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Combined Chapters 1,2,14,15,16,17

Thrombotic Stroke

- type of ischemic stroke
- arterial occlusions caused by thrombi formed in arteries supplying the brain or in intracranial vessels
- transient ischemic attacks (for short period of time; decrease blood supply)
- blockage in brain

Embolic Stroke

- fragments that break from a thrombus formed outside of the brain
- high-risk sources for the onset of embolic stroke are atrial fibrillation (15 to 25% of strokes, left ventricular aneurysm or thrombus, left atrial thrombus, recent myocardial infarction, rheumatic valvular disease, mechanical prosthetic valve, nonbacterial thrombotic endocarditis, patent foramen ovale & primary intracardiac tumors
- moving from another area of body; like DVT
- arterial defibrillation = irregular contraction of atria; many Ps before QRS

Hemorrhagic stroke

- lacunar stroke: a microinfarct smaller than 1 cm in diameter; b/c of the subcortical location & small area of infarction, these strokes may have pure motor & sensory deficits
- cerebral infarction
-cerebral hemorrhage

Subarachnoid Hemorrhage

- blood escapes from defective or injured vasculature into the subarachnoid space
- manifestations: meningeal irritation & inflammation causing neck stiffness (nuchal rigidity); photophobia, blurred vision, irritability, restlessness & low-gradefever
*positive Kernig sigh: straightening the knee w/ the hip & knee in a flexed position produces pain in the back & neck regions
*Brudzinksi sign: passive flexion of the neck produces neck pain & increased rigidity may appear


- chronic headache
- trigger factors

Cluster Headache

- several attacks can occur during the day for days followed by a long period of spontaneous remission
- pain mainly in temporal lobe that last 2-4 hours
- chronic
- usually begin with warning & is characterized by severe, unilateral tearing, burning, periorbital & retorbulbar or temporal pain lasting 30 min to 2 hours

Chronic paroxysmal hemicrania

- cluster-type headache that occurs w/ more daily frequency but w/ shorter duration

Tension-type headache

- mild to moderate bilateral headache w/ a sensation of a tight band or pressure around the head

Multiple Sclerosis

- progressive, inflammatory, demyelinating, autoimmune disorder of the CNS
- degeneration of the myelin sheath in CNS neuron & loss of axons

Amyotrophic Lateral Sclerois

- ALS- Lou Gehrig's disease
- diffusely affects upper & lower motor neurons of the cerebral cortex, brainstem & spinal cord (corticospinal tracts & anterior roots)
- progressive weakness leading to respiratory failure & death
- person has normal intellectual & sensory function until death

Guillain-Barre syndrome

- acquired inflammatory disease causing demyelination of the peripheral nerves w/ relative sparing of axons
- acute onset, ascending motor paralysis
- humoral & cellular immunologic reaction
- considered to be an autoimmune disease triggered by a preceding bacterial or viral infection

Myasthenia Gravis

- MG
- chronic autoimmune disease
- IgG antibody produced against acetylcholine receptors (anti-acetylcholine receptor antibodies) at the acetylcholine-binding site of the postsynaptic membrane
- weakness & fatigue of muscles of the eyes & the throat, causing diplopia, difficulty chewing, talking, swallowing
- characterized by exertional fatigue & weakness that worsens with activity, improves with rest & recurs w/ resumption of activity


- viewed as having 2 distinct components: arousal & awareness
- arousal: an attentional system, is the state of awakens that an individual exhibits; level of arousal
- mediated by the reticular activating system
-awareness: all the cognitive functions that embody awareness of self, environment, & affective states (i.e. moods)
- content of


- produced by either bilateral hemisphere damage or suppression or brainstem lesions or metabolic derangement that damages or suppresses the reticular activating system


- the area located above the tentorium cerebellum
- contains the cerebrum


- the area of the brain located below the tentorium cerebelli,
the infratentorial region contains the cerebellum
- disease process include compression of the brainstem resulting from hematomas, hemorrhage & aneurysm as well as cerebellar hemorrhage, infarcts, abscesses, enoplamsa & demyelinating disorders

Clinical Manifestations of Alterations in Arousal

- level of consciousness changes
- pattern of breathing: posthyperventilation apnea and Cheyne-Stokes respirations
- Pupillary changes: consensual reaction- when pupil will react due to other reacting
- oculomotor responses (Doll's eyes)
- motor responses
- normal ICP is 10-15 mmHg
- when neural control at this center is lost as consciousness decreases, the lower brainstem centers regulated the breathing pattern by response only to changes (increases) in PaCO2 levels; result is the irregular breathing associated w/ PHVA
- rhythmic breathing returns when the PaCO2 returns to normal
- vomiting is associated particularly w/ CNS injuries that: (1) involve the vestibular nuclei (located in the lower pons & medulla oblongata) or their immediate projections, particularly when double vision (diplopia) is also present

Posthyperventilation Apnea

- aka PHVA
- pattern of breathing
- response to changes in PaCO2
- respiration stops until PaCO2 levels are normal
- normal: 7.35- 745 mmHG

Cheyne-Stokes Respirations

- aka CSR
- repeated cycle of increased rate & depth of breathing, then creased rate & depth of breath (cycle of hyperventilation & apnea)
- happens in a number of conditions

Doll's Eyes

- oculomotor response
- a clinical sign for evaluating brainstem function in a comatose patient
- in a normal person, as the head is turned rapidly to one side (contraindicated if there is a possibility of brainstem injury) the eye conjugately deviate in the direction opposite to the head's movement
- loss of this reflex implies dysfunction of brainstem or oculomotor nerves
- inferolateral deviation of the eyes in combination w/ pupillary dilation implies dysfunction of the 3rd cranial nerve, possibly due to tentorial herniation

