Unit 4 Study Guide

Question 1

23. Describe the pathophysiology and signs and symptoms of Myasthenia Gravis

Answer 1

Myasthenia Gravis is an acquired chronic autoimmune disease. A result of IgG antibodies being produced against ACh receptors, so ACh can’t bind. If this continues, the autoantibodies will destroy receptor sites. When this occurs, there is a decrease in nerve impulse transmission at the NMJ and, consequentially, decreased muscle depolarization. MG can also happen if, instead of anti-AChR antibodies, there are antibodies against muscle-specific kinase (MuSK) (an enzyme involved in NMJ functioning).

S/S: weakness/fatigue of eye muscles and throat (i.e. diplopia), difficulty chewing, talking, and swallowing.

Question 2

1. Describe Transient Ischemic Attack. Be sure to list how long an attack lasts. Identify the difference between TIA and a true stroke (hint—it’s related to time).

Answer 2

A transient ischemic attack is caused by a temporary blockage of blood flow to the brain, which results in a brief episode of neurologic dysfunction. TIAs usually last no more than an hour, which differentiates them from a true stroke. TIAs can lead to a true stroke, but it only occurs in 12% of individuals. p.396

Question 3

2. Describe arteriovenous malformations. What are these? How do they form? What problems do they cause?

Answer 3

Describe arteriovenous malformations. What are these? How do they form? What problems do they cause?

An arteriovenous malformation is dilated blood vessels that are between the arterial and venous systems without a capillary bed. Also known as AVMs, they are formed from birth but symptoms are delayed, which usually start showing before the age of 30. AVMs form because of its abnormally thin walls. It’s also caused by an unusual pattern of arterial blood which causes the vessels to become dilated to the point of rupture. Symptoms tend to vary, with 20% having migraines, 50% having seizures, and 50% having neurologic deficits. If it bleeds into the subarachnoid space, it can even cause symptoms that are similar to a ruptured aneurysm. If an AVM is large, noncommunicating hydrocephalus can even form with it. On the other hand, some people may never have any symptoms at all.

Textbook pages 399-400

Slide 11 of Intracranial Hemorrhage Aneurysms PowerPoint

Question 4

3. Describe a “saccular (aka Berry)“ aneurysm. Address the risk factors for developing this and what can occur as a result.

Question 5

4. Describe a “Fusiform“ aneurysm. Address the risk factors for developing this and what can occur as a result.

Answer 5

a Fusiform shape is an oval-like bulge on both sides of the blood vessel, not on one side like other common aneurysms. Causes of this aneurysm include arteriosclerosis, elastin/collagen disorders, infections (syphilis), pregnancy, hypertension, smoking, trauma, systemic lupus erythematosus, and fibromuscular dysplasia. S/S: include dizziness, neurologic deficits, severe headaches, loss of consciousness, pain, tachycardia, moist skin, and nausea/vomiting.

Question 6

5. Describe Decorticate posturing. Explain what the patient will look like AND where the injury is in the brain.

Answer 6

Decorticate posturing is described as a posture where the person’s arms are tucked in towards the core and the feet are flexed. We can remember this by hearing “core” in the middle of the word decorticate. This is considered to be representative of a severe brain injury. Decorticate posturing may be present when the brainstem isn’t inhibited by the cerebral cortex area. The midbrain controls motor movement and it lies between the brain and spinal cord. In short, decorticate positioning is due to an injury in the midbrain.

This information can be found on slide 6 of the “Assessment of Neurologic Changes” slides, as well as page 894 of our textbook.

Question 7

6. Describe Decerebrate posturing. Explain what the patient will look like AND where the injury is in the brain.

Answer 7

Decebrate posturing is an abnormal motor response, it’s a disorder of posture. Disorders of posture are due to inequity of tone in muscles because there is some damage that leads to loss of normal postural reflexes. With decerebrate posture/response the tonic neck reflexes are active and there is an increase in tone in extensor muscles and truck muscles. The patient’s head will be neutral while all four limbs will be ridgely extended. It results from severe injury to the brain and brainstem, usually involving the midbrain and upper pons.

Found on text book pages 845, 846, and 894

Question 8

7. Thoroughly describe the types and classifications of seizures. Be sure to indicate which seizures involve loss of consciousness.

Answer 8

During a partial seizure, the abnormal activity is only present in a local/focal part of the brain. Partial seizures can also be divided into 2 groups, either simple or complex. Simple partial seizures occur when there is no loss of consciousness. A complex partial seizure is when consciousness is lost.

