Alterations in mobility Test 4 Flashcards
1
Q
Static encephalopathy
A
cerebral palsy
2
Q
Brain injury that is a non-progressive disorder of posture and movement
A
Encephalopathy
3
Q
most common type of cerebral palsy
A
rigid-spastic
4
Q
Often associated with epilepsy, speech problems, vision compromise, & cognitive dysfunction
A
cerebral palsy
5
Q
issues with balance and coordination. Problems with depth perception
A
ataxic
6
Q
very unique abnormal movement. Writhing. Can effect hands, feet, tongue thrusting, often times there are challenges in feeding
A
athetoid
7
Q
have severely decreased motor tone. Kind of like rag dolls
A
atonic
8
Q
combination of two or more of the different types of cerebral palsy
A
mixed (usuallty rigid-spastic with the athetoid)
9
Q
Hemiplegic
A
one side of the body is affected
10
Q
triplegic
A
three sides of the body are affected
11
Q
Diplegic
A
all four extremities are effected, but lower extremities are more affected than the upper
12
Q
most common topographic presentation of cerebral palsy
A
diplegic
13
Q
Infection, anoxia, toxic, vascular, Rh disease, genetic, congenital malformation of brain
A
Prenatal etiology of cerebral palsy
14
Q
anoxia, traumatic delivery, metabolic
A
natal etiology of cerebral palsy
15
Q
Big concern of infection in prenatal women as far as cerebral palsy
A
Ruebella
16
Q
Trauma, infection, toxic etiology
A
Post natal etiology of cerebral palsy
17
Q
Could cause baby to develop athetoid cerebral palsy
A
Severe jaundice
18
Q
A risk factor for development of cerebral palsy
A
prematurity
19
Q
- Persistent primitive reflexes
- Poor head control after afe 3 months
- Stiff or rigid limbs
- Arching back, pushing away
- Floppy tone
- Unable to sit without support at age 8 months
- Clenched fists after age 3 months
A
Possible motor signs of CP
20
Q
- Excessive irritability
- No smiling by age 3 months
- Feeding difficulties
- Persistent tongue thrusting - Frequent gagging or choking with feedings
A
Possible behavioral signs of Cerebral Palsy
21
Q
- Establish locomotion, communication, and self-help skills
- Gain an optimal appearance and integration of motor functions
- Correct associated defects as effectively as possible
- Provide adapted educational opportunities
- Promote socialization experiences with other affected and unaffected children
A
Therapeutic Nursing Goals for individuals with CP
22
Q
- Spasticity
- Weakness
- Increase reflexes
- Clonus
- Seizures
- Articulation & Swallowing difficulty
- Visual compromise
- Deformation
- Hip dislocation
- Kyphoscoliosis
- Constipation
- Urinary tract infection
A
CP complications
23
Q
Management of Cerebral Palsy (5)
A
- Promote growth and development
- OT and PT
- Speech
- Adaptive equipment
- Surgical
- Rhizotomy, Baclofen pumps, Botoxin
24
Q
What is substantially disabling Cerebral Palsy
A
- Mobility
- Communication
- Learning
- Self Care
- Self Direction
- Independent Living
- Economic Sufficiency
25
Surgery where they cut nerves very close to where they're coming off the spinal cord
Rhizotomy
26
Baclofen pump
Continuous infusion of baclofen intrathecally to decrese the spacicity
27
* Defects of closure of neural tube during fetal development
* Congenital (present at birth)
* Believed to be caused by genetic or environmental factors, but exact etiology is unknown
Neural tube disorders: one of the most common neural defects
28
Common in women with poor folic acid intake before and during pregnancy
Neural tube defects
29
* Not visible externally
* Lamina fail to close but spinal cord does NOT herniate or protrude through the defect
* No motor or sensory defects
* Tuft of hair
Spina Bifida occulta
30
* External sac that contains meninges and CSF
* Protrudes through defect in vertebral column
* Not associated with neurologic deficit – good prognosis
* Hydrocephalus may be an associated finding, or aggravated after repair (large heads)
Spina Bifida Meningocele
31
* Same as above, but the spinal cord and meninges protrude through the defect in the bony rings of the spinal cord
* Contains nerves therefore the infant will have motor and sensory deficits below the lesion
* Visible at birth, most often in the lumbaosacral area
* Covered with a very fragile thin membrane/sac which can tear easily, allowing CSF to leak out
Spina Bifida Cystica Myelomeningocele
32
Three areas we focus on for nursing interventions for neural tube defects
* Protect the sac from injury
* _Keep free from infection_: Position: prone or side lying. Cover sac with sterile, moist non-adherent dressing, sterile technique imperative
* Parents need emotional support & education regarding short and long term needs of infant
33
When does surgical repair occur with neural tube defects?
