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Pathophysiology Exam 1

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.
Mr. White, 39, a construction worker, was admitted to the E.R. w/ a ruptured disk. He & another worker were carrying a 125-pound bag of concrete when his partner tripped on a rock & fell. Mr. White tried to hold the bag but felt excruciating pain in his lower back. The x-ray revealed a ruptured disk in L4. What happened to Mr. White?
Ans: When Mr. White's partner let go of the bag of concrete, it caused undo stress on his lower back. The disk ruptured & protruded through the spinal canal. The action caused the spinal cord to compress.
Mrs. Bronnell was brought to the E.R. department after suffering a seizure at home. Which diagnostic test is appropriate for this person & why?
Ans: Electroencephalography would be the appropriate test. The purpose of the test is to record electrical impulse impulses from the brain. It's helpful in determining the foci that caused the seizure activity.
Mr. Black was working in his garage when one of the shelves gave way & landed on his head. He was brought to the ER & was diagnosed w/ a subarachnoid hemorrhage. What causes subarachnoid hemorrhage?
Ans: A subarachnoid hemorrhage occurs when there is trauma to the inter cranial vessels. Signs & symptoms include neck stiffness, Kernig sign, & low back pain
Why are spinal nerves called "mixed nerves"?
Ans: Spinal nerves are called mixed nerves b/c they have sensory & motor neurons.
How do the 31 pairs of spinal nerves correspond to the to the vertebral column?
Ans: The names of the spinal nerves are derived from where they exit at the vertebral location. ONly the first cervical vertebra has the nerve exit above it. The remaining spinal nerves exit below the appropriate vertebrae.
Ms. Spinosa has increased intracranial pressure of 30 mmHg caused by a massive closed head injury. Explain the process of increasing intracranial pressure & discuss possible complications if the pressure is not decreased.
Ans: Supratentorial processess that cause a decreased level of consciousness are caused by injury somewhere above the tentorium. In this case, Ms. Spinosa suffered diffuse bilateral cortical dysfunction that caused widespread injury throughout the cerebral cortex & in the subcortical white matter. IN Ms. Spinosa's injury, her intracranial pressure increased from a normal 5 to 15 mmHg because of intracerebral hemorrhage or edema. The brain tissue is displaced, & the blood vessels are distorted...In stage 1 the increasing pressure forces the cerebrospinal fluid out of the cranial vault, compresses the intracranial veins, & increases venous vasoconstriction. Often intracranial pressure will not change during this stage b/c blood volume & CSF volumes are reduced...Stage 2 occurs when pressure is not relieved. Arterial blood vessels constrict, compromising oxygen supply. The systemic arterial system will also constrict to increase BP. There elevated system BP is an attempt to overcome the intracranial pressure...When intracranial pressure increases & approaches arterial pressure, stage 3 intracranial hypertension occurs. During the stage tissue hypoxia, hypercapnia, & acidosis occur. Autoregulation of blood vessel diameter is lost. Hypercapnia causes local vasodilation w/ subsequent increasing capillary permeability. As increasing cerebral edema occurs., ICP increases. Small changes in volume cause dramatic increases in pressure w/ decreased cerebral perfusion pressure...Stage 4 is characterized by herniation of the brain from the compartment of greater pressure to one of lower pressure. In Ms. Spinosa's case, the brain herniated downward (supratentorial herniation), causing central or uncal herniation. Blood supply & brain tissue are markedly compromised or completely cut off, causing further ischemia, hypoxia & hemorrhage in the herniated portion of the brain. When mean systolic pressure equals ICP, the blow to the brain sops
Injury to the extrapyramidal motor system does not cause paralysis of voluntary movement & general spasticity. Explain why, & discuss the major motor symptoms seen in extrapyramidal motor disorders.
Ans: The extrapyramidal motor system includes all motor pathways in the brain & brainstem that are not part of the corticospinal or pyramidal motor pathways. This system includes the basal ganglia, reticular formation, & parts of the cerebellum. Disorders are classified as either basal ganglia motor or cerebellar motor syndroms. Both are characterized by little or no paralysis of voluntary movement; normal or slightly increased tendon reflexes; presence of tremor, chorea, athetosis, or dystonia; & rigidity or intermittent rigidity. Muscle tone & equilibrium are also affected
Sally's husband has recently been diagnosed with late-onset familial Alzheimer disease (FAD). She wants to know what caused it and what the disease course will be.
Ans: In late-onset FAD there is a genetic defect on chromosome 19 that may be linked to aggregation & precipitation of insoluble amyloid (senile plaques) in brain tissue & blood vessels. The disease course varies from one individual to another, but eventually all persons affected with the disease will pass through 3 stages. IN stage 1, which lasts 1 to 3 years, her husband will seem apathetic, irritable or depressed, His memory will show impaired remote recall & defective new learning. He will have difficulty drawing simple pictures. His language will deteriorate, & he will be unable to recall the names of some objects. In stage 2, which lasts 2 to 10 years, her husband will seem indifferent & apathetic, will have a severely impaired recent & remote recall, will have fluent aphasia, will be unable to perform calculations or copy simple drawings, & will exhibit ideomotor apraxia. In stage 3, which lasts 8 to 12 years, her husband will have severely deteriorated intellectual functions, exhibit limb rigidity & flexion posture & be incontinent for urine & feces.
Bobby, an energetic 10 year old is swinging on his swing set when he suddenly falls to the ground, shaking uncontrollably. His family lives out in the country & 40 min have gone by before the rescue team arrives. His mother who saw the incident said that he never stopped shaking the entire time. What happened to him?
Ans: Bobby is suffering from status epilepticus It occurs due to failing to take anti-seizure medications as scheduled or it may be due to not being effectively treated for epilepsy. It is considered a medical emergency because of the complication of cerebral hypoxia. In addition, Bobby is at risk for mental retardation, dementia, other types of brain injuries, aspiration & even death.
Mr. Smith is suffering from head trauma due to a severe car accident. The computed tomography (CT) scan indicated that he has cerebral edema. Why is cerebral edema dangerous?
Ans: Cerebral edema is the fluid that accumulates in the brain. Once the trauma occurs on the brain, there is an increase of extracellular or intracellular tissue volume to the area. Cerebral edema can also cause infection, hemorrhage, tumor, ischemia, infarct or hypoxia. The dangerous effects are caused by blood vessel distortion, brain tissue displacement, & herniation of brain tissue from one brain compartment to another.
What is spinal shock?
Ans: Spinal shock is a complete cessation of spinal cord functions below lesion of injury. Physical characteristics include complete flaccid paralysis, no reflexes & extreme disturbances of bowel & bladder function.
Two individuals come to the emergency department with head injuries. One, 25 years old, has just been in a motor vehicle accident (MVA) and has a temporal lobe injury. The other, 65 years old, has increasing confusion after a fall that happened earlier in the week. How could you clinically differentiate between the individual with the extradural hematoma and the individual with the subdural hematoma? Which one of these individuals requires priority surgical treatment?
Ans: An extradural hematoma or epidural hemorrhage is a rapidly accumulating arterial bleed occurring between the skull and dura mater. Injuries to the temporal lobe are often associated with extradural hematomas because the middle meningeal artery runs in a groove on the surface before entering the skull. Extradural hematomas are most commonly caused by MVAs and are frequently associated with temporal lobe injuries. An epidural hemorrhage is characterized by loss of consciousness at the time of injury, followed by a lucid period. Within a few hours symptoms progress from severe headache, vomiting, and drowsiness to confusion, seizures, ipsilateral pupillary dilation, and contralateral hemiparesis. An extradural hematoma is always a medical emergency, so the individual in the MVA requires priority surgical treatment...A subdural hematoma is a venous bleed occurring between the dura mater and the arachnoid mater. Subdural bleeds occur more slowly, ranging from hours to weeks. The range in the delay depends on how many veins were torn, the size of the epidural space, and the amount of compression on the bleeding veins. Once a vein is torn, it will bleed and compress the brain. As intracranial pressure increases, the bleeding veins are compressed, slowing the amount of bleeding. A subdural hematoma can also be caused by an MVA but is commonly the result of falls in older adults, in whom the symptoms vary from a chronic headache and drowsiness to slowed cognition, confusion, progressive dementia, and paratonia (generalized rigidity). A subdural hematoma requires surgery to evacuate the clot but does not take priority over the individual with the extradural hematoma.
Ms. Evans has a flexion injury with resultant incomplete spinal cord transection at level C4-C5. What symptoms would you expect Ms. Evans to have 1 month after her injury?
She would have Brown-Séquard syndrome with (1) ipsilateral paralysis below C4-5 with return of Babinski reflexes and ankle and knee reflexes; (2) ipsilateral loss of touch, pressure, vibration, and proprioception with possible paresthesia below the level of transection; and (3) contralateral loss of pain and temperature. She may experience autonomic hyperreflexia (dysreflexia). She may also have some reappearance of defecation and urination reflexes.
Alex is going backpacking over spring break. He wants you to tell him about Lyme disease so he will know how to avoid it. How would you respond?
