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NU 545
Unit 2 Study Guide
Advanced Pathophysiology
University of South Alabama.
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NU 545 Unit 2 Study Guide
- Review the anatomy of the brain. Which portion is responsible for keeping you awake, controlling thought, speech, emotions and behavior, maintaining balance and posture? P. 454- - Allows individuals to reason, function intellectually, express personality and mood and interact with environment Approx. 3 lbs and consistency of tofu 15%-20% of total cardiac output Midbrain, medulla oblongata and pons= brainstem Collection of nuclei within the brainstem= reticular formation - Reticular Formation (regulates vital function- cardio and respiratory) essential for maintaining wakefulness conjunction with cerebral cortex= reticular activating system - Prefrontal area- goal oriented behavior, short term/ recall memory, and elaboration of thought and inhibition on the limbic (emotional) areas of the CNS. - Broca Speech Area- responsible for motor aspects of speech (on left hemisphere) damage to this area as a result of CVA results in inability to form words (expressive aphasia and dysphasia) - Wernicke Area- superior temporal gyrus; responsible for reception and interpretation of speech - The Limbic System- primitive behavioral responses, visceral reaction to emotion, feeding behaviors, biologic rhythms, and sense of smell. Emotional and behavioral states= connections with the limbic system and prefrontal cortex - Cerebellum- responsible for conscious and unconscious muscle synergy-- for maintaining balance and posture.
- Know the function of the arachnoid villi. P. 468
- Arachnoid villi— protrude from the arachnoids space, through dura mater, and lie within the blood flow of the venous sinuses.
- CSF is reabsorbed by means of a pressure gradient btw the arachnoid vili and cerebral venous sinuses
- Vili function as one way valves they direct CSF outflow into the blood but preventing blood from into the subarachnoid space.
- Helps CSF circulate through the CNS and return to the blood
- Where is the primary defect in Parkinsons disease and Huntingtons p. 457 - Defects of the basal ganglia - Various involuntary and exaggerated motor movements
- What is the function of the CSF? Where is it produced? Where is it absorbed? P. 465 - Intracranial and spinal cord structures float in the CSF and are thereby partially protected from jolts and blows.
- Cause reflex withdraw of affected body part BEFORE pain sensation is perceived C- Fibers— unmyelinated, small- stimulated by mechanical, thermal and chemical nociceptors
- Slowly transmit dull, aching or burning sensations that last longer A-beta Fibers—large, myelinated fibers
- transmit touch and vibration sensations
- DO NOT normally transmit pain but play role in pain modulation
- Where in the CNS does pain perception occur?
- Pain Perception—conscious awareness of pain
- Sensory-discriminative System— somatosensory cortex Identifies the presence, character, location, and intensity of pain
- Affective-motivational System— reticular formation, limbic system, and brainstem with projections to the prefrontal cortex Determines individuals conditioned avoidance behaviors and emotional responses to pain.
