SEMINAR Neuro Hand-Outs

7/31/2019 SEMINAR Neuro Hand-Outs

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INTRODUCTION

Medical conditions associated with neuromuscular and skeletal impairment, plus

problems in body senses such as the eye, are currently increasing in prevalence in this

generation. These may be associated with a variety of factors to include genetics in origin,

autoimmunity, familial, environmental, and among others.The nervous system plays a major and extensive role in the body since it is the maste

controlling and communicating system of the body. The muscular system is essentially

responsible for body movement, acting as machines of the body, while the skeletal system is

the bodys internal framework.

According to World Health Organization (WHO, 2011), Glaucoma is considered as the

second leading cause of blindness in the world with rough estimate of 4 million Americans

affected, while, on the other hand, 5.5 million suffer in Cataract. There are also approximately

200 million women affected worldwide with osteoporosis; whereas, 62.9% among 50 patients

in the Philippine Orthopedic Center suffered fractures in line with this. For Guillane-Barre

Syndrome (GBS), approximately 1 in 100,000 is affected with this or 2,720 people in United

States (US); while in the Philippines involved 862 people only. It is also believed that there are

currently about 250,000 to 350,000 people in US who have been diagnosed with Multiple

Sclerosis.

This seminar is geared to the enhancement of knowledge to promote quality nursing

education, research, and practice. In nursing education, this is a great tool to be used in

reviewing concepts related to perception and coordination especially because nurses need

continuous knowledge even if they are already outside the four corners of the classroom. In

nursing research, this will serve as a guide and basis to expound the knowledge recently

acquired through further investigation. This may involve the statistics of each diseases, the

prognosis, and even the latest treatment or management to promote quality care. In nursing

practice, since all of these diseases needed critical attention especially because it concerns

the mastermind system of the body which is the brain, effective nursing care is needed. The

usual routine care may be involved with special consideration on the neuro-vital signs, level of

consciousness, and activity level of the clients.


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OBJECTIVES

General Objective

At the end of our 5 hour seminar, the participants will acquire and develop knowledge

and skills related to the concept of perception and coordination to promote quality, effective,

and efficient nursing care.

Specific Objectives

Specifically, the participants will be able to:

a. present a brief introduction about concept of perception and coordination with the

associated statistics per disease;

b. formulate a specific, measurable, attainable, realistic, and time-bounded objectives;

c. present an overview of the anatomy and physiology of the optic, skeletal, and

neuromuscular system;

d. describe the different diseases concerning the concept of perception and coordination in

this order: glaucoma, cataract, osteoporosis, Guillain-Barre syndrome, myasthenia

gravis, and multiple sclerosis;

e. discuss the etiology, risk factors, clinical manifestations, diagnostic tools

pathophysiology, medical-surgical management, and nursing management of each

disease; and

f. evaluate the participants learning on the discussion through creative and mind-bogglinggames/drills.


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ANATOMY AND PHYSIOLOGY

OPTIC (VISUAL) SYSTEM

External and Accessory Structures

Extrinsic eye muscles. The extrinsic muscles of the eye come from the bones of the orbit

and are movable due to broad tendons in the eyes tough outer surface. There are sixextrinsic eye muscles that function to move the eye in various directions:

1. Superior rectus muscle rotates the eye upward and toward the midline

2. Inferior rectus muscle rotates the eye downward and toward the midline

3. Medial rectus rotates the eye toward the midline

4. Lateral rectus rotates the eye away from the midline

5. Superior oblique rotates the eye downward and away from the midline

6. Inferior oblique rotates the eye upward and away from the midline

Eyelids. The eyelids protect the eyes anteriorly which meet at the medial and the latera

corners of the eye.

Conjunctiva. The conjunctiva is a mucous membrane that begins at the edge of the cornea

and lines the inside surface of the eyelids and sclera, which serves to lubricate the eye. It is

the thin, transparent tissue that covers the outer surface of the eye. This structure is

nourished by tiny blood vessels that are nearly invisible to the naked eye. The conjunctiva

is composed of 3 sections:

Palpebral Conjuctiva covers the posterior surface of the eyelids Bulbar Conjuctiva coats the anterior portion of the eyeball

Fornix the transition portion, forming the junction between the posterior eyelid and the

eyeball

Lacrimal Apparatus. The lacrimal apparatus consists of the lacrimal gland and a number of

ducts that drain the lacrimal secretions into the nasal cavity. Located above the lateral end

of each eye are the lacrimal glabds that continually release a dilute salt solution, known as

tears, onto the anterior surface of the eyeball through several small ducts.

Internal Eye structures

The Eyeball

The eye, commonly called the eyeball, is a hollow sphere and is composed of:

3 tunics or coats


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Humors the interior filled with fluids that help maintain the shape of the eye

Lens the main focusing apparatus of the eye. This structure is supported within the eye

cavity dividing it into two chambers.

TUNICS of the EYEBALL

Fibrous Tunic this is the outermost tunic and is also known as the sclera, the thick and

white connective tissue. Vascular tunic this is the middle coat of the eyeball and has three distinguishable regions

namely:

1. Choroid this is located posteriorly and lies between the sclera and the retina. It

contains the blood vessels that provide nourishment to the outer layers of the retina.

2. Ciliary Body the ciliary body is made up of ciliary muscles and ciliary processes. It lies

just behind the iris. They secrete aqueous humour.

3. Sensory Tunic this is the innermost tunic of the eye and is called the retina. This

structure extends anteriorly only to the ciliary body. It converts images into electrica

impulses that are sent along the optic nerve to the brain where the images are

interpreted.

LENS

The crystalline lens is located just behind the iris. Light entering the eye is focused on the

retina by the lens. The lens is divided into two segments namely:

1. Anterior (aqueous) segment located anterior to the lens and contains a clear wayetry fluid

called aqueous humor. The aqueous humor helps to nourish the cornea and the lens. It iscontinually produced by the ciliary body.

2. Posterior (vitreous) segment located posterior to the lens and is filled with a gel-like

substance called the vitreous humor or the vitreous body. The vitreous humor helps

maintain the shape of the eye.

