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Pathophysiology > Patho Unit 5 > Flashcards

Patho Unit 5 Flashcards

Understand: - Pain, Temperature Regulation, Sleep, and Sensory Function (Ch 13) - Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor Function (Ch 14) - Disorders of the Central and Peripheral Nervous Systems and the Neuromuscular Junction (Ch 15)

1
Q

Pain

A

A complex interaction, between physical, cognitive, spiritual, emotional, and environmental factors

  • Can’t be characterized as only a response to injury
  • “Whatever the experiencing person says it is, existing whenever he says it does”
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2
Q

Gate Control Theory

A
  • Pain transmission is modulated by a balance of impulses conducted to the spinal cord
  • Cells in the gray matter of the dorsal spinal cord act as a pain gate
  • A-δ and C fibers open the gate (neurons carrying pain)
  • Other sensations may close the gate (stimulating touch receptors)
  • Doesn’t explain all observable pain
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3
Q

Neuromatrix Theory

A
  • The brain produces patterns of nerve impulses drawn from various inputs including genetic, psychologic, and cognitive experiences
  • Neuromatrix patterns are generally activated by sensory inputs
  • Other stimuli that do not produce pain may trigger pain patterns (phantom limb pain)
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4
Q

Pain Perception

A

Conscious awareness of pain, the result of the interaction of 3 systems

  • Sensory-Discriminative
  • Affective-Motivational
  • Cognitive-Evaluative
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5
Q

Sensory-Discriminative System

A

Somatosensory Cortex identifies presence, character, location, and intensity of pain

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6
Q

Affective-Motivational System

A

Individual’s emotional response to pain

- Mediated through reticular formation, limbic system, brain stem

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7
Q

Cognitive-Evaluative System

A

Can modulate pain by overlying learned behavior

- Mediated through cerebral cortex

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8
Q

Pain Threshold

A

The lowest intensity of pain that a person can recognize

  • Pain in one location may increase the threshold in another
  • Influenced by genetics, gender, culture, expectations, and physical and mental health
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9
Q

Pain Tolerance

A

The greatest intensity of pain that a person can tolerate

- Influenced by genetics, gender, culture, expectations, and physical and mental health

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10
Q

3 portions of the nervous system that are responsible for sensation and perception of pain?

A
  • Afferent pathways
  • Interpretive centers
  • Efferent pathways
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11
Q

Afferent Pathways

A

Begin with pain receptors (nociceptors), travel to spinal gate in dorsal horn, then ASCEND to higher centers in CNS

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12
Q

Interpretive Centers

A

Located in brain stem, midbrain, diencephalon, and cerebral cortex

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13
Q

Efferent Pathways

A

Descend from CNS back to dorsal horn of spinal cord

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14
Q

Nociceptors

A
  • Chemoreceptors (detect chemicals from damaged tissue, and products of blood and inflammation)
  • Means “receiving noxious information” i.e. pain information
  • Anatomically, appears as free nerve ending in skin
  • Same anatomical type receives temp information
  • Axon carries information to CNS
  • A-δ and C
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15
Q

A-δ Nociceptors

A
  • Myelinated
  • Fast, “bright” pain
  • Acute pain
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16
Q

C Nociceptors

A
  • Unmyelinated
  • Itching, Slow, “dull” pain
  • Chronic pain
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17
Q

Pain Transduction

A

Begins when tissue is damaged by exposure to chemical mechanical, or noxious stimuli stimulating nociceptors

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18
Q

Chemicals detected by Nociceptors

A
  • K+
  • Prostaglandins (vascular permeability, chemotaxis & pain)
  • Leukotrienes (slower, prolonged histamine like effect)
  • Aspirin works as an analgesic (pain reducer) by blocking prostaglandin E2 synthesis
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19
Q

Blood Products detected by Nociceptors

A

Serotonin from platelets, Bradykinin from plasma

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20
Q

Products of Inflammation detected by Nociceptors

A

Histamine

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21
Q

Pain Transmission

A

The conduction of pain impulses to the spinal cord

  • Axons in spinal cord and brainstem on opposite side from where they entered (info from the left side is carried in right Spinothalamic tract and right Brainstem)
  • Relayed in Thalamus
  • Info ends up in Somatosensory Cortex (postcentral gyrus)
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22
Q

Transmitters of Ascending Pain Pathways

A
  • Glutamate
  • Substance P (for pain)
  • Nitric Oxide (NO)
  • All are excitatory neuromodulators of pain
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23
Q

Transmitters of Descending Pain Pathways

A
  • Serotonin
  • GABA
  • Norepinephrine
  • Endogenous Opioids (Endorphin, Enkephalin)
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24
Q

Endorphins and Enkephalins

A

Peptide neurotransmitters made by the brainstem and released in the spinal cord

  • Attach to Opiate receptors (the same as opium, heroin, morphine, and related drugs)
  • Stress, excessive physical exertion, acupuncture and sex all increase them
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25
Q

Action of Opioids

A

Within the posterior (dorsal) horn, receptors for opioids shut off pain signal at synapses