- Cognitive-eevaluative System—cerebral cortex Overlies the individuals learned behavior concerning the experience of pain and can modulate perception of pain
- Know different clinical descriptions of pain (acute, chronic, neuropathic); pain threshold/tolerance p. 491-
- Acute Pain- protective mechanism that alerts the individual to a condition or experience that is immediately harmful to the body and mobilizes individual to take prompt action. Lasts seconds to days and up to 3 months Relieved after chemical mediators that stimulate pain receptors are removed Stimulation of ANS increase HR, HTN, diaphoresis, dilated pupils Acute somatic (superficial), Acute visceral (internal organs and lining of body cavities), Referred Pain (pain felt in an area removed or distant from its point of origin)
- Chronic Pain- lasting at least three months and lasting well beyond the expected healing time following onset. Serves no purpose and is poorly understood Changes in peripheral and central nervous system cause dysregulation of nociception and pain modulation process that are thought to lead to chronic pain Persistent pain allows for physiologic adaptation, producing normal heart rate and BP
- Neuropathic Pain- results from pain injury to the peripheral or central nervous system and is not the result of pain signaling from peripheral organs or tissues abnormal processing of sensory information by the PNS and CNS
Peripheral Neuropathic pain- peripheral nerve trauma; alcohol abuse, diabetics, HIV, carcinoma Central Neuropathic pain- brain/ spinal cord trauma, tumors, MS, Parkinson’s, phantom limb pain, vascular lesions Hemiagnosia Pain- central pain assoc with stroke that produces paralysis and hypersensitivity to one side of the body Phantom Limb Pain- pain in an amputated limb/ stump after healed Sympathetically Mediated Pain- peripheral nerve/ extremity damage- 1- 2wks after an extremity injury
- Pain Threshold— the point at which a stimulus is perceived as pain, does not vary significantly among people or in the same person over times. Intense pain at one location may increase threshold in another location
- Pain Tolerance—the duration of time or the intensity of pain that an individual will endure before initiating over pain responses. Decreased with repeated exposure to pain Influenced by culture, perceptions, expectations, role behaviors, physical and mental health, gender, fatigue, anger, boredom, apprehension and sleep deprivation Tolerance may be INCREASED by: alcohol, persistent use of pain meds, hypnosis, warmth, distraction, and strong faith beliefs.
- Endogenous opioids p. 490-
- Family of morphine-like neuropeptides that inhibit transmission of pain impulses in the spinal cord, brain and periphery. Their receptors also play a role in various CNS, gastrointestinal system, immune system, and other organ system disorders.
- Found to bind to almost all tissues in the body and this affect numerous biologic functions
- There are 4 types of neuropeptides: Enkephalins—best known and most prevalent; 1st endogenous opioid extracted in research, concentrated in the hypothalamus, PAG matter, nucleus raphe magnus of the medulla and the dorsal horn in the spinal cord. 2 types: methionine-enkephalin and leucine-enkephalin (ratio is 4:1) Endorphins— first discovered in human PAG.
- B-endorphin is synthesized and concentrated in the hypothalamus and pituitary gland; produces a greater sense of exhilaration, or “high,” than all the other types of endorphins; Strong u-receptor agonist and believed to provide substantial natural pain relief Dynorphins—most potent endogenous neurohormone; found in the hypothalamus, brainstem, PAG-RVM system, and spinal cord; generally, serve to impede pain signals but can in certain circumstances incite pain through mechanism of up-regulation Endomorphins—most potent analgesia, GI and anti-inflammatory effects. Can modulate stress and anxiety, feeding behavior, cough suppression, immune and inflammatory responses, and alcohol intake.
not evaporate and instead remains on the skin or drips, humidity low evaporates quickly) Increased Pulmonary Ventilation – exchanging air with the environment; minimal in humans; Hyperventilation associated with hyperthermia Voluntary Mechanisms- people physically “stretch out” and increase body surface area; “dress for warm weather” Adaptive to Warmer Climates – individual who goes from a cooler to a much warmer climate undergoes period of adjustment
- Know heat exhaustion and heat stroke? P. 500
- Heat Exhaustion— collapse is the result of prolonged high core/ environmental temperatures Vasodilation and profuse sweating Hypothalamic response produces dehydration, decreased plasma volume, hypotension, decreased cardiac output and tachycardia Weak, dizzy, nauseated and faint Lying down redistributes vascular volume