SKELETAL SYSTEM

The Skeletal System provides support for the human body through a framework that allows

muscles to pull on something that is rigid.

The skeletal system is involved in:

1. Structural Support;

2. Protection;

3. Movement;


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4. Mineral Storage;

5. Red Blood Cell production; and

6. Fat Storage.

A. APPENDICULAR SKELETON

Bones of the shoulder: The shoulder joint provides a connection between the chest and the

arm. Clavicle: The clavicle, or collar bone, is a long bone that articulates with the sternum in

the chest and the scapula in the shoulder. It provides a rigid support from which the

scapula and arm are suspended and transfers stress, due to physical impact to the axia

skeleton.

Scapula: The scapula, or shoulder blade, is a triangular shaped flat bone that connects

the humerus with the clavicle. It has a large oblong process, called the acromium.

Humerus: The humerus bone makes up the upper arm between the elbow and the

shoulder. It has a large process called the head, which articulates with the scapula in

the gleonhumeral joint. At the opposite end, is a medial and lateral epicondyle, where it

forms the elbow joint with the bones of the forearm.

Bones of the upper extremity

Elbow joint: The bones of the elbow include the humerus, radius and ulna. This joint is

a pivot point for the forearm and plays a major role in hand movement and function.

Humerus: The humerus has a depression called the olecranon fossa. This depression

receives the olecranon of the ulna, while the forearm is extended. The olecranonforms the prominence of the elbow.

Radius: The radius is the lateral bone of the forearm (located on the thumb side). The

radial head articulates with the humerus and the radia notch of the ulna.

Ulna: The ulna is the medial bone of the forearm (located on the little finger side), which

articulates with the humerus in the elbow joint and the carpals in the wrist.

The wrist: or carpal bones, is made up of 8 small bones held together by ligaments

The carpal bones articulate with the radius and ulna and include the: The scaphoid,

lunate, triquetrium, pisiform, hamate, trapezium, trapezoid and the capitate.

The hand is made up of: The hand is made up of the metacarpal bones and phalange

bones. There are 5 metacarpal bones, which make up the palm. There are a total of 14

phalanges, which make up the fingers.


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Bones of the pelvis: The pelvis is located at the base of the spine and contains two sockets

for articulation with the lower extremities.

Ilium: The ilium bone articulates with the sacrum at the sacroiliac joint. This joint, along

with its ligaments, connects the lower extremities with the torso.

Ischium: The ischium bone forms the lower and back part of the pelvis. The ischium

bone also makes up part of the acetabulum and contains the obturator foramen. Pubis: The pubis bone is between the ilium and the ishium, and it forms part of the

acetabulum.

Bones of the lower extremity: the leg bones are the largest bones of the body and, along

with the ankle and feet, provide support for standing and walking.

Femur: The femur, or thighbone, is the largest and strongest bone of the human body.

It articulates with the hip at the hip joint and the bones of the lower leg at the knee joint.

Tibia: The tibia is the larger of the two shinbones. It articulates with the fibula and femur

at the knee joint and the tarsal bones of the ankle.

Fibula: The fibula is the smaller shinbone; it is more posterior than the tibia. It forms the

lateral portion of the ankle joint.

The Tarsal bones are a group of bones that make up the ankle, and the foot is made up

of meta-tarsal ones and phalange bones.

B. AXIAL SKELETON

The spine is made up of a curved stack of 33 irregular bones, known as vertebrae. This stack

can be divided into 5 regions which are, from the top, cervical (7 vertebrae), thoracic (12vertebrae), Lumbar (5 vertebrae), sacral (5 fused vertebrae) and coccygeal (4 fused

vertebrae). Two adjacent vertebrae, and all the soft tissue between them make up one

Motion segment. The vertebrae are irregular in shape, with the spinal cord running down the

neural arch or the vertebrae. Between each vertebrae is a intervertebral disc. This is a

fibrocartilaginous disc, that cushions the two bones.

NERVOUS SYSTEM

It is the master controlling and communicating system of the body.

Organization:

A. Structural: Central Nervous System or CNS (brain and spinal cord) and Peripheral

Nervous System or PNS (nerves and ganglia)


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B. Functional: Somatic Nervous System or SNS (stimulate skeletal muscle) and Autonomic

Nervous System or ANS (stimulate smooth/cardiac muscle)

Structure:

A. Supportive connective tissue cells

Neuroglia support and protect neurons in the CNS. Specific glial cells are phagocytes.

Schwann cells myelinate neuron processes in the PNS.B. Neurons

1. Axons. These typically generate and conduct impulses away from the cell body an

release a neurotransmitter.

2. Dendrites. These typically carry electrical currents toward the cell body.

I. Central NS

- Location: within the cranial cavity of the skull

- Parts:

A. Cerebral Hemispheres. These two form the largest part of the brain. This involves

logical reasoning, moral conduct, emotional responses, sensory interpretation, and the

initiation of voluntary muscle activity.

B. Diencephalon.

1. Thalamus. This encloses the third ventricle and is the relay station for sensory

impulses passing to the sensory cortex for interpretation.

2. Hypothalamus. This makes up the floor of the third ventricle and is the most

important regulatory center of the autonomic nervous system.3. Epithalamus. This includes the pineal body and the choroid plexus.

C. Brain stem: Midbrain, Pons, and Medulla oblongata

D. Cerebellum. It coordinates muscle activity and body balance.

- Protection of the CNS:

A. Skull and vertebral column are the most external protective structures.

B. Meninges: dura mater, arachnoid mater, and pia mater

C. Cerebrospinal fluid (CSF), provides watery cushion around the brain and cord.

D. Blood-brain barrier.

- Spinal Cord is a reflex center and conduction pathway.

II. Peripheral NS

1. Cranial Nerves: 12 pairs of nerves that extend from the brain to serve the head and

neck region.


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2. Spinal Nerves: 31 pairs of nerves are formed by the union of the dorsal and ventra

roots of the spinal cord of each side.

III. Autonomic NS

1. Parasympathetic is the housekeeping system responsible for rest-and-repair

response.2. Sympathetic is the fight-or-flight response.