  • Reduce the release of pain transmitters (Substance P and Glutamate)
  • Reduce the response of postsynaptic cells (block Nitric Oxide NO)
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26
Q

Acute Pain

A
  • Protective mechanism against bodily harm
  • Transient, usually lasting seconds to days
  • Autonomic nervous system stimulated (increased heart rate, hypertension, diaphoresis, dilated pupils)
  • Classified as Somatic and Visceral
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27
Q

Somatic Acute Pain

A

Superficial and well-localized pain

- Sharp, dull, aching, or throbbing

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28
Q

Visceral Acute Pain

A

Pain in internal organs and linings of body cavities

  • Poorly localized, aching, gnawing, throbbing, cramping
  • Often radiates from original site
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29
Q

Referred Pain

A

Your mind constructs a rough map of where your organs are, depending on what nerve roots are shared with information coming in from skin and organs. Based on this the brain decides where pain is “referred” to.

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30
Q

Chronic Pain

A

Pain lasting 3-6 months or well beyond normal healing time

  • Doesn’t respond to usual therapy
  • Dysregulation of nociception and pain modulation
  • Neuroimaging studies have demonstrated brain atrophy leading to decreased ability to cope with pain
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31
Q

Common Chronic Pain Conditions

A
  • Low back
  • Postoperative
  • Cancer
  • Hyperesthesia
  • Hemiagnosia
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32
Q

Hyperesthesia

A

Increased sensitivity and decreased pain threshold to tactile and painful stimuli

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33
Q

Hemiagnosia

A

Loss of ability to identify source of pain on one side of the body
- Associated with stroke

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34
Q

Myofascial Pain Syndrome
Fibromyalgia
Chronic Fatigue Syndrome

A
  • Interrelated chronic pain syndromes
  • Borders between them aren’t clear
  • Compression of trigger points cause referred pain, movement disorders, and autonomic responses
  • Little is known, and only effective treatment is antidepressants
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35
Q

Neuropathic Pain

A

Chronic pain characterized as burning, shooting, shock-like, or tingling

  • Caused by primary lesion or dysfunction in the nervous system
  • Leads to long term changes in pain pathway structure and abnormal processing of sensory function
  • Hyperalgesia and Allodyina
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36
Q

Hyperalgesia

A

Abnormally heightened sensitivity to pain

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37
Q

Allodyina

A

Pain from stimuli that are not normally painful

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38
Q

Peripheral Neuropathic Pain

A

Trauma or disease to one or more peripheral nerves

- Nerve Entrapment

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39
Q

Nerve Entrapment

A

Nerves that are compressed or entrapped

- ex: Carpel Tunnel Syndrome

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40
Q

Diabetic Neuropathy

A

Lack of nutrition to nerve axons damages them

- Pain receptors activated and “always on”

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41
Q

Central Neuropathic Pain

A

Phantom Pain

  • Brain perceives pain in amputated limb
  • Obviously no receptors exist
  • Recent studies suggest this is because of reorganization of the somatosensory cortex and “fight” for brain territory in remaining areas (ex: right leg info tries to occupy space vacated by right arm after amputation)
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42
Q

Body Temperature

A

37° C / 98.6° F

- Controlled by the Hypothalamus

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43
Q

Fever

A

Resetting of the “Hypothalamic Thermostat” to a higher setting by Exogenous/Endogenous Pyrogens

  • During fever, factors are released to help diminish the febrile response in a (-) feedback loop
  • Endogenous cryogens released
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44
Q

Exogenous Pyrogens

A

Bacteria

- Destroyed and absorbed by phagocytes

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45
Q

Endogenous Pyrogens

A

Inflammation

  • Stimulate increased metabolism and body temp
  • Interleukin 1
  • Tumor Necrosis Factor Alpha (TNF-α)
  • Interferons
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46
Q

Endogenous Cryogens

A

Set the hypothalamic thermostat back to normal when fever breaks
- Argenine Vasopressin

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47
Q

How is Fever beneficial?

A
  • Kills some organisms directly, and affects the growth of others by sequestering needed nutrients (iron, copper and zinc)
  • Promotes lysosomal breakdown with autodestruction of cells to prevent viral replication in infected cells
  • Increases lymphocyte transformation and phagocyte motility
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48
Q

Hyperthermia

A

Overheating, causes nerve damage, coagulation of cell proteins, and cell death

  • 41° C / 105.8° F produces convulsions
  • 43° C / 109.4° F causes death
  • Heat cramps, exhaustion, and stroke are forms of accidental hyperthermia
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49
Q

Heat Cramps

A

Spasmodic cramps in abdomen and limb muscles related to prolonged sweating and sodium loss

  • Usually in people not accustomed to warm climates
  • May be accompanied by fever, rapid pulse, and increased blood pressure
  • Administer dilute salt solutions
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50
Q

Heat Exhaustion

A

Collapse due to prolonged high body core or environmental temperature

  • Cause hypothalamic induction of large-scale vasodilation and profuse sweating
  • Dehydration, hypovolemia (low blood volume), decreased cardiac output, hypotension, and tachycardia
  • Individual feels weak, dizzy, nauseated, and faint
  • Treat with warm fluids to replace fluid loss
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51
Q