Pontine Dysfunction

- causes pupils to be pinpoint size & fixed in position
- patients w/ fixed dilated pupils are dead

prefrontal lobe

- mediates several cognitive functions including vigilance, reasoning, & executive functions

Brainstem Death

- occurs when brain damage is so extensive that the damage is irreversible & the brain has not potential for recovery
- the brain has lost reflex function & body cannot maintain internal homeostasis
- criteria: completion of all appropriate, therapeutic procedures; unresponsive coma (absence of motor & reflex responses); no spontaneous respirations (apnea); no cephalic (ocular or caloric) reflexes; isoelectric EEG & EKG; persistence for 1 hour & 6 hours after onset
- apnea is viewed as a criterion of brainstem death, whereas vegetative state, coma & Locked in Syndrome reflect cerebral death

Flaccid State

- little or no motor response to stimuli; is characteristic of damage to the pons


- an abnormal posture associated with severe brain injury, characterized by abnormal flexion of the upper extremities and extension of the lower extremities

Decerebrate posturing

- includes opisthotonos (hyperextension of the vertebral column w/ clenching of the teeth
- extension, abduction & hyperpronation of the arms
- extension of the lower extremities including plantar extension

Cerebral Death

- irreversible coma
- death of the cerebral hemisphere exclusive of the brainstem & cerebellum
- no behavioral or environmental responses
- the brain can continue to maintain normal respiratory & cardiovascular functions, temperature control, & GI function
- Survivors: remain in coma; emerge into a vegetative (wakeful unconscious) state; progress into a minimal conscious state: akinetic mutism (AK) & locked-in syndrome


- a sudden, transient alteration of brain function caused by an abrupt explosive, disorderly discharge of cerebral neurons
- disruption in balance of excitation & inhibition
- motor, sensory, autonomic or psychic
- convulsion: tonic-clonic (jerky,contract-relax) movements associated w/ some seizures

Partial (focal) seizure

- simple partial: starts in the fingers & progressively spreads up the arm & extends to the left
- complex partial: results in impaired consciousness as well as the inability to response to exogenous stimuli

Status epilepticus (seizure)

- second seizure before the first has ended
before the person has fully regained consciousness from the preceding seizure or a single seizure lasting more than 30 min
- a true medical emergency b/ a single seizure can last more than 30 min resulting hypoxia of the brain

"Development of Seizures"

- resting potential instability
- bursting of actin potentials (hypersynchronization)
- epileptogenic focus: group of neurons that appear to hypersensitive to paroxysmal depolarization
- tonic phase
- clonic phase
- postictal state: state that follows the seizure

Seizures: Consequences

- 250% increase in ATP
- cerebral oxygen consumption increased by 60%
- cerebral blood increases approx. 250%
- available glucose & oxygen are depleted
*with severe seizures, the brain tissue may require more ATP than can be produced
*lactate accumulates in the brain tissues
* may produce secondary hypoxia, acidosis & lactate accumulation
* may result in progressive brain tissue injury & destruction
* cellular exhaustion & destruction


- some people have a distinctive feeling or some other warning sign when a seizure is coming
- they can be helpful b/c they can give time to prepare for the seizure & prevent injury; most injuries due to no warning, or not recognizing it
- vary btw ppl; maybe immediate or several min to hrs earlier
- common signs: changes in bodily sensations, changes in ability to interact w/ things happening outside of you & changes in how familiar the outside world seems; depression, irritability, sleep disruption, nausea & headache


- an early symptom that a disease is developing or than an attach is about to occur


- data processing deficit
- loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss
- usually associated w/ brain injury or neurological illness
- tactile, visual, auditory, etc


- the loss of speech & comprehension of the written language

Receptive Dysphasia

- w/ receptive dysphasia (fluent), the individual is able to comprehend speech, but not respond verbally
- may result in expressive deficits

Transcortical Dysphasia

- the association cortex adjacent to Wernicke's and/or Broca's areas maybe become disconnected
- there are 3 forms: transcortical sensory, transcortical motor, mixed transcortical dysphasia
- in all forms of transcortical dysphasia repetition of speech is conspicuously normal

Acute Confusional States

- acquired mental disorder w/ deficits in attention & coherence of thoughts & action
- secondary to drug intoxication, metabolic disorder, or nervous system disease
- disruption of reticular activating system of upper brainstem & its projections to thalamus, basal ganglion & specific areas of the cortex & limbic areas
- abrupt onset

Intracranial Pressure

- normal: 5 to 15mmHG
- increases caused by an increased intracranial content: tumor growth, edema, excessive CSF or hemorrhage

Cerebral Edema

- an increase in the fluid content of brain tissues
- a net accumulation of water within the brain
- leads to increased intracranial pressure

Vasogenic Edema

- caused by the increased permeability of the capillary endothelium of the brain after injury to the vascular structure
- leads to increased ICP

Alterations in Movement

- Hyperkinesia: excessive movement; chorea, wandering, tremor @ rest, postural tremor etc
- Paroxymal dyskinesias
- Tardive dyskinesia: the involuntary movement of the face, trunk & extremities; antipsychotic drugs cause denervation hypersensitivity so that it mimics the effect of too much dopamine
- Hypokinesia: decreased movement, akinesia, bradykinesia, loss of associated movement

Disorders of Posture (Stance)

- Dystonia: dystonic postures & movements; decorticate posture; decerebrate posture; basal ganglion posture; senile posture

Parkinson's Disease

- severe degeneration of the basal ganglia (corpus striatum) involving the dopaminergic nigrostriatal pathway
- manifestations: rigidity, bradykinesia, tremor; postural abnormalities; autonomic & neuroendocrine symptoms; cognitive-affective symptoms