Within the first 24 hours
34
What to look for after neural tube defect surgery?
observe for early signs of infection: elevated temp, irritability, lethargy, nuchal rigidity
observe for signs of increasing ICP (may indicate hydrocephalus)
35
* _Degeneration of skeletal muscle fibers_: undergoes necrosis and replacement with fat. Loss of muscle mass is progressive.
* Duchenne’s
* Becker’s
* Facioscapulohumeral
* Scapluloperoneal
* Limb Girdle
Muscular Dystrophy
36
* X-linked disorder
* Etiology: Genetic defect
- Defective dystrophin protein (need it for attachment of skeletal muscles to attachment of the basement membrane that attaches to surrounding bone tissue
* Most common type
Duchene's Muscula Dystrophy
37
Weak muscle attachment
↓
Fiber tearing with repeated use
↓
Muscle cell regeneration (initially) produces more defective cells
Later - muscle necrosis--\>Replacement with adipose and fibrous tissue
## Footnote
Pathogenesis of Duchene's Muscular Dystrophy
38
_Postural muscles in the hips & shoulders affected_
* Frequent falling
\*Age?
Age 3-5 for DMD clinical manifestation
39
1. Imbalances between agonist and antagonist muscle groups
* Kyphoscoliosis, contractures & joint immobility
* Wheelchair dependent
* Cardiomyopathy
\*age?
Age 7-12 DMD clinical manifestations
40
Which disorder?
Changes seen with DMD
41
Kyphoscoliosis
Being an abnormality in terms of skeletal structure. Posterior spine being changed in terms of the normal curvatures. Exaggerated thoracic and lateral curve
42
* ↓ depth of respiration--\>Hypercapnea
* (increased PaCO2)
* hypoxemia (↓ PaO2)
* ineffective cough
* Decreased clearance of secretions
Effects of Kyphoscoliosis
43
Diagnosis of kyphoscoliosis
* physical assessment
* Elevated creatine kinase (CK): serum blood test for damage to muscles
* muscle biopsy
* DNA testing
44
Complications of kyphoscoliosis
recurrent respiratory infections
45
Causes of death related to kyphoscoliosis
* Heart failure
* Respiratory Failure
46
1. Demyelinated plaques in white matter of the central nervous system
2. Etiology
* Genetic predisposition
* Northern European decent, twice as common in women than men in 20-30s
1. 3. Precipitating event: pregnancy, stress, consequence following a viral infection
Multiple Sclerosis
47
* ? immune mediated
* Macrophage, CD4 & CD8 cell invasion of plaques
* Injury to Oligodendrocytes ------\>demyelination --\>degeneration of the nerve
* Slowed conduction at first
* Blocked impulse conduction later
MS pathogenesis
48
* Changes in visual fields
* Abnormal gait
* Bladder and sexual dysfunction
* Vertigo
* Nystagmus
* Fatigue
* Speech problems
* Paresthesias: numbness, tingling, burning sensation
* Psychological symptoms
Clinical manifestations of MS
49
* Shakiness, difficulty walking
* Fatigue, muscle weakness
* Numbness, tingling
* Tinnitus
* Visual problems
* Difficulty chewing and speaking
* Incontinent; impotent
\*subjective or objective s/s of MS
Subjective
50
* Ataxia
* Changes in behavior & emotions
* Nystagmus
* Spasticity, tremors, dysphagia, facial palsy, speech impaired, fatigue
* Urinary Incontinence
* Impaired judgment
\*subjective/objective s/s of MS?