NEUROMUSCULAR SYSTEM

Nerves:

1. Sensory nerves - send sensory information to the spine

2. Motor nerves - send signals to the muscles

Motor Unit - is the motor nerve and all of the fibers it innervates.

Different muscles have different innervation ratios:

a. 1:10 for occular muscles- smaller motor units

b. 1:10,000 for quadriceps muscles - larger motor units

This is what results in fine versus gross motor movement.

A. Sensory Receptors

Proprioceptors - sensory receptors - sense changes in the environment.

B. Cutaneous receptors - deep pressure and touch

C. Joint and skin receptorsjoint- ruffinni endings

skin touch - (meissner)

pressure ( pacinian)

pain (free nerve endings)

D. Musculotendinous receptors

Golgi tendon organs - sensitive to stretch of the tendon due to muscular contraction and

causes the muscle to relax.

Muscle spindle - responsive to active or passive stretch. as well as the rate (phasic) and

length (tonic) of stretch.

Labyrinthine and neck proprioceptors:

labyrinthine system- orientation of the head

neck proprioceptors- orientation of the neck relative to the head.

Reflexes - preprogrammed motor patterns or nerve muscle patterns

- They do not require voluntary activation


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NEUROMUSCULAR JUNCTION

- is the synapse or junction of the axon terminal of a motor neuron with the motor end

plate, the highly-excitable region of muscle fiber plasma membrane responsible for

initiation of action potentials across the muscle's surface, ultimately causing the muscle to

contract. In vertebrates, the signal passes through the neuromuscular junction via

the neurotransmitter acetylcholine (ACh).NMJ Actions:

1. Release of ACh

When a nerve pulse reaches a synaptic end bulb, it triggers release of the

neurotransmitter ACh from synaptic vesicles that contain ACh. ACh then diffuses

across the synaptic cleft between the motor neurone and the motor end plate.

2. Activation of ACh receptors

The motor end plate contains receptors onto which the free ACh binds after diffusing

across the synaptic cleft. This binding of ACh to ACh receptors in the motor end plate

causes ion channels to open & so allow the sodium (Na+) ions to flow across the

membrane into the muscle cell.

3. Generation of muscle action potential

The flow of sodium (Na+) ions across the membrane into the muscle cell generates

a muscle action potential. This action potential then travels along the sarcolemma and

through the T-Tubules.

4. Breakdown of AChThe ACh that is released at Step (1.) is only available to take part in step (2.) for a short

time before it is broken down by an enzyme called acetylcholinesterase (AChE). This

breakdown of ACh occurs within the synaptic cleft.


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GLAUCOMA

DEFINITION: It is a disease of the major nerve of vision (optic nerve). It is characterized by a

particular pattern of progressive damage to the optic nerve that generally begins with a subtle

loss of side vision (peripheral vision). If not diagnosed and treated, it can progress to loss of

central vision and blindness.

ETIOLOGY: Elevated pressure in the eye is the main factor leading to glaucomatous damage

to the optic nerve.

RISK FACTORS:

- Age over 45 years

- Family history of glaucoma

- Black racial ancestry

- Diabetes

- History of elevated intraocular pressure

- Nearsightedness (high degree of myopia), which is the inability to see distant objects

clearly

- history of injury to the eye

- Use of cortisone (steroids), either in the eye or systemically (orally or injected)

- Farsightedness (hyperopia), which is seeing distant objects better than close ones(Farsighted people may have narrow drainage angles, which predispose them to acute

[sudden] attacks of angle-closure glaucoma.)

MANIFESTATIONS:

- Open-Angle: Visual field loss; Haziness; Halo among lights

- Close-Angle: severe eye pain, headache, nausea and vomiting, and visual blurring.

DIAGNOSTICS:

- Tonometry; Pachymetry; Gonioscopy; Ophthalmoscopy; Visual Field testing


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PATHOPHYSIOLOGY

MANAGEMENT:

Medical:

- timolol (Timoptic), levobunolol (Betagan), carteolol (Ocupress),

and metipranolol (Optipranolol)

- Prostaglandin analogs

- Adrenergic agonists

- Carbonic anhydrase inhibitors

- Parasympathomimetic agents, which are also called miotics

- Osmotic agents

Surgical:

- Laser iridotomy, Laser trabeculoplasty, Laser cyclo-ablation

Nursing Diagnosis:

Disturbed sensory perception: Visual, related to myopia and lens extraction

Anxiety, related to anticipated surgery

Deficient knowledge: lack of information regarding postoperative care

Impaired home maintenance, related to activity restrictions and impaired vision

Predisposing Factors

Age, Sex, Race, Genetics, Familial History

Precipitating Factors

Myopia/Hyperopia, Injury, Cortisone

Mircocirculation causing Ischemia/Hypoxia

Abberant Immunity

Inflammatory Cytokines in Microglia and Astrocytes causing excessive glutamate stimulation

Blockade of neutrophin and other target derived factors

Increased intraocular pressure

Optic nerve damage

GLAUCOMA


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Nursing Management:

- Provide a safe environment, placing the call light and personal care items within easy

reach.

- Encourage to express fears about surgery and its potential effect on vision.

- Explain all procedures related to surgery and recovery.- Instruct to avoid shutting the eyelids tightly, sneezing, coughing, laughing, bending over

lifting, or straining to have a bowel movement.

- Teach to wear glasses during the day and an eye shield at night to prevent injury to the

surgical site.

- Explain and demonstrate the procedure for administering eye drops.

- Provide verbal and written instructions about postoperative care, including a schedule of

follow-up examinations, potential complications, and actions to take in response.

- Refer to a discharge planner or social worker to help establish a plan for home

maintenance.


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CATARACT

DEFINITION: It is an opacity or cloudiness of the normally transparent crystalline lens. It is

also an eye disease in which the clear lens of the eye becomes cloudy opaque, causing

decrease in vision, progressing to blindness.