Parkinson & Dementia

- 50% of persons have depression, an inherent part of the pathologic state & not a situational response
- 30% treated on outpatient basis have dementia; 80% of persons requiring institutional care have dementia
- disorientation, confusion, memory loss, distractibility & difficulty w/ concept formation, abstraction, calculations, thinking & judgement
- symptoms fluctuate & progressively worsen
- anxiety disorders; impulse-control disorders; & punding
- excessive daytime sleepiness is experienced in more than 50% of persons


- characterstice of parking & dementia
- disorder of stereotypic motor behavior in which there is intense fascination w/ repetitive handling & examining of mechanical objects

Blunt Brain Trauma

- close, non-missile
- head strikes hard surface or rapidly moving object strikes the head
- the dura remains intact; brain tissues not exposed to the environment
- causes focal (local) or diffuse (general) brain injuries

Open Brain Trauma

- penetrating, missile
- injury breaks the dura & exposes the cranial contents to the environment
- causes primarily focal injuries

Brain Trauma

- compound fractures
- basilar skull fracture
- subdural & epidural (extradural) hematomas

Epidural Hematomas

- aka extradural hematomas
- 90% have skull fracture
- almost always arterial bleeds (85%); meningeal vein or dural sinus injury (15%)
- most involve the middle meningeal artery in the temporal fossa
- bood accumulates quickly & the individual is in imminent danger of death if not diagnosed & treated expediently

Subdural Hematomas

- venous bleeds that can be acute (w/in 48 hours, often located at the top of the skull) or chronic (develops over weeks to months-older adults, alcohol abuse)
- chronic: complain of chronic headaches & have tenderness at site of injury
- 10 to 20% of person w/ traumatic brain injury
- MVAs are the most common cause
- also occur due to falls (older adults, substance abuse)
- usually located in the top of the skull & most often resulting from tearing of the bridging veins
- 50% associated w/ skull fractures
- may need surgical removal, depending on their size

Severity of Brain Injury

- 75% to 90% of head injuries are not severe
- focal brain injury & diffuse axonal injury (DAI) each account for 1/2 of all injuries
- focal brain injury accounts for more than 2/3 of head injury deaths; DAI less than one 1/3 of deaths
- DAI accounts for the greatest number of severely disabled survivors; most severe diffuse brain injury caused by rotational acceleration is most likely to be located in the diencephalon to brainstem
- hallmark of severe brain injury: loss of consciousness for 6+ hours; decreased level of consciousness

Diffuse Axonal Injury

- formerly called primary brainstem injury or brainstem contusion
- involves severe mechanical disruption of many axons in both cerebral hemispheres & those extending in the diencephalon & brainstem

Focal Brain Injury

- observable brain lesion
- cerebral edema
- coup injury or contrecoup injury
- force of impact typically produces contusions
- contusions can cause: epidural hemorrhage or hematoma; subdural hematoma; intracerebral hematoma; clinical manifestations of contusion

Coup Injury

- injury directly below the point of impact

Contrecoup Injury

- injury on the pole opposite the site of impact

Spinal Cord Trauma

- commonly occurs from vertebral injuries: simple fracture, compressed fracture & comminuted fracture
- traumatic injury of vertebral & neural tissues to compressing, pulling or shearing forces
- most common locations: C1,C2,C4-C7 & T1-L2 lumbar vertebrae; in the cervical region, S.C. swelling may be life threatening due to possible impairment of the diaphragm function (phrenic nerves C3-C5)
- older adults are particularly at risk for minor trauma resulting in serious s.c. injury from falls, etc
- manifestations: complete loss of reflex function in all segments below the level of the lesion; severe impairment below the level of the lesion is obvious; paralysis & flaccidity in muscles, absence of sensation, loss of bladder & rectal control, transient drop in BP & poor venous circulation

Spinal Shock

- normal activity of the s.c. ceases at & below the level of injury
- sites lack continuous nervous discharges from the brain
- complete loss of reflex function (skeletal, badder, bowel, sexual, thermal control; autonomic control)
- indications of termination: reappearance of reflex activity, hyperreflexia, spasticity, & reflex emptying of the bladder

Neurogenic Shock

- spinal cord trauma
- loss of sympathetic outflow: vasodilation, hypotension, bradycardia, hypothermia

Autonomic Hyperreflexia

- dysreflexia
- massive, uncompensated cardiovascular response to stimulation of the sympathetic nervous system
- stimulation of the sensory receptors below the level of the cord lesion
- visceral distention, spinothalamic tract to level of lesion, reflex stimulus to sympathetic outflow, increase BP stimulation of carotid sinus receptors, cranial & vagus nerve stimulation, bradycardia & autonomic response to hypertension

Spinal Cord Trauma (tissues)

- chemical & metabolic changes in tissues
* release of toxic excitatory amino acids, accumulation of endogenous opiates, lipid hydrolysis w/ production of active metabolites & local free radical release
* produce further ischemia, vascular damage & necrosis of tissues
* necrosis consumes 40% of cross-secetional cord w/in 4 hours of trauma & 70% w/in 24 hours
* cord swelling increases degree of dysfunction; distinguishing functions to be lost permanently from those that are impaired temporarily become difficult; in the cervical region, cord swelling may be life threatening

Specificity Theory

- pain theory
- amount of pain is related to the amount of tissue injury
- accounts for many types of injuries but does not explain psychologic contributions

Gate Control Theory

- pain theory
- explains the complexities of the pain phenomenon; physical pain is not a direct result of activation of pain receptor neurons, but rather its perception is modulated by interaction btw different neurons

Nociception (nociperception)

- perception of pain
- "the neural process of encoding & processing noxious stimuli; the afferent activity produced in the peripheral & central nervous system by stimuli that have the potential to damage tissue
- activity is initiated by nociceptors (pain receptors), that can detect mechanical, thermal or chemical changes above a set threshold
- once stimulated, a nociceptor transmits a signal along the spinal cord to the brain