- Heat stroke—potentially lethal result of breakdown in control of an overstressed thermoregulatory center The brain cannot tolerate temperatures greater than 40.5C (104.9F) Sweat cools the person starting with the face and forehead (fanning increases mechanism) When Temperatures range 40-43degrees C (104-109.4F) the cardiovascular and thermoregulatory centers may cease to function properly Irritable, confused, stuporous, comatose, visual disturbances Cerebral edema, swollen dendrites, renal tubular necrosis, multiple organ failure and DEATH in treatment not initiated quickly Use cooling blankets, ice packs on head, neck, axillae, and groin area *Children more susceptible to heat stroke: 1. they produce more metabolic heat when exercising 2. they have greater surface area to body mass ratio 3. their sweating capacity is less
- Define the different stages of sleep. P. 502 o Normal sleep has two phases that can be documented by EEG: rapid eye movement (REM) sleep non REM (NREM) sleep o NREM sleep is divided into 3 stages followed by REM sleep o Awake: wakefulness with eyes closed and predominant with alpha waves o N1: light sleep, with alpha waves, slow eye movements o N2: presences of sleep spindles and slow-eye movements o N3: low-frequency high-amplitude delta waves with occasional sleep spindles; no slow eye movement o REM: sleep- time of most dreaming (20-25% of sleep time)
o NREM- (slow wave sleep)-75%-80% of sleep time Initiated by the withdrawal of neurotransmitters from the reticular formation and by the inhibition of arousal mechanisms in the cerebral cortex. Respiration is DEPENDENT and controlled by metabolic processes Basal metabolic rate is decrease by 10-15% Temperature decrease 1degrees C HR decreases by 10-30beats per min Respiration, BP and muscle tone all decrease, pupils constrict and knee jerk reflexes are absent N1 and N2= cerebral blood flow to brainstem and cerebellum is decreased N3= cerebral blood flow to cortex is decreased and growth hormone released, decreased corticosteroids o REM sleep (rapid eye movement)- 20-25% of sleep time and is characterized by low voltage, fast activity that occurs for 5-60minutes about every 90minutes. Vivid dreaming Paradoxic sleep- EEG pattern is similar to the normal awake pattern bursts of conjugate rapid eye movement in all directions atonia of antigravity muscles suppressed temperature regulation and alteration in HR, BP and Respirations penile erection in men, clitoral enlargement in women high rate of memorable dreams steroids released in short bursts respiratory control INDEPENDENT of metabolic requirements Respiratory obstruction common because of loss of tongue muscle control Cerebral blood flow to both hemispheres is increased. REM sleep controlled by the pontine reticular formation Loss of REM sleep impairs memory and learning
- Discuss disorders of the conjunctivia of the eye. P. 507 · Conjunctivitis- inflammation of the conjunctiva (covers front part of eyeball) Redness, edema, pain and lacrimation · Acute bacterial conjunctivitis- highly contagious, caused by gram positive bacteria (staphylococcus and haemophilus) acute onset, handwashing 10- days, in children haemophilus may lead to otitis media as well · Viral Conjunctivitis- adenovirus, some strains also cause pharyngitis, contagious- watering, redness and photophobia. Tx= symptomatic · Allergic Conjunctivitis- assoc. with antigens such as pollen. Burning, gritty feel in eye. Tx= antihistamines, corticosteroids · Chronic Conjunctivitis- persistent conjunctivitis, · Trachoma- (chlamydial conjunctivitis) caused by Chlamydia- poor hygiene and the leading cause of preventable blindness in the world. Corneal scarring from distorted eyelashes; Surgery for inturned lashes, antibiotics, facial cleanliness, and environment improvement
· Status Epilepticus—in adults is a state of continuous seizures lasting more than 5 min. OR rapidly recurring seizures before the person has fully regained consciousness from the preceding seizure, or a single seizure lasting more than 30min. · The onset of seizures may point to the presence of an ongoing primary neurological disease OR hypoglycemia, fatigue, emotional or physical stress, fever, hyponatremia, use of stimulant drugs, loud noises and withdrawal from drugs/ alcohol* · Etiological factors in seizures include: Cerebral lesions Biochemical disorders Cerebral trauma Epilepsy · Febrile Seizures— (pg. 679) seizures assoc. with fever in the absence of central nervous system infection Simple febrile seizures= benign febrile seizures and occur in 2%-5% of children Most common childhood seizure and patho is unknown · Distinguish febrile seizures from complex seizures precipitated by fever: Simple are rare before 9 months or after 5 years of age Rise in temp greater than 102. Acute resp tract infection or ear infection is usually present with no CNS infection Most occur during the first 24 hrs of illness Short, generalized and tonic Interictal EEG is normal Usually does not recur with the same infection No acute systemic metabolic disorder is present
- Know the characteristics of closed head injury. P. 582 and 587
- Involves head striking a hard surface or rapidly moving object striking the head.