Ans: Ticks are carriers of Lyme disease, the most common arthropod-borne bacterial infection in the United States. Regions of infestation include the northeast coast, the Midwest, and western wooded and coastal areas. The causative organism, Borrelia burgdorferi, incubates for 3 to 32 days and then migrates to the skin, lymph nodes, and other body systems...The disease occurs in three stages: Stage I: An acute localized reaction occurs 3 weeks after the bite and is characterized by a bull's-eye-like burning rash about the bite, generalized malaise, flu-like symptoms, stiff neck, and headache...Stage II: Cardiac and neurologic involvement predominates in this stage and includes the following signs and symptoms: palpitations, dizziness, shortness of breath, dysrhythmias, first-degree heart block, headache, chronic aseptic meningitis, Bell palsy, encephalitis, and radiculitis...Stage III: The chronic stage may occur up to 2 years after the bite and involves arthritis and involvement of brain parenchyma with encephalitis, chronic neuropathy, and encephalopathy. ..Antibiotics successfully treat the disease in 50% of individuals, but 50% will have minor recurring symptoms following antibiotic treatment.
A physician suspects that her 23-year-old patient has either bacterial or viral (aseptic) meningitis. What diagnostic information does she need to make her decision?
Ans: The physician will likely order a complete blood count (CBC), a white cell differential, and cerebrospinal fluid (CSF) analysis to include culture, Gram stain, cell count, and protein and glucose levels....Both types of meningitis demonstrate an increased white cell count, but the physician will look for a neutrophilic (bacterial) versus a lymphocytic (viral) response to help her make the decision. CSF cell counts should also show a neutrophilic response in bacterial meningitis and a lymphocytic response in viral...Gram-stain testing should reveal a bacterial organism with bacterial meningitis. Neisseria meningitidis is a common organism based on the age of this person...CSF protein levels increase in both types, but the increase is usually greater in bacterial meningitis because of the greater intensity of inflammation present in bacterial meningitis...Because of the consumption of glucose by the bacteria for metabolism and reproduction, the CSF glucose result will be out of the normal range on the low end. Viruses do not use the glucose present in the CSF, so the CSF glucose result will likely be in the normal range.
Mr. Blane was driving his 1954 Chevy Impala to a Red Sox baseball game when a deer jumped out in front of him on the highway. He swerved his car and hit a telephone pole instead. His head hit the windshield and he suffered severe head trauma. What specific kind of head injury did he suffer?
Ans: Mr. Blane suffered a coup and contrecoup brain injury. As his car hit the telephone pole, it threw Mr. Blane's head forward (coup) breaking the windshield, and then his head went backward (contrecoup).
Why is autonomic dysreflexia dangerous?
Ans: Autonomic dysreflexia is a condition that occurs after spinal shock has resolved. A stimulus of the sympathetic nervous system causes a severe, uncompensated cardiovascular response. It is considered life threatening and requires immediate response. This syndrome occurs mainly in lesions at the T6 level or above. Signs and symptoms include paroxysmal hypertension (300 mmHg systolic), pounding headache, blurred vision, sweating that occurs above the lesion level, skin flushing, nasal congestion, nausea, piloerection, and bradycardia (30 to 40 beats/minute).
Sally, a nurse, injured her lower back while helping a nursing assistant get Mr. Pod from his chair back into bed. He weighs 300 pounds and was not steady on his feet in the transfer. Sally's diagnosis was a herniated L4 disk. What are her treatment options?
Ans: Conservatively, treatment options include traction, bed rest, heat and ice to painful areas, and effective analgesic anti-inflammatory medications. Surgical interventions may be needed if severe compression is apparent or if the conservative approach is not successful
What are the causes and risk factors associated with a hemorrhagic stroke?
Ans: A hemorrhagic stroke has several causes. These include hypertension (56% to 81%), ruptured aneurysm, vascular malformations, bleeding into the tumor, hemorrhage linked to bleeding disorders or anticoagulation, head trauma, and illegal drug use. The risk factors include hypertension, previous cerebral infarct, coronary artery disease, and diabetes mellitus
Explain the differences between bacterial meningitis, aseptic meningitis, fungal meningitis, and tubercular meningitis.
Ans: Meningitis in general is an infection of the meninges caused by bacteria, viruses, fungi, parasites, or toxins. Bacterial meningitis mainly affects the pia mater and arachnoid, subarachnoid space, ventricular system, and the CSF. Meningococcus and pneumococcus are the common causes. Aseptic meningitis is an inflammation thought to be limited to the meninges. This type is mainly caused by viruses such as enteroviruses, mumps, herpes simplex 1 and 2, West Nile virus, Epstein-Barr, Colorado tick fever, and influenzavirus types A and B. Fungal meningitis is a chronic condition and much less common. Some of the most common infections include histoplasmosis, candidiasis, and aspergillosis. It frequently occurs in people with immune response impairment or problems with normal body flora. Syphilis, tuberculosis, and Lyme disease are also associated with fungal meningitis. Tubercular meningitis is the common and dangerous form of CNS tuberculosis. Mycobacteria enter the CSF causing a hypersensitivity reaction that results in a purulent exudate that affects the basal meninges, cerebrum, and spinal nerves. Recovery is 90% effective if caught early and treated with appropriate medications.
What are the major chemical components of the cell membranes?
Ans: Lipids and Proteins
Explanation: The major chemical components of all cell membranes are lipids and proteins, but the percentage of each varies among different membranes.
What organic compound facilitates transportation across cell membranes by acting as receptors, transport channels for electrolytes & enzymes to drive active pumps?
Ans: Proteins
Explanation: Proteins act a (1) recognition & binding units (receptors) for substances moving in & out of the cell; (2)pores or transport channels for various electrically charged particles called ions or electrolytes & specific carriers for amino acids & monosaccharides; (3) specific enzymes that drive active pumps that promote concentration of certain ions, particularly K+, w/in the cell while keeping concentration of other ions, like Na+ below concentrations found in the extracellular environment
What prevents water-soluble molecules from entering cells across the plasma membrane?
Ans: Phospholipid bilayer
Exp: The bilayer's structure accounts for one of the essential functions of the plasma membrane-it is impermeable to most water-soluble molecules b/c they are insoluble in the oily core region. The bilayer serves as a barrier to the diffusion of water & hydrophilic substances while allowing lipid-soluble molecules, such as O2 and CO2 to diffuse through it readily
Using the fluid mosaic model, a cell is actively capable of protecting itself against injurious agents by:
Ans: altering the number & patterns of receptors to bacteria, antibodies & chemicals
Exp: Hormones, bacteria, viruses, drugs, antibodies, chemicals that transmit nerve impulses, & other substances attach to the plasma membrane by means of receptor molecules on its outer layer. The number of receptors present may vary @ different times, and the cell is capable of modulating the effects of injurious agents by altering receptor # and pattern. This aspect of the fluid mosaic model has drastically modified previously held concepts concerning the onset of disease
Which form of cell communication is used to communicate within the cell itself & with other cells in direct physical contact?
Ans: Plasma membrane-bound signaling molecules (involving receptors)
Exp: Cells communicate in 3 ways: (1) they form protein channels (gap junctions) that directly coordinate the activities of adjacent cells; (2) they display plasma membrane-bound signaling molecules (receptors) that affect the cell itself & other cells in direct physical contact; & (3) (the most common means) they secrete chemicals that signal to cells some distance away
Which mode of chemical signaling uses blood to transport communication to cells some distance away?
Ans: Hormone Signaling
Exp: It involves specialized endocrine cells that secrete hormone chemicals (e.g. thyroid-stimulating hormone) released by one set of cells & travel though the tissue & through the bloodstream to produce a response in other sets of cells
Which mode of chemical signaling uses local chemical mediators that are quickly taken up, destroyed or immobilized?
Ans: Paracrine Signaling
Exp: In paracrine signaling, cells secrete local chemical mediators that are quickly taken up, destroyed, or immobilized
Neurotransmitters affect the postsynaptic membrane by binding to:
Ans: Receptors
Exp: In each type of chemical signaling, the target cell receives the signal by first attaching to is receptors
How do cells receive communication from the extracellular fluid surrounding them?
Ans: Chemical messengers such as ligands
Exp: Channel opening & closing can be initiated in 1 of 3 ways: (1) by binding a ligand to a specific membrane receptor that is closely associated w/ the channel (G-proteins); (2) by changes in electric current in the plasma membrane, altering flow of Na+ & K+; & (3) by stretching or other chemical deformation of the channel
The mammary glands enlarge during pregnancy primarily as a consequence of:
Ans: Hormonal Hyperplasia
Exp: Hormonal occurs chiefly in estrogen dependent organs, such as the uterus & breast
What is a consequence of leakage of lysosomal enzymes during chemical injury?
Ans: Enzymatic digestion of the nucleus & nucleolus occurs, halting DNA synthesis
Exp: Enzymatic digestion of cellular organelles, including the nucleus & nucleolus, ensures, halting synthesis of DNA & ribonucleic acid (RNA)
What organs are affected by the type of necrosis that results from hypoxia caused by severe ischemia or caused by chemical injury?
Ans: Kidneys and heart
Exp: Coagulative necrosis, which occurs primarily in the kidneys, heart & adrenal glands, commonly results from hypoxia caused by severe ischemia or hypoxia caused by chemical injury, especially ingestion of mercuric chloride
What effect does fetal alcohol syndrome (FAS) have on infants?
Ans: Cognitive impairment & facial anomalies
Exp: FAS can lead to growth restriction, cognitive impairment, facial anomalies, & ocular disturbances
What physiologic changes occur during heath exhaustion?
Ans: Hemoconcentration occurs because of the loss of salt & water.
Exp: Heat exhaustion occurs when sufficient salt & water loss results in hemoconcentration.
What is the common site of lipid accumulation?
Ans: Liver
Exp: Although lipids sometimes accumulate in heart & kidney cells, the most common site of intracellular lipid accumulation or fatty change, is liver cells.
Which of the following transmit a never impulse at the highest rate?
Ans: Large myelinated axons
Exp: If the myelin layer is tightly wrapped many times around the axon forming nodes of Ranvier, it increases conduction velocity & the neuron is referred to as myelinated. Larger myelinated axons transmit impulses at a faster rate
The ___ is the membrane that separates the cerebellum from the cerebrum.
Ans: tentorium cerebelli
Exp: The tentorium cerebelli is a membrane that separates the cerebellum below from the cerebral structures above. The remaining options do not perform the function described in the stem
Where is the neurotransmitter norepinephrine secreted?
Ans: In the sympathetic postganglion
Exp: Most postganglionic sympathetic fiber release norepinephrine (adrenaline). The remaining options do not reflect the correct site of norepinephrine secretion.
Which nerves are capable of regeneration?
Ans: Myelinated nerves in the peripheral nervous system
Exp: Nerve regeneration is limited to myelinated fibers & generally only in the PNS.
The ability of the eyes to track moving objects through a visual field is primarily a function of the ___ colliculi
* voluntary & involuntary visual motor movements (e.g. the ability of the eyes to track moving objects in the visual field
Ans: Superior
Exp: The superior colliculi are involved w/ voluntary & involuntary visual motor movements (e.g. the ability of the eyes to track moving objects in the visual field). This is not the primary function of the remaining options.
What parts of the brain mediate the expression of affect, both emotional & behavioral states?
Ans: Limbic system & prefrontal cortex
Exp: Expression of affect (emotional & behavioral states) is mediated by extensive connections w/ the limbic system & prefrontal cortex. The remaining options are not involve in these expressions
Pricking one's finger w/ a needle would cause minimal pain, whereas cutting one's finger w/ a knife would produce more pain. This is an example of the ___ theory of pain
Ans: Specificity
Exp: According to the specificity theory, there is a direct relationship between the intensity of pain & the extent of tissue injury> The remaining options are not related to the intensity of perceived pain>
The ___ theory proposes that pain results from excessive stimulation of sensory receptors.
Ans: Intensity
Exp: Rene Descartes proposed that the body works like a machine that can be studied by scientific methods & that injury activates specific pain receptors & fibers that project to the brain. He further postulated that the intensity of pain is directly related to the amount of associated tissue injury resulting in the stimulation of sensory receptors. The remaining options are not related to the resultant of pain.
What type of nerve fibers transmit pain impulses?
Ans: A-delta fibers
Exp: These two receptors are associated w/ lightly myelinated, medium-sized A-delta (Ad) fibers. Other types of mechanical, thermal & chemical nociception are transmitted by excitation of polymodal nociceptors and & are carried on small, unmyelinated C fibers
Where do primary efferent pain fibers enter the spinal cord?
Ans: Dorsal root ganglia
Exp: The cell bodies of primary-order neurons or pain-transmitting neurons reside in the dorsal root ganglia just lateral to the spine along the sensory pathways the penetrate the posterior part of the cord
Where is the gate located that is referred to in the gate control theory of pain?
Ans: Substantia gelantinosa
Exp: The synaptic connections between cells of primary & secondary order neurons located in the substantia geliatinosa & other rexed laminae function as a "pain gate". The remaining options do not act in the function.
Which spinal tract carries the most nociceptive information?
Ans: Lateral Spinothalamic tract
Exp: Most nociceptive information travels by means of ascending columns in the lateral spinothalamic tract (also called the anterolateral funiculus.)
Where is the major relay station of sensory information?
Exp: Although the organization of all the ascending tracts is complex, the principal target for nociceptive afferents is the thalamus (major relay station of sensory information in general.) The remain options do not fulfill this objective-basal ganglia,midbrain,hypothalamus)
Where in the central nervous system does pain perception occur?
Ans: Parietal
Exp: On the postcentral gyrus of the parietal lobe is topographically organized representation of the body that mirrors the concentration of peripheral sensory receptors known as the sensory homunculus. This area of the brain is thought to be involved in the discriminative & cognitive aspects of pain, that is, what we think about the pain
Massage therapy relieves pain by stiumalting the ___ that close the pain gate.
Ans: A-beta fibers
Exp: Afferent A-beta (Ab) fibers carry non-noxious low-threshold mechanical information gained by touch, vibration, & pressure
What part of the brain provides the emotional response to pain?
Ans: Limbic System
Exp: The limbic & reticular tracts are involved in alerting the body to danger, initiating arousal of the organism, & emotionally processing the perceived afferents signals not just as stimuli, but as pain
Which neurotransmitters inhibit pain in the medulla & pons?
Ans: Norepinephrine & serotonin
Exp: Norepinephrine & 5-hydroxytryptamine (serotonin) contribute to pain modulation (inhibition) in the medulla & pons.
Which endogenous opioid is located in the hypothalamus & pituitary & is a strong mu-receptor?
Ans: Endorphins
Exp: Endorphins were first discovered in the human PAG in 1979, b-endorphin being the best studied of the group. The synthesis & activity of b-endorphin are concentrated in the hypothalamus & pituitary gland
What are the characteristics if visceral pain?
Ans: It is perceived as poorly localized & is transmitted by the sympathetic nervous system
Exp: Visceral pain refers to pain in the internal organs & the abdomen & is transmitted by sympathetic afferents. It is poorly localized b/c of fewer nociceptors in the visceral structures.
How do enkephalins & endorphins act to relieve pain?
Exp: These substances are neurohormones that act as neurotransmitters by binding to one or more G protein-coupled opioid receptors.
Release (increase) of epinephrine increases body temperature by increasing?
Ans: heat production
Exp: Epinephrine and norepinephrine produce a rapid transient increase in heat production by raising the body's basal metabolic rate
Using a fan to reduce body temperature is an example of which mechanism of heat loss?
Ans: Convection
Exp: Convection is the transfer of heat through currents of gases or liquids
Heat loss from the body via convection occurs by:
Ans: transfer of heat through currents of liquids or gas
Exp: Convection is the transfer of heat through currents of gases and liquids
Which disorder of temperature regulation is caused by prolonged high environmental temperatures that produce dehydration, decreased plasma volumes, hypotension, decreased cardiac output & tachycardia?
Ans: Heat Exhaustion
Exp: heat exhaustion, or collapse, is a result of prolonged high core or environmental temperatures resulting in dehydration, decreased plasma volumes, hypotension, decreased cardiac output & tachycardia.
Children are more susceptible to heat stroke than are adults because:
Ans: Children are more susceptible to heat stroke than are adults because (1) they produce more metabolic heat when exercising; (2) they have a greater surface area-to-mass ration & (3) their sweating capacity is less than that of adults
In acute hypothermia, what physiologic change shunts blood away from the colder skin to the body core in an effort to decrease heat loss?
Ans: Peripheral vasoconstriction
ExP: Tissue hypothermia slows the rate of chemical reactions (tissue metabolism), increases the viscosity of the blood, slows blood flow through the microcirculation, facilitates blood coagulation, & stimulates profound vasoconstriction
A medication used to reverse effects of malignant hyperthermia is:
Ans: Dantrolene Sodium
Exp:Treatment includes withdrawal of the provoking agents & administration of dantrolene sodium (a skeletal relaxant that inhibits calcium release during muscle contraction). The other options are not effective in the treatment of malignant hyperthermia.
What are expected changes in sleep patterns of older adults?
Ans: They experience frequent awakenings during the night with less time spent in stage IV sleep.
Exp: The sleep pattern of the older adult includes total decreased sleep time & takes longer to fall asleep. Older adults tend to go to sleep earlier in the evening & awaken more frequently during the night & earlier in the morning. REM & slow wave sleep decreases on EEG, the spindle indicating stage II sleep is well formed
Open-angle glaucoma occurs because of ___ humor
Ans: Obstructed outflow of aqueous humor
Exp: Open-angle glaucoma is characterized by intraocular pressures above the normal pressures of 12 to 20 mmHg maintained by the inadequate outflow of aqueous fluid
How dos glaucoma cause blindness?
Ans: By pressure on the optic nerve
Exp: Loss of visual acuity results from pressure on the optic nerve
A sensorineural hearing loss may be a result of:
Ans: Meniere dieses, aging, diabetes mellitus & noise exposure all apply.
Exp: A sensorineural hearing loss is caused by impairment of the organ of Corti or its central connections. The hearing loss may be gradual or sudden. Conditions that commonly cause sensorineural hearing loss include congenital & hereditary factors, noise exposure, aging, Meniere disease, ototoxicity, & systemic disease (syphilis, Paget disease, collagen disease, diabetes mellitus). Outer ear trauma is not a typical cause of sensorineural hearing loss.
Define Scotoma
Ans: Defect in central field
ExP: a scotoma is a circumscribed defect of the central field of vision
Define Nystagmus
Ans: Involuntary movement of eyeballs
Exp: Nystagmus is an involuntary unilateral or bilateral rhythmic movement of the eyes
Define Hemianopia
Ans: Defective vision in half of a visual field
Exp: Hemianopia describe defective vision in half of a visual field
Define Anosmia
Ans: Loss of ability to smell
Exp: Anosmia is the complete loss of smell
Define Parageusia
Ans: Perversion of sense of taste
Exp: Parageusia is a perversion of taste in which substances possess an unpleasant flavor
What causes stage 1 of intracranial hypertension? Stage 1 intracranial hypertension is caused by the:
Ans: Displacement of cerebrospinal fluid (CSF) followed by compression of the cerebral venous system
Exp: If intracranial pressure remains high after CSF displacement out of the cranial vault, cerebral blood volume is altered, which causes state 1 intracranial hypertension. Vasoconstriction & external compression of the venous system occur in an attempt to further decrease intracranial pressure
Dilated & sluggish pupils, widening pulse pressure & bradycardia are clinical findings evident of which stage of intracranial hypertension?
Ans: Stage 3
Exp: Stage 2 of intracranial hypertension presents clinical manifestations that include decreasing levels of arousal, Cheyne-Stokes respiration or central neurogenic hyperventilation, pupils that become sluggish & dilated, widened pulse pressure & bradycardia.
Dilation of the ipsilateral pupil following uncial herniation is the result of pressure on which of the following cranial nerves?
Ans: Oculomotor (CN III)
Exp: The oculomotor cranial nerve (CN III) is involved in this manifestation of pupil dilation
Which of the following is the most critical index of nervous system dysfunction?
Ans: Level of consciousness
Exp: Level of consciousness is the most critical clinical index of nervous system function or dysfunction. An alteration in consciousness indicates either improvement or deterioration of a person's condition
Diagnostic criteria for a vegetative state (VS) include:
Ans: Return of autonomic functions such as gastrointestinal function
Exp: Diagnostic criteria for VA includes return of so-called vegetative (autonomic) functions, including sleep-wake cycles & normalization of respiratory & digestive system functions
Uncal herniation occurs when:
Ans: The hippocampal gyrus shifts from the middle fossa through the tentorial notch into the posterior fossa
Exp: Uncal herniation (hippocampal herniation, lateral mass herniation) occurs when the uncus or hippocampal gyrus (or both) shifts from the middle fossa through the tentorial notch into the posterior fossa, compressing the ipsilateral their cranial nerve impairing parasympathetic function carried in the periphery of the nerve, then the contralateral third cranial nerve, & finally the mesencephalon, including coma
Which assessment finding marks the end of spinal shock?
Ans: Spinal reflexes gradually return
Exp: A gradual return of spinal reflexes marks the end of spinal shock
In amyotrophy, paresis & paralysis are segmental. Why is the segmental character of weakness difficult to recognize? The weakness resulting from the segmental paresis & paralysis characteristic of amyotrophy is difficult to recognized because:
Ans: Each muscle is supplied by 2 or more nerve rods
Exp: The paresis & paralysis associated w/ anterior horn cell injury are segmental, but because each muscle is supplied by two or more roots, the segmental character of the weakness may be difficult to recognize.
Clinical manifestations of Parkinson disease are cause by a deficit in which neurotransmitter?
Ans: Dopamine
Exp: Parkinson disease is a commonly occurring degenerative disorder involving deficits of dopamine
What pathologic alteration produces tremors at rest, rigidity akinesia, & postural abnormalities?
Ans: Atrophy of neurons in the substantia nigra that produce dopamine
Exp: The hallmark characteristics of Parkinson disease are a result of a loss of dopaminergic pigmented neurons in the substantia nigra (SN) pars compacta w/ dopaminergic deficiency in the putamen portion of the striatum includes the putamen & caudate nucleus
Define Expressive Dysphasia
Ans: Broca dysphasia
Exp: Broca dysphasia is an expressive dysphasia of speech & writing but with retention of comprehension
Define Receptive Dysphasia
Ans: Wernicke aphasia
Exp: Wernicke dysphasia is a disturbance in understanding all language-verbal & reading comprehension
Describe decrease in voluntary movement
Ans: Akinesia
Exp: Akinesia is an absence, poverty, or lack of control of associated & voluntary muscle movements. There is a disturbance in time it takes to perform a movement
Describe abnormal involuntary movement
Ans: Paroxysmal dyskinesia
Exp: Paroxysmal dyskinesias are abnormal, involuntary movements that occur as spasmas
Describe lower motor neuron disorders
Ans: Flaccidity
Exp: Lower motor neuron syndromes manifest with impaired voluntary & involuntary movements (i.e. hypotonia)
Describe upper motor neuron disorders
Ans: Spasticity
Exp: An upper motor neuron syndrom is characterized by paresis or paralysis, hypertonia (spasticity), & hyperreflexia
What complication is occurring for a person who has a spinal cord injury above T6 & is experiencing paroxysmal hypertension as well as piloerection & sweating above the spinal cord lesion?
Ans: Autonomic hyperreflexia
Exp: Individuals most likely to be affected have lesions at the T6 level or above. Autonomic hyperreflexia is characterized by paroxysmal hypertension (up to 300 mmHg systolic), a pounding headache, blurred vision, sweating above the level of the lesion w/ flushing of the skin, nasal congestion, nausea, pilorection caused by pilomotor spasm, & bradycardia (30 to 40 beats/minute)
Why does a person who has a spinal cord injury experience faulty control of sweating?
Ans: The hypothalamus is unable to regulate body heat as a result of sympathetic nervous system damage.
Exp: The condition also results in disturbed thermal control b/c the hypothalamus is unable to regulate a damaged sympathetic nervous system. This damage causes faulty control of sweating & radiation through capillary dilation.
Multiple sclerosis & Guillain-Barre syndrome (GBS) are similar in that they both?
Ans: Result from demyelination by an immune reaction
Exp: The condition also results in disturbed thermal control b/c the hypothalamus is unable to regulate a damaged sympathetic nervous system. This damage causes faulty control of sweating & radiation through capillary dilation
What sequence causes autonomic hyperreflexia-induce bradycaria?
Ans: Stimulation of the carotid sinus to the vagus nerve to the SA node.
Exp: The intact autonomic nervous system reflexively responds w/ an arteriolar spasm that increases blood pressure. Baroreceptors in the cerebral vessels, the carotid sinus, & the aorta sense the hypertension & stimulate the parasympathetic system. The heart rate decreases, but the visceral & peripheral vessels do not dilate because efferent impulses cannot pass through the cord.
Of the following people, who is at the highest risk for a cerebrovascular accident (CVA)?
Ans: Black women older than 70 years age
Exp: 50% of CVAs occur in persons older than 70 years. Strokes, however, do occur in a 3:10 ration (28%) in individuals younger than 65 years. Stroke tends to run in families. The incidence of stroke 2.5x higher in blacks in whites. Stroke prevalence in 2005 for black mean was 2.3 million compared to 3.4 million in black women. The risk of first ever stroke in blacks is almost twice of whites
A right hemisphere emoblic cerebrovascular accident has resulted in left-sided paralysis & reduced sensation of the left foot & leg. The vessel most likely affected by the emobli is the right ___artery.
Ans: Anterior cerebral
Exp: Symptomatology of an embolic stroke in the right anterior cerebral artery would include left-sided contralateral paralysis or paresis (greater in foot and thigh) and mild upper extremity weakness with mild contralateral lower extremity sensory deficiency with loss of vibratory and/or position sense and loss of two-point discrimination.
A man was in an automobile accident in which his forehead struck the windshield. A blunt force injury to the forehead would result in a coup injury to the ___region.
Ans: Frontal
Exp: The focal injury may be coup (directly below the point of impact). Objects striking the front of the head usually produce only coup injuries (contusions and fractures) because the inner skull in the occipital area is smooth.
A blunt force injury to the forehead would result in a countercoup injury to the ___ region.
Ans: Occipital
Exp: The focal injury may be coup (directly below the point of impact) or contrecoup (on the pole opposite the site of impact). Objects striking the back of the head usually result in both coup and contrecoup injuries because of the irregularity of the inner surface of the frontal bones.
The most likely rationale for body temperature fluctuations after cervical spinal cord injury is that the person:
Ans: Has sympathetic nervous system damage resulting in disturbed thermal control
Exp: The condition in disturbed thermal control b/c the sympathetic nervous system is damaged
A man who sustained a cervical spinal cord injury 2 days ago suddenly develops severe hypertension & bradycardia. He reports severe head pain & blurred vision. The most likely explanation for these clinical manifestations is that he is:
Ans: Developing autonomic hyppereflexia
Exp: Autonomic hyperreflexia is characterized by paroxysmal hypertension (up to 300 mm Hg systolic), a pounding headache, blurred vision, sweating above the level of the lesion with flushing of the skin, nasal congestion, nausea, piloerection caused by pilomotor spasm, and bradycardia (30 to 40 beats/minute).
Cranial Nerve I
- Name: Olfactory
- Function: Purely Sensory
- Origin & Course: Fibers arise from nasal olfactory epithelium & form synapses w olfactory bulbs that transmit impulses to temporal lobe
- To Test: Pt sniff aromatic substances i.e. oil of cloves & vanilla & identifies them
Cranial Nerve II
- Name: Optic
- Function: Sensory
- Origin & Course: fibers arise from retina of eye to form optic nerve, which passes through sphenoid bone; two optic nerves then form optic chiasm & eventually end in occipital cortex
- To Test: vision & visual field tested w/ an eye chart; inside of eye viewed to observe blood vessels of eye interior
Cranial Nerve III
- Name: Oculomotor
- Function: Both; motor fibers to eye muscles (inferior oblique & superior,inferior & medial rectus extraocular) that direct eyeball, levator muscles of eyelid, smooth muscles of iris & ciliary body & propioception (sensory) to brain from extraocular muscles
- Origin & Course: fibers emerge from midbrain & exit from skull & extend to eye
- To Test: pupils examined & reflexes tested w/ a penlight; ability to follow moving objects
Cranial Nerve IV
- Name: Trochlear
- Function: Both; proprioceptor & motor fibers for superior oblique muscle of eye (extraocular muscle-downward & inward movement)
- Origin & Course: fibers emerge from posterior midbrain & exit from skull to run to eye
- To Test: tested in common with cranial nerve III:pupils examined & reflexes tested w/ a penlight; ability to follow moving objects
Cranial Nerve V
- Name: Trigeminal
- Function: Both motor and sensory for face; sensory impulses from mouth, nose, surface of eye & dura mater; motor fibers that stimulate chewing muscles
- Origin & Course: fibers emerge from pons & form 3 divisions that exit from skull & run to face & cranial dura mater
- To Test: sensations of pain, touch & temp; corneal reflex tested with wisp of cotton; motor branch tested by asked subject to clench teeth, open mouth against resistance, & move jaw from side to side
Cranial Nerve VI
- Name: Abducens
- Function: Both; motor fibers to lateral rectus muscle; propioceptor fibers from same muscle to brain, allowing eyes to move laterally
- Origin & Course: fibers leave inferior pons & exit from skull & extend to eye
- To Test: tested in common with cranial nerve III relative to ability to move each eye laterally
Cranial Nerve VII
- Name: Facial
- Function: Mixed; supplies motor fibers to muscles of facial expression & to lacrimal & salivary glands; carries sensory fibers from taste buds of anterior part of tongue
- Origin & Course: fibers leave pons & travel through temporal bone & extend to face
- To test: anterior 2/3 tongue test for ability to taste sweet, salty, sour & bitter; symmetry of face; pt closes eyes, smiles,w whistles; test tearing w/ ammonia
Cranial Nerve VIII
- Name: Vestibulocochlear (acoustic)
- Function: Purely Sensory; vestibular branch transmits impulses for sense of equilibrium; cochlear branch transmits or sense of hearing
- Origin & Course: fibers run from inner ear (hearing & equilibrium receptors to temporal bone) to enter brainstem just below pons
- To test: hearing checked by bone condution by use of a tuning fork; vestibular tests: Barany & caloric tests
Cranial Nerve IX
- Name: Glossopharyngeal
- Function:Mixed: motor fibers serve pharynx & salivary glands; sensory fibers carry impulses from pharynx, posterior tongue (taste buds) & pressure receptors of carotid artery
- Origin & Course: fibers emerge from midbrain & leave skull & extend to pharynx, salivary glands & tongue
- To test: gag & swallow reflexes checked; pt asked to speak & cough; posterior 1/3rd of tongue may be tested
Cranial Nerve X
- Name: Vagus
-Function: Both; fibers carry sensory & motor impulses for pharynx; a large part of this nerve is parasympathetic motor fibers, which supply smooth muscles of abdominal organs; receives sensory impulses from the viscera
- Origin & Course: fibers emerge from the medulla, pass through the skull & descend through neck region into thorax & abdominal region
- To Test: same as IX; gag & swallow reflexes checked; pt asked to speak & cough; posterior 1/3rd of tongue may be tested
Cranial Nerve XI
- Name: Spinal Accessory
- Function: Both; provides sensory & motor fibers for sternocleidomastoid & trapezius muscles & muscles of soft palate, pharynx, and larynx
- Origin & Course: fibers arise from medulla & superior spinal cord & extend to muscles of neck & back
- To Test: sternocleidomastoid & trapezius muscles checked for strength by asking Pt to rotate head & shrug shoulders against resistance
Cranial Nerve XII
- Name: Hypoglossal
- Function: Both: carries motor fibers to muscles of tongue & sensory impulses from tongue to brain
- Origin & Course: fibers arise from medulla & exit from skull & extend to tongue
- To test: Pt asked to stick out tongue & any position abnormalities are noted
Resting Membrane Potential
- the difference in electrical charge/voltage across the plasma membranes as a result of differences in ionic composition of ICF and ECF (-70 mV to -85mV)
- Na+ have a higher conc in the ECF and K+ in the ICF; the concetration diff. is maintained by active transport of Na+ and K+
Action Potential
- occurs when a nerve or muscle cell receive a stimulus that exceeds the membrane threshold value causing a rapid change in the resting membrane potential
- carries signals along the cell & conveys info from one cell to another
- net movement of Na+ into the cell causes the membrane potential to decrease from a negative value to zero
- the depolarized cell is more positively charged & its polarity is neutralized
- a critical value that must be reached in order to generate an action potential
- once reached, the cell will continue to depolarize w/ no further stimulation
- the Na+ gates open & Na+ rushes into the cell, causing the membrane potential to reduce to zero & then become positive
- period in which the negative polarity of the resting membrane potential is reestablished
- as voltage-gated Na+ channels begin to close, voltage-gated K+ channels open
- membrane permeability to Na+ decreases & K+ permeability increases w/ an outward movement of K+ ions
- Na+ gates close & w/ outward movement of K+, the membrane potential becomes negative
- the Na+-K+ pump then returns the membrane to resting potential by pumping K+ back into the cell & Na+ out of the cell
Absolute Refractory Period
- the time during the action potential in which the plasma membrane cannot respond to an additional stimulus
- related to changes in permeability to Na+
Relative Refractory Period
- the latter phase of the action potential, when permeability to K+ increases, a stronger-than-normal stimulus can evoke an action potential
- when the membrane potential is more negative than normal, the cell is in a less excitable state
- a larger-than-normal stimulus is required to reach the threshold potential & generate an action potential
- occurs as K+ continues to leave the cell, after the Na+ gates have close, and (undershoots) causing a drop in membrane potential
- when the membrane potential is more positive than normal
- a more excitable than normal state & a smaller-than-normal- stimulus is required to reach the theshold potential
preganglionic neurons
- myelinated neurons with cell bodies located in the CNS
- axons terminate in the autonomic ganglia.
postganglionic neurons
- unmyelinated
- ANS neurons that exist outside the brain and spinal cord and innervate the major organ systems -- ACh used as a transmitter in parasympathetic postganglionic neurons
Sympathetic Nervous System
- functions to mobilize energy stores in time of need
- aka "Fight or Flight" response
- prepares the body for emergencies and stress by increasing the breathing rate, heart rate, and blood flow to muscles
- cell bodies located from T1 to L of the spinal cord
- mediated by epinephrine & norepinephrine
Parasympathetic Nervous System
- functions to conserve and restore energy
- cell bodies are located in the cranial nerve nuclei & the sacral region o the spinal cord
- division of the ANS that is most active in ordinary conditions; it counterbalances the effects of the sympathetic system by restoring the body to a restful state after a stressful experience
*Central Nervous System
- the brain and spinal cord
- densely packed cell bodies are nuclei
*Peripheral Nervous System
- consists of the 12 pairs of cranial nerves: sensory, motor & mixed
- cranial nerves III (oculomotor), VII (facial), IX (glossopharyngeal), X (vagus) contain parasympathetic nerves
- consists of 31 spinal nerves: afferent (ascending:sensory to spinal) & efferent (descending: enervate effector) pathways
- names correlate w/ the vertebral level from which they exit; mixed nerves; arise from the anterior & posterior horn cells of the spinal cord
- densely packed cell bodies are called ganglia
*Somatic Nervous System
- motor & sensory pathways regulating voluntary motor control of skeletal muscle
- NT: acetylcholine
- spinal cord or brain ---> skeletal muscle
*Autonomic Nervous System
- motor and sensory pathways regulating the body's internal environment through involuntary control of organ systems (maintains steady state)
- include the sympathetic and parasympathetic nervous systems
- contains both preganglionic neurons (myelinated) & postganglionic (unmyelinated)
- epinephrine will vasoconstrict, increasing BP, dilates bronchioles, elevates blood glucose level
*Sympathetic Nervous System
- mobilized energy stores in time of need- "fight or flight" response
- receives innervation from he cell bodies located from the 1st thoracic thru the 2nd lumbar (thoracolumbar division)
- sympathetic (paravertebral) ganglia
*Parasympathetic Nervous System
- functions to conserve & restore energy- "rest or digest/repose response"
- receives innervation from cell bodies located in the cranial nerve nuclei & sacral region of the spinal cord (craniosacral)
- preganglionic neurons travel to ganglia close to the organs they innervate
- long threadlike extensions of motor neurons, which travel bundled within nerves , to muscle cells they serve; ends are called axon terminals
- Nodes of Ranvier: regular interruptions of the myelin sheath
- saltatory conduction: flow of ions between segments o myeline rather than along the entire length of the axon
- divergence: ability of branching axons to influence many neurons
- convergence: branches of numerous neurons converging on one for a few neurons
*Nerve Injury & Regeneration
- Wallerian degneration
- occurs distal to the cut :swelling appears, neurofilaments hypertrophy, myeline sheath shrinks & disintegrates, axon portion degenerates & disappears
- proximal to the cut: swelling & dispersal of the Nissl substance; cell increases in metabolic activity, protein synthesis & mitochondrial activity; new terminal sprouts project from proximal segment; process limited to myelinated axons (usually only in PNS); depends on locate, type of injury, inflammatory response, & scar tissue formation
Neurotransmitters & Neuroreceptors
- one NT can have different effects in different postsynaptic cells; one type of NT can bind to several types of receptors in the postsynaptic PM, each type producing different effects when stimulated
- sympathetic nervous system w/ the NT norepinephrine and alpha & beta receptors
- the exceptions; for example, Beta receptors in the conductive tissues of the heart mimic alpha effects
- sympathetic preganglionic fibers: acetylcholine & cholinergic receptors
- sympathetic postganglionic fibers: norepinephrine & adrenergic receptors
- parasympathetic pre- and postganglionic fibers: acetylcholine & cholinergic receptors (spinal cord or brain -->(ACh) @ peripheral ganglion --> (ACh) @ organ: post-ganglionic)
Sympathetic Stimulation
- promotes responses that are concerned w/ the protection of the individual that would include increased blood sugar levels & temperature & BP
- the primary response from norepinephrine (levophed) is stimulation of alpha1-adrenergic receptors that cause vasoconstriction
- the binding of the NT at the receptor site changes the permeability of the postsynaptic neuron & consequently, its membrane potential
Synaptic Transmission
- PM of presynaptic & postsynaptic neurons are close, but do not touch. The synaptic cleft is filled w/ interstitial fluid
- for a nerve impulse to cross the SC, a # of structures are required: voltage-gated Ca2+ channels, synaptic vesicle containing a NT, postsynaptic neuron receptor & postsynaptic ligand-gated channels
- for the stimulus to eventually discontinue, an enzyme must be present to break down the excitatory or inhibitory NT
- disease can effect one or more of these structures, thus causing a prolonged excitatory or inhibitory response
Central Nervous System
- forebrain: cerebral hemispheres
- midbrain: corpora quadrigemina, tegmentum & cerebral peduncles
- hindbrain (brain stem): cerebellum, pons & medulla
- part of the hindbrain in the brain steam
- the cerebellum is responsible for conscious & unconscious muscle synergy & for maintaining balance & posture
Reticular Formation
- network of connected nuclei that regulate vital reflexes, such as cardiovascular & respiratory function
- together w/ the cerebral cortex is referred to as the reticular activating system
- the reticular formation is a large network of neurons w/in the brainstem that is essential for maintaining wakefulness
Frontal lobe
- prefrontal: goal-oriented behavior i.e. ability to concentrate, short-term or recall memory & the elaboration of though & inhibition of the limbic (emotional areas)
- premotor: basal ganglia-Parkinson disease & Huntington disease are conditions associated w/ defects of the basal ganglia
- primary motor area: Brodmann area 4 is located along the precentral gyrus forming the primary voluntary motor area. Electrical stimulation of specific areas of this cortex causes specific muscles of the body to move
- Broca speech area: responsible for the motor aspects of speech. articulation of words
Parietal lobe
- somatic sensory input
Occipital lobe
- primary visual cortex (Brodmann area 17)
- receives input from the retinas
- visual association
Temporal lobe
- Wernicke area (speech) responsible for
- composed of the superior, middle & inferior temporal gyro
- primary auditory cortex (Brodmann area 41) & its related association area (Brodmann area 42) lie deep w/ the lateral sulcus on the superior temporal gyrus
- epithalamus
- thalamus
- hypothalamus: functions in maintenance of a constant internal environment & implementation of behavioral patterns
- subthalamus
- corpora quadrigemina (tectum): superior & inferior colliculi
- tegmentum: red nucleus & substantia nigra
- basis pedunculi
Hindbrain (metencephalon)
- cerebellum
- pons: the nuclei of cranial nerves V through VIII are located in the pons
- medulla oblongata: makes up the myelencephalon & is the lowest portion of the brainstem; reflex activities, such as heart rate, respiration, blood pressure, coughing, sneezing, swallowing, & vomiting
- the nuclei of cranial nerves IX through XII are located here
- telecephalon: cerebrum --> gyric, sulci, & fissures; gray matter & white matter
- cerebral nuclei (basal ganglia)
Spinal Cord
- secretions: cervical, thoracic, lumbar & sacral
- horns: posterior, lateral, anterior
- blood supply provided by the vertebral arteries (anterior & posterior spinal arteries) & aorta
Upper Motor Neurons
- efferent pathways primarily relaying information from the cerebrum to the brainstem or spinal cord
- synapse w/ interneurons
- destruction= partial recovery
-upper motor neurons (i.e. corticospinal tract) are the classfication of motor pathways completely contained w/in the CNS; their primary roles include directing, influencing, & modifying spinal reflex arcs, lower-level control centers, & motor (and some sensory) neurons
Lower Motor Neurons
- neurons having direct influence on muscle
- cell bodies originate in gray matter of spinal cord, but their axons extend into the PNS
- destruction=permanent paralysis
Sensory Pathways
- anterior spinothalamic
- lateral spinothalamic
- posterior (dorsal): 3 neuron chain, ipsilateral transmission (on the same side), contralateral transmission (on the opposite side)
Protective Structures
- Meninges: protective membranes surrounding the brain & spinal cord: dura mater, arachnoid, pia mater
- unlike the dura mater & arachnoid & inner dura, the delicate pia mater closely adheres to the surface of the brain & spinal cord & even follows the sulci fissures
- cerebrospinal fluid (CSF) & the ventricular system; a clear colorless fluid similar to blood plasma & interstitial fluid; 125 to 150 ml; produced by the choroid plexuses in the lateral, third, and fourth ventricles; reabsorbed through the arachnoid villi
- vertebral column: 33 vertebrae (7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral & 4 fused coccygeal; intervertebral disks (nucleus pulposus)
Motor Pathways
- lateral corticospinal
- corticobulbar
- basal ganglia
- vestibulospinal
Blood-Brain Barrier
- the capillary walls of the brain serve as barriers for the movement of selected chemicals & molecules from the blood to the brain tissue
- an example of a set of sieves w/ different gauges of mesh helps illustrate how some substances are allowed to pass through & others are not, depending on the composition & size of the substance in relation to the mesh size of the sieve
Blood Supply to the Brain
- the brain receives approx. 20% of the cardiac output or 800 to 1000 ml of blow flow per minute
- CO2 is the primary regulator for CNS blood flow
internal carotid & vertebral arteries
- arterial circle (circle of Willis): a structure credited w/ the ability to compensate for reduced blood low from any one of the major contributors (collateral blood flow)
- the choroid plexuses, structures that produce CSF, arise from the pia mater
- CSF is reabsorbed by means of a pressure gradient btw the arachnoid villi & the cerebral venous sinuses
The Cranial Nerves
Aging & the Nervous System
- Structural changes: decrease in the # of neurons; decreased in brain weight & size; increased adherence of the dura mater to the skull; fibrosis & thickening of the meninges; narrowed gyro & widened sulci w/a corresponding increase in the size of the subarachnoid space; basal ganglia & ventricular system (aberrations in vascular structures)
- cellular changes: deposition of lipofuscin; presence of senile plaques; multiple neurofibrillary tangles; lewy bodies
- functional changes: slowed response to neural signals
*Cellular Adaptation
- an alteration that enables the cell to maintain a steady state despite adverse conditions
- decrease in the size of cells due to a decrease in work demand, disuse (casts), denervation (paralyzed limbs), lack of neurologic or hormonal stimulation, ischemia/decreased blood flow, inadequate nutrition
- mechanisms probably include decreased protein synthesis, increased protein catabolism or both
- result in reduced tissue mass
*Physiologic Atrophy
- occurs with early development i.e. the thymus gland involutes and atrophies
*Pathologic Atrophy
- occurs as a result of decreases in workload, use, pressure, blood supply, nutrition, hormonal stimulation & nervous stimulation
- an increase in the size of cells by increased work demands or hormonal stimulation i.e. cardiac muscular enlargement
- can be physiologic or pathologic
- amounts of protein in the plasma membrane, endoplasmic reticulum, microfilaments & mitochondria are increased
- results in enlarged tissue mass
- increased number of cells caused by an increased rate of cellular division
- results in an enlarged tissue mass
- can occur simultaneously with hypertrophy
- occurs in response to a stimulus & ceases after stimulus removed
- compensatory hyperplasia enables certain organs to regenerate
- i.e. thyroid with goiter or gum size
*Cellular Changes
- cells change in response to different stimuli (hormonal or environmental
- can be reversible & can be normal (increased breast tissue during pregnancy
- disease may develop from these changes which can cause permanent tissue damage, tumors, cancer if DNA is altered
*Hormonal Hyperplasia
- cellular adaptation; stimulated by hormones to replace lost tissue or support new growth
- occurs chiefly in estrogen-dependent organs such as the uterus and breast
- after ovulation, estrogen stimulates the endometrium growing/thickening during fertilization
*Pathologic Hyperplasia
- cellular adaptation
- abnormal proliferation of normal cells & can occur as a response to excessive hormonal stimulation or the effects of growth factors on target cells (as the result of disease)
*Compensatory Hyperplasia
- an adaptive mechanism that enables certain organs to regenerate
- i.e. removal of part of the liver leads to hyperplasia of the remaining liver cells
*Dysplasia/ Atypical Hyperplasia
- an abnormal change in the size, shape & organization of mature tissue cells due to chronic irritation or inflammation
- increased rate of mitosis can occur
- may be precancerous
- potentially reversible
- i.e. pap smear
- the reversible replacement of one mature cell type by another less differentiated (mature) cell type
- Develops from a reprogramming of stem cells existing in most epithelia or of undifferentiated mesenchymal cells in connective tissue
- can be from Vit A deficiency
- Results from chronic irritation & inflammation
- continued exposure can lead to a cancerous transformation
- i.e. replacement of normal columnar ciliated epithelial cells of the bronchial lining by stratified squamous epithelial cells
- Undifferentiated cells: various nuclei and structures
- characteristic of cancers & are the basis for staging cancers & tumors for aggressiveness
- "new growth"
- commonly called a tumor
- can be benign or malignant (cancer)
- deficit of oxygen in the cells as a result in a decrease in blood supply to the tissues
- can lead to necrosis
- reduced oxygen in tissues
- the single most common cause of cellular injury
- can lead to anoxia
- loss of oxygen
- cellular suicide or programmed cell death (active process) can occur in normal as well as pathologic tissue changes & is a difficult concept for students
- can happen quicker if cell development is abnormal or cells are injured or aged
- cells self-destruct, digest themselves enzymatically & then disintegrate
*Cell Injury
- initial cell damage leads to loss of cell function (less oxygen to the area as well as ATP --> less function)
- the damage can be reversible, if not, structural changes occur => cell death
*Post Cell Death
- Ischemia -> Tissue Injury -> Cell Death
- Lysis occurs
- Enzymes are released into the surrounding tissues (can be detected by diagnostic lab tests)
- Inflammation occurs which damages nearby cells
- MONA - Morphine Oxygen Nitroglycerin Aspirin
- occurs when a group of cells die (autolysis)
- includes liquefaction necrosis, coagulative, fat, caseous, and Infarction- lack of oxygen (MI)
- an area of dead cells lose function, blood can not be pumped effectively & scar tissue replaces the cells
- an infected necrotic area (bacterial)
- can be wet or dry depending on location (such as intestines or limb)
- removed surgically to prevent spread of infection
*Hypoxic Injury
- cellular injury mechanism; single most common cause of cellular injury
- ischemia (decrease of blood flow into vessels that supply oxygen & nutrients
- anoxia (total lack of oxygen)
- cellular responses: decrease in ATP (metabolic failure), causing failure of sodium-potassium pump and sodium-calcium exchange --> cellular swelling (Na+ influxes the cell and K+ outfluxes, water comes into the cell with the Na+ & the cell swells) --> cell death
- dissolution of all cellular membranes is occurring simultaneously
- reperfusion injury: return of blood to the site of injury, which can cause inflammation
*Cellular Damage Secondary to Accumulations
- due to osmosis, cells may shrink or swell which result in impaired function
- accumulations of pigments, lipids, calcium, enzymes etc also occurs in multiple disorders can alter the cell's ability to function properly
*Free Radicals
- difficult to control and initiate chain reactions
- can cause: lipid peroxidation or destruction of unsaturated fatty acids, alteration of proteins & alterations in DNA
- "steal" electrons or give one up to become stable & thus hurt the "normal population" of cells; capable of injurious chemical bond formation w/ proteins, lipids, carbohydrates- key molecules in membranes & nucleic acids
- i.e. ALS, cancer, heart disease and function decliness associated w/ aging
- emerging date indicates that reactive oxygen species play major roles in the initiation & progression of cardiovasuclar alterations associated w/ hyperlipidemia, DM, hypertension, ischemic heart disease & chronic heart failure
- antioxidants: react with oxidants to disarm them (vit C)
*Lead (cellular injury)
- causes chemical injury
- interferes with the functions of calcium & affects include the nervous system, the hematopoietic system (tissues that produce blood cells), & the kidneys
- alterations in calcium may interfere w/ NTS which may cause hyperactive behavior & proliferation of capillaries of the white matter & intercerebral arteries
- can occur in adults who work w/ metal, environmental exposure, pottery
*Carbon Monoxide (cellular injury)
- has a higher affinity for hemoglobin (300x) so it quickly binds w/ the hemoglobin, preventing oxygen molecules from doing so
*Ethanol (cellular injury)
- acute alcoholism mainly affects the CNS but may induce reversible hepatic & gastric changes
*Blunt Force Injuries
- application of mechanical energy to the body resulting in the tearing, shearing, or crushing of tissues i.e. car accidents & falls
- bleeding into the skin or underlying tissues as a consequence of a blow
- collection of blood in soft tissues or an enclosed space
- scrape; removal of the superficial layers of the skin caused by friction between the skin & injuring object
- tear or rip resulting when tensile strength of the skin or tissue is exceeded
- blunt force blows also can cause bone to break or shatter
*Sharp Force Injuries
- incised wounds
- stab wounds
- puncture wounds
- chopping wounds
*Asphyxial Injuries
- caused by a failure of cells to receive or use oxygen
- suffocation
- strangulation: hanging, ligature & manual
- chemical asphyxiants
- drowning
*Infectious Injuries
- injury from microorganism lies in their ability to survive & proliferate in the human body (to invade & destroy cells, produce toxins, & produce damaging hypersensitivity reactions
- pathogenicity of a microorganism, virulence of a microorganism; disease-producing potential (invasion & destruction, toxin production, production of hypersensitivity reactions
*Phagocytic cells
- ingest & digest bacteria and cellular particulate
- immunologic & inflammatory injury
- immunologic/inflammatory injury
- active amine produced by mast cells to dilate capillaries, regulate gastric acid production, causes symptoms of allergic reactions
- H1 (allergies): cause vasodilation & inflammation, redness, edema, swelling, immune system
- H2 (GI tract): ulcers, etc
- immunologic/inflammatory injury
- type of serum protein products of the adaptive immune response
- plasma protein produced by the t cells, direct the antigen-antibody response by signaling between the cells of the immune system causing either a direct inflammatory response or via a component
*Injurious Genetic Factors
- nuclear alterations
- alterations in the plasma membrane structure, shape, receptors, or transport mechanism
- i.e. sickle cell anemia & muscular dystrophy
*Injurious Nutritional Imbalances
- essential nutrients are required for cells to function normally
- deficient in take; starvation-lack of all nutrients & vitamins (serious tissue damage)
- excessive intake
-obesity & high fat diets predispose to atherosclerosis
- iron-deficiency anemia
*Atmospheric Pressure Changes
- injurious physical agents include temperature extremes, changes in atmospheric pressure, ionizing radiation, illumination, mechanical stress (repetitive body movements) & noise
- sudden increases or decreases in atmospheric pressure: blast injury or decompression sickness/caisson disease (the bends)
*Hypothermic Injury
- temperature extreme
- slows cellular metabolic processess
- ROS production
*Hyperthermic Injury
- temperature extremes
- heat cramps
- heat exhaustion
- heat stroke
*Illumination Injury
- cellular injury
- eyestrain, obscured vision & cataract formation
- caused by light modulation
*Mechanical Stresses
- cellular injury
- repetitive body movements
- physical impact, irritation ,overexertion
*Manifestations of Cellular Injury
- accumulations of water, lipids, carbs, glycogen, proteins, pigments hemosiderin, bilirubin, calcium & urate; caused by cellular uptake of the substance exceeds cell's ability to catabolize or use, cellular anabolism (synthesis) exceeds use
- crowing of organelles causing excessive (sometimes harmful) metabolites to produced during catabolism and released into the cytoplasm or extracellular matrix
- cell swelling due to failure of transport mechanisms
- dystrophic calcifiation (accumulation of Ca2+ salts); only occurs in injured or dead cells; free Ca2+ in the cytosol can cause activation of protein kinases, activation of phospholipases & membrane damage & damage of cytoskeleton; also occurs during hyercalcemia to uninjured cells
- disturbances in urate metabolism can result in hyperuricemia & deposition of sodium urate crystals in tissue --> gout
- fever, leukocytosis (increase in wt. blood cells), increased HR, pain & serum elevations
- cellular death
- nuclear dissolution & chromatin lysis from the action of hydrolytic enzymes
- cellular death
- clumping/shrinkage of the nucleus into a small, dense mass of genetic material; karyolysis follows
- fragmentation of the nucelus into smaller particles or "nuclear dust"
*Coagulative Necrosis
- occurs primarily in the kidneys, heart, & adrenal glands
- cell proteins are altered or denaturation
- commonly results from hypoxia caused by severe ischemia or hypoxia caused by chemical injury (esp. mercuric chloride)
*Liquefactive Necrosis
- results from ischemia injury to neurons & glial cells in the brain
- dead cells liquefy due to release of hydrolytic enzymes
*Wet Gangrene
- develops when neutrophils invade the site causing liquefactive necrosis
*Caseous necrosis
- tuberculous pulmonary infection
- combination of coagulative & liquefactive necrosis
- thick, yellowish "cheesy" substance forms
*Fat necrosis
- fatty tissue is broken down into fatty acids
- an area of dead cells as a result of oxygen deprivation
Subdural Hematoma
- a collection of blood between the inner surface of the dura mater & the surface of the brain, resulting from the shearing of small vins that bridge the subdural space
- can result from blows, falls, or sudden acceleration/deceleration of the head i.e. shaken baby syndrome
Epidural hematoma
- collection of blood between the inner surface of the skull and the dura
- caused by a torn artery & is almost always associated w/ a skull fracture
Lipid Accumulation
- occurs after cellular injury sets
- increased synthesis of triglycerides from FA (increases in the enzymes, a-glycerophosphatase, which can accelerate triglyceride synthesis) & decreased synthesis of apoproteins (lipid-acceptor proteins)
Hemoprotein Accumulations
- caused by excessive storage of iron, which is transferred to the cells from the bloodstream
- condition in which excess iron is stored as hemosiderin in the cells of many organs & tissues
*Signs of Normal Aging
- muscle atrophy, loss of subcutaneous fat; reduction in immune function; loss of cells in CNS; decreased sense of taste, smell, hearing, & propioception; atrophy of the thyroid gland & reduced secretion of hormones; reduced estrogen/testosterone secretion; cardiac cell & coronary blood vessel stiffening; decreased chest wall expansion & recoil; reduced kidney function; reduced esophageal & gastric motility & decreased hydrochloric acid secretion
*Frailty Syndrome
- imprecisely defined as a wasting syndrome of aging that leaves a person vulnerable to falls, functional decline, disease, & death
- women have a higher risk than men
*Somatic Death
- Algor mortis (reduction of body temp)
- livor mortis (skin discoloration)
- rigor mortis (muscle stiffening)
postmortem autolysis: putrefactive changes are associated with the release of enzymes & lytic dissolution
- cellular injury
- acoustic trauma & noise-induced hearing loss
* Mercury Toxicity
- long-lived fish
- dental fillings
- vaccines (themerasol)
*Cytoskeleton and Movement
- the cell rapidly constructs the cytoskeleton & disassembles it allowing movement of phagocytosis, diapedesis, mitosis, & more
- maintains cell's shape and internal organization
- permits movement of substances with the cell and movement of external projections
Cellular Function
- each cell needs to obtain O2, & other nutrients from the environment
- metabolize nutrients
- removes waste materials (CO2)
- most replicate themselves
*Plasma Membrane
- mosaic of lipids, proteins, and carbs; made of 2 layers of phospholipids
- allows cells to communicate w/ one another thru physical contact and by providing receptors for chemicals (hormones, neurotransmitters, enzymes, nutrients, & antibodies)
-semi-permeable; molecules cross by diffusion and osmosis
- the membrane is constantly changing depending on the body's needs
*Proteins in PM
-types: integral, peripheral, transmembrane
- functions: receptors, transport, enzymes, surface markers, adhesion molecules
*Gap Junctions
- communicating junctions; provide cytoplasmic channels between adjacent cells
*Cellular Communication
- form protein channels (gap junctions) that directly coordinate the activities of adjacent cells
- display membrane-bound signaling molecules(receptors) that affect the cell itself and other cells that are in direct physical contact
- secrete chemicals that signal cells some distance away (most common)
*Hormonal Signaling
- a type of long-distance signaling where an endocrine excretes hormones in a blood vessel to travel to a target cell
- e.g. thyroid-stimulating hormone
*Paracrine Signaling
- a molecule secreted by one cell binds to a receptor on or inside neighboring cells and then are taken up, destroyed or immobilized
- aka intracellular communication
*Autocrine Signaling
- cells secrete signaling molecules that bind to their own cell surface or neighboring cells of the same type & serve as a growth-regulatory mechanism
- chemical messengers that cross the synaptic gaps between neurons. When released by the sending neuron, neurotransmitters travel across the synapse and bind to receptor sites on the receiving neuron, thereby influencing whether that neuron will generate a neural impulse
*Direct Linkup
- cellular communications, receptor to receptor
*Neurohormonal Signaling
- hormones are released into the blood by neurosecretory neurons
- i.e. neurons of the hypothalamus & pituitary gland secrete hormones that circulate to influence function of endocrine glands
- cells receive communication from the extracellular fluid surround them by chemical messengers such as ligands
- channel opening and closing can be initiated by 1 of 3 ways: by binding a ligand to a specific membrane receptor closely associated w/ the channel (G-protein); changes in electrical current in the PM, altering flow of Na+ & K+; stretching or other chemical deformation of the channel
*Cell receptor proteins- 1st messengers
- involved in signal transduction
- ion-channel linked (Na+,K+,Ca2+), G-protein linked or enzyme linked that "accept" the ligand and "open the door"
- convey instructions to the cell's interior (transfer, amplify, distribute and modulate)
*Second Messengers
- involved in signal transduction
- cAMP G protein and/or calcium 'middlemen" interpret the message & trigger the appropriate function of a specific cell
- a second messenger derived from adenosine triphosphate (ATP) and used for intracellular signal transduction in many different organisms, conveying the cAMP-dependent pathway.
* Electrical Properties of Cells
- cell membranes maintain a small voltage or electical "potential" across the membrane
- the process during the action potential when sodium is rushing into the cell causing the interior to become more positive
*Threshold potential
- the electrical charge or potential difference at which an action potential will occur
- after Na+ ions have rushed into the cell, K+ ions rush out of the cell to restore the balance and the original polarity
*Absolute Refractory Period
- the minimum length of time after an action potential during which another action potential cannot begin
*Relative Refractory Period
- a period after firing when a neuron is returning to its normal polarized state and will fire again only if the incoming message is much stronger than usual
- when axon is repolarizing, more K+ ions leave the cell, causing the cell to become MORE polarized than before it started
- changes membrane potential toward the point of threshold potential (less negative), promoting the excitatory effect of propagation of the impulse or neuron firing
*Membrane Potential
- when the cell is inactive, its a resting potential
- at resting state the inside of the cell membrane is negative (-70mV to 90 mV)
- to balance positive charges, the inside of the cell contains proteins that have a negative charge & are too large to pass thru the cell membrane easily
*Structure of Plasma Membrane
- Contain Caveolae: are a special type of lipid rat, are small invaginations of the plasma membrane. These flask-shaped structures are rich in proteins & lipids such as cholesterol & have several functions in signal transduction. They are also believed to play a role in endocytosis & the uptake of pathogenic bacteria & certain viruses
- Lipid Bilayer: Amphipathic lipids (hydrophilic & hydrophobic); phospholipids, glycolipids & cholesterol
- Carbohydrates
*Membrane Transport: Cellular Intake & Output
- cell membranes act as a barrier to most, but not all molecules
- cell membranes are semi-permeable barriers separating the inner cellular environment from the outer cellular environment
- In general, the mechanisms of cellular exchange (intake and output) can be divided into passive & active movement across the cell membrane
*Plasma Membrane Transport
- the PM is a barrier to many solutes
- a solute has a greater likelihood of crossing the plasma membrane if one or more of the following criteria are met: small molecular size, neutrally charged, lipid soluble, or presence of a specific transport protein
- water soluble substances cannot get through the hydrophobic cell membrane without help; the fatty cell membrane repels water
*Active Transport
- occurs across membranes that have receptors that are capable of binding w/ the substances to be transported
- other molecules cannot be driven across the plasma membrane solely by forces of diffusion, hydrostatic pressure, or osmosis b/c they are too large or are ligands that have bound w/ receptors on the cell's plasma membrane
- protein mediated; active transport pumps; transport by vesicle formation (endocytosis-pinocytosis, phagocytosis, potocytosis)
*Passive Transport
- water and small electrically uncharged molecules move easily through pores in the plasma membrane's lipid bilayer; occurs naturally through any semipermeable barrier
- driven by osmosis , hydrostatic pressure & diffusion
- does not require energy expenditure & substances move down a concentration or pressure gradient by diffusion, osmosis, filtration & carrier-mediated facilitated diffusion
- the most widely referred to passive transport system is that for glucose in erythrocytes
* Mediated (Protein) Transport
- passive & active
- involves integral or transmembrane proteins with receptors having a high degree of specificity for the substance being transport
- inorganic anions & cations (Na+, K+, etc) & charged & uncharged organic compounds (e.g. amino acids, sugars) require specific transport systems to facilitate movement through different cellular membranes
- Ex: in type 2 DM, the cell membrane protein (receptor) for insulin is deficient in # or function; many drugs increase the # of receptors for insulin
*Membrane Transport Mechanisms: Osmosis and Diffusion
- osmosis involves the body's attempts to maintain the same concentration of solvent (water) to solute (sodium) across all 3 body fluid compartments (intracellular, vascular, interstitial)
- Ex: if hydrogen moves into the cell, a K+ moves out of the cell so that the electrolyte make up of all the cell remains neutral; it is compensatory, but ultimately can cause problems such as high blood potassium in acidosis as K+ moves out of the cell to "make room" for H+ inside the cell
- when water osmoses into or out of the cell in excess, the cell will or shrink
- the greater the force of blood flow (hydrostatic pressure) within a capillary, the greater the filtration out of the capillary
*Hypertonic & Hypotonic Solutions
- NaCl 0.9% is isotonic. >0.9% is hypertonic and <0.9% is hypotonic
- a hypertonic solution has a concentration of more than 285 to 294 mOsm/kg
- an example of a hypertonic solution is 3% saline solution
- water can be pulled out of the cells by a hypertonic solution, so the cells shrink
- water can pulled into the cells by hypotonic solution, so the cells swell
*Action Potential
- initiated when adequate positive stimulus is applied to the cell
- cellular membrane poteintial exists due to the ionic concentration difference across the membrane's permeability characteristics & active transport systems that maintain the ion concentration acorss the membrane; in the resting state, the inside of the cell membrane is negative w/ respect to the outside
- the voltage arises from differences in concentration of the electrolyte ions K+ & Na+
*What causes the rapid change in the resting membrane potential that initiates an action potential?
- when a resting cell is stimulated through voltage-regulated channels, the cell membranes become more permeable to Na+. There is a net movement of Na+ into the cell & membrane potential decreases.
- Na+ gates open & Na+ rushes into the cell, changing the membrane potential from negative to positive (depolarization)
- when it becomes sufficiently positive, the Na+ channels close & the K+ channels open
- Now K+ leaves the cell, & the membrane potential becomes more negative (repolarization)
- Hyperpolarization (undershoot)
- the return of the membrane potential to the resting level is completed by the Na+/K+ pump, which exchanges the inside Na+ for the outside K+