Heat Stroke

A

Breakdown of thermoregulatory control (the brain doesn’t tolerate temps >40° C / 104° F)

  • Sweating ceases, skin becomes dry, internal core temp rises rapidly
  • Leads to vascular collapse
  • Causes Rhabdomyolysis
  • Death will result without gentile cooling (rapid cooling is dangerous, causing peripheral vasoconstriction and prevents core cooling)
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52
Q

Rhabdomyolysis

A

The degeneration of the CNS and muscles

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53
Q

Hypothermia

A

Extreme cold, causes depression of CNS and respiratory symptoms

  • Cognitive and muscular processes become sluggish, chemical reactions slows, increases blood viscosity, encourages coagulation and vasoconstriction and can lead to ischemic tissue damage
  • In severe cases, ice crystals form on the inside of cell causing lysis and death
  • Hypothalamic center stimulates shivering to increase heat production
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54
Q

Hypothermia Treatment

A

Gradual re-warming of tissues is required

  • Superficial
  • Core rewarming with warm IV fluids, gastric or peritoneal lavage, or inhalation of warmed gases
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55
Q

Therapeutic Hypothermia

A

Protects the brain by reduction in metabolic rate, ATP consumption, and reduces critical threshold for oxygen delivery

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56
Q

Temperature Regulation in Infants and the Elderly

A
  • Both have difficulties with temp regulation
  • Infants have little subcutaneous fat, greater ratio of body surface to body weight, inability to shiver
  • Elderly have slow blood circulation, slowed activity levels, decreased shivering, slowed metabolic rate, and decreased vasoconstrictor response and ability to sweat
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57
Q

REM Sleep

A

Rapid Eye Movement

  • Occurs about every 90 minutes
  • Roughly equivalent to dream sleep
  • Body is paralyzed, eyes move
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58
Q

Non-REM Sleep

A

Stages 1 (light sleep) through 4 (deep sleep)

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59
Q

Dysomnias

A

Disorders of initiating and maintaining sleep and disorders of excessive sleeping
- Insomnia, Sleep Apnea, and Narcolepsy

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60
Q

Insomnia

A

Inability to fall or stay asleep
- Long therm insomnia may be associated with drug or alcohol abuse, chronic pain disorders, chronic depression, use of certain drugs, obesity, and aging

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61
Q

Sleep Apnea

A
  • Lack of breathing during sleep (at least 10 seconds between breaths)
  • Can be central or obstructing apnea or a combination
  • Produces low O2 saturation, pulmonary hypertension, polycythemia, cyanosis, edema, and right-sided heart failure
  • Treatment: weight loss, O2 therapy (CPAP), respiratory stimulant, surgery to relieve the obstruction
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62
Q

Narcolepsy

A

Symptoms:

  • Periods of extreme drowsiness for ~15 minutes every 3-4 hours
  • Dream-like hallucinations during the transition from sleep to wakefulness
  • Inability to move at both sleeping and waking transitions
  • Often includes cataplexy
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63
Q

Cataplexy

A

Loss of muscle tone while awake

- Can be triggered by emotional excitement

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64
Q

Parasomnias

A

Unusual behaviors during sleep

- Somnambulism, Night Terrors, and Enuresis

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65
Q

Somnambulism

A

Sleep walking

  • Individual functions at a very low level of arousal with no memory of the event
  • Individuals can end up in dangerous situations
  • Usually occurs in children during the first third of the night and resolves over time
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66
Q

Night Terrors

A

Characterized by extreme terror and a temporary inability to regain full consciousness

  • Patient awakens abruptly gasping, moaning, or screaming
  • No memory of the episode (nightmares can usually be recalled)
  • Calm the person and convince them to “go back to sleep” (they are already in stage 4 sleep)
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67
Q

Enuresis

A

“Bed-wetting”

  • Occurs when a child is difficult to arouse
  • Developmental delay, and is usually outgrown
  • Thought to have a hereditary component
  • Rule out medical causes: child is evaluated for infections, obstructions, neurogenic bladder, and decreased nocturnal antidiuretic hormone
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68
Q

Restless Leg Syndrome

RLS

A

More prevelent in women than men
Iron deficiency and Substantia Nigra appears to be the main cause
Symptoms:
- An urge to move the legs, with an accompanying uncomfortable sensation
- Worse during rest or inactivity, and at nigth
- Relieved by movement

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69
Q

Strabismus

A

Deviation of one eye from the other when looking directly at a specific object

  • May often, but not always, lead to Amblyopia
  • Treatment: botulinum toxin injection to partially paralyze stronger muscle of the pair
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70
Q

Amblyopia

A

If one eye doesn’t focus or produce what the brain decides is an unreliable image during the critical period, then the information is discarded and only one eye is “wired into” the brain