objective
51
Relapsing-remitting of clinical course of MS
Clear relapses with complete or partial recovery, no progression between “attacks”
52
Primary progressive clinical course of MS
Steady progression with plateaus or minor improvements
53
Secondary progressive course of MS
Early relapses and recovery with later progression between “attacks”
54
Progressive-relapsing clinical course of MS
Steadily progressive aggravated by acute attacks
55
Pharm management of MS
1. _Corticosteroids (given during an attack or exacerbation)_: ACTH, Solu Medrol, Prednisone
2. _Muscle Relaxants_: Baclofen, Dantrolene (muscles of the bladder), Valium
3. I_mmunosuppressants (given during an attack or exacerbation)_: Imuran, Cytoxan
4. I**_mmunomodulators_**: Avonex, Betaseron, Copaxone
56
1. Degeneration of the basal ganglia of the substantia nigra
2. Etiology
* _Primary_: really don't know why they have itidiopathic
* _Secondary_: Trauma, infection, Drugs,Toxins
Parkinsons disease
57
* Degeneration of the dopaminergic pathways
* Loss of basal ganglia dopamine receptors
Parkinsons disease pathways
58
Cardinal symptoms of Parkinsons disease
* Tremors: pill rolling
* Rigidity
* Akinesis or bradykinesis: shuffling
* Postural abnormalities: mask-like facial appearance
59
Clinical course of Parkinson's disease
* insidious onset
* slow progression of symptoms
60
Pharm management of Parkinson's disease
1. Dopaminergics: levodopa, sinemet, symmetrel
2. Dopamine agonists: Parlodel, Permax, Mirapex, Requip
3. Anticholinergics (controlling drooling, tremors, rigidity): Artane, Cogentin, Parsidol, Akineton
4. Monoamine Oxidase Inhibitors: Eldepryl (selegiline)
61
* Defect in nerve impulse conduction at the neuromuscular junction
* Etiology: autoimmune disorder,
1. acetylcholine receptor antibody (Ach-R IgG)
2. More common in women
3. Thyoma or Thymic hyperplasia
* More likely diagnosed in young to middle adulthood
Myasthenia Gravis
62
* Blockage and gradual destruction of Ach-R
* Low amplitude end plate potential
* Weak muscle contraction
Myasthenia Gravis pathogenesis
63
Initial signs and symptoms of myasthenia gravis
* diplopia
* ptosis
64
Tremors at rest, tremor decreases or goes away with intentional activity
Parkinson's disease
65
* Huge complication we're worried about in Myasthenia Gravis
Difficulty swallowing leading to respiratory insufficiency
66
* History and physical
* Nerve stimulation tests
* Presence of the Ach-R IgG
* Tensilon test: IV edrophonium chloride (Tensilon®) → improvement in muscle weakness
Myasthenia gravis dx
67
* Too little acetylcholine
* Infection
* Exacerbation of MG symptoms
* Respiratory arrest
* \*\*TENSILON TEST TO DISTINGUISH
\*type of myasthenia complication
Myasthenia Crisis
68
* Too much acetylcholine
* Excess medication
* Sudden extreme weakness
* Respiratory arrest
\*type of myasthenia complication
Cholinergic crisis
69
Myasthenia Gravis medication and other procedure management
* Anticholinesterases: Mestinon, Prostigmin, Mytelase
* Immunsuppressives: Prednisone, Imuran
* Other Procedures: Plasmapheresis (filter the blood to remove antibodies that are destroying acetylcholine), Thymectomy (removal of the thymus, may take several years before full effects are experienced)
70
Factors in exacerbation in Myasthenia Gravis?—infection, stress, surgery, hard physical exercise, sedatives, enemas, strong cathartics
Avoid overheating, crowds, overeating, erratic changes in sleeping habits, emotional extremes
* infection, stress, surgery, hard physical exercise, sedatives, enemas, strong cathartics
Avoid overheating, crowds, overeating, erratic changes in sleeping habits, emotional extremes
71
* No muscle nutrition
* Lou Gehrig's disease
* Destruction of upper and lower motor neurons
- Anterior horn cells (LMN)
- Motor nuclei (brain stem)
- Cerebral cortex motor neurons (UMN)
* Amyotrophy: atrophy of muscles that hardens tissues of the spinal cord in the lateral column
* 50-60 years of age, usually men. Lifespan is usally 2-5 years
Amyotrophic lateral sclerosis
72
* muscle weakness and atrophy that leads to a flacid quadriplegia
* Atrophy of tongue, facial muscles
* Fasciculations: localized twitching
Amyotrophic lateral sclerosis
73
Famous scientist with Atrophic lateral sclerosis
Stephen Hawking
74
Diagnosis of amyotrophic lateral sclerosis
* EMG: differentiates neuropathy with myelopathy
* Muscle biopsy: demonstrates atrophy and loss of muscle fiber
* Medication: Rilutek (riluzole)