Generalized seizures are seizures that occur when abnormal brain activity is happening across the whole brain. These are seizures such as absence petit mal, myoclonic, clonic, tonic, tonic-clonic, and atonic. An absence petit mal, usually occurs in children, and they will just appear to be spaced out/daydreaming, but really having a seizure. This does not involve a loss of consciousness. Myoclonic seizures usually appear as twitching. Clonic is alternating contractions and relaxing of the muscles. Tonic seizures are when the muscles get more toned and stiffen. Tonic-clonic seizures occur when the patient is going back and forth between constant contraction, relaxation, and stiffening. Atonic seizures are also referred to as a “drop attack” when the muscles lose their tone and just give out altogether. Last, any seizures that don’t fall under any of these descriptions would be referred to as an unclassified epileptic seizure.

Question 9

8. Describe what happens to blood oxygen and glucose during a seizure.

Answer 9

During a seizure, because of all the excitation and firing that is happening cerebral blood flow increases drastically. This means all the blood that would be going everywhere else in the body goes straight to the brain. The brain then takes as much of the oxygen and glucose that it can (60% greater than the normal rate), depleting it fairly quickly. This is even more problematic if hypoglycemia led to the seizure. Irreversible damage can be caused if this severe seizure action is continued.

Because of this after a seizure nurses check both the patient’s oxygen level and the capillary blood glucose.

Seizures & Epilepsy PowerPoint Slide 5

Understanding Pathophysiology Page 367

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Question 10

9. Describe the pathophysiology of bacterial and viral meningitis

Answer 10

Bacterial meningitis is the entry of bacteria like meningococci and pneumococci, into the CSF, pia mater, arachnoid villi, the subarachnoid space, and the ventricular system. These bacteria can be inhaled from a sneeze, then they cross the mucosal barrier, enter the blood stream, travel to cerebral blood vessels, cross the blood brain barrier, and infect the meninges. The bacterial infection causes neutrophils to go to the subarachnoid space. Cytotoxic inflammatory agents and bacterial toxins change the blood brain barrier. This causes cerebral edema and damage to the brain tissue. The inflammation thickens the CFS, which changes the way the CFS flows around the brain and spinal cord. In viral meningitis, viruses like enteroviral viruses, arboviruses, and herpes simplex type two cross the blood brain barrier and enter the nervous system. It can also spread along peripheral nerves, or through the choroid plexus epithelium. The immune system recognizes the viral antigens and activates the inflammatory response.

Textbook page 402,403

Question 11

10. Describe the pathophysiology of encephalitis

Answer 11

Encephalitis is characterized by inflammation of the brain’s active tissue caused by an infection. These are common in cases of viruses such as measles, mumps, and rubella. Additionally, they can be triggered by autoimmune responses. An individual’s likelihood of developing encephalitis can be influenced by biological and environmental factors such as where they live due to increased exposure to viruses, which can more likely progress to inflammation in the brain and people who are already immunocompromised which can increase due to the body’s reactive response. In environmental cases, encephalitis is most common in cases of mosquito bites and other insects. There are different signs and symptoms one may encounter with encephalitis. A common symptom would be a headache due to the brain’s swelling which may progressively get worse and long in duration. Because the body is battling an infection, one may also experience high fevers and decreased mental status as one starts to become more confused and lethargic. In the pathophysiology of encephalitis, the viruses enter through the bloodstream to access the central nervous system. They always enter through the meninges and the irritation causes more pressure and inflammation.

Information about this topic can be found in the “Understanding Pathophysiology” textbook on pages 948 and 1000

Question 12

11. Describe the signs and symptoms of meningitis (including the positive Brudzinski and Kernig’s tests)

Answer 12

Meningitis is inflammation of the brain or spinal cord and can be bacterial, viral, or fungal.

Bacterial meningitis

Signs and symptoms of infection: fever, tachycardia & chills

Meningeal signs: Irritation of meninges causes sever throbbing headache, severe photophobia, nuchal rigidity, and positive Kernig and Brudzinski signs
Neurologic signs: Decreased consciousness, cranial nerve palsies, focal neurologic deficits (hemiparesis, hemiplegia, ataxia) and seizure

Viral meningitis

Signs and symptoms of infection: all signs and symptoms are like bacterial but typically milder.

Fungal meningitis

Signs and symptoms of infection: fever, headache, stiff neck, nausea, vomiting, discomfort with bright lights, confusion, sleepiness, can take weeks to show up

Brudzinski and Kernig’s tests

Brudzinski: severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed.

Kernig’s: severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.

Both can be used to assess for meningitis.