- Dura matter remains intact, brain tissue not exposed
- Most closed trauma is mild and causes mild concussion and classic cerebral concussion.
- Mild concussion—CSF pressure rises, ECG and EEG changes occur without loss of consciousness, Glasgow coma scale 13-15, and confusion 1-several mins.
- Grades: Grade I: transient confusion and disorientation followed by amnesia, no loss of consciousness, resolve within 15min Grade II: transient confusion and retrograde amnesia that develops after 5- 10min, symptoms last more than 15min Grade III: any loss of consciousness, confusion and amnesia remain present from impact and persist for several mins.
- Define dyskinesia. Types? Characteristics? P. 561
- Dyskinesias—unnatural movements
- Hyperkinesia—excessive movements
- Paroxysmal dyskinesia—abnormal, involuntary movements that occur as spasms
- Tardive Dyskinesia—involuntary movement of face, trunk, and extremities. Side effect of prolonged use of psychiatric drugs OR Parkinson’s Continual chewing with protruding of the tongue, lip smaking, facial grimacing; excessive dopaminergic activity
- Hypokinesia—decreased amplitude of movement
- Bradykinesia—decreased speed of movement
- Akinesia— absence of voluntary movements Parkinson’s disease is the hallmark for lack of movement*
- Know the stages of intracranial hypertension p. 556
- ICP is normally 5-15mmHg or 60-180 mm H20.
- Increased ICP may result from an increased intracranial content (tumor growth), edema, excess CSF, or hemorrhage. It necessitates an equal reduction in volume of the other cranial contents. The most readily displaced content is CSF. If ICP remains high after CSF displacement out of the cranial vault, cerebral blood volume and blood flow are altered.
- Stage 1: vasoconstriction and external compression of venous system occur to decrease ICP ICP may not change or May cause a small increase in pressure and takes longer to return to baseline
- Stage 2: expansion of intracranial contents Pressure begins to compromise neuronal oxygenation and arterial vasoconstriction occurs in an attempt to elevate BP sufficiently to overcome the increase in ICP Confusion, restlessness, drowsiness, slight pupil and breathing changes
- Stage 3: ICP began to approach arterial pressure Brain tissues experience hypoxia and hypercapnia Condition of person deteriorates; decreased LOC, hyperventilation, widened pulse pressure, bradycardia and pupils small and sluggish
- Know normal intracranial pressure. How does body compensate for increased ICP?
- ICP is normally 5 to 15 mmHg, OR 69 to 180mm H2O
- Body compensates by equally reducing volume of other cranial contents, most readily is CSF
- Know the most critical index of nervous system dysfunction/function.
- What is responsible for the tremors associated with Parkinsons Disease?
- Immediately after a spinal cord injury, normal activity of spinal cords cells at and below the level of injury ceases because of loss of the continuous tonic discharge from the brain or brainstem and inhibition of suprasegmental impulses thus causing spinal shock.
- Spinal Shock—completes loss of reflex function, flaccid paralysis, sensory deficit, and loss of all bladder/ rectal control in all segments below level of injury. Disruption of central communication with sympathetic spinal nerves causes a transient drop in BP, poor venous circulation, and disturbed thermal regulation. Hypothalamus cannot regulate body temperature through vasoconstriction and increased metabolism, therefore, the individual’s body temperature assumes the temp of the air.