Delta Fibers

- transmit through the CNS
- type of sensory fibers; associated w/ cold & pressure, & as nociceptors they convey fast pain information
- thinly myelinated, so conduct signals more rapidly than unmyelinated C fibers, but more slowly than other, more thickly myelinated "A" class fibers

Lateral Spinothalamic tract

- part of transmission thru the CNS
- has 2 pathways for nociceptive information to reach brain
-1. neospinothalamic tract- "fast spontaneous pain"
-2. paleospinothalamic tract- "slow increasing pain"

Neospinothalamic tract

- "fast spontaneous pain"
- fast pain travels via type Adelta fibers to terminate on the dorsal horn of the S.C where they synapse w/ the dendrites of the neospinothalamic tract;
- the axons of these neurons travel up the spine to the brain
- fast pain is felt w/in a tenth of a second of application of the pain stimulus & is a sharp, acute, prickling pain felt in response to mechanical & thermal stimulation
- can be localized easily if Adelta fibers are stimulated together w/ tactile receptors

Paleospinothalamic tract

- "slow increasing pain"
- slow pain is transmitted via slower type C fibers to laminae II and III of the dorsal horns, together are then transmitted to nerve fibers that terminate in lamina V, also in the dorsal horn, synapsing w/ neurons that join fibers from the fast pathway
- slow pain is stimulated by chemical stimulation, is poorly localized & is described as an aching, throbbing or burning pain

Segmental Inhibition

-neuromodulation of pain
- low-threshold mechanical information
- touch, vibration, & pressure
- can distract from injury pain
- i.e. sucking thumb after hitting w/ hammer
- all converge on the spinal dorsal horns

Diffuse noxious inhibitory controls

- neuromodulation of pain
- integration of: peripheral sensory axon terminals; spinal interneurons; top-down control pathways
- all converge on the spinal dorsal horns

Chemicals & Neurotransmitters of Pain

- Pain excitatory: Glutamate, sapartate
- pain inhibitory: serotonin, GABA, endorphins
- modulators of pain

Direct Excitation

- threshold depolarization from direct stimuli

Indirect Excitation

- threshold depolarization from inflammatory mediators after tissue injury
- increased sensitivity due to inflammatory mediators
- i.e. sunburn


- an exaggerated sense of pain


- pain that result from a non-injurious stimulus to the skin

Pain Threshold

- the point at pain beings to be felt; entirely subjective; the intensity @ which a stimulus (e.g. heat, pressure) beings to evoke pain is the threshold intensity
- does not vary significantly among people or in the same person over time
- the intensity @ which a stimulus beings to evoke pain varies from individual to individual & for a given individual
- intense pain @ one location may cause an increase in the threshold in another location

Threshold intensity

- the intensity @ which a stimulus (eg. heat, pressure) beings to evoke pain
- so if a hotplate on your skin begins to hurt at 107degF, then it is the pain threshold temp for that bit of skin at that time

Pain Tolerance

- duration of time or intensity of pain that a person will endure (tolerate) before initiating pain responses
- influenced by cultural perceptions, expectations, role behaviors & physical & mental health
- decreased w/ repeated pain, fatigue, anger, boredom, apprehension & sleep deprivation
- generally increased by alcohol consumption, persistent used of pain medication, hypnosis, warmth, distracting activities & strong beliefs or fain
- varies greatly among people & in the same person over time

Nociceptive Pain

- pain w/ normal tissue injury
- somatic, visceral
- ex: sprains, bone fractures, burns, bumps, bruises, inflammation (from an infection or arthritic disorder), obstructions

Non-nociceptive Pain

- neuropathic pain (e.g. diabetic neuropathy)
- peripheral & central
- ex: post herpetic (or post-shings) neuralgia, components of cancer pain, phantom limb pain, entrapment neuropath (e.g. carpal tunnel syndrome), and peripheral neuropathy (widespread nerve damage)

Acute Pain- Protective Mechanism

- acute pain begins suddenly & is usually sharp in quality
- serves as a warning of disease or threat to the body
- might be caused by many events or circumstances
- e.g. surgery broken bones, dental work, burns or cuts, labor &childbirth

Manifestations of Acute Pain

- fear and anxiety
- tachycardia, hypertension, fever, diaphoresis, dilated pupils, outward pain behaviors, elevated blood sugar levels, decreased gastric acid secretion & intestinal motility, decrease in blood blow

Acute Somatic Pain

- arises from connective tissue, muscle, bone & skin
- A-delta fibers: pain is sharp & well localized
- C fibers: dull, aching, & poorly localized

Acute Visceral Pain

- pain in the internal organs & abdomen
- poorly localized due to the lesser number of nociceptors

Referred pain

- pain perceived at a site adjacent to or at a distance from the site of an injury's origin
-ex: during ischemia brought on by a myocardial infarction where pain is often felt in the neck, shoulders, & back rather than in the chest, the site of injury
- area of referred pain is supplied by the same spinal segment as the actual site

Chronic Pain

- misinterpretation of nociceptive input
- persists despite the fact that the injury has healed; pain signals remain active in the nervous system for weeks, months or years
- physical effects: tense muscles, limited mobility, lack of energy, & changes in appetite
- emotional effects: depression, anger, anxiety & fear of the re-injury; might hinder a person's ability to return to normal work or leisure activities
- complaints: myofascial pain syndrome (injury to the muscle & fascia), headache, low back pain, cancer pain, arthritis pain

Neurogenic Pain

- type of chronic pain
- pain resulting from damage to nerves

Psychogenic Pain

- type of chronic pain
- pain not due to past disease or injury or any visible sign of damage inside
- imbalance of neuromodulation controls
- ex: decreased level of endorphins; predominance of C-neuron stimulation