Meningitis and encephalitis ppt. slides 3-7

Question 13

12. Describe the pathophysiology and signs and symptoms of Huntington’s disease.

Answer 13

Huntington disease is an autosomal hereditary-degenerative disorder. There is severe degeneration of the basal ganglia and frontal cerebral cortex, which occurs between ages of 25 to 45. The Huntington gene is located on the short arm of chromosome 4. The clinical manifestations are Involuntary jerking and other abnormal movements as well as progressive dysfunction of intellectual processes.

Textbook page 306

Question 14

13. Explain the pathophysiology and signs and symptoms of Alzheimer’s disease. Be sure to explain how it is different from other forms of dementia.

Answer 14

Alzheimer’s disease refers to a specific brain disease and can be a type of dementia rather than an overall general term used to described the symptoms associated with a decline in cerebral functioning (e.g. memory loss, decrease in intellectual functioning) . It is characterize by memory loss, disorientation to place and time, loss of facial recognition, and progressive cognitive, language, abstraction, and judgement impairment. In the initial stages of Alzheimer’s disease, the symptoms are often attributed to forgetfulness,, emotional upset, or other illness. However, these symptoms become progressively worse over time. Changes in mental status in turn result in behavioral changes such as irritability, agitation and restlessness. In the end stages of Alzheimer’s disease, there may be no significant cognitive function and/or the person may be nonambulatory and have difficulties eating (failure to sense hunger and swallowing.

Although the cause of Alzheimer’s disease is unknown, there are genetic associations. Mutations on chromosome 21 (early-onset familial) and chromosome 19 (late onset) are thought to be related to the disease. It is thought to be a result of the degeneration of the basal forebrain cholingeric neurons with loss of ACH. (The accumulation of neuritic plaque results in the death of neurons and eventual atrophy of the brain).

Alzheimer’s disease is different from other forms of dementia such as vascular dementia which is a result of cerebrovascular disease, frontotemporal dementia which involves the frontal and temporal regions of the brain, and Creutzfeldt-Jakob disease which is genetic.

This information can be found in the Pathophysiology textbook and powerpoint on Dementia and Alzheimer’s disease.

Question 15

14. Describe the area of stroke damage that typically results in receptive aphasia

Answer 15

Receptive Aphasia (aka~ Wernicke aphasia), is the inability to understand written or spoken language. Therefore, words that people speak, will have no meaning to the person experiencing this type of aphasia. Moreover, the area of the brain that controls language (aka the Wernicke area) is damaged (or rather a lesion is discovered in this area). To be specific, the Wernicke area is found in the Left posterosuperior temporal lobe.

Textbook Page 360

Question 16

15. Describe the pathophysiology and signs and symptoms of Tardive dyskinesia.

Question 17

16. Describe the pathophysiology and signs and symptoms of Parkinson’s disease

Answer 17

Parkinson disease is a disease more commonly known for its late onset, typically around age 40 and older. It is a difficult disease to catch and diagnose early. Primary PD is based on genetic predisposition, due to mutations being passed on. The primary pathology is based on the degeneration of the basal ganglia, which is very important in voluntary movement and emotional and cognitive functions; there is also an accumulation of misfolded/dysfunctional alpha-synuclein protein. A significant loss of dopamine-producing neurons is also noted with PD. Secondary PD can occur due to other brain-neural disorders, such as head trauma, infection, neoplasm, atherosclerosis, toxins, and drug use.

Signs and symptoms of Parkinson Disease include tremors of the hands, arms, and legs when at rest (involuntary tremors), rigidity, bradykinesia (slow voluntary movements), difficulty with keeping and correcting posture, and issues with speaking (dysarthria) or swallowing (dysphagia). These symptoms may not initially develop bilaterally or concurrently, but eventually will all present together. Symptoms can be treated as they occur, but side effects can further hinder the individual. These individuals also have a higher disposition for development of dementia.

Source: Pg. 306 (Basal Ganglia) and Pgs. 374-375 (Parkinson Disease in Understanding Pathophysiol

Question 18

17. Describe the pathophysiology and signs and symptoms associated with Multiple Sclerosis

Answer 18

Multiple sclerosis (MS) is a chronic inflammatory disease of the CNS that involves the demyelinating, scarring, and loss of axons. It is mediated by the immune system. The pathophysiology of multiple sclerosis is the formation of plaques when myelin is attacked by autoreactive T and B cells that cross the blood-brain barrier. This attack stimulates the release of mediators of the inflammatory process and the loss of myelin-producing cells (called oligodendrocytes). Brain macrophages called glia cells also play a role in inflammation and injury. This can lead to a disruption in nerve conduction, the wasting of brain tissue (brain atrophy), and neuron death. All of this can occur even before symptoms appear. Signs and symptoms consist of the sensation of tingling and pricking (paresthesia) of the face, limbs and trunk; this is the most common initial symptom. Other symptoms include weakness, urinary incontinence, impaired gait, and changes in vision. Symptom onset, severity, and duration are different between each person and the kinds of symptoms change depending on which parts of the body are involved. There would be visual impairment if there is inflammation involving the optic nerve. If there is corticospinal and cerebellar involvement, nystagmus, ataxia, and weakness would be the symptoms. Symptoms can temporarily worsen if delayed or blocked conduction persists.