- Clinical manifestations of Acute Spinal Cord Injury: Rapid loss of voluntary movements in body parts below the level of injury Sensations in the lower extremities and possibly lower trunk (depending on the level of injury) Spinal and autonomic reflexes below the level of injury
- Spinal Cord Injuries are life threateningbecause they could possibly lead to autonomic dysreflexia
- Know diagnostic criteria for vegetative state and brain death. P. 534
- Brain Death— is death of the cerebral hemispheres exclusive of the brainstem and cerebellum; brain damage is permanent and severe, person will likely never behaviorally respond to environment Medical criteria for brain death:
- Complete all therapeutic procedures with no possibility of brain function recovery
- Unresponsive coma (absence of motor and reflex movements)
- No spontaneous respiration (apnea)- a PaCO2 that rises above 60mmhg without breathing efforts
- No brainstem function (dilated fixed pupils, no gag or corneal reflex)
- Isoelectric EEG(flat)
- Persistence of these signs for an appropriate observation period
- Vegetative State—complete unawareness of the self or surrounding environment and complete loss of cognitive function Diagnostic criteria:
- Periods of eye opening
- Reponses to pain such as posturing, tachycardia, diaphoresis
- Normal respiratory and digestive system function
- Occasional eye movements with tracking ability
- Brainstem motor functions intact
- Person does not speak any comprehensible words or follow commands
- Define and discuss the different types of stroke, which affected artery causes what data processing deficits (agnosia, dysphasia, etc). p. 598- 602
- Thrombotic Strokes (cerebral thrombosis)—arise from arterial occlusion cause by thrombi formation in the arteries supplying the brain or in the intracranial vessels Arthrosclerosis and inflammatory disease damage arterial walls Plaques form at branching and curves in the cerebral circulation Platelets and fibrin adhere to the damaged wall, and clots form— occluding the artery Clots detach and travel to distant sites where occlusion occurs, producing stroke symptoms
- Transient Ischemic Attack (TIA)—transient episodes of neurologic dysfunction (weakness, numbness, sudden confusion, loss of balance and loss of vision and h/a resulting from focal cerebral ischemia
- Embolic Stroke—involves fragments that break from the thrombus formed outside the brain or in the heart, aorta, or common carotid artery. Other sources include fat, air, tumor, bacteria and foreign bodiescauses ischemia Emobolization is usually distributed in the middle cerebral artery
- Cerebral infarction— when an area of the brain loses blood supply and becomes ischemic because of vascular occlusion (embolic or thrombotic)
- Lacunar Stroke—microinfarct smaller than 1cm in diameter and involves occlusion of the small perforating arteries, predominantly in the basal ganglia, internal capsules and pons. Assoc with hyperlipidemia, smoking, HTN and DM May have pure motor and sensory deficits
- Hemmorhagic Stroke—spontaneous bleeding in the brain Most common cause of primary hemorrhage strokes are HTN Most common sites: putamen in basal ganglia, thalamus, cortex, pons, and cerebral hemispheres Focal neurologic deficits are in 80% on people experiencing hemorrhagic strokes
- Know all types of cerebral edema and what causes each type. P. 557- 558
- Cerebral edemaan increase in the fluid content of the brain tissue, a net accumulation of water within the brain
- Vasogenic edema—most important, caused by increased permeability of the capillary endothelium of the brain after injury to the vascular structure Disruption of the blood brain barrier Plasma proteins leak into the extracellular spaces, drawing water to them, and the water content of the brain parenchyma increases Focal neurological deficits, disturbed consciousness, and severe increase in ICP Resolves by slow diffusion
Risk factors—possible autoimmune, associated with immunizations, frequently preceded by mild respiratory or intestinal infection
- Clinical manifestations Progress over hours to days, minimal musical atrophy, symmetrical paralysis Causes problems with respiration, talking, swallowing, bowl and bladder function Begins in lower extremities and ascends bilaterally weakness, ataxia, bilateral paresthesia progressing to paralysis
- Mysthenia Gravis p. 624-
- Pathophysiology chronic, autoimmune disease mediated by acetylcholine receptor antibodies that act at the neuromuscular junction. Results from a defect in nerve impulse transmission at the neuromuscular junction, Autoantibodies block acetylcholine or cause loss of acetylcholine from neuromuscular junction T-cell dependent formation of autoantibodies against receptors at the Ach- binding sites on postsynaptic membrane.