ETIOLOGY:

o Senile- associated with aging

o Congenital- may be hereditary

o Traumatic- associated with injury

o Secondary- associated with systemic disease (such as Diabetes)

RISK FACTORS:

- Age. Some people develop cataracts during their middle-aged years (40s and 50s), but

these cataracts tend to be very small. It is after age 60 that cataracts are most likely to

affect vision. Nearly half of people age 75 and older have cataracts.

- Gender. Women face a higher risk than men.

- Family History.

- Race and Ethnicity. African-Americans seem to have nearly twice the risk of developing

cataracts than do Caucasians. This difference may be due to other medical illnesses,

particularly diabetes. African-Americans are much more likely to become blind from

cataracts and glaucoma than Caucasians, mostly due to lack of treatment. Hispanic

Americans are also at increased risk for cataracts. In fact, cataracts are the leading cause

of visual impairment among Hispanics.

- Diabetes and Other Medical Conditions.

Diabetes. People with diabetes type 1 or 2 are at very high risk for cataracts and are much

more likely to develop them at a younger age. They also have a higher risk for nuclear

cataracts than nondiabetics. Cataract development is significantly related to high levels of


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blood sugar (hyperglycemia), and cataracts in people with diabetes are sometimes referred to

as so-called sugar cataracts.

Autoimmune Diseases and Conditions Requiring Steroid Use. Medical conditions

requiring high use of corticosteroids (commonly called steroids) pose a particularly high risk.

Many of these medical conditions are autoimmune diseases, including rheumatoid arthritis,

psoriasis, multiple sclerosis, systemic lupus erythematosus, Behcet's disease, and others.

Eye Conditions. People who are nearsighted (myopia) are at increased risk of developing

cataracts. Physical injuries to the eye (such as a hard blow, cut, or puncture) or eye

inflammation can also increase risk. Previous intraocular eye surgery increases cataract risk.

- Obesity.

- Overexposure to Sunlight

Exposure to even low-level UVB radiation from sunlight increases the risk for cataracts

especially nuclear cataracts. The risk may be highest among those who have significant sun

exposure at a young age. People whose jobs expose them to sunlight for prolonged periods

are also at increased risk.

- Smoking and Alcohol Use

- Environmental Factors

Long-term environmental lead exposure may increase the risk of developing cataracts. Gold

and copper accumulation may also cause cataracts. Prolonged exposure to ionizing radiation

(such as x-rays) can increase cataract risk.

MANIFESTATIONS:

Early:

Painless blurred vision

Decreased colour perception

Late:

Opaque or cloudy white pupil


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Vision that is better in dim light with pupil dilation

Gradual loss of vision progressing to blindness

Absence of red reflex

DIAGNOSTICS:

- Laboratory test as preoperative screening process to detect coexisting diseases (e.gdiabetes mellitus, hypertension, and cardiac anomalies).

- Ocular imaging studies: ultrasound, MRI, CT scan

- Routing visual acuity testing

- Testing for brightness acuity and contrast sensitivity

- Confrontation visual field testing

- The following tests may be performed to evaluate macular function: Maddox rod test

photostress recovery test, blue-light entoptoscopy, Purkinje entoptic phenomenon, and

visual-evoked response and electroretinography (VER-ERG).

PATHOPHYSIOLOGY:

MANAGEMENT:

Medical-Surgical:

Predisposing Factors:

Age,

Gender,

Family History,

Race & Ethnicity

Precipitating Factors:

Diabetes & Other Medical

Conditions, Obesity,

Overexposure to Sunlight,

Smoking & Alcohol, Environment

Age > 40 y/o Heredity Eye injury Systemic dse.

e. . DM II

Poor hydration

to the eye

Irregular hydration & change in connective

tissue proteinGlycosylation

of proteins

Increase advanced glycation end-products (AGE) and accumulation of sorbitol in the lens

Cloudiness and opacification of the lenses leading to blurry of vision progressing to blindness

Senile

Cataract

Congenital

CataractTraumatic

Cataract

Secondary

Cataract


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- Extracapsular Cataract Extraction (ECCE)

The lens is lifted out without removing the lens capsule may be performed with

Phacoemulsion(the lens is broken up by ultrasonic vibration & extracted)

- Intracapsular Cataract Extraction (ICCE)

The lens is removed within its capsule through a small incision

Nursing:

Pre-operative nursing care:

Instruct measures to prevent or decrease IOP

a. Avoid heavy lifting, violent coughing, bending lower than waist, reading (but

watching TV is allowed)

b. Avoid prolonged anger and sexual activity

Administer pre-op eye medications including mydriatics and cycloplegics asprescribed (i.e. Atropine)

Post-operative Nursing Care:

Elevate the head of the bed 30-45 degrees

Turn the client to the back or un-operative side

Pharmacologic: antibiotic- steroids: TobraDex; Acetominophen for minor pains

No aspirin due to its clotting effects

Instruct measures to decrease or prevent the increase of IOP

Wear glasses during the day until the pupils responds to light

Eye-shield at night while sleeping

Shower or bathing is allowed

Care of the dressing

Stool softeners

Instruct to report pain with nausea and vomiting


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OSTEOPOROSIS

DEFINITION: It is a disease characterized by low bone mass and loss of bone tissue that may

lead to weak and fragile bones.

ETIOLOGY: Osteoporosis occurs when there is an imbalance between new bone formationand old bone resorption. The body may fail to form enough new bone, or too much old bone

may be reabsorbed, or both. Two essential minerals for normal bone formation are calcium

and phosphate.

RISK FACTORS:

European or American ethnic background

Personal history of fracture as an adult

Poor general health

Smoking tobacco

Low body weight, less than 127 pounds

Estrogen deficiency

Early menopause, before age 45

Surgical removal of the ovaries before age 45

Irregular menstruation

Taking medical therapy that lowers estrogen levels, such as for breast cancer or

endometriosis

Lifelong low calcium intake

Alcoholism

Falling

Inadequate physical activity

MANIFESTATIONS:

Back pain, caused by a fractured or collapsed vertebra

Loss of height over time

A stooped posture

A bone fracture that occurs much more easily than expected

Dowagers hump


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Low calcium level

DIAGNOSTICS:

Dual X-ray absorptiometry (DXA) of the lower (lumbar) spine and hip.