75
* Autosomal dominant
- Chromosome 4
* Clinical onset = 30 to 50 years of age
- Progressive
- Fatal within 15 - 20 years
Huntington's Disease
76
1. Early motor effects of Huntington's disease early or late?
* Restlessness
* Fidgety feeling
* Minor gait changes
* Posture disturbances
* Positioning disturbances
* Protruding tongue
* Slurred speech
Early motor effects of huntington's disease
77
1. Early motor effects of Huntington's disease early or late?
* Chorea
* Facial grimacing
* Dysphagia
* Unintelligible speech
* Impaired diaphragmatic movement
Late effects of huntington's disease
78
1. Early or late psychosocial clinical manifestations of Huntington's disease?
* Irritability
* Outbursts
* Depression
* Risk for suicide
Early psychosocial clinical manifestations of Huntington's disease
79
1. Early or late psychosocial clinical manifestations of Huntington's disease?
* Decreasing memory
* Loss of cognitive skills
* Dementia
* Total dependence
Late psychosocial clinical manifestations of Huntington's disease
80
Medications for Huntington's disease
* antipsychotics
* antidepressants
81
* Acute inflammatory polyneuropathy resulting in demyelination of peripheral nerves
* Precipitating infection: Campylobacter jejuni, Cytomegalovirus, Mycoplasma pneumoniae
* CAN recover from this
Guillian-Barre Syndrome
82
Macrophage destruction of peripheral nerve myelin
↓
Demyelination
↓
Blocked impulse conduction
Guillien-Barre Patho
83
Clinical manifestations of Guillien-Barre syndrome regarding paralysis and autonomic nervous system
* _ASCENDING paralysis and paresis_: Rapid progression from lower extremity symptoms to paralysis of respiratory muscles
* _Autonomic nervous system dysfunction_: Tachycardia or bradycardia. Hyper or hypotension, Facial flushing, Excessive sweating
84
* Paresthesias
* Weakness of lower extremities
* Gradual progressive weakness of upper extremities & facial muscles
* Possible respiratory failure / arrest
Clinical manifestations of Guillain-Barre
85
DX of Guillain-Barre
* Physical exam and history
* CSF analysis: increased proteins
* EMG studies: nerve conduction decreased
* _Nerve biopsy_: visualize demyelination of peripheral nerves
86
Medication, Other proceedures and treatments of Guillain-Barre syndrome
* _Medications_: Analgesics, Antibiiotics, Anticoagulants, Vasopressors
* _Other Procedures_: Tracheostomy, Plasmaphoresis
* _PT / OT_
87
Long bones are _____ and ______ dense and can bend, buckle or break easily
porous, less dense
88
growth takes place in ________ and if these are injured it can cause \_\_\_\_\_\_?
epipheseal plates, abnormal growth
89
* A congenital abnormality in which the foot is twisted out of its normal position.
* Muscles, tendons, and bones are involved in the abnormality.
- adduction and supination of forefoot
- inversion of the heel
- fixed plantar flexion
clubfoot, or talipes equinovarus
90
goal of care for clubfoot
stretch tightened ligaments and tendons gently to
Return the foot to a maximal anatomic position
91
* AKA Developmental Dysplasia of Hip
* Abnormal development of the femoral head in the acetabulum
congenital dislocated hip
92
* Limited abduction of the affected hip during Ortolani maneuver. May hear a click upon movement.
* Asymmetry of gluteal and thigh fat folds when lying with legs extended.
* Telescoping of thigh
* Limp and abnormal gait in older child
developmental displaisia of hip clinical manifestation
93
* Ensures hip flexion and abduction and does not allow hip extension or adduction.
* It maintains correct position of the femoral head in the acetabulum.
Pavlik harness for developmental hip displaisia
94
type of cast
Spica cast for developmental hip dysplasia
95
type of harness for?
Pavlik harness for developmental dysplasia of hip
96
* Most common spinal deformity
* Lateral curvature of spine
* Can cause alterations in spine, chest, pelvis
* Most frequent in girls during adolescent growth spurt
scoliosis
97
For scoliosis treatement, a curve Less than _____ - Watch for Progression – Not Braced
curve less than 25%
98
What is the priority psychosocial nursing diagnosis for the adolescent diagnosed with scoliosis?
distorted body image, could be self esteem issues
99
* Family history
* ↑ age
* Female
* Menopause
* Thin, small frame
* Caucasian or Asian
* Cigarette smoking
* Excessive use of alcohol
* ↓ calcium intake
* Sedentary lifestyle
\*risk factors for?
Risk factors for osteoporosis
100
Osteoporosis primary
we don't know what causes it, risk factors increase risk of developing it. Usually happens when aging.
101
osteoporosis planning and implementation
* Goal = Pain relief
* Nursing interventions:
- Administer analgesics, muscle relaxants, anti- inflammatory med
- Encourage use of firm mattress
- Back brace
102
secondary osteoporosis
can occur for a variety of reasons, usually a side effect of medications such as corticosteroids
103
* A break or disruption in the continuity of a bone
* Risks: Trauma