Treatment: alternately patch each eye

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71
Q

Nystagmus

A

Involuntary unilateral or bilateral rhythmic movement of the eyes

  • May be caused by an imbalanced reflex activity of the inner ear (inner ear sends a signal in the absence of movement, eyes move as if head is rotating)
  • May also be caused by drugs, retinal disease, and disease involving the cervical spinal cord
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72
Q

Cataract

A

Clouding of the lens

  • Caused by UV light exposure, diabetes, infections, trauma, and drugs
  • Treatment: lens is liquified inside its capsule and intraocular lens is implanted in its place
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73
Q

Glaucoma

A

Abnormal pressure in the anterior chamber

  • Measure intraocular pressure with tonometer (puff of air)
  • Increased pressure can reduce blood supply to retina and cause permanent vision loss
  • Can result from overproduction by ciliary processes, obstruction in flow, or scleral venous sinus)
  • Drugs which cause pupil dilation tend to close the sinus and make glaucoma worse
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74
Q

Macular Degeneration

A

Loss of critical neurons in the Macula for unknown reasons

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75
Q

Presbyopia

A

As we age, the lens loses its elasticity, which prevents it from taking on a round shape when relaxed (needed to focus on near objects)
- Treatment: reading glasses

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76
Q

Retinal Detachment

A

Neurons of the retina lose their nutritional support and die
- Since neurons can’t repair; treatment is to limit spread of damage by “spot welding” retina to the sclera with either cold or heat

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77
Q

Emmetropia

A

Normal vision

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78
Q

Myopia

A

Near-sighted, eyeball is too long

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79
Q

Hypermetropia

A

Far-sighted, eyeball too short

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80
Q

Astigmatism

A

Unequal curvature of the cornea or lens

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81
Q

Alterations in Color Vision

A

Mutations in the green pigment gene is most common

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82
Q

Conjunctivitis

A

Inflammation of the Conjunctiva (pinkeye)

  • Highly contagious acute bacterial infection
  • May lead to otitis media in children under 6
  • Also caused by viruses, allergies, or chemical irritants
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83
Q

2 categories of Hearing Loss

A

Conductive and Sensorineural

84
Q

Conductive Hearing Loss

A

Occurs when a change in the outer and/or middle ear impairs conduction of sound waves

  • Foreign bodies, cerumen impaction (ear wax), neoplasms, auditory tube dysfunction
  • Infection: Acute Otitis Media (AOM), especially in children from 6 months to 5 years
85
Q

Sensorineural Hearing Loss

A

Involves the inner ear structures and cranial nerve VIII

  • Due to congenital, hereditary, or environmental factors
  • Streptomycin and related antibiotics, loud noises, aspirin at toxic levels
86
Q

Vertigo

A

Sensation of spinning that is caused by inflammation or other disorders of the semicircular canals
- Causes loss of balance, disorientation, nausea, and severe sensations that the room is spinning

87
Q

Meniere Disease

A

A not uncommon vestibular disorder of unknown etiology
- Results in loss of proprioception, inability to walk or drive a car (affects gait and vision by causing vertigo) and persistent ringing in the ears

88
Q

Proprioception

A

Knowing how your body is oriented without looking at it (“How you know you have a butt”)

89
Q

Consciousness

A

A function of arousal and content of thought

- Activity in the cerebral cortex

90
Q

Reticular Activating System

RAS

A

Neurons that control state of arousal

  • Projects to all areas of the cortex
  • Inputs to RAS from sensory system
  • Outputs of RAS to cerebral cortex, regulating arousal
91
Q

Unimpaired

A

“Fully functional”, alert and oriented to person place and time (Oriented x3)
- Normal speech, voluntary movement, oculomotor activity, respirations, and pupillary responses

92
Q

Structural Alterations of Arousal

A
  • Infections
  • Vascular
  • Neoplastic
  • Traumatic
  • Congenital
  • Degenerative
93
Q

Metabolic Alterations of Arousal

A
  • Hypoxia
  • Electrolyte disturbances
  • Hypoglycemia
  • Drugs
  • Toxins
94
Q

Psychogenic Alterations of Arousal

Unresponsiveness

A

Patient may appear unconscious but is physiologically awake

- May signal a general psychiatric disorder

95
Q

Confusion

A

Loss of ability to think rapidly and clearly

96
Q

Disorientation

A

Disorientation to time, and then place (usually person is preserved

97
Q

Lethargy

A

Limited spontaneous movement, easily aroused, not oriented x3

98
Q

Obtundation

A

Mild to moderate reduction in arousal

  • Falls asleep if not continuously stimulated
  • Single syllable answers to questions
99
Q

Stupor

A

Can only be aroused with vigorous and continuous stimulation

100
Q

Light Coma

A

Purposeful movement on stimulation

101
Q

Coma

A

Nonpurposeful movement on stimulation

102
Q

Deep Coma

A

No response

103
Q

Skeletal Muscle Decorticate Posture

A
  • Loss of connections between cortex and spinal cord/muscles
  • Upper extremities flexed at elbows and held close to the body
  • Lower extremities extended with toes pointed
104
Q