Aging & Pain

- research studies are conflicting
- increase in pain threshold: peripheral neuropathies, skin thickness changes
- decrease in pain tolerance
-alteration in metabolism of drugs & metabolites

Temperature Regulation

- peripheral thermoreceptors
- hypothalamic control
- heat production & conservation: chemical reactions of metabolism, skeletal muscle contraction, chemical thermogenesis, vasoconstriction, voluntary mechanisms

Heat Loss

- radiation
- conduction
- convection
- vasodilation
- decreased muscle tone
- evaporation
- increased respirations
- voluntary measure
- adaption to warmer climates

Temperature Regulation

- pediatrics: produced sufficient body heat but are unable to conserve heat produced
- small body size & high body surface-to-weight ration; thin subcutaneous layer
- aging: slow blood circulation, vasoconstrictive response, & metabolic rate
- decreased sweating & perception of heat & cold


- resetting of hypothalamic thermostat
- activate heat production & conservation measures to a new set point
- Pyrogen is a substance that produces a fever (exists as exogenous, endogenous)
- endogenous cryogens: existing in the blood of a hypothermic patient
- pathogenesis: certain disease set through elaboration of exogenous pyrogens, stimulate monocytes & macrophages to produce endogenous pyrogens; these pyrogenic cytokines act @ the endothelial surface of the circumventricular organ of the preoptic area of the anterior hypothalamus to induce the production of PGE2, which elevates the body's thermal set point; physiologic & behvaioral response may be invoked to raise body temp to a new set point; some central & systemic anipyretics exert their effects by decreasing levels of PGE2, decreasing the "set point" & lowering body temp

Benefits of Fever

- helps kill or helps prevent the replication of many microorganisms by decreasing serum iron, zinc & copper needed for bacterial replication & causing lysosomal breakdown & autodestruction of cells
- enhances the body's immune response to microorganisms by increasing the motility of polymorphonuclear leukocytes (PMNs), intensifying phagocytosis, increasing lymphocytic transformation, & augmenting the production of antiviral interferon
- deprives bacteria of food
- promotes lysosomal breakdown & autodestruction of cells
- increases lymphocytic transformation & phagocyte motility


- not mediated by pyrogens
- no resetting of the hypothalamic set point
- 41degC (105.8degF): nerve damage produces convulsions
- 43degC (109.4degF): death results
- forms: heat exhaustion, heat stroke

Heat Exhaustion

- collapse due to prolonged high core or environmental temperatures
- prolonged vasodilation, profuse sweating
- dehydration, depressed plasma volumes, hypotension, decreased cardiac output, tachycardia
- manifestations: dizziness, weakness, nausea & syncope

Heat Stroke

- potentially lethal result of a breakdown in an overstressed thermoregulatory center
- brain cannot tolerate temps greater than 40.5degC (104.9degF)
- temp maintained by blood flow through the veins in the head & face
- cardiovascular & thermoregulatory centers may cease functioning in high temps

Manifestations of Heat Stroke

- cerebral edema (treated w/ osmotic diuretic mannitol or diamox --> degeneration of the CNS, swollen dendrites & renal tubular necrosis
- rapid peripheral cooling causes peripheral vasoconstriction & limits core cooling
- children are more susceptible b/c produce more metabolic heat when exercising; greater surface area-to-mass ration; sweating capacity is less than adults

Malignant Hyperthermia

- complication of inherited disease that causes a rapid rise in body temp (fever) & severe muscle contractions when the affected person receives general anesthesia
- not the same as hyperthermia that is due to medical emergencies such as heat stroke or infections

Symptoms of Malignant Hyperthermia

- rapid rise in temp to 105 degF or higher
- muscle rigidity & stiffness
- dark brown urine
- muscle ache w/o obvious exercise to explain sore muscles, bleeding

Treatment of Malignant Hyperthermia

- wrapping the patient in a cooling blanket can help reduce fever & the risk of serious complications
- drugs such as dantrolene, lidocaine, or beta-blocker can help w/ heart rhythm problems. Fluids (PO or IV)
- precipitated by the administration of volatile anesthetics & neuromuscular-blcoking agents: increased calcium release or decreased calcium uptake w/ muscle contraction; causes sustained muscle contractions which leads to increased oxygen consumption & lactic acid production


- body temp less than 35degC (95degF)
- produces: vasoconstriction, alterations in the microcirculation, coagulation, & ischemic tissue damage; ice crystals, which form inside he cells, causing them to rupture & die
- tissue hypothermia: slows chemical reaction; increases blood viscosity & slows blood through the microcirculation; facilitates blood coagulation & stimulates vasoconstriction
- accidental hypothermia: commonly caused by a sudden immersion in cold water or prolonged exposure to cold
- therapeutic hypothermia: used to slow metabolism & preserve ischemic tissue during surgery or limb reimplantation (may lead to ventricular fibrillation & cardiac arrest
- could also be caused by using refrigerated blood during a blood transfusion


- active multiphase process
- hypothalamus is the major sleep center
- two phases: REM and NREM


- rapid eye movement sleep: 20% to 25% of sleep time
- also known as paradoxic sleep
- occurs every 90 min beginning after 1 to 2 hours of sleep
- shows little variation in the different age groups; however stage IV sleep decreases w/ age & older adults awaken frequently & show a marked increase in total time awake


- non-rapid eye movement (NREM) sleep: 75% to 80% of sleep time
- stages evaluated by EEG
- stage I; stage II; stage III; stage IV

EEG stages of Wakefullness & Sleep

- Stage W or 0: awake, low-voltage, fast acuity
- State 1: falling asleep
- Stage II: light sleep w/ sleep spindles
- Stage III: moderately deep sleep
- Stage IV: deep sleep w/ slow delta waves
- REM sleep looks similar to awake & stage I