-uses fan beam technology allowing for rapid scanning with very low-energy X-

rays.

Ultrasound of the heel.

-Bone density of the heel predicts overall fracture risk.

Quantitative computerized tomography (QCT) of the lower (lumbar) spine.

-This exam uses a standard CT scanner.

PATHOPHYSIOLOGY:

MANAGEMENT:

Medical-Surgical:

1. regular exercise regimen of weight-bearing exercises


Age, Gender,

Genetics, Race/Ethnicity,

History of Fracture,

Poor general health

Precipitating Factors:Smoking, Low weight, Estrogen

deficiency, early menopause,

oophorectomy, irregular menstruation,

low calcium, alcohol, fall, inactivity

Low dehydrocholesterol

Low UV light

Poor diet intake of Vit. D

Liver FailureRenal Failure

Calcitrol formation

Low

hos hate

Hypocalcemia

Genetics

Hypoparathyrodism

Stimulates Ca2+

receptors

Increase PTH

glucocorticoids

estrogen

DM II

insulin

mechanical

stress

Osteoid breakdown (skeletal pain, vertebral prolapse, fractures)

OSTEOPOROSIS


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2. Vitamin D. A daily intake of 400 IU

3. daily calcium intake of 1,000 mg per day

4. Kyphoplasty

5. Medications

a. Alendronate (Fosamax)

b.Risedronate (Actonel, Atelvia)

c. Ibandronate (Boniva)

d. Zoledronic acid (Reclast, Zometa)

e. Bisphosphonates

f. Calcitionin

g. Parathyroid Hormone (PTH)

Nursing Diagnosis:

Chronic pain

Disturbed body image

Dressing or grooming self-care deficit

Imbalanced nutrition: Less than body requirements

Impaired physical mobility

Risk for impaired skin integrity

Risk for injury

Nursing Management:

- Focus on careful positioning, ambulation, and prescribed exercises.

- Administer analgesics and heat to relieve pain as ordered.

- Include the patient and his family in all phases of care.

- Encourage the patient to perform as much self-care as her immobility and pain allow.

- Provide the patient activities that involve mild exercise.

- Check the patients skin daily for redness, warmth, and new pain sites.

- Monitor the patients pain level, and assess her response to analgesics, heat therapy, anddiversional activities.

- Explain all treatments, tests, and procedure to the patient.

- Make sure the patient and her family clearly understand the prescribed drug regimen.

- Tell the patient to report any new pain sites immediately, especially after trauma.

- Provide emotional support and reassurance to help the patient cope with limited mobility.
http://nursing-concept.blogspot.com/2009/02/free-nursing-care-plans-for-pneumonia.htmlhttp://nursing-concept.blogspot.com/2009/02/free-nursing-care-plans-for-pneumonia.html


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GUILLAIN-BARRE SYNDROME

DEFINITION: It is an autoimmune attack of the peripheral nerve myelin. The result is acute

rapid segmental demyelination of peripheral nerves and some cranial nerves, producing

ascending weakness with dyskinesia, hyporeflexia and paresthesia.

Stages of GBS:

Acute the symptoms show between one to three weeks.

Plateau the symptoms show between several days to 2 weeks.

Recovery This is the stage wherein there is remyelination which may last up to 2 years.

ETIOLOGY:

- autoimmune disease triggered by a preceding bacterial or viral infection.

- lung infection or gastrointestinal infection

- commonly identified antecedent pathogens: Campylobacter jejuni, cytomegalovirus,

Epstein-Barr virus and Mycoplasma pneumoniae

RISK FACTORS:

The syndrome may occur at any age, but is most common in people of both sexes

between ages 30 and 50.

Precipitating factors may also include post infection e.g. to Campylobacter jejuni, poor hygienestress, poor diet and lifestyle.

MANIFESTATIONS:

- Paresthesia tingling and numbness of the lower extremities

- Muscle weakness of legs progress rapidly ascending paralysis involving the trunk

upper extremities and facial muscles which may mean complete paralysis.

- Difficulty in chewing, swallowing and talking. The cranial nerves are now involved.

- Loss of sensation and sphincter disturbances of bladder and rectum.

- Areflexia or absence of reflexes is also observed.

- Respiratory failure is the respiratory muscle function is affected.


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DIAGNOSTICS:

- Lumbar puncture: CSF sample

- ECG

- Electromyography (EMG) tests the electrical activity in muscles

- Nerve conduction velocity test: allow decreased conduction velocity of peripheral nerves

due to demyelination.- Pulmonary function test

PATHOPHYSIOLOGY

MANAGEMENT:Medical:

- No specific treatment instead they prefer symptomatic treatment

- plasmapheresis, used to remove the antibodies from the blood

- high dose immunoglobulin therapy (IVIG) that blocks the antibodies that causes

inflammation

Predisposing Factors

Age, Sex, Autoimmunity

Precipitating Factors

Infection, Poor Hygiene, Stress, Lifestyle, Diet

Infectious pathogens enter the body by the use of multinfenestrated cells or other mechanisms

Innate immune response causes uptake of the pathogens by immature antigen-presenting cells

Migrates to lymph nodes, activates T-cells and B-cells causing humoral response, activation of

complement system and phagocytosis of the bacteria

Molecular mimicry

Immune res onses directed to ca sular com onents; roduce Ab to cross-react with myelin

Lym hocytes and macro hages circulate the blood and find the myelin

Lymphocytic infiltration of spinal roots and peripheral nerves, followed by macrophage-

mediated, multifocal stri in of m elin and axonal dama e

Defects in the ro agation of electrical nerve im ulses, with conduction block

GUILLAIN-BARRE SYNDROME


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- ETT/ Tracheostomy with mechanical ventilator

- 4As: Antibiotics, Analgesic, Anticoagulants, Azathiprine & cyclophosphamide(

Immunosuppresants to decrease production)

- feeding tube may be used to prevent choking during feeding if the muscles used for

swallowing are weak

Nursing:

- Monitor vital signs, muscle weakness, gag reflex and swallowing ability.

