and confusion are followed by progressively decreasing loc from somnolence to coma
    thyroid storm - loc decreases suddenly and can progress to coma; irritability, restlessness, confusion, and psychotic behavior precede the deterioration
    tia - loc decreases abruptly (with varying severity) and gradually returns to normal within 24 hours
    west nile encephalitis - severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death
    other causes
    alcohol - alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.
    drugs - sedation and other degrees of decreased loc can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.
    poisoning - toxins, such as lead, carbon monoxide, and snake venom, can cause varying degrees of decreased loc. confusion is common, as are headache, nausea, and vomiting. other general features include hypotension, cardiac arrhythmias, dyspnea, sensorimotor loss, and seizures.
    special considerations
    reassess the patient's loc and neurologic status at least hourly. carefully monitor icp and intake and output. ensure airway patency and proper nutrition. take precautions to help ensure the patient's safety. keep him on bed rest with the side rails up, and maintain seizure precautions. keep emergency resuscitation equipment at the patient's bedside. prepare the patient for a computed tomography scan of the head, magnetic resonance imaging of the brain, eeg, and lumbar puncture. keep the head of the bed elevated at least 30 degrees. don't administer an opioid or a sedative because either may further decrease the patient's loc and hinder an accurate, meaningful neurologic examination. apply restraints only if necessary because their use may increase his agitation and confusion.
    pediatric pointers
    the primary cause of decreased loc in children is head trauma, which usually results from physical abuse or a motor vehicle accident. other causes include accidental poisoning, hydrocephalus, and meningitis or brain abscess following an ear or a respiratory infection. to reduce the parents' anxiety, include them in the child's care. offer them support and realistic explanations of their child's condition.
    patient counseling
    talk to the patient even if he appears comatose; your voice may help reorient him to reality. explain all treatments and procedures to the patient and his family. explain all safety and seizure precautions. discuss quality-of-life decisions with the patient and his family, and make the appropriate referrals to other sources of support such as hospice care."
    hope this information was helpful for you.
  7. by   jesa
    thanks everyone! this information is really helpful! I am now prepared to go back and write this section...when I have enough time to sift through the info! and will use the information re: different levels and different causes, boil it down to the assumed cause for my patient (over-medication) and go to the patho of how over-medication of his specific drugs could induce altered consciousness.
  8. by   MB37
    I got in trouble on something similar - my pt was admitted for hemoptysis, and the doctors hadn't figured out what was causing it. We aren't allowed to write the patho section on a symptom, so I correctly didn't do hemoptysis, but apparently we're supposed to do it on whatever medical diagnosis/diagnoses they suspect or are trying to rule out. I did my patho section on one of her comorbidities, and it wasn't what my teacher wanted. So for your patient we'd have to do it on schizophrenia. Make sure you know what your instructor requires for each section.