This information can be found on pages 403-404 in the textbook and on slide 1 of the “Demyelinating and PNS disorders” PowerPoint.

Question 19

18. Describe the pathophysiology and signs and symptoms of Age-related macular degeneration

Answer 19

This is a severe and irreversible loss of vision, and also recognized as a major cause of blindness in older individuals. Some risk factors include hypertension, cigarette smoking, diabetes mellitus, as well as a family history of AMD are risk factors. Typically, this degeneration occurs after the age of 60 years. As a whole this is an irreversible loss of vision with either atrophic (dry) or neovascular (wet) forms.

textbook pg. 338/339

Question 20

19. Describe the area of damage from stroke that typically results in expressive aphasia

Answer 20

The area that is damaged from a stroke that causes expressive aphasia is Broca’s area. This causes the person to be unable to speak or write, but they can still comprehend language well.

Textbook page 360

Question 21

20. Explain the occurrence of coup and contre-coup injuries that occur with traumatic brain injury.

Question 22

21. Describe “spinal shock”. What is happening and what should the nurse look for?

Answer 22

Spinal shock is when the normal spinal cord activity stops below the site of injury. It stops working immediately. Anything below the site of injury is damaged and will not work for about 2 to 3 days. However, this can last for months. It could be caused by hemorrhage, trauma, or edema. I think of this like a train track. If you remove a piece of the train track, the train will not be able to move further down the tracks. This is similar to spinal shock because the nerve impulses will not be able to move past the damaged area to get to the lower body or send signals back to the brain. Since impulses cannot travel past the damaged area, the muscles become flaccid and stop working. The person will have no sensation in the regions affected. Reflexes also stop functioning, as well as control of the bladder and bowels. There is also uncontrolled blood pressure and no perspiration. When reflexes, muscle stiffness, and hyperreflexia occur, it means that spinal shock has ended.

I found this information on page 389 in the textbook and on slide 3 in the Spinal Cord Trauma PowerPoint.

Question 23

22. Explain autonomic dysreflexia (hyperreflexia). Describe what is happening in the body and the signs and symptoms. Be sure to be specific about the response of the cardiovascular system, sweating, and all signs and symptoms a nurse should look for.

Answer 23

Autonomic dysreflexia happens to a patient after the initial spinal shock and inflammation process of an injury at T6 or above sorts out. It happens because nerve impulses can’t get through the part of the spinal cord that has suffered the injury. This syndrome is characterized by a large uncompensated cardiovascular response when the parasympathetic nervous system is stimulated, it is considered a life-threatening condition. The parasympathetic system is stimulated by sensory receptors stimulated below the injury caused by a full bladder or bowel, once stimulated, the intact autonomic system responds by spasming out the arterioles which is the cause for the increased blood pressure. Signs and symptoms include a systolic BP that can reach up to 300 as well as pounding headache, blurred vision, sweating above the level of injury, nasal congestion, nausea, goosebumps, and bradycardia. These symptoms can occur in combinations or simultaneously. It’s important for a nurse to be constantly checking for bowel movement and urine output in a patient who suffers from a spinal cord injury.

Page 391 in the textbook

Spinal cord injuries, spinal shock, and autonomic hyperreflexia/dysreflexia narrated PowerPoint

Question 24

24. Differentiate between the neural tube defects of meningocele and myelomeningocele.

Answer 24

Neural tube defects are an arrest of the normal development of the brain and spinal cord injury during the first month of embryonic development. Meningocele is a saclike cyst of meninges filled with spinal fluid and is a mild form of spina bifida. It develops when the neural tube fails to close completely. The cystic dilation of meninges protrudes through the vertebral defect but does not involve the spinal cord or nerve roots. Myelomeningocele is a hernial protrusion of a saclike cyst containing meninges, spinal fluid, and a portion of the spinal cord and nerve roots. The spinal cord and nerve roots are malformed below injury resulting in loss of motor, sensory, reflex, and autonomic functions.