Pediatrics & Sleep

- newborns sleep 16 to 17 hours per day
- 53% of that time is spent in active (REM) sleep
- the infant sleep cycle is about 50 to 60 minutes
- infants enter REM sleep immediately on falling asleep

Aging & Sleep

- total sleep time is decreased
- older adults take longer to fall asleep; awaken more frequently during the night
- amount of time in stage IV decreases
- causes: physical ailments (illness); lack of daily routine; circadian (daily) rhythm changes & medications

Sleep Disorders

- Disorders initiating sleep: insomnia
- sleep-disordered breathing: upper airway resistance syndrome; obstructive sleep apnea; obesity hypoventilation syndrome
- disorders of sleep-wake cycle: parasomnias, somnambulism (sleep walking); night terrors; enuresis (bed wetting)


- involve abnormal & unnatural movements, behaviors, emotions, perceptions, & dreams that occur while falling asleep, sleeping, between sleep stages, or arousal form sleep
- most are dissociated sleep states which are partial arousals during the transitions btw wakefulness & NREM sleep or wakefulness & REM sleep

Sleep & Disease

- secondary sleep disorders: alterations in the quality &/or quantity of sleep due to primary disease
-depression, pain, sleep apnea syndromes & alterations in thyroid hormone secretion
- sleep-provoked disorders: sleep stage alterations produced in certain disease states

Vision (disease)

- blepharitis: inflammation of the eyelids
- hordeolum (stye): infection of sebaceous glands of the eyelids
- chalazion: infection of the meiboian (oil-secreting) gland
- keratitis: infection of the cornea
- conjunctivitis: inflammation of the conjunctiva
- acute bacterial conjunctivitis (pinkeye): highly contagious, mucopurulent drainage from one or both eyes
- viral conjunctivitis
- allergic conjunctivitis
- trachoma (chlamydial conunctivitis)

Vision Changes and Aging

- eyesight is often one of the first senses affected by aging
- cornea, anterior chamber, lens, ciliary muscles, retina

Visual Dysfunctions

- alterations in ocular movements: strabismus: diplopia (double-vision), nystagmus: pendular or jerk
- alterations in visual acuity: cataracts, papilledma, glaucoma, age-related macular degeneration (AMD)
- alterations in accommodation (the process whereby the thickness of the lens change); oculomotor nerve changes; decreased flexibility of the lens
*manifestations: diplopia; blurred vision; & headache
- alterations in refraction: myopia (nearsighted); hyperopia (farsighted); astigmatism: may coexist w/ myopia or hyperopia
- alterations in color vision: age-related yellowing of the lens; color-blindness
- neurologic disorders: hemianopia/hemianopsia (loss of vision in either the whole left of the whole right half of the field of vision; injury to the optic chiasm; homonymous hemianopsia (a type of partial blindness resulting in a loss of vision in the same visual field of both eyes

Aging & Hearing

- cochlear hair cell degeneration
- loss of auditory neurons in spiral ganglia of organ of corgi
- degeneration of basilar conductive membrane of the cochlea
- decreased vascularity of cochlea
- loss of cortical auditory neurons

Ear Infections

- Otitis externa: infection of the outer ear; commonly caused by prolonged moisture exposure, i.e. swimmer's ear
- Otitis media: acute otitis media; otitis media w/ effusion

Auditory Dysfunction

- Conductive hearing loss: impaired sound condition
- sensorineural hearing loss: impairment of the organ of Corti or its central connections; presbycusis (age-related hearing loss)
- mixed hearing loss
- functional hearing loss

Age-Related Olfaction & Taste Changes

- Olfaction: decline in odor sensitivity; loss of olfactory sensory neurons & cells in the olfactory bulbs; causes diminished appetite, food selection
- Taste: higher concentration of flavors is required; decline in the number of fungiform papillae located on the top (dorsal) surface of the tongue

Olfactory Dysfunction

- hyposmia: reduced ability to smell & detect odors
- anosmia: no odors can be detected
- olfactory hallucinations
- parasmia: also know as troposmia
- some of the causes are allergies, nasal polyps, viral infections & head trauma
- up to 4 million people in the US have hyposmia or related anosmia
- hyposmia might be a very early sign of Parkinson's Disease


- aka troposmia
- an olfactory dysfunction that is characterized by the inability of the rain to properly identify an odor's "natural" smell
- the natural odor is transcribed into unpleasant aroma: burnd, rotting, feca or chemical smell

Taste Dysfunction

- hypgeusia: diminished taste sensation
- dysegueisa: altered taste sensation
- ageusia: lose of taste sensation
- parageusia: a bad taste in the mouth

Explain why O2 can easily cross a plasma membrane, whereas Na+ are unable to cross a plasma membrane

Ans: Oxygen is able to easily cross the plasma membrane because oxygen is soluble in the lipid core of the plasma membrane. Na+ is insoluble in the lipid core of the membrane & thus is actively transported by a pump that uses ATP for energy

Discuss why proteins & lipids in plasma membranes are dynamic & asymmetrically distributed.

Ans: According to the fluid mosaic model, biologic membranes are dynamic & change in response to cell needs. Lipids are very fluid & mobile in the PM. They are not asymmetrically distributed but are also capable of fairly free lateral & rotational mobility. Asymmetric distribution of lipid changes plasma fluidity, which affects the flexibility & curvature of membranes. The type of fatty acid & the length of the fatty acid chains affect fluidity. For example, cholesterol, a small molecule w/ a small OH head group occurs @ he bilayer surface, decreasing fluidity & increasing the mechanical strength & stability of the membrane. Proteins define the specific function of the membrane b/c they are asymmetrically distributed. They can be either integral (intrinsic) or peripheral & float either singly or in an aggregate w/in the membrane. Integral proteins are associated directly w/ the lipid bilayer. Peripheral membrane proteins are associated ionically w/ hydrophilic lipid molecule heads or other proteins

What the difference between the absolute refractory period & the relative refractory period of the repolarization phase of impulse generation?