Skeletal Muscle Decerebrate Posture

A
  • Upper extremities now extended (thought to involve loss of input to arms from Red Nucleus in midbrain) - Lower extremities the same as Decorticate Posture
  • Seen in extensive brain stem damage
  • Death is imminent
105
Q

Outcomes of Alterations of Arousal

A

Range from full recovery to permanent disability or death
2 categories:
- Extenet of disability
- Mortality

106
Q

Brain Death

A

Irreversible cessation of function of the entire brain, including the brain stem and cerebellum

107
Q

Cerebral Death

A

Death of cerebral hemispheres exclusive of the brain stem and cerebellum
- The brain stem may respond but individual is unable to respond to their environment

108
Q

Persistent Vegetative State

A
  • Complete unawareness of self or environment with complete loss of cognitive function
  • Brain stem reflexes intact
  • Recovery unlikely if the state persists for more than 12 months
109
Q

Minimally Conscious State

A

Individuals may follow simple commands, have intelligible speech, and may blink or smile

110
Q

Locked-in Syndrome

A
  • Complete paralysis of voluntary muscles except eye muscles

- Content of thought and level of arousal are intact but efferent pathways are blocked

111
Q

Anterograde Amnesia

A
  • Inability to form new memories

- Usually damage to hippocampus

112
Q

Retrograde Amnesia

A
  • Inability to recall memories from before traumatic event
  • May be a few seconds
  • May be years (Damage to brain structures where memory is stored)
  • Distant events stored more strongly/in more locations and less likely to be lost
113
Q

Seizure

A

Abnormal electrical activity in the brain

114
Q

Epilepsy

A

A transient occurrence of signs and/or symptoms as a result of abnormal excessive or enhanced synchronous neuronal activity in the brain

115
Q

Generalized Seizures

A
  • Abnormal activity over a wide area of the brain
  • Consciousness impaired or lost
  • Most common type: absence seizures (“spacing out”)
116
Q

Partial Seizures

A

Focal seizures, unilateral

  • Specific area affected
  • May progress to generalized seizures
117
Q

Prodroma

A

(symptom) Early clinical manifestation a few days or hours preceding a seizure
- Maliase, headaches, depression

118
Q

Aura

A

(symptom) Partial seizure, feeling that “something is about to happen”
- Gustatory, visual, auditory, dizziness, numbness, funny feeling

119
Q

Tonic Phase

A

(sign) Contraction of muscle(s)

120
Q

Clonic Phase

A

(sign) Alternating contraction and partial relaxation of muscles

121
Q

Ictus

A

Time that seizure is occurring

122
Q

Postictal State

A

Period immediately following end of seizure activity

123
Q

Status Epilepticus

A

Life threatening emergency

  • Patient has a string of seizures with no respite
  • Usually caused by discontinuation of prescribed seizure medications
124
Q

Agnosia

A

Defect of pattern recognition

  • Generally only one sense is affected (tactile, visual, auditory)
  • Ex: an individual may be able to identify an object by touch but not by site)
125
Q

Dysphasia

A

Impairment of production or comprehension of language

126
Q

Aphasia

A

More severe form of dysphasia and ability to communicate

127
Q

Broca Aphasia

A

“Non-fluent aphasia”, Patient unable to produce written or oral speech

  • May have one syllable that he uses for all speech
  • Appears frustrated or angry
128
Q

Wernicke Aphasia

A

“Fluent aphasia”, Patient can speak, but language makes no sense and lacks grammatical structure

129
Q

Testing for Aphasia and Other Brain Disorders

A 
Comprehension:
What is happening in the picture?
  - Word Salad = Wernicke
  - Inability to speak = Broca
  - Ignores left side of picture = Contralateral Hemineglect 
Naming Ability:
Name the objects.
  - Does the patient need prompting?
  - Are names correct?
  - Are answers slow or vague?
130
Q

Dementia

A

Progressive failure of cerebral functions

  • Patient loses orientation to person, place and/or time
  • Memory loss
  • Decline in intellectual ability leads to altered behavior
131
Q

Major Causes of Dementia

A
  • Alzheimers (>50%)
  • Alcoholism
  • Parkinsons
  • Neoplasms of CNS
  • Neurosyphilis
  • Prion disease (Creutzfeld-Jacob)
  • Chronic Meningitis
132
Q

Alzheimer Disease

A
  • Leading cause of dementia
  • Declarative memory most severely affected
  • Neuropsychological testing suggests diagnosis, but only definitive diagnosis is post-mortem examination of the brain
133
Q

Alzheimer Brain

A
  • As neurons die, brain shrinkage occurs
  • Memory, language, and judgment areas most affected
  • Using imaging, it is difficult to distinguish between normal aging and Alzheimers
134
Q

Alzheimer Therapy

A
  • Acetylcholinesterase Inhibitors (AChEIs), which make more acetylcholine available at the remaining synapses
  • Only shifts the course of a 10 year+ disease by a few months
135
Q

Cerebral Hemodynamics

A

Injuries to the brain may induce alterations in cerebral blood flow, intracranial pressure and O2 delivery
- Increases in intracranial pressure may cause a decrease in blood perfusion