Understanding Pathophysiology pg 416

Question 25

25. Differentiate between anencephaly and microencephaly

Answer 25

Anencephaly is when a soft and/or bony piece of the brain or skull is missing. Those with anencephaly tend to be stillborn or die within a few days after their birth. The reason it occurs is unknown but it can be diagnosed before birth by ultrasound and testing maternal serum alpha-fetoprotein.

Microencephaly is when an individual’s brain is underdeveloped, causing it to be much smaller than an average-sized brain. There is an issue in brain cell proliferation that causes the brain to not fully develop, usually caused by reduced proliferation or even accelerated apoptosis. With microencephaly, the size is due to an issue with the cell growth process in the brain, unlike anencephaly which has an unknown cause. Microencephaly is not considered microcephaly, which is an underdeveloped skull and brain.

(Bonus info) There are 2 types of microcephaly: primary and secondary. Primary microcephaly occurs because of either a chromosomal or autosomal recessive defect. Secondary microcephaly is acquired due to either: intrauterine infection (e.g. Zika Virus), metabolic disorder(s), maternal anorexia during the 3rd trimester, trauma, or exposure to alcohol, specific medications, or other toxins.

Found in “Neuro Issues in Children” PPT and pp. 416 and 419 in the online “Understanding Pathophysiology” textbook

Question 26

26. Differentiate between the neural tube disorders of cyclopia and encephalocele

Question 27

27. Explain how morphine reduces pain in the body (describe the specific neurotransmitter involved).

Question 28

28. Describe the patient responses to stimuli that the nurse would expect to seen for the three levels of coma: light coma, coma, deep coma (for example, what would you expect to happen if you touch them with something hot? What would the person in light coma do vs someone in a coma or deep coma?)

Answer 28

Light coma: associated with purposeful movement on stimulation. May be physically reactive by moving away from a cold hand’s touch or hot object.
Coma: associated with nonpurposeful movement only on stimulation. May jerk or twitch in response to hot/cold touch, but movement does not benefit accordingly to action.
Deep Coma: associated with unresponsiveness or no response to any stimulus. Patient is completely unresponsive to any shaking, loud noises, or a hot/cold object.

Causes of coma can be structural or from toxins and metabolic effects. The cause and region affected may determine the level of coma seen in the patient and the treatment plan for reversal if possible.

Altered consciousness and coma lecture video – Dr. Peggy Hill
Pathophysiology textbook pg. 840

Question 29

28. Describe the patient responses to stimuli that the nurse would expect to seen for the three levels of coma: light coma, coma, deep coma (for example, what would you expect to happen if you touch them with something hot? What would the person in light coma do vs someone in a coma or deep coma?)

Answer 29

Light coma: associated with purposeful movement on stimulation. May be physically reactive by moving away from a cold hand’s touch or hot object.
Coma: associated with nonpurposeful movement only on stimulation. May jerk or twitch in response to hot/cold touch, but movement does not benefit accordingly to action.
Deep Coma: associated with unresponsiveness or no response to any stimulus. Patient is completely unresponsive to any shaking, loud noises, or a hot/cold object.

Causes of coma can be structural or from toxins and metabolic effects. The cause and region affected may determine the level of coma seen in the patient and the treatment plan for reversal if possible.

Altered consciousness and coma lecture video – Dr. Peggy Hill
Pathophysiology textbook pg. 840

Question 30

29. Differentiate between somatic, visceral, and neuropathic types of pain. Be sure to describe the pathophysiology and the specific signs and symptoms unique to each type of pain.

Answer 30

Somatic pain: Tends to arise from the skin (examples: abrasion or laceration, joints (examples: arthritis or joint injury), and muscles (examples: overexertion or muscle injury). Somatic pain can be a sharp, well-localized pain and this fast pain is carried by alpha delta fibers; or it can be a dull, aching, throbbing, poorly localized pain seen in polymodal C fiber transmissions.

Visceral pain: This type of pain is transmitted by C fibers and occurs in internal organs or the lining of body cavities. Visceral pain is typically a poorly localized with a throbbing, gnawing, aching, or intermittent cramping quality sensation. Visceral pain is carried by sympathetic fibers and is associated with nausea and vomiting, hypotension and, sometimes shock. This pain often radiates which is known as referred pain (pain that moves from the initial or actual site of pain).