- Etiology unknown, some persons have genetic susceptibility related to variants in acetylcholine genes, as well as the major histocompatibility genes, and they can present with varying clinical phenotypes
- Clinical manifestations Exertional fatigue and weakness that worsens with activity and improves with rest Recent hx of recurring upper resp tract infections Muscles of the eye, face, mouth, throat and neck are affected 1st Diplopia, ptosis and ocular palsies Facial droop and expressionless face Difficulty chewing and swallowing, drooling Weakness of arms and legs and eventually weakness of diaphragm impairing ventilation
- Parkinsons disease p. 564- Pathophysiology: o Parkinsonism tremor appears to result from instability of feedback from the basal ganglia to the cerebral cortex cause by the loss of the inhibitory influence of dopamine in the basal ganglia* Etiology: o Parkinson disease (PD) is a complex motor disorder accompanied by systemic nonmotor and neurologic symptoms. The main disease feature is degeneration of the basal ganglia involving the dopaminergic (dopamine-secreting) nigrostriatal pathway. Onset occurs after 40 years of age, with mean onset of 60 years of age.
The pathogenesis of primary PD is unknown although several PD genes have been identified. Clinical manifestations: o Resting tremor, bradykinesia/akinesia (poverty of movement), muscular rigidity, and postural abnormalities. Manifestations may develop alone or in combination; as disease progresses, all 4 usually present to some degree; No true paralysis.
- Huntington disease p. 562-
- Pathophysiology relatively rate, autosomal dominant disease; onset usually btw 25-45 years of age, when trait is already passed to children severe degeneration of the basal ganglia, particularly the caudate and putamen nuclei and the frontal cerebral cortex* degeneration of the basal ganglia leaves enlarged lateral ventricles expression of the huntingtin gene produces tangles of protein that collect in brain cells and chains of glutamine on the abnormal molecules that adhere to each other GABA depletion on dopamanergic neuronsin the substantia nigra
- Etiology genetic defect on the short arm of chromosome 4
- Clinical Manifestations hypotonia and hyperkinesias (chorea- excess of dopamanergic activity) emotional lability progressive dysfunction of cognitive processes (dementia) chorea can be combined with athetosis (twisting and writhing) short term memory loss, decreased ability to plan, slow thinking and attention deficits (frontal lobe defect) euphoria and depression
- Prenatal and perinatal factors may result in what psychiatric condition?
- Some of the prenatal and perinatal factors that may result in schizophrenia are: exposure to prenatal infection, prenatal nutritional deficiencies, perinatal complications (such as birth defects and neonatal hypoxia).
- What is schizophrenia? What part of the brain is associated with the S/S of this disorder? P. 642-
- Schizophrenia is a serious psychiatric illness, describes collection of illnesses characterized by thought disorders which reflect a break in reality or splitting of the cognitive from the emotional side of one’s personality.
- a feeling of happiness when recollecting a terrible event or emotional indifference when describing a joyful occasion
- positive and neg. symptoms including hallucinations, paranoid delusions, and cognitive deficits
- Pathological changes in the dorsal prefrontal cortex are believed to contribute to negative symptoms of schizophrenia
- Major Depression— The illness is complex and stems between susceptible genes and environmental influences. Life stressors and a potentially dysfunctional serotonin (5-HT) systems appears to elevate the risk of depression (p. 648). Monoamine hypothesis of depression found a deficit in the concentration of brain norepinephrine, dopamine, and serotonin = underlying cause of depression; also found a reduction of monoamine metabolites in the CSF in depressed clients (p. 648). Chronic activation of the HPA system and elevated glucocorticoid secretion are found in depression. There is also an altered hypothalamic-pituitary-thyroid (HPT) system (p. 648). There is also norepinephrine receptor alterations found in the frontal cortex of suicide victims.