136
Q

Sources of Intracranial Pressure

A
  • Space-occupying lesion
  • Hydrocephalus
  • Brain Edema
137
Q

Space-Occupying Lesions

A
  • Hematomas

- Brain Tumors

138
Q

Increased ICP

Stage 1

A

Vasoconstriction and external compression of venous system to decrease ICP

  • Few symptoms
  • ICP may not change due to compensation
139
Q

Increased ICP

Stage 2

A

Continued expansion of intracranial content

  • Systemic arterial vasoconstriction in an attempt to overcome increased ICP
  • Patient may be confused restless, drowsy, and may have slight pupillary and breathing changes
140
Q

Increased ICP

Stage 3

A

ICP begins to approach arterial pressure

  • Brain tissues begin to experience hypoxia and hypercapnia
  • Patient’s condition rapidly deteriorates
  • Decreased levels of arousal, widened pulse pressure, bradycardia, and small, sluggish pupils
  • Dramatic rises in ICP when compensatory mechanisms exhausted
141
Q

Increased ICP

Stage 4

A

Brain tissue herniates

142
Q

Uncal Herniation

A

When there is more pressure in the Supratentorial compartment than the Infratentorial compartment, the brain tries to “leave” (herniates) past the Tentorium Cerebelli

  • The Uncus is in the way
  • Underneath the Uncus are the structures for DECLARATIVE MEMORY (facts, dates, and events)
143
Q

Tonsillar Herniation

A

If Supratentorial pressure continues, or pressure begins in the Infratentorial compartment, Cerebellar Tonsils and Medula try to “leave” skull at same time through the Foramen Magnum

  • This part of the medulla controls HEARTBEAT AND RESPIRATION
  • Death can result
144
Q

White Matter in Spinal Cord

A

Contains ascending (sensory) and descending (motor) tracts

145
Q

Gray Matter in Spinal Cord

A

Where neural information is processed

  • Posterior/Dorsal Horn processes sensory information
  • Anterior/Ventral Horn contains cell bodies of neurons which control voluntary muscles
146
Q

Motor Pathway

A

Lateral Corticospinal Tract

  • Axons from motor cortex
  • Cross at pyramidal decussation
  • In the spinal cord, motor fibers are on the same side as the muscles they will eventually innervate
147
Q

Hypotonia

A

Decreased muscle tone, caused by decreased neuronal activity

148
Q

Hypertonia

A

Increased muscle tone

149
Q

Hyperkinesia

A

Excessive movement

150
Q

Dyskinesia

A

Abnormal involuntary movements

151
Q

Hypokinesia

A

Decreased movement

152
Q

-paresis

A

weakness

153
Q

-plegia

A

paralysis

154
Q

Hemiparesis

A

Weakness of the upper and lower extremity on one side (common after stroke)

155
Q

Diplegia

A

Paralysis affecting both arms or both legs

- Due to brain damage

156
Q

Paraplegia

A

Partial or total paralysis in the lower extremities

- Dut to spinal cord damage

157
Q

Tetraplegia

Quadriplegia

A

Partial or total paralysis in all four extremities

- Due to spinal cord damage

158
Q

Lower vs Upper Motor Neurons

A
  • Lower motor neurons in the spinal cord directly innervate skeletal muscle
  • Upper motor neurons are all the others (including cortex neurons)
159
Q

Flaccid Paralysis

A

Loss of LOWER MOTOR NEURON

  • There is no way to “drive” the muscle
  • Patient exhibits HYPOREFLEXIA
160
Q

Spastic Paralysis

A

Loss of UPPER MOTOR NEURON is thought to remove inhibition of reflexes

  • AKA Rigidity
  • Patient exhibits HYPERREFLEXIA
161
Q

Upper Motor Neuron Lesion

A

Loss of control from brain means reflexes operate without modification
Ex: The Babinski Sign (stroke the sole of the foot)
- In normal adults, response is PLANTAR FLEXOR
- In spinal cord damage, brain damage or in babies less than 1, response is PLANTAR EXTENSOR

162
Q

Neurotransmitters in the Basal Nuclei

A
  • Basal Nuclei control smooth movement
  • Motor cortex signal is processed through this system
  • Interactions between motor inhibiting neurotransmitters (GABA, Dopamine) and excitatory neurotransmitters (Acetylcholine) control movement
163
Q

Parkinson Disease

A
  • Neurons in the Substantia Nigra make dopamine and send axons to the basal nuclei, where dopamine is release
  • In Parkinson Disease, these neurons die for unknown reasons
164
Q

Parkinson Disease Symptoms

A
  • “Pill-Rolling” tremor at rest
  • Slow movement (bradykinesia)
  • Stooped posture
  • Chracteristic gait (trouble getting through doorways
  • About 40% have dementia
165
Q

Huntington Disease

A

Trinucleotide repeat disease, 40 or more repeats of CAG in the Huntington Gene (normal is 10-29)

  • Causes Dementia and Chorea (writhing, dance-like movements)
  • Degeneration of Basal Nuclei with degeneration of GABA producing neurons (inhibitory) leads to Hyperkinesia
  • More repeats means more severe disease and earlier onset
166
Q