- Position patient with the head of bed elevated to provide for maximum chest excursion.

- Avoid giving opioids and sedatives that may depress respirations.

- Position patient correctly and provide range-of-motion exercises.

- Provide good body alignment, range-of-motion exercises, and change of position to prevent

complications such as contractures, pressure sores, and dependent edema.

- Ensure adequate nutrition without the risk of aspiration.

- Provide assistive devices as needed (cane or wheelchair) to maximize independence and

activity.

- If verbal communication is possible, discuss the patients fears and concerns.

- Provide choices in care to give the patient a sense of control.

- Teach patient about breathing exercises or use of an incentive spirometer to reestablish

normal breathing patterns.

- Instruct patient to wear good supportive and protective shoes while out of bed to preveninjuries due to weakness and paresthesia.

- Instruct patient to check feet routinely for injuries because trauma may go unnoticed due to

sensory changes.


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MYASTHENIA GRAVIS

DEFINTION: It is an autoimmune disease that presents as muscular weakness and fatigue

that worsens with exercise and improves with rest. The manifestations result from a loss of

ACh receptors in the postsynaptic neurons of the neuromuscular junction.

Onset:

EARLY: 20-30 years old and Women are more affected than men

LATE: After age 50 and Men are more often affected

Classifications:

a. Ocular Form b. Generalized Form

Stages of Generalized Form:

I. Mild

II. Moderate

III. Acute Fulminating

IV. Late Severe

ETIOLOGY: The cause of MG is unknown, but 80% of people with the generalized form

of the disease have elevated titers of antibodies to the ACh receptor in their serum.

RISK FACTORS:

a. Predisposing Factors

Gender: Female and Male

Age: In female: 20-40 years old; Male: 60-70 years old

Race: Asian

b. Precipitating Factors

Thymic tumor

Occult Infection

Stress

MANIFESTATIONS:

Increasing weakness with sustained muscle contraction; muscle weakness is

greatest after exertion or at the end of the day


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Ptosis- drooping of the upper eyelid

Diplopia-double vision

Neck flexion/extension (Head-drop)

Dysarthria

Expressionless face; tendency for mouth to hang open

Dysphagia

Masticatory weakness

Dyspnea

Extreme quardiparesis/ quadriplegia

Increased salivation

Increased sweating

DIAGNOSTICS:

a. TENSILON TESTING

Edrophonium (Tensilon) is a short-acting drug that is given intravenously (Tensilon

test). A test dose of 2 mg. (for adults) is injected first. If no untoward reaction occurs

(such as increased weakness, change in heart rate or rhythm, nausea, or abdominal

cramps), the remaining 8 mg. is injected. The client is then observed for objective

manifestations of improvement in muscle strength. The effect is transitory, wearing off

after 3 to 5 minutes. Another drug, neostigmine methylsulfate (Prostigmin), may be usedbecause of its longer duration of effect on muscle strength (1 to 2 hours), which allows

better analysis of its effect.

When either drug is used, IV atropine sulphate should be available to inject as an

antidote. This medication counteracts any severe cholinergic reactions (cardiac

dysrhythmias or abdominal cramping).

b. ELECTROMYOGRAPHY (EMG)

EMG helps in confirm the diagnosis. Repetitive stimulation of the nerve with

recording from the involved muscle shows a characteristic decrementing response of

the muscle action potential. Generally, after the initial diagnostic testing is performed by

the practitioner, referral to a neurologist and/or pulmonologist may be necessary for

long-term management.


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c. ACETYLCHOLINE RECEPTOR ANTIBODIES

Acetylcholine receptor antibody is a protein found in the blood of most people with

myasthenia gravis. The antibody attacks receptors for a chemical called acetylcholine

which sends signals from nerves to muscles and between nerves in the brain.

MANAGEMENT:

Medical:

1. DRUG THERAPY

Short-acting anticholinesterase drugs- pyridostigmine (Mestinon) and

neostigmine (Prostigmin)

Dosages are highly individualized, based on physiologic response to the medication

The goal is to achieve the maximum benefit (muscle strength and endurance) with the

fewest side effects (excessive salivation, sweating, nausea, diarrhea, abdominal crampsor tachycardia).

Corticosteroids- prednisone

This drug is directed toward reducing the levels of serum ACh receptor antibodies.

Corticosteroids may temporarily worsen manifestations; however this is followed by

gradual improvement in muscle strength. A low dose of alternate-day prednisone may

be effective for many months or years. Precautions with any steroid therapy are

important, including potassium supplements if indicated and liberal use of antacids.

Potential complications of steroid use are cataracts, hypertension, diabetes, fluid

retention, delayed wound healing, and osteoporosis.

Cytotoxic and immunosuppressive drugs- azathioprine (Imuran) and cyclosporine

(Sandimmune), which reduce the level of circulating ACh receptor antibodies.

Plasmapheresis

Plasmapheresis is an adjunctive therapy for clients with refractory MG. It is a

processby which plasma is separated from formed elements of blood. The plasma is

discarded and the packed red blood cells are joined with albumin, normal saline, and


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electrolytes and returned to the client. The purpose is to remove plasma proteins

containing antibodies that are believed to cause MG.

Usually, three to five treatments given once daily over 5 to 7 days are required

Potential complications include myasthenic or cholinergic crisis and, rarely,

hypovolemia. Muscle strength should be assessed before and after the procedure , with

particular attention paid to vital capacity, swallowing ability, diplopia, and ptosis to

evaluate the effectiveness of treatment.

Intravenous Immunoglobulin (IVIG)

Intravenous immunoglobulin (IVIG) is a blood

product administered intravenously. It contains the

pooled IgG (immunoglobulin (antibody) G) extracted from the plasma of over one

thousand blood donors. IVIG's effects last between 2 weeks and 3 months. Intravenous

immune globin (IVIG) is the opposite of plasmapheresis - instead of drawing off the

offending antibodies, IVIG swamps the body with pooled gamma globulin antibodies

from many donors.