Ans: During the absolute refractory period the plasma membrane cannot respond to an excitatory stimulus, not matter how strong the stimulus is. The concentration of Na+ ions is too high w/in the cell to permit generation of an action potential. During the relative refractory period the cell is considered to be hyperpolarized or less excitable. Potassium ions are returning into the cell, & sodium ions are leaving. A stronger than normal excitatory stimulus can result in generation of an action potential

Explain how cells are connected to form tissues & organs.

Ans: Cells can be bound together via the extracellular matrix that the cells secrete around themselves. It is an intricate network of fibrous proteins embedded in a watery gel-like substance composed of complex carbohydrates. It is like glue, but it provides a pathway for diffusion of nutrient wastes & other water-soluble traffic between the blood & tissue cells. Interwoven w/in the matrix are 3 types of protein fiber: (1) collagen: forms cable-like fibers or sheets that provide tensile strength or resistance to longitudinal stress; (2) elastin: a rubber-like protein fiber that is most abundant in tissues that are capable of stretching & recoiling; (3) fibronectin: promotes cell adhesion & cell anchorage..The matrix is not just for cellular attachment, it also helps regulate the functions of cell w/ which it interacts. The matrix helps regulate cell growth & differentiation.

If aqueous solution A & aqueous solution B are separated by a membrane that is impermeable to solutes, & solution A has a concentration of 300 mOsm/kg & solution B has concentration of 500 mOsm/kg, the net movement of the water (solvent) will be in which direction?

Ans: Osmosis is the movement of water across a semipermeable membrane from a region of higher water concentration to a region of lower concentration

Why is cellular communication important to the survival of cells?

Ans: In order to maintain a stable environment, cells must have communication w/ each other. They communicate by forming protein channels that assemble nearby cell activities, activate receptors that affect the cells, & secrete chemicals that alert other cells of a change. Any discourse in cell communication leads to the onset of disease & affects the progression.

Explain the role of electrolyes & non-electrolytes in body fluids.

Ans: Electrolytes consist of polarity in which they gravitate to a positive or negative pole. They are electrically charged ions make up 95% of the molecules of solute in body water. The concentrations of the anions & cations are responsible for how the electrical impulses transmit across the muscle & nerve cells

How does the variety of cells differ in cell division?

Ans: Cells differ in variety of ways. First, adult cells from the nerves, lens of the eye, & muscle cells cannot replicate & divide. However, epithelial cells found in the intestine. lung, & skin can divide. These types of cells rapidly divide & complete the cycle in less than 10 hours.

Explain the fourth different type of tissues

Ans: (1) Epithelial tissue is found on most internal & external surfaces of the body. B/c of their different locations, epithelial tissues have different functions. Ex: the epidermis provides protection from outside trauma. Epithelial cells found in the respiratory passages assist in moving particles out of the body. (2) connective tissue: provides strength in binding different types of tissues & organs together. As opposed to the epithelial tissue, connective tissue contains an enormous amount of extracellular matrix & is classified as either dense or loose. (3) Muscle tissue is made up of long, slim fibers that highly contract. there are different types of muscle tissue: skeletal, cardiac & smooth. (4) Neural tissue is composed of highly specialized cells that quickly receive & transmit nerve impulses across synapses. The total number of neurons is determined at birth.

Explain the difference between osmosis, osmolality, and osmolarity.

Ans: Osmosis is the ability of water to move a cross a concentration (semipermeable membrane) from a higher concentration of water to a lower concentration of water. Osmolality is responsible for how the body compartments control the distribution and water movement. The measurement of osmolality is determined by the number of milliosmoles per kilogram of water. Body fluids have the normal osmolality of 280 to 294 mOsm/kg. Osmolarity is the concentration of the active particles in the solution.

Ms. Ellis has an annual Pap smear & gynecologic examination. 3 years ago, before her 3rd pregnancy, the pathology report of her Pap smear indicated she had hormonal hyperplasia. Her current Pap smear indicates she has atypical hyperplasia or dysplasia. What is the difference between these?

Ans: Hyperplasia- an increase in the # of normal cells. Ms. Ellis had normal hormonal hyperplasia cause by increased by increased cellular division. Estrogen was stimulating the uterine endometrium to grow & thicken in preparation for the ovum's implantation. Dysplasia or atypical hyperplasia-an abnormal change in the size, shape, or organization of mature cells. It most commonly occurs in epithelial membranes such as the uterus. It is strongly associated w/ neoplasia (malignant growth.) She will need more tests, eg biopsy.

Mr. Crane has suffered an acute myocardial infarction. Describe the cellular process of this disease

Ans: The gradual narrowing of the arteries has occurred over the years. Suddenly, there is an obstruction of the coronary artery that may cause cell death of the myocardium if the blood supply is not recovered

A victim of poisoning present with cherry-red appearance. How wold you determine what type of poisoning this victim has?

Ans: Toxins, eg, carbon monoxide, hydrogen sulfide, & hydrogen cyanide, directly interfere w/ cellular respiration; carbon monoxide & hydrogen cyanide cause a cherry-red appearance; to differentiate, lab tests must be done-presence of carboxyhemoglobin is diagnostic for carbon monoxide, drug test for cyanide.

Joey is 16 & is the pitcher for the high school baseball team. In the 9th inning, Joey pitches a perfect knuckle ball. The batter swings hard & the ball hits him directly in the head. What kind of concussion did Joey experience?