Traumatic Brain Injury

Open Trauma

A

Penetrating or Open head injuries occur from missile trauma

  • Injuries break the dura and expose the cranial contents possibly causing infection or loss of CSF
  • Produce FOCAL/observable injuries
167
Q

Traumatic Brain Injury

Blunt Trauma

A

Brain is not exposed
Focal:
- Observable
- Epidural (extradural) hematoma, Subdural hematoma, Intracerebral hematoma, Contusion

Diffuse:

  • Not observable
  • Concussion, Diffuse Axonal Injury (DAI)
168
Q

Focal Brain Injury

A

Closed-head injuries usually present as COUP and COUNTERCOUP contusions

169
Q

Coup Injury

A

The direct impact between the brain and skull

170
Q

Countercoup Injury

A

Directly opposite the Coup injury, from the brain “bouncing” and impacting the opposite side of the skull

171
Q

Epidural Hematoma

A

Focal brain injury

  • Bleeding usually ARTERIAL, between skull and dura mater
  • Can be insidious (slow onset)
  • Usually lens shaped on CT/MRI
  • Symptoms: increasingly sever headache, vomiting, drowsiness, confusion, and seizure
  • Can produce paralysis on opposite side of body
  • May cause brain herniation
172
Q

Subdural Hematoma

A

Focal brain injury

  • Bleeding usually VEINOUS
  • More difficult to see on CT/MRI
  • Symptoms insidious and chronic: headache, drowsiness, slowed cognition, and confusion
  • May cause brain herniation
173
Q

Intracerebral Hematoma

A

Focal brain injury

  • Usually seen in falls and motor vehicle crashes
  • Shearing forces tear blood vessels inside the brain
  • May cause weakness and paralysis
  • May progress to herniation
174
Q

Cortical Contusion

A

Focal brain injury

  • Like a brain bruise
  • Edema because of injury
  • Can be very difficult to see on CT/MRI
175
Q

Concussion

Mild: Grades I-III

A

Diffuse brain injury

- Temporary axonal disturbances causing attention and memory deficits but no loss of consciousness

176
Q

Concussion

Classic: Grade IV

A

Diffuse brain injury

  • Disconnection of cerebral systems and the brain stem reticular activating system causing loss of arousal
  • Physiologic and neurologic dysfunction with no anatomic disruption
  • Loss of consciousness (<6 hours)
  • Anterograde and retrograde amnesia
177
Q

Diffuse Axonal Injury

A

Diffuse brain injury

  • Soft gray matter shifts against firmer white matter and axons get torn (shear injuries)
  • Difficult to see on conventional imaging
  • Range from mild to severe
178
Q

Hyperextension and Hyperflexion of Spinal Cord

A

Commonly seen in motor vehicle accidents

  • Hyperextension: head back
  • Hyperflexion: head forward
179
Q

Spinal Cord Injury

A
  • Cord is usually injured from broken fragments of injured vertebrae
  • Most common location is where cord is large and tightly packed in the vertebral canal (cervical and lumbar)
180
Q

Spinal Shock

A

Temporary cessation of cord function below a spinal lesion

  • Causes flaccid paralysis, areflexia or hyporeflexia and bowel/bladder disfunction
  • If spinal cord is not permanently damaged, in about 10-14 days cord function returns, increased reflexes, and possibly Autonomic Hyperreflexia
181
Q

Autonomic Hyperreflexia

A

Massive, uncompensated cardiovascular response to stimulation of the sympathetic nervous system

  • Stimulated by visceral distention of bowel, bladder, or abdomen
  • Sensory afferent neurons stimulate reflex of major sympathetic outflow
  • Parasympathetic response above the lesion but not below
  • BP up, pounding headache, blurred vision, sweating above lesion, flushed skin, bradycardia
182
Q

Diagnosis and Treatment of Spinal Cord Injuries

A

Diagnosis
- By physical examination (loss of reflexes) or by radiological exam: CT/MRI

Treatment
- Immobilization, surgery, administration of corticosteroids to reduce secondary cord swelling, and symptomatic treatment of Autonomic Hyperreflexia

183
Q

Degenerative Disc Disease

A

Dehydration and loss of disc structure

184
Q

Herniated Disc

A

Herniation of Nucleus Pulposus can lead to nerve impingement

185
Q

Ischemic Stroke

A

Vessel blocked by clot that develops in place, or moves from another location to lodge in artery

  • Limited blood flow
  • Causes loss of oxygen and glucose to affected brain tissue (Infarction)
186
Q

Hemorrhagic Stroke

A

Rupture of blood vessel

- Ex: Aneurysm (weak spot in artery)

187
Q

Stroke Symptoms and Territories

A

Location of leaky or blocked vessel is the key to symptoms

- Use homunculus to determine correlation between stroke location and symptoms

188
Q

Aneurysm

A

If they rupture, hemorrhagic stroke occurs

  • Often found as “incidentalomas” because they are asymptomatic
  • Death is common