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PATHOPHYSIOLOGY:

Predisposing Factors:Gender; Age;

Familial tendency; Genetics; Race

Precipitating Factors:Thymus/Thyroid problems; Occult

infection; Medications; Autoimmunedisorders; Chemical exposure; Stress

Genetic abnormality/ Autoimmune Response

Affinity of IgG-Ab Abnormal Thymus/Hyperplasia

IgG-4 toneuromuscular junction

Muscular specifickinase (MuSK) - Ab

Impaired postsynapticmembrane differentiation

& clustering of AChR

Anti-MuSK MG

Seronegative MG

Dxcs:(+)Anti-MuSK-Ab

Dxcs:(+) Anti-MuSK-Ab;(-) Anti-AChR-Ab

Abnormal T-helpercell production

Th1/Th2

Dxcs:MRI;Chest CT scan

Abnormal proliferation of B-cell producingAcetylcholine receptor antibodies (AChR-Ab)

Anti-AChR-Ab (IgG1/IgG3 isotype)

Binds to AChR Crosslinks receptors Activates complement system

Blocks binding ofAch to receptor

sites

Endocytosis ofAChR molecules

AChR degradation

Complement-mediated lysis ofpostsynaptic membrane

Anti-AChR MG

MYASTHENIA GRAVIS

Impaired nerve impulse transmission at neuromuscular junction

muscular depolarization

Voluntary muscle weakness

Dxcs:single-fiber electromyography;repetitive nerve stimulation

Dxcs:Tensilon Test


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IIIA:Predominant

limb/axial muscle weakness

IIIB:Predominant oropharyngeal/

respiratory muscle weakness

Moderate ocular muscle weakness accompanied withIII

MYASTHENIA GRAVIS

Extraocular muscles Levator palpebrae

S/sx:Diplopia S/sx:Ptosis

Ocular muscle weakness d/t scarcity of junctional foldsI

IIA:Predominant


IIB:Predominant oropharyngeal/

res irator muscle weakness

Mild ocular muscle weakness accompanied withII

IVA:Predominant


IVB:Predominant oropharyngeal/

respiratory muscle weakness

Severe ocular muscle weakness accompanied withIV

S/sx:Limb:

descendingparalysis

Axial:Neck

flexion/extension

(Head-drop)

S/sx:Bulbar:

Dysarthria;Dysphagia;Dysphonia;Masticatoryweakness

Facial:Poor eyelid

closure;Poor cheek

puff;Drooling

Respi:Dyspnea;

Orthopnea;Tachypnea

Needed IntubationV

Management:Medical: O2 admin, ETT, MV, Plasmapheresis/IVIG; Pharm: AChE

inhibitor, immunosuppressants; Surgical: Thymectomy

If treated: Good Prognosis If not: Complications

Myasthenic Crisis Cholinergic Crisis

S/sx:Extreme quadriparesis/ quadriplegia,respiratory insufficiency, aspiration

S/sx:Diarrhea, bradycardia, pupillary

constriction, salivation, sweating

Respiratory Arrest

If treated: Fair Prognosis If not: DEATH


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Complications of Drug Therapy:

A. MYASTHENIC CRISIS

-It is precipitated with intercurrent infection or sudden withdrawal of anticholinestrase

drugs.

CLINICAL MANIFESTATIONS

Sudden marked rise in blood pressure because of hypoxia

Increased heart rate

Severe respiratory distress and cyanosis

Absent cough and swallow reflexes

Increased secretions, increased diaphoresis, and increased lacrimation

Restlessness, dysarthria

Bowel and bladder incontinence

INTERVENTION

Increased doses of cholinergic drugs as long as the client responds positively

to edrophonium treatment

Possible mechanical ventilation if respiratory muscle paralysis is acute

B. CHOLINERGIC CRISIS

-It is caused by depolarization block resulting from excessive medication.

CLINICAL MANIFESTATIONS

Weakness with difficulty swallowing, chewing, speaking, and breathing

Apprehension, nausea and vomiting

Abdominal cramps and diarrhea

Increased secretions and saliva

Sweating, lacrimation, fasciculations and blurred vision

INTERVENTION

Discontinue all cholinergic drugs until cholinergic effects decrease


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Provide adequate ventilatory support

Administration of 1 mg. intravenous atropine may be necessary to counteract

severe cholinergic reactions, as ordered

SURGICAL:

THYMECTOMY

Thymectomy is the surgical removal of the thymus gland. Located in the upper chest

below the thyroid gland and behind the breastbone, the thymus gland is part of the

body's immune system. During the formation of the fetus, the thymus migrates from the

neck into the chest, and in adults it lies beneath the breastbone (sternum). Like tonsils

and adenoids, the thymus is large in infants and gets smaller, to be replaced by fat, as

we get older, making it hardly functional. It transforms certain white blood cells

(lymphocytes) into disease-fighting T-cells, an important part of the body's defenseagainst viruses and other infections.

Indication

The most common indication for thymectomy is the presence of a tumor (thymoma)

in the thymus gland. Thymomas can be noncancerous (benign), but are potentially

cancerous (malignant) and are known to invade nearby tissue (local metastasis)

Metastasis to more distant tissue is not typical of a thymoma. Thymomas can also be

associated with myasthenia gravis (MG), an autoimmune condition in which the muscles

become weak when the individual's antibodies attack the neuromuscular junction

Thymectomy is indicated for treatment of both non-MG-associated and MG-associated

thymoma.

If most of the thymus gland is removed at surgery, myasthenic symptoms usually

lessen and in some individuals go away completely. Although the relation of the thymus

gland to myasthenia gravis is not totally understood, it appears that the thymus gland islinked to the production of acetylcholine receptor antibodies or other substances that

interfere with neuromuscular transmission.