Ans: Joey suffered a blow to the head. The injury will mirror the shape of the object. Bleeding will occur under the tissues b/c of the force of the injury which caused rupture of the blood vessels

Can a crime scene investigation team determine the location of an assailant to the victim based on entrance wound characteristics?

Ans: yes; gunshot entrance wounds are classified as contact range, intermediate range, or indeterminate range

Is a nutritional deficiency the only form of nutritional imbalance?

Ans: No. Nutritional deficiencies limit lipids, proteins, carbohydrates, vitamins & minerals that cells need to function normally, but excessive nutritional intake can also lead to pathphysiologic damage to cells. Excess nutritional intake can lead to glycogen storage disease, damage to cells from excess cholesterol, & chronic diseases related to obesity

Explain how a deep-sea diver develops decompression sickness ("the bends")

Ans: As a diver descends, the pressure of gases in the body increases & more gas goes into solution. If the diver surfaces too quickly, the gases dissolved in the blood bubble out of solution. Oxygen dissolves very quickly back into solution but nitrogen does not. The gases form gaseous emboli that can obstruct blood vessels & cause ischemia. The gases can also accumulate in the joints & muscles. causing the diver to double up in pain, thus causing the bends.

Can a dental hygienist observe that person has been persistently biting is cheek?

Ans:Yes, habit of unconsciously biting the mucosa of one's cheek produces a hyperkeratotic lesion in the irritated area

Mrs. Jones is 95 years old & is frustrated because of constant stiffness she suffers. What are some examples of a decrease in her tissue & systemic function as a result of her aging process?

Ans: Increase in peripheral resistance to blood flow is causing her stiffness; decrease in diffusion capacity of her lungs affects her breathing; decrease in renal plasma flow causing decreased production; muscle atrophy (decreased motor tone & contractility) affecting her mobilization

Explain the process of frailty

Ans: Frailty-degenerative process that happens to individuals who are aging. This syndrome makes them vulnerable to falls, decrease in health, & even death. The condition involves protein synthesis decrease, neuro-endocrine & muscular deterioration, immune dysfunction, sarcopenia; osteopenia, cognitive impairment, anemia; decreased skeletal muscle mass (difficulty with weakness, fatigue, imbalance, unsteady gait, & speed)

Explain changes that occur in a body during the first 48 hours after death

Ans: First 6 hours after death-rigor mortis begins; withing 12-24 hours-affects entire body; after 24 hours-body temperature equilibrates w/ environmental temperature, rigor mortis reverses & the body becomes flaccid over a period of 12 to 14 hours, & signs of putrefaction occur (24 to 48 hours after death); most visible change; a greenish discoloration to the skin, particularly on the abdomen. Slipping or loosening of the skin occurs followed by swelling or bloating

Compare & Contrast the sympathetic (SNS) & parasympathetic nervous (PNS)

Ans: The SNS is the "fight or flight" system & when activated produces a generalized & widespread response that mobilizes energy stores...Sympathetic stimulation promotes responses that are concerned w/ protection of the individual. The single most important function of this system is regulation of vasomotor tone, allowing it to shunt blood to areas of highest need in the body...In contrast, the PNS can be thought as the "rest and digest" system. It lacks the general widespread response of the sympathetic nervous system & functions to conserve & restore energy store...The actions of the two systems are usually antagonistic. However, exception to this include unopposed parasympathetic control of the shape of the lens of the eye for near vision & unopposed sympathetic regulation of vasomotor tone

Explain normal changes in the central nervous system occurring with aging.

Ans: Normal changes in the CNS that occur w/ aging are structural, cellular, & functional...Structural changes include decreased brain weight, decreased size of primarily the frontal hemispheres, adherence of the dura mater to the skull, fibrosis & thickening of the meninges, narrowed gyri, widened sulci, increased size of the subarachnoid space, aberrations in vascular structures of the basal ganglia & enlarged ventricles...Cellular changes include decreased number of neurons, changes in dendrite structure, lipofuscin deposition, & presence of neurofibrillary tangles, senile plaques, & Lewy bodies...The major functional change that results from the structural & cellular changes is a progressive slowing in response seen w/ aging

Brett reach into a clogged snowblower to clear the chute while it was still running. He completely severed one finger & partially severed another on hi left hand. AFter lengthy surgery to reattach his fingers, he has regained much of his motor ability but he has lost some of his sensory function. What factors are involved that affect the regeneration of Brett's neurons & neuron function?

Ans: For regeneration of neurons, the cell bodies must be intact. Cell bodies are in or near the CNS so Brett's injury did not involve the cell bodies. B/c his PNS neurons were involved, the chances of his neurons regenerating increases, but the Schwann cells must be functional. The newly created gap between the severed pieces cannot be too large or fill too rapidly w/ collaged fibers. Accumulation of collagen inhibits the excitability of the tissue.

What specific mechanisms could be targeted by a drug that would block the transmission of impulses across a synapse?

Ans: A drug could block the release of the neurotransmitter, block the binding of the neurotransmitter to the postsynaptic neuron, or encourage the removal of the neurotransmitter from the synaptic cleft. All three of these mechanism could block the transmission of an impulse across a synapse

A bacterium is producing a toxin that causes flaccid paralysis. How might this toxin be the cause of this condition?

Ans: The toxin could block the release of an acetylcholine; block acetylcholine receptors, thus limiting the effects of acetylcholine; or increase the production of acetylcholinesterase

A bacterial toxin is producing a toxin that causes large groups of skeletal muscle to contract at the same time. How might this toxin be causing this condition?

Ans: The toxin could block the release or action of acetylcholinesterase, block inhibitory neurotransmitters to antagonistic muscles so antagonists contract w/ prime movers, or mimic the action of acetylcholine on postsynaptic receptors.

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