2 Treatments:

  • Coil: intravascular “nest” of wire, causing clot to form
  • Clip: external clamp over “neck” of aneurysm
189
Q

Arteriovenous Malformation

A

Nest-like structure with anastomosing arteries and veins

  • May appear as holes in CT/MRI
  • Difficult to treat, frequently prone to rupture and hemorrhagic stroke
190
Q

Ischemic Penumbra

A

The area surrounding the direct, immediate, and irreversible damage from a stroke
- This tissue can be saved if the right treatment is administered, but will die otherwise

191
Q

Transient Ischemic Attack

TIA

A

All Penumbra, No Infarction

Symptoms:

  • Unilateral weakness
  • Unilateral sensory disturbance
  • Slurred speech
  • Transient blindness in one eye
  • Difficulty speaking
  • Unsteady gait
  • Dizziness
192
Q

Headaches

A

One of the most common neurological disorders, poorly understood
- Common types: Tension, Migraine, and Cluster

193
Q

Tension Headaches

A
  • Gradual onset
  • Bilateral
  • Self-limiting
  • Possible Causes: hypersensitivity of Trigeminal Nerve, contraction of jaw and neck muscles
194
Q

Migraine Headache Criteria

A

5,4,3,2,1, criteria:

  • 5 or more attacks
  • 4 hours to 3 days duration
  • 2 of: unilateral, pulsating, moderate to severe pain, aggravation by physical activity
  • 1 of: nausea, vomitting, photophobia, phonophobia
195
Q

Migraine Headaches

A
  • Vascular origin: blood vessel dilation
  • 2x as common in women
  • Triggers like stress, hunger, certain foods, weather, and hormonal changes in women are usually involved
196
Q

Cluster Headaches

A
  • Occur in groups: several in one day for several days, then remit for a time
  • 5x more common in men, age 20-50
  • Severe unilateral stabbing pain behind eyes (retro-orbital) with eye watering and nausea
197
Q

Meningitis

A

Inflammation of the Pia and Arachnoid

  • Usually caused by infectious agents (viruses, bacteria, fungi, parasites)
  • Drugs, toxins, or radiation trigger Chemical Meningitis
  • All types exhibit increased ICP: increased production, impaired circulation, or impaired resorption of cerebrospinal fluid
198
Q

Viral Meningitis

A

Aseptic/Non-purulent Meningitis

  • Develops more gradually and is less severe
  • CSF will be clear
  • Lumbar puncture with Gram Stain may show Lymphocytes, but NO BACTERIA
  • Chemistry analysis may show elevated protein but not glucose
  • WBC count slightly elevated, differential shows elevated Lymphocytes
199
Q

Bacterial Meningitis

A

Extends beyond Meninges to involve the CSF in subarachnoid space and ventricular system

  • More severe, can be life threatening within hours
  • CSF will be cloudy
  • Lumbar puncture with Gram Stain WILL SHOW BACTERIA
  • Chemistry analysis will show markedly elevated protein, and decreased glucose
  • WBC count significantly elevated, differential shows elevated Neutrophils and Monocytes
200
Q

Meningitis Symptoms

A
  • Throbbing headache
  • Nausea/vomiting
  • Nuchal rigidity (neck stiffness)
  • Petechial rash on palms
  • Progresses to altered mental status
201
Q

Encephalitis

A

Acute inflammation of the brain matter; usually viral

  • Caused by arthropod-born viruses and HSV-1
  • Can occur due to systemic viral disease
  • Causes widespread nerve cell degeneration
  • Increased intracranial pressure may progress to herniation
202
Q

Encephalitis Symptoms

A
  • Fever
  • Delirium
  • Dementia
  • Seizures
  • Palsies
  • Paralysis
203
Q

Multiple Sclerosis

A

Autoimmune; Patient’s immune system attacks the myelin sheaths surrounding nerve axons in CNS

  • As myelin sheaths are destroyed the body releases more antigen and problems get worse
  • Because demyelination can occur anywhere in the nervous system, it can mimic almost any other neurological problem
204
Q

Amyotropic Lateral Sclerosis

ALS, Lou Gehrig’s Disease

A

Affects upper and lower motor neurons

  • Leads to progressive weakness beginning in a single muscle group, muscle wasting, and death
  • Patients have normal intellectual and sensory function until death
  • Respiratory paralysis may cause death in <1 year
205
Q

Guillian-Barre Syndrome

A

An acute inflammatory demyelinating disorder of the peripheral nerves (Schwann cells)

  • Signs: rapid onset of weakness, paralysis of legs/arms/facial muscles, paralysis of the respiratory muscles is possible
  • Most common cause of rapidly acquired paralysis in the U.S.
206
Q

Myasthenia Gravis

A

Autoimmune; and IgG antibody is produced against the ACh receptor

  • Muscles innervated by cranial nerves affected earliest, later progresses to upper body and diaphragm
  • Weakness and fatigue affect the muscles of the eyes and the throat causing diplopia (double vision), difficulty chewing, talking, and swallowing

Pathophysiology (11 decks)

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