- Stress-Induced Depression—Uncontrollable stress activates the HPA system and immune response system. Psycho-social stress increases secretion of proinflammatory cytokines, such as interleukin - 1α (IL-1α) and IL-β, tumor necrosis factor –alpha (TNF-α), and IL-6, which modulates signaling pathways throughout the periphery and brain and augments further secretion of HPA hormones and monoamine metabolism. There is also a chronic elevation in cortisol levels, atrophy in neurons in the hippocampus (neurogenesis), and a deficit in hippocampal brain- derived-neurotrophic factor (BDNF) levels.
- In depressed individuals there is a widespread decrease in serotonin 5-HT1a receptor subtype binding in the frontal, temporal, and limbic cortex as well as serotonin transporter binding in the cerebral cortex and hippocampus.
- How Does ECT (electroconvulsive therapy) treat depression? P. 652
- Mechanism of action of the ECT is not clear, the procedure is known to produce alterations in monoamine systems.
- ECT effectively alleviates depressive sx in 50%-80% of people. Used when patients fail on antidepressants, severely, depressed, pregnant, psychotic or suicidal.
- Define generalized anxiety disorder. What is the underlying defect? Know characteristics. P. 655
- Generalized anxiety disorder (GAD)— hallmark s/s are excessive and persistent worrying. The individual worries about life events, job performance, health, money, and social status. 6 major s/s of GAD are:
- Restlessness
- Muscle tension
- Irritability
- Being easily fatigues
- Difficulty concentrating
- Difficulty sleeping
Other characteristics include startles easily and frequently suffer from depression and panic attacks.
- Underlying defects: abnormalities in nor epinephrine and serotonin systems. reduction in the α2-adrenergic receptor binding decrease in the serotonin levels in CSF reduced platelet binding of paroxetine, an SSRI reduction of BZ (GABA-Benzodiazepine) binding in the left temporal hemisphere.
- Anticipatory anxiety was associated with elevated cingulate cortex activity and both the heightened anxiety and cingulate cortex activation were reduced after 8 weeks of treatment. A decrease in pathophysiologic cingulate cortex activity is a predictor of GAD.
- *In children and adolescents heightened right amygdala activation corresponds positivity with severity of anxiety.
- Define Panic Disorder. What are the complications? P. 654
- consists of multiple disabling panic attacks and is characterized by intense autonomic arousal involving a wide variety of sx: lightheadedness a rapid heart rate (tachycardia) difficulty breathing chest discomfort generalized sweating general weakness trembling abdominal distress Chills or hot flashes
- Between panic attacks the person often worries about future panic attacks and fear of losing control and dying.
- Sx occur spontaneous and can last a few minutes to an hour.
- Complications: Hyperventilation, elevated heart rate and respiration rates, tachycardia, and a possible addiction to over use of anxiolytics.
- Define encephalocele, meningocele, spina bifida, myelomeningocele. Where is the defect located in each? P. 663-
- Encephalocele—herniation or protrusion of various amounts of brain and meninges through a defect in the skull, resulting in a saclike structure. Occurs during first weeks of pregnancy Most contain neural tissue and meninges and occur in the occipital area, with the remainder found in the frontal, parietal, or nasopharygeal areas.
- Spina Bifida—birth defects in which there is failure of closure of the vertebrae (split spine) 2 types:
- Meningocele—cystlike dilation of meninges protruding through a defect in the posterior arch of the vertebrae; spinal cord intact