Neuropathic pain: Chronic pain associated with dysfunction in the nervous system causing abnormal processing of sensory information via changes in pain pathway structure known as neuroplasticity. This pain is described as a shooting, burning, tingling, or shocking sensation. Hyperalgesia (increased pain sensation from painful stimuli), allodynia (pain caused by a stimulus that shouldn’t cause pain), and spontaneous pain accompany the sensations described. Neuropathic pain is classified as either central (pain pathway dysfunction in the brain or spinal cord) or peripheral (pain pathway dysfunction outside the brain and spinal cord) sensitization. Central sensitization is typically caused by and seen in brain or spinal cord trauma, tumors, vascular lesions, multiple sclerosis, Parkinson disease, postherpetic neuralgia, and phantom limb pain. The most likely causes of peripheral sensitization and conditions is which it is seen include nerve entrapment, diabetic neuropathy, and chronic pancreatitis.

Source: Huether, S. E., & McCance, K. L. (2019). Understanding Pathophysiology (7th ed.). Elsevier Health Sciences (US). https://yuzu.vitalsource.com/books/9780323672818Links to an external site.

Pages 330-331

Question 31

30. Describe the thermo-regulation mechanism associated with fever.

Answer 31

Temperature regulation is controlled by the hypothalamus and the endocrine system. If the hypothalamus senses that the temperatures are too low or high the hypothalamus then produces or conserves the heat depending on the situation. If the body senses infection then the body will raise the temperature using therm regulation to help fight off the infection resulting in fever.

Page 326 and 327 of the Understanding Pathophysiology book.

Question 32

31. Thoroughly describe Glaucoma including the pathophysiology and signs and symptoms

Answer 32

Glaucoma is the second leading cause of blindness. It characterized by intraocular pressures > 12-20mmHg, with the death of retinal ganglion cells, their axons, and irreversible loss of vision. There are 3 primary types of glaucoma.
* Open angle: Characterized by outflow obstruction of aqueous humor even when there is enough space for drainage. Signs/ symptoms: very few
* Angle closure: Displacement of iris toward cornea with obstruction of outflow of aqueous humor from anterior chamber. It may occur acutely with a sudden rise in intraocular pressure. Signs/ symptoms: pain & visual disturbances.
* Congenital closure: This type is rare. it associated with congenital malformations and genetic anomalies.

Source of information: Textbook page 339

Question 33

32. Describe “conjunctivitis” (all types)

Question 34

33. Describe Meniere’s disease including the pathophysiology and signs and symptoms.

Answer 34

Ménière disease (endolymphatic hydrops) is an episodic, chronic disorder of the inner ear (labyrinth) where there is an excessive amount of the fluid called endolymph, causing pressure in the membranous labyrinth that disrupts both vestibular and hearing functions. The labyrinth consists of the cochlea, the vestibule, and the semicircular canals; inside their walls (bony labyrinth) is the endolymph-filled membranous labyrinth. The cause of the abnormal buildup of endolymph in Ménière disease is unknown, and it can be in one or both ears.
There are four symptoms: recurring episodes of vertigo (which could lead to nausea and vomiting), hearing loss, tinnitus (ringing in the ears), and a feeling of fullness in the ear. Treatment is symptomatic with medical management and surgery if prescriptions fail.
(Pages 812-815 in Understanding pathophysiology textbook)

Question 35

34. Describe “Wind up” of the pain response.

Question 36

35. Differentiate between the types of headaches: migraine, cluster, and tension

Answer 36

Migraine headaches: Last 4 to 72 hours, Classical features include: unilateral head pain, throbbing pain, worsening of pain due to activity, nausea and/or vomiting, photophobia and phonophobia (Diagnosis only requires 2 of these features). Migraines have 3 classifications: migraine with aura, migraine without aura (most common), and chronic migraine. Migraines are most common between the ages of 25-55. Migraines are caused by various genetic and environmental factors. To diagnose migraines, medical history and examination is required. Starts in occipital region and soon begins to spread. Treatment for migraines include pain relievers, triptans, Botox shots, and other medications

Cluster headaches: Last minutes to hours for some days (around 8 attacks per day) with long periods of remission. Occur on one side of the head, changing sides from one episode to the next. These types of headaches are seen in men ages 20 to 50. The pain experienced is severe, typically associated with a stabbing and throbbing sensation around the eye. Prophylactic drugs are utilized to treat cluster headaches, however acute attacks are managed with oxygen, sumatriptan, or inhaled ergotamine.

Tension headaches: Can last for several hours or days and is not aggravated by physical activity. This is the most common type of headache. Pain is often categorized as mild to moderate (feels like a tight band around the head). Mild versions are treated with ice and more severe versions are treated with aspirin or a nonsteroidal anti-inflammatory drug.