Nursing Diagnosis:

a. Ineffective Breathing Pattern related to respiratory muscle weakness secondary

to Myasthenia Gravis


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b. Impaired gas exchange related to respiratory muscle weakness secondary to

Myasthenia Gravis

c. Ineffective airway clearance related to absence of coughing reflex secondary to

Myasthenia Gravis

d. Activity intolerance related to generalized weakness secondary to Myasthenia

Gravise. Risk for aspiration related to weakness of oropharyngeal muscles secondary to

Myasthenia Gravis

NURSING MANAGEMENT

Encourage deep breathing and coughing;

Provide suction equipment available at bedside;

Encourage adequate nutrition;

Instruct to sit upright when eating, to swallow only when the chin is tipped

downward the chest and never to speak while food is in the mouth;

Promote effective breathing pattern such as mechanical ventilation and

oxygenation;

Increase activity tolerance by providing a carefully planned activities to include

rest periods to conserve energy and muscles have a chance to regain their

strength;

Assist client in ADLs and decrease complications of immobility;

Provision of optimum vision

s


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MULTIPLE SCLEROSIS

DEFINITION: It is a disease in which the nerves of the central nervous system (brain

and spinal cord) degenerate.

Myelin, which provides a covering or insulation for nerves, improves the

conduction of impulses along the nerves and also is important for maintaining the health

of the nerves. In multiple sclerosis, inflammation causes the myelin to disappear.

Consequently, the electrical impulses that travel along the nerves decelerate,

that is, become slower. In addition, the nerves themselves are damaged. As more and

more nerves are affected, a person experiences a progressive interference with

functions that are controlled by the nervous system such as vision, speech, walking

writing, and memory.

ETIOLOGY: The cause of multiple sclerosis is still unknown, but researchers claimedthat it may be associated with autoimmune responses of our body.

RISK FACTORS:

Although its role is unclear, genetics may play a role in multiple sclerosis.

European gypsies, Eskimos and African Bantu essentially do not develop multiple

sclerosis, while Native Indians of North and South America, Japanese and other Asian

groups have a low incidence. The general population has less than a one-percen

chance of developing multiple sclerosis.

The chance increases in families where a first-degree relative has the disease.

Thus, a brother, sister, parent, or child of a person with multiple sclerosis stands a one-

percent to three percent chance of developing multiple sclerosis. Similarly, an identica

twin runs a nearly 30% chance of acquiring multiple sclerosis whereas a non-identica

twin has only a 4% chance if the other twin has the disease. These statistics suggest

that genetic factors play a major role in multiple sclerosis.

However, other data suggest that environmental factors also play an important

role.

MANIFESTATIONS:

- visual disturbances,

- limb weakness,

- muscle spasms,

- loss of sensation,
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- speech impediment,

- tremors,

- dizziness,

- depression,

- manic depression,

- paranoia, or

- uncontrollable urge to laugh and

weep

DIAGNOSTICS:

- MRI (magnetic resonance imaging) scans with intravenous gadolinium helps to

identify, describe, and in some instances date lesions in the brain (plaques).

- An electro-physiological test, evoked potentials, examines the impulses traveling

through the nerves to determine if the impulses are moving normally or too

slowly.

- Finally, examining the cerebrospinal fluid that surrounds the brain and spinal cord

may identify abnormal chemicals (antibodies) or cells that suggest the presenceof multiple sclerosis.

PATHOPHYSIOLOGY:

MANAGEMENT:

Medical:

- There are many issues for the patient and physician to consider in treating

multiple sclerosis. Goals may include:


Age, Sex, Heredity,

Genetics, Autoimmunity

Precipitating Factors:

Environment, Respiratory

infections, stress, fatigue

MS T-cells infiltrate the BBB

Virus reduces the strength of the junctions forming the blood-brain barrier (BBB)

T-cells locked in the brain perceives myelin as an alien agent

T-cells attack the myelin

Activation of inflammatory response

MULTIPLE SCLEROSIS
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1. improving the speed of recovery from attacks (treatment with steroid

drugs);

2. reducing the number of attacks or the number of MRI lesions; or

3. attempting to slow progression of the disease (treatment with disease

modifying drugs or DMDs).

4. An additional goal is relief from complications due to the loss of function ofaffected organs (treatment with drugs aimed at specific symptoms).

- Corticosteroids: prednisone (Deltasone, Liquid Pred, Deltasone, Orasone,

Prednicen-M) ormethylprednisolone (Medrol, Depo-Medrol)

- Interferons for relapsing MS

Nursing Diagnosis:

Self-Care Deficit Self-Esteem Disturbance

Potential for Ineffective Family Coping: Compromised

Sleep Disturbance

Social Isolation

Nursing Management:

- Provide emotional and psychological support for the patient and family.

- Increase patient comfort with massages and relaxing baths.

- Administer medications as needed.

- Promote emotional stability. Help the patient establish a daily routine to maintain

optimal functioning.

- Keep bedpan or urinal readily accessible because the need to void is immediate.

- Encourage adequate fluid intake and regular urination.

- Watch for adverse reactions to administered medications.

- Monitor bowel and bladder function during hospitalization.- Assess patients neurologic status for deficits.

- Educate the patient nad her family about this chronic disease.

- Emphasize the importance of exercise.

- Teach the patient about bowel and bladder training if necessary.
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REFERENCES

Black, J. and Hawks, J., (2009). Medical-Surgical Nursing: Clinical Management for

Positive Outcomes. 8th Edition. Missouri: Saunders Elsevier.

Doenges, M., et.al., (2008). Nurses Pocket Guide: Diagnoses, Prioritized Interventions

and Rationales, 11th ed. Pennsylvania: F.A. Davis Company.

Huether, S. and McCance, K., (2008). Understanding Pathophysiology, 4th ed

Singapore: Elsevier Pte Ltd.

Marieb, E., (2008). Essentials of Human Anatomy and Physiology, 9 th ed. Singapore

Pearson Education South Pte Ltd.

McCann, J., et.al., (2010). Professional Guide to Pathophysiology, 3 rd ed. Philadelphia

Lippincott Williams and Wilkins.

Silbernagl, S., et.al., (2010). Color Atlas of Pathophysiology, 2nd. Ed. Germany: Georg

Thieme Verlag KG.

WHO, (2011). World Health Organization. Retrieved January 29, 2012 from

http://www.who.int/en/.
http://www.who.int/en/http://www.who.int/en/

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