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204 Cards in this Set
- Front
- Back
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Cerebral edema is an increase in the fluid content of:
a. ventricles b. brain tissue c. CNS neurons d. None of the above |
B. Brain tissue
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Risk factors for hemorrhagic stroke include:
a. Arteriosclerosis (thrombotic – ischemia) b. dysrhythmias (embolotic—ischemia d/t afib) c. acute HTN d. sedentary lifestyle |
c. acute HTN
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Encephalitis is usually:
a. due to bacterial infection w/in the CNS (meningitis) b. fatal c. due to viral infection of brain cells d. asymptomatic |
c. due to viral infection of brain cells
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The most important preventative measure for hemorrhagic stroke is
A. Anticoagulation (embolotic-with afib) B. blood pressure control C. thrombolytics (arteriosclerosis – ischemia) D. management of dysrhythmias (afib-embolotic ischemia) |
B. blood pressure control
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Rupture of a cerebral aneurysm should be suspected if the patient reports
a. ringing in the ears b. transient episodes of numbness c. transient episodes of vertigo d. sudden, sever headache |
d. sudden, sever headache
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Subarachnoid hemorrhage causes communicating hydrocephalus by obstructing:
a. the cerebrospinal fluid flow between the ventricles b. the cerebrospinal fluid flow into the subarachnoid space (b/c hemorrhage is taking up that space) c. blood flow to the arachnoid villi d. the absorption of cerebrospinal fluid by the arachnoid villi |
b. the cerebrospinal fluid flow into the subarachnoid space (b/c hemorrhage is taking up that space)
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Cerebral edema is an increase in the fluid content of the:
a. ventricles b. brain tissue c. neurons d. meninges |
b. brain tissue
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With receptive dysphasia (fluent), the individual is able to
a. respond in writing, but not in speech b. speak back, but not comprehend speech c. comprehend speech, but not respond verbally d. respond verbally, but not comprehend speech |
c. comprehend speech, but not respond verbally
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Status epilepticus is considered a medical emergency because of the:
a. loss of consciousness b. development of cerebral hypoxia c. possibility of a head injury during the seizures d. decrease in brain metabolism |
b. development of cerebral hypoxia
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A sudden, explosive, disorderly discharge of cerebral neurons is termed:
a. reflex b. seizure c. epilepsy d. convulsion |
b. seizure
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Most dysphasias are associated with cerebrovascular accidents involving which artery?
a. anterior communicating artery b. posterior communicating artery c. circle of willis d. middle cerebral artery |
d. middle cerebral artery
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Clinical manifestations of Parkinson disease rare caused by a deficit in which neurotransmitter?
a. GABA b. Dopamine c. Norepinephrine d. Acetylcholine |
b. Dopamine
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What damage is most likely to occur to the brain in a classic cerebral concussion?
a. diffuse cerebral disconnection from the reticular activating system b. cerebral edema throughout the cerebral cortex c. cerebral edema throughout the diencephalon d. disruption of axons extending from the diencephalon and brainstem |
a. diffuse cerebral disconnection from the reticular activating system
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14. A blunt force injury to the forehead would result in a contrecoup injury to the UUU?
a. frontal b. temporal c. parietal d. occipital (polar) |
d. occipital (polar)
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15. All of the following may contributre to the development of osteoporosis except
a. parathyroid hormone dysfxn b. decreased estrogen levels c. smoking d. increase intake of vitamin C |
d. increase intake of vitamin C
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16. The chief pathological feature of osteoarthritis is degeneration and loss of
a. the epiphyses b. articular cartilage c. synovial fluid d. muscle function |
b. articular cartilage
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How many pairs of cranial nerves are there?
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12
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What type of cells are cranial nerves myelinated with?
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Schwann cells
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Where do the cranial nerves originate?
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in the brainstem, except CN I and II, which originate in the diencephalon
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Which cranial nerves contain parasympathetic neurons?
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Cranial nerves III, VII, IX, and X and spinal nerves S2 and S3
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CN II is myelinated with a different type of cell. what type of cell is CNI meylinated by?
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oligodendrocytes
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Does the right visual field project to the right hemisphere of the brain?
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No. Right visual field projects to left hemisphere of brain.
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What is it called when damage to one hemisphere (stroke) interrupts visual signals from the corresponding side of each retina?
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Homonymous hemianopsia
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What is the mnemonic to remember which cranial nerves are sensory, motor, or both?
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Some Say Marry Money, But My Brother Says Big Brains Matter More
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What is the mnemonic to remember the order of cranial nerves?
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On Occasion Our Trusty Truck Acts Funny, Very Good Vehicle Anyhow.
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Name the cranial nerves in order.
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I: Olfactory
II: Optic III: Oculomotor IV: trochlear V: Trigeminal VI: Abducens VII: facial VIII: vestibulochlear IX: glossopharyngeal X: vagus XI: accessory XII: hypoglossal |
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What is the function of the oculomotor nerve and where does it originate?
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movement of eyeball, eyelid, constriction of pupil. originates in midbrain
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What is the function of the trochlear nerve and where does it originate?
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lateral eye movements. Originates in lower midbraine
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What is the function of the trigeminal nerve? where does it originate?
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ophthalmic: originates in forehead, eyes. sensation from forehead, eye scalp
Maxillary: originates in upper jaw, lip. sensation from cheek, upper lip Mandibular: originates in lower jaw area. sensation from chin and lower jaw, motor chewing |
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What is the function of the abducens nerve? where does it originate?
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lateral eye movements. originates in lower pons.
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What is the function of the facial nerve? where does it originate?
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controls muscles of facial expression, taste from anterior tongue. originates in pons
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What is the function of the vestibulocochlear nerve? where does it originate?
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transmits sound (cochlea) and equilibrium from inner ear to brain
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What is the function of the glossopharyngeal nerve? where does it originate?
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bitter and sour taste (posterior tongue), swallowing. use gag reflex to assess. secretion of saliva. Originates in medulla.
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What is the function of the vagus nerve? where does it originate?
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Monitors oxygen, CO2, and pH levels in blood; sense blod pressure; inhibits cardiac action, has extensive GI activities. Originates in medulla
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What is the function of the accessory nerve? where does it originate?
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controls sternocleidomastoid and trapezius muscles (head and shoulders), voice production. originates in medulla and cervical cord
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What is the function of the hypoglossal nerve? where does it originate?
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controls tongue movements required for speech, swallowing. originates in medulla
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What is this reflex called? vestibular neurons of cranial nerve VII interact w/neurons of cranial nerves III and VI to reflexively control eye movements during head rotation, such that a visual image can remain fixed on the retina
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Oculovestibular reflex
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What is important about the oculovestibular reflex for pt assessment?
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dolls eyes assessed in unconscious pt to evaluate brain stem fxn
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What is the normal ICP?
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0 to 15 mm Hg
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What are groups of cell bodies in the PNS called?
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ganglia
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What are groups of cell bodies in the CNS called?
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nuclei
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What 3 elements is the volume of the cranium composed of?
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brain tissue, CSF, blood
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What are 3 common causes of increased ICP?
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w/space-occupying lesions, vasogenic or cytotoxic edema, or w/obstruction or excessive production of CSF (hydrocephalus)
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How does increased brain tissue volume lead to increased ICP?
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tumor blocks ventricles of brain, bleeds, contusion, anything causing swelling = increased volume and pressure
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What happens in IICP? or what does it result in?
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results in compression of vessels and brain tissue leading to ischemia and brain damage
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What are some treatments for IICP?
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bone flap, hyperventilate pt, take off CSF
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What is decorticate posturing?
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flexor posturing indicating corticospinal lesion (less severe than decerebrate)
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What is decerebrate posturing?
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posturing indicating brain stem injury
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What are some clinical manifestations of IICP?
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Headache, projectile vomiting, altered LOC (drowsy), widening pulse pressure (difference between systolic/diastolic – epidural hematoma show this quickly, subdural more slowly), bradycardia
Blurry vision, edema of optic disk (papilledema) As ICP rises to higher levels, LOC decreases, pupil responsiveness to light becomes impaired; altered resp patterns and unresponsive to stimulation; unable to move, verbalize, or open eyes |
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In reference to ICP, what is protrusion of brain tissue through an opening in supporting dura of brain; deadly?
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herniation
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What can IICP do to neural tissue and blood vessels?
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As ICP rises, it can compress neural tissue and blood vessels
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What is the excessive accumulation of CSF called, also contributes to increased ICP called?
This is an increase in the amount of cerebrospinal fluid attributable to blocked circulation or absorption and the consequent enlargement of the ventricles |
hydrocephelus
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How does elevated CSF volume cause IICP?
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elevated CSF volume → ventricles enlarge → pressure on cerebral brain structures
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How is congenital hydrocephalus caused?
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viral infx or other neurotoxic agents acquired during pregnancy
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How can a person have hydrocephalus with normal ICP?
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due to increase in volume of CSF w/o change in pressure. Ventricles dilate.
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What type of hydrocephalus does this describe: d/t an obstruction to flow of CSF (usually a tumor outside CSF system compressing ventricles)?
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obstructive/noncommunicating
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How do dilated ventricles in the brain during hydrocephalus contribute to no net change in ICP?
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Ventricles dilate → compress brain tissue and cerebral vessels
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What are the triad of symptoms associated with obstructive/noncommunicating hydrocephalus?
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gait instability, urinary incontinence, dementia
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What congenital abnormality contributes to obstructive/noncommunicating hydrocephalus?
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Stenosis of the foramina of the 4th ventricle or spina bifida cystica
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What type of hydrocephalus does this describe: abnormality in the capacity to absorb fluid from the subarachnoid space (there is NO obstruction) d/t infection, trauma, tumors?
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abnormality in the capacity to absorb fluid from the subarachnoid space (there is NO obstruction) d/t infection, trauma, tumors
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What is the most effective treatment concerning hydrocephalus?
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surgical correction employing a shunt
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Describe how the clinical manifestations of communicating hydrocephalus originate?
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blockage of fluid flow in subarachnoid space around basal regions of brain OR blockage of arachnoid villi → fluid collects both inside ventricles and outside brain → in infants head swells tremendously
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Describe how the clinical manifestations of noncommunicating/obstructive hydrocephalus originate?
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Block of aqueduct of Sylvius d/t premature closure before birth or from brain tumor → fluid formed by choroid plexus in ventricles, volumes increases in ventricles → flattens brain into a thin shell against skull → in neonates increased pressure causes entire head to swell b/c skull bones aren’t fused yet
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What are the 2 primary functions of the CNS?
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1. Receiving and processing sensory information
2. Creating appropriate responses to be relayed to muscles and glands |
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Where is the site of emotion, memory, cognition, and learning.
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CNS
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What are fine motor skills?
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The coordination of small muscle movements which occur in body parts such as the fingers, usually in coordination with the eyes
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What/where are hand movements initiated by?
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Commands originating from a region of the primary motor cortex that contain a high number of specialized corticospinal (CST) neurons, termed corticomotoneuronal (CM) cells.
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What are some causes for fine motor impairment?
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injury, illness, stroke, congenital deformities, cerebral palsy, and developmental disabilities. Problems with the brain, spinal cord, peripheral nerves, muscles, or joints can decrease control.
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What produces voluntary motor movement?
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interaction among basal ganglia, the cerebellum, and several regions of the cortex.
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What transmits the final program of voluntary muscle activity?
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transmission from the brain down the spinal cord by way of the lateral corticospinal tracts
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What does the corticospinal tract control?
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controls distal muscles of the arms, wrists, finger, lower legs, feet and toes
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Where do corticospinal tract neurons originate?
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primary motor cortex
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How do corticospinal neurons execute voluntary motor commands?
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Corticospinal neurons from the primary motor cortex, in association with neuronal output from the premotor area and the supplemental motor cortex, activate α motor neurons to execute voluntary motor commands.
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What determines the speed of which action potentials travel?
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axonal diameter and myelination
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What type of neurons conduct impulses more quickly?
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larger and myelinated
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Where are action potentials generated in myelinated neurons?
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nodes of Ranvier
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How do nodes of Ranvier assist with quick impulse conduction of myelinated neurons? (saltatory conduction)
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impulse “hops” quickly from node to node down the axon
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How does exocytosis of neurotransmitters occur?
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Voltage-gated channel opens in response to AP → Ca2+ enters synapse →Synaptic vesicle fuses with presynaptic membrane → release of neurotransmitter
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Which neurotransmitter is metabolized in the synapse?
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acetylcholine
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Which neurotransmitter is taken up by neurons following exocytosis?
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catecholamines
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What changes the membrane potential?
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when concentration of K+ changes and when permeability of membrane to other ions changes
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What are the most important voltage-gated ion channels in nerves ?
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Na+ fast channels and K+ channels
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What happens in Na+ channels during upstroke of action potential?
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allow Na+ influx
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What happens in K+ channels during upstroke of action potential?
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allow K+ to leave cell and help repolarize membrane
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How is an action potential initiated?
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when neurotransmitters bind to receptors on the dendrite and cell body and allow cations to leak in (Ligand gated channel)
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How do ligand gated channels open?
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open in response to neurotransmitter binding to their receptor domain
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What does this describe:
charge inside the cell when there is no net ion movement across the plasma membrane; K+ concentration is 30x greater inside than outside;At rest, membrane permeable to K+, but not Na+ or Ca+;Described by the K+ equilibrium potential |
Resting membrane potential
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What creates a resting membrane potential?
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separation of charge across the membrane at rest
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What is the presence of hypertension and bradycardia associated with increased intracranial pressure known as?
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Cushing Reflex
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Is the Cushing Reflex an early or late sign of IICP?
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late sign of increasing intracranial pressure and indicates that brainstem herniation is imminent.
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What is the purpose of the Cushing Reflex?
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helps save brain tissues during periods of poor perfusion.
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What is the Cushing Triad composed of?
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Cheyne stokes respirations (irregular/deep), widening pulse pressure, bradycardia
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What is a sudden onset of neurologic dysfx d/t cardiovascular disease that results in an area of brain infarction?
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Stoke
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What manifestations would you see with a Left hemorrhagic stroke?
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R sided weakness, R droop, speech issues, gait/balance disturbance
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What would you hear over carotid arteries when assessing for TIA?
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listen for bruit on carotid arteries (narrowing of arteries)
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This type of stroke results from sudden occlusion of a cerebral artery 2/2 a thrombus (arteriosclerosis) or embolus (afib).
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Ischemic stroke
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What type of stroke does this describe:
Oxygenation of neurons are reduced, Na pump and neurotransmitters fail leading to cerebral edema leading to vasospasm and reduced cerebral perfusion? |
Ischemic Stroke
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What clinical manifestations are present with anterior cerebral blockage?
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Contralateral hemiparesis; contralateral sensory loss; impaired cognition and decision making; aphasia (left-sides stroke); incontinence
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What clinical manifestations are present with middle cerebral blockage?
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Contralateral hemiplegia; contralateral sensory loss; aphasia (left-sided stroke); homonymous hemianopsia; altered consciousness; neglect syndrome
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What clinical manifestations are present with posterior cerebral blockage?
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Visual defects including homonymous central blindness and color blindness; memory impairment
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What clinical manifestations are present with basilar and vertebral artery blockage?
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Sensory loss; mild hemiparesis; disturbances of gait, speech, swallowing, and vision
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Where is the hemorrhage when a pt has a hemorrhagic stroke?
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brain parenchyma
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Which has higher morbidity/mortality: ischemic or hemorrhagic stroke?
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Degree of secondary injury and associated morbidity and mortality is much higher in hemorrhagic stroke than ischemic stroke
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What is homonymous hemianopsia?
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visual field loss on the left or right side of the vertical midline
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How does homonymous hemianopsia occur?
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Homonymous hemianopsia occurs because the right half of the brain has visual pathways for the left hemifield of both eyes, and the left half of the brain has visual pathways for the right hemifield of both eyes
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What type of aphasia is it when verbal motor/expressive-understands what you’re saying but can’t answer appropriately back) consists of poor articulation and sparse vocabulary?
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broca aphasia
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What type of aphasia is it when sensory, acoustic, *receptive –does not understand what you’re saying to them) characterized by impaired auditory comprehension and speech that is fluent but does not make sense
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Wernicke aphasia
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What is a transient neurological event of paroxysmal abnormal or excessive cortical electrical discharges that are manifested by disturbances of skeletal motor fxn, sensation, autonomic visceral fxn, behavior, or consciousness?
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Seizure disorder/epilepsy
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What is the pathophysiology causing a seizure?
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Due to an alteration in membrane potential that makes certain neurons abnormally hyperactive and hypersensitive to changes in their environment
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What is the seizure etiology?
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Genetic, Acquired from pathologic conditions, Head injury, Infxn, Space-occupying lesions, Metabolic-electrolyte imbalance (hypoglycemia), hypoxia, acidosis, renal failure, Drugs, idiopathic
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Is normal neuronal activity synchronized or non synchronized?
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nonsynchronized
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Is seizure activity synchronized or non synchronized?
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synchronized. Seizures occur when neurons are activated synchronously
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What does the kind of seizure depend on?
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The location of the abnormal activity and the pattern of spread to different parts of the brain
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What type of seizure is this:
entire brain surface involved from the onset of the seizure |
Generalized
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What type of seizure is this:
part of brain surface involved. Abnormal electrical activity is restricted to one brain hemisphere |
Partial Seizure
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What type of seizure is this:
continuing series of seizures w/o a period of recovery between seizure episodes and can be life-threatening (b/c of hypoxia) (may see with first dx of seizure d/o) |
status epilepticus
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What is the subjective sense of impending seizure called?
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aura/prodrome
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Generalized seizures usually have what kind of etiology?
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metabolic or toxin-induced seizures
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What type of seizure does this describe:
usually only occur in kids, Brief- 2-10 seconds, Staring spells that last only seconds, Onset & termination of attacks are abrupt, Person is unaware of environment, can be motionless, walking or performing a motor task, may miss words or pause in convo, usually resolve by age 20, although another seizure type may occur later |
Absence (petite mal)
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What type of seizure does this describe:
brief; single or multiple jerks of one or more muscle groups? |
Myoclonic
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How are seizures diagnosed?
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EEGs, lab studies (poss. metabolic abnormalities and serum drug levels), lumbar puncture with suspicion of CNS infection; CT or MRI
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What disease do these characteristics describe:
degeneration of neurons in temporal and frontal lobes (clinical manifestations) brain atrophy, amyloid plaques, neurofibrillary tangles Extracellular neuritic plaques in cerebral cortex and in walls of meningeal and cerebral blood vessels, Plaques contain a dense core of amyloid material surrounded by axons and dendrites, Structural changes include the formation of intraneuronal neurofibrillary tangles, neuronal and synaptic loss |
Alzheimers
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What is the pathophysiology of Alzheimers?
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Synthesis of brain acetylcholine is deficient and tx is aimed at increasing acetylcholine levels by reducing acetylcholine reuptake
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How long is the course of Alzheimers?
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It is slowly progressive d/o that runs a course of 5-10 years and typically begins w/impairment of learning and recent memory
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How is a diagnosis of Alzheimers made?
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Diagnosis by exclusion!
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What pathological findings are found on autopsy of Alzheimers pt?
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amyloid plaques, neurofibrillary tangles, cerebral atrophy and large ventricles
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Alzheimers disease effects what lobes of the brain?
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frontal and temporal lobe
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These clinical manifestations describe what disease?
Increasing difficulty with judgment, abstract thinking, problem solving and communication, Assistance for completing ADLs, Difficulty with eating and swallowing, weigh loss, Loss of bladder and bowel control and eventual complete loss of ability to ambulate, Personality and behavior changes |
Alzheimers
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What causes motor impairment in relation to Parkinson's?
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Dopamine deficiency in basal ganglia
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What disease do these clinical manifestations describe?
Difficulty initiating and controlling movements results in akinesia, tremor, rigidity; Tremor occurs at rest and hand tremors exhibit pill-rolling movements; Attempts to passively move the extremities are met with cogwheel rigidity; Progressive gradual neurological degenerative d/o of the brain; Clinical syndrome of rigidity, bradykinesia, termor, and postural instability; Affects brain centers that control movement; Neurons in the basal ganglia/substanta nigra degenerate and are deficient in production of dopamine |
Parkinson's
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What does this pathology cause:
When dopamine levels fall, acetylcholine is not inhibited allowing increased excitation --> |
tremors
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At what age does Parkinson's usually develop?
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65 y/o
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What are 3 common causes of Parkinson's?
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infection, intoxication, trauma
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What meds result in drug toxicity causing Parkinson's?
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1. Drug class phenothiazine- chlorpromazine, prochlorperazine, thioradizine
2. Drug class butyrophenone –haloperidol |
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What type of pain does this describe:
is perceived in an area other than the actual source of injury (the area of referred pain is supplied by the same spinal segment as the actual site? |
Referred Pain
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What is the cause of referred pain?
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Thought to occur because of the convergence of visceral nociceptor activity with primary somatic afferents in the posterior horn of the cord
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What do these examples describe?
MI that is felt in the jaw or left armShoulder pain after pelvic procedures Diaphragmatic irritation from peritonitis Cutaneous abdominal pain experienced with visceral irritation or tension |
Referred Pain
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When one leg is longer than the other. A unilateral injury to which portion of the bone during a growing phase will result in one leg being longer than the other?
• Diaphysis • Epiphysis • Metaphysis • Epiphyseal plate |
Epiphyseal plae
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What allows for lengthening of long bone and is site of continuous growth (by osteoblasts)?
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Epiphyseal plate
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Regarding the epiphyseal plate, what causes the epiphysis to move away from the metaphysis?
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Growth and thickening of cartilage cells of the plate move the epiphysis away from the metaphysis. .
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Where does calcification and replacement of cartilage occur?
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on the metaphyseal surface
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Which zone of the epiphyseal plate has very thin line of chondrocytes; weakest segment of the epiphyseal plate?
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zone of calcifying cartilage
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Which zone of the epiphyseal plate has enlarged/mature cartilae cells migrating toward metaphysis
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maturing cartilage
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What zone of the epiphyseal plate has the most active cell growth?
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proliferating cartilage
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What zone of the epihyseal plate maintains adherence of plate to the epiphysis
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resting cartilage
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What is the resorption per osteoclasts and formation per osteoblasts called?
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bone turnover
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What are the 2 ways a bone heals?
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1. periosteal or external callus forms in fractures managed by closed methods
OR 2. Medullary callous formation takes place with rigid immobilization at fracture site |
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What stage of bone healing does this describe:
Hematoma formation and aseptic inflammation at fracture site. occurs on days 1-3 |
Stage 1
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What stage of bone healing does this describe:
Formation of granular tissue (fibrocartilage formation) with blood vessels, fibroblasts, and osteoblasts. occurs on days 3-5 |
Stage 2
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What stage of bone healing does this describe:
Granulation tissue matures. occurs after 2-6 weeks |
Stage 3
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What stage of bone healing does this describe:
Space in bone is bridged and fracture ends are united (ossification), callus slowly replaced by trabecular bone along lines of stress, unnecessary callus is reabsorbed. occurs after 3 weeks to 6 months |
Stage 4
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What stage of bone healing does this describe:
Consolidation and remodeling (balanced coupling of bone resorption and new bone formation) occur as the medullary canal is reestablished. Bone is reabsorbed and deposited along stress lines as bone reshapes to meet its mechanical requirements. occurs after 6 weeks to 1 year. |
Stage 5
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. When an x-ray of a fractured humerus shows that the callus is formed, this coincides with which stage of fracture healing?
• Stage 1 • Stage 2 • Stage 3 • Stage 4 |
Stage 3
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A child presents with bone deficiency and a bowlegged appearance. This assessment data supports a diagnosis of
• Rickets • Osteoporosis • Osteomalacia • Paget disease |
Rickets
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What is a deficit in mineralization of newly formed bone matrix in the growing skeleton with resulting soft osteopenic (bone mineral density is lower than normal) bone known as?
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Rickets
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What does a deficiency of vitamin D preventing maintenance of normal levels of Ca++ and Phosphate cause?
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Rickets
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What type of Rickets might children have?
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Vitamin D resistant rickets or congenital hypophosphatasia
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What disease does this describe:
Cartilage in the growing epiphyses fails to calcify. Cartilage is not replaced by bone and continues to enlarge, leading to widening of epiphyseal plates and irregularity of the junction with the metaphyses. Bone is poorly calcified and less rigid. |
Rickets
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Kyphosis, genu valgum (knock knee) is common with what type of bone disease?
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Rickets
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Genu varum (bow leg) is a common deformity with what type of bone disease?
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Rickets
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Regarding teeth and muscles, what type of dysfunction would be seen in a person with Rickets?
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Delayed eruption of teeth, enlargement of costochondral junctions and decreased muscle tone
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What is this called:
The adult form of rickets. It is always caused by inadequate concentration of calcium or phosphorus in the body. |
Osteomalacia
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What is this disease:
A slowly progressive disease of excessive resorption followed by excessive formation of bone |
Pagets disease
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What is the most common metabolic disease that occurs when rate of bone resorption is greater than that of bone formation?
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Osteoporosis
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What are 3 common factors in rate of bone loss with osteoporosis?
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Hormone deficiencies (estrogen, androgen), poor intake of calcium, lack of use
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This is the treatment for what disease:
calcium and Vit D supplement, exercise, estrogen replacement therapy, bisphosphonates, recombinant human parathyroid hormone |
Osteoporosis
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How do you know if a pt has osteoporosis?
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Changes in height, bone density scan.
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How often should bone density be done?
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Every 5 years, especially after menopause
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What bone density scan result indicates osteoporosis?
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Bone density based on age, wt, sex. Bone density >2.5 standard deviation below standardized young adult mean
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What is the relationship between smoking and osteoporosis?
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Smoking Thins bone. idiopathic
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A patient with osteoporosis will have a history of what, and what clinical manifestations present?
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History – fractures
Decreased height, back pain Dowager’s hump Difficulty bending over |
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Are blood/urine tests helpful for osteoporosis diagnosis?
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No
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Why is an x-ray not helpful in diagnosing osteoporosis early on?
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X-ray 25-35% of bone mass lost before able to visualize
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Which is a cause of decreased bone mass or weakness of bone? (select all that apply)
• Old age • Young age • Lost estrogen • Immobilization • Internal fixation |
old age, lost estrogen (post-menopausal), immobilization, internal fixation
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What is a chronic autoimmune disease that affects the neuromuscular fxn of voluntary muscles and characterized by profound muscle weakness and fatigability?
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Myasthenia Gravis
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Is myasthenia gravis a disorder of voluntary or involuntary muscles?
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D/o of voluntary muscles
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What are 2 causes of myasthenia gravis?
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Thymic tumors, Autoimmune
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A defect in nerve impulse transmission at neuromuscular jxn and destruction of acetylcholine receptor sites is the pathophysiology of what disorder?
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Myasthenia Gravis
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These clinical manifestations describe with disorder?
Insidious onset; Fatigue after exercise; Muscles of eyes, face, mouth, throat, neck first affected; Diagnosis made with Tensilon: if given and muscle strength improves = increased amt of acetylcholine; Unpredictable progression |
Myasthenia Gravis
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When is peak onset of Myasthenia Gravis?
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20-30 yrs of age
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Who are at greater risk of Myasthenia Gravis diagnosis, men or women?
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Women
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Which muscles are commonly first affected by Myasthenia Gravis?
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Weakness usually begins with ocular cranial muscles and then limb muscles
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This pathophysiology describes what disorder:
Acetylcholine receptor antibodies are produced→destroy or block acetylcholine receptors of the muscle-end plate of the neuromuscular junction→impair transmission of acetylcholine across the junction=muscle weakness and fatigability |
Myasthenia Gravis
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How does treatment of Myasthenia gravis with Anticholinesterase Inhibitors (pyridostigmine, bromide, neostigmine) help the pt?
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Inhibit breakdown of acetylcholine in the neuromuscular synapse
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How does the use of Corticosteroids, IV immunoglobulin, plasmapheresis, and immunosuppressive drugs help in the treatment of Myasthenia Gravis?
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These are sometimes used to regulate the immune system if autoimmune etiology
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When would mechanical ventilation be indicated in Myasthenia Gravis?
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In severe cases when respiratory muscle fatigue occurs
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What is this disease:
Chronic multisystem, inflammatory, autoimmune disease characterized by periods of exacerbations and remission with multiple organs affected |
SLE
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B-lymphocytic overactivity (autoimmune) results in what disease?
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SLE
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These common clinical manifestations are seen with what disease:
arthralgias and synovitis, skin lesions, butterfly rash |
SLE
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What are the treatments of choice for SLE?
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topical corticosteroids, avoidance of sun, NSAIDS and/or antimalarial drugs, and immunosuppressive agents
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Where does Discoid Lupus Erythematous occur?
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only affects the skin. It causes superficial lesions- typically over the cheeks and bridge of the nose-that leave scars after healing.
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If a pt complains of fever, anorexia, weight loss, malaise, fatigue, abdominal pain, nausea, vomiting, diarrhea, constipation, rashes and polyarthralgia (multiple joint pains). You would suspect what disease?
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Systemic Lupus Erythematous
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What blood disorders would you look for with SLE?
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Anemia, leukopenia, lymphopenia, thrombocytopenia, and an elevated ESR, occur because of circulating antibodies. Women may report irregular menstruation or amenorrhea, particularly during exacerbations.
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What cardiopulmonary s/sx would a pt with SLE have?
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Cardiopulmonary signs and symptoms occur in about 50% of patients. They include: chest pain, indicating pleuritis; dyspnea, suggesting parenchymal infiltrates and pneumonitis; tachycardia central cyanosis; and hypotension. These signs and symptoms may signal pulmonary embolism.
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What neurological s/sx would a pt with SLE exhibit?
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Seizure disorders and confusion may indicate neurologic damage. Other CNS signs and symptoms include emotional liability, psychosis, headaches, irritability, stroke and depression.
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What Urinary (GU) system s/sx would a pt with SLE exhibit?
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Be especially alert for infrequent urination, which may signal renal failure, and urinary frequency, painful urination, and bladder spasms, which are signs and symptoms of UTI. UTIs and renal failure are the leading causes of death for SLE patients.
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What medications may trigger SLE and activate it?
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procainamide, hydralazine, isoniazid, methylodopa, anticonvulsants, penicillins, sulfas, and hormonal contraceptives
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What tests would you run on a pt you suspect has SLE?
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blood tests may show a decreased platelet count and an elevated ESR.
Antinuclear antibodies are elevated. |
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What will CBC with Diff show in a pt with SLE?
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CBC with Diff may show anemia and a reduced WBC count
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What effect will serum electrolytes show in SLE?
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Serum electrophoresis may show hypergammaglobulinemia
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Active SLE disease is diagnosed by what?
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Active disease is diagnosed by decreased serum complement levels, leukopenia, mild thrombocytopenia and anemia.
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What would a CXR show in a pt with active SLE?
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Chest X-rays may reveal pleurisy or lupus pneumonitis
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What theory of pain does this describe:
Capacity for interneurons in the spinal cord to modify the transmission of nociceptor impulses. Impulses carried by large myelinated cutaneous fibers could “close the gate” on nociceptor ipulses = pain blocked in spinal cord, not allowed to progress centrally to brain. A. referred pain B. gate control theory C. theory of blocked pain D. myelinated pain block |
B. gate control theory
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What are the 5 stages of bone healing?
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1. Hematoma formation
2. Fibrocartilage formation 3. Callous 4. Ossification 5. Remodeling |