Textbook: Pages 942-944

PowerPoint: Headaches (slides 2-7)

Question 37

36. Differentiate between the pathophysiology of hordeolum and chalazion

Answer 37

Hordeolum and chalazion are very closely related. Clinically, a hordeolum is a stye, and consists of swelling of the eyelid. A hordeolum does not affect vision nor does it present with discharge. This is the same with chalazion, however where the two conditions differ is etiology. Hordeolum is caused by inflammation whereas chalazion is caused by a glandular obstruction. The hordeolum tends to present with tender pain, while the chalazion does not. Treatment for both includes a warm compress.

Textbook page 341

Slide 9 of Eyes Powerpoint

Question 38

37. Explain hypoperfusion stroke.

Answer 38

A hypoperfusion, or hemodynamic stroke occurs when there is inadequate blood supply to the brain caused by cardiac failure, a pulmonary embolism or bleeding. This results in a hemodynamic stroke and symptoms of this stroke are bilateral and diffuse.

Understanding Pathophysiology pg. 396

Question 39

38. Explain Increased Intracranial Pressure, including what causes it, and what can happen as a result. Be sure to list the s/s the nurse should monitor for in these patients.

Answer 39

Normal intracranial pressure is between 1-15 mmHg, but in increased intracranial pressure (IICP) cerebral perfusion pressure is between 70-90 mmHg. IICP can result from an increase in intracranial content which happens when there is a tumor growth, excess CSF, cerebral edema, or a hemorrhage. The cranium is unable to tolerate increased volume since it is not able to expand. If intracranial pressure remains high, alterations in cerebral blood flow (CBF) and excessive cerebral blood volume (CBV) occur. There are 4 progressive stages of IICP, and at first there may be no detectable symptoms. In stage 2, the nurse may see subtle manifestations including episodes of confusion, restlessness, drowsiness, and slight pupillary and breathing changes. In stage 3, the brain tissues experience hypoxia and hypercapnia, and the patient’s condition deteriorates rapidly while experiencing decreased arousal or central neurogenic hyperventilation, widened pulse pressure, bradycardia and small, sluggish pupils. In stage 4, brain tissue shifts (herniates) furthering ischemia and hypoxia, and herniation into the brainstem can lead to death by impairing the cardiovascular and respiratory systems.

Slides 1-4 of “Increased ICP and cerebral edema” powerpoint

Page 869-870 of textbook

Question 40

39. Differentiate between non-REM and REM sleep and Explain how conditions like age and apnea impact sleep.

Answer 40

Non-REM sleep is no random eye movement, and one would obtain 75-80% of sleep and no dreaming is involved. This happens when inhibitory signals are released from the hypothalamus.Non-REM sleep is divided into three stages (N1,N2,N3). For example, Stage one is very light sleep, stage two is a light stage of sleep and is the slowing down of brain waves and stage three is a stage of deep sleep, where when we are woken up, we are often confused and or disoriented. While REM sleep happens, rapid eye movement occurs, dreams commonly occur and there is an increased blood flow and memory consolidation. It occurs about every 90 minutes and starts 1 to 2 hours after non-REM sleep begins. Age can impact sleep due to the fact that as you age, the likelihood of non-REM sleep increases and occurs. Also, there is less sleep time and it takes longer to fall asleep when age increases. Apnea impacts sleep due to the fact that there’s a partial or total upper airway obstruction to airflow which causes constant gasping and snoring. In short, this breathing repeatedly stops and starts, which causes major disruption in a night’s sleep.

(Textbook pages: 797-799)

Question 41

40. Thoroughly describe Tay-Sachs disease.

Question 42

41. Explain the “reflex arc” and how it shortens the response type to painful or dangerous stimuli

Answer 42

This is a process that can occur if you touch a hot stove, for example. Instead of touching the stove and having to wait for the signal to go from your finger to your spinal column, from the spinal column to your brain, then back down through your spine to your finger, thankfully you have a reflex arc in order to shorten that pathway. Basically, the receptor in your finger takes the pain and sends it to the spinal column where it senses through the afferent sensory neurons that “woah, we don’t have enough time to send this all the way up to the brain” and immediately sends a response through the efferent motor neurons that makes you take your finger off the stove. This shortened process aiming to minimize damage in called a reflex arc.

Answer found on Slide 10 of the “CNS and Reflec Arc” ppt

Question 43

42. Explain hemorrhagic stroke. Include the pathophysiology and differentiate between the types. Include a discussion of the signs and symptoms.

Answer 43

Hemorrhagic strokes occur when there is bleeding in the brain and one of the main causes is chronic hypertension. It can occur in the subarachnoid or subdural spaces. Subarachnoid hemorrhages are due to a ruptured aneurysm and can cause meningeal irritation to occur which leads to nuchal rigidity. Subdural hemorrhage is associated with brain trauma and the patient may not have any signs. Once the hemorrhage resolves the end result is scar tissue in the brain which leads to decreased neurological ability. To determine if a patient has a hemorrhagic stroke look for both positive Kernig and Brudzinski signs.

Powerpoint: Intracranial Hemorrhage ppt. slide 4

Book page:934

Question 44

43. Explain the area of “penumbra” that can occur in an ischemic stroke and the importance of this concept to patient care.

Answer 44

When an ischemic stroke occurs, the irreversible ischemia and necrosis presents in the center zone of the infarct. The area surrounding the core of the infarct acts as a border of hypoxic tissue that is referred to as the penumbra. Within this bordering area, the hypoxia cannot cause any structural damage, because the hypoxia is not severe enough. Because of this, the penumbra acts almost as a buffer when it comes to patient care. By restoring the penumbra in a timely manner, we can prevent necrosis in the brain and maintain the neurologic function. It is important to note that there is a limited window of opportunity in which this restoration must occur. 3 hours is the approximate amount of time healthcare providers have to prevent damage and degeneration within the brain. This is extremely important because this concept of the area of penumbra, could essentially be the difference between a patient surviving an ischemic stroke to the point of retaining brain function, or not.

Understanding Pathophysiology pg 397

Question 45

44. Differentiate between thrombotic and embolic strokes. Describe the pathophysiology of each and the signs and symptoms.

Question 46

45. Describe Lacunar stroke including the pathophysiology and the signs and symptoms.

Answer 46

Lacunar stroke is caused by the occlusion of one, “deep perforating artery that supplies” tiny penetrating subcortical vessels, this causes ischemic lesions, mainly inside of “the basal ganglia internal capsules, and pons.” They are uncommon due to the location as well as the small area that the infarction occurs in. The person may have sensory or motor deficits.

Understanding Pathophysiology 6th edition pg.403

Question 47

46. Explain the manifestations of an ischemic stroke that occurs in the anterior cerebral artery or the middle cerebral artery, basilar artery, posterior cerebral artery, and cerebellar artery (a table would be helpful)

Question 48

47. Thoroughly describe the disorder Phenylketonuria (PKU) including the pathophysiology, potential problems, and dietary management.

Answer 48

This is an example of an error of metabolism characterized by phenylalanine hydroxylase deficiency and the body is unable to convert the essential amino acid (phenylalanine) to tyrosine. It is an autosomal recessive inborn error. Brain damage occurs before the metabolites can be detected in the urine, and the damage continues as long as the phenylalanine levels remain high. Developmental abnormalities can also happen in the cerebral cortical layers, defective myelination, and cystic degeneration of the white and gray matter. The treatment includes a reduction of dietary phenylalanine. The PKU diet is a low protein diet and it needs to be strictly followed, fruits and vegetable are able to be eaten as well.

This information was found in our textbook Understanding Pathophysiology on page 421.

Question 49

48. Thoroughly describe hydrocephalus. Include the impact of this condition on the signs and symptoms.

Answer 49

Hydrocephalus happens when there is excess fluid within the cerebral ventricles subarachnoid space, or both.

The cause of it is due to an interference in the cerebral spinal fluid that can be a result of:

Decreased reabsorption, increased fluid production, or an obstruction within the ventricular system.

There are two types of hydrocephalus: Noncommunicating and Communicating.

Noncommunicating hydrocephalus happens due to an obstruction of ventricular drainage of CSF.

Communicating hydrocephalus happens because of defective reabsorption of CSF

In adults the pressure in the brain will increase, and as a result the brain will try to compensate but it needs a shunt.

In a child, the head expands if the fontanel is not fused.
Hydrocephalus powerpoint slides 1 and 2

Question 50

49. Describe “Dandy-Walker deformity” and the resultant neurologic issue that occurs.

Question 51

50. Differentiate between a Neuroblastoma and a retinoblastoma. Include a discussion of the pathophysiology, signs and symptoms, and possible outcomes.

Answer 51

Neuroblastoma- tumors arising from neural crest cells of the peripheral sympathetic nervous system.
S/S: weight loss, irritability, fatigue, and fever. Hard to manage diarrhea occurs in some children
Possible outcomes:associated with spontaneous remission, commonly in infants. Prognosis is worse for children older than 2 years of age with spread of tumor.

Retinoblastoma- rare congenital eye tumor of young children that originates in the retina of one or both eyes.
Patho: Inherited as an autosomal dominant trait with incomplete penetrance, asymptomatic genetic mutation (~40% of cases)
Acquired (~60% of cases)

S/S: leukocoria, strabismus (misalignment of the eyes), red, painful eyes and limited vision.
Possible outcomes:greater than 90% long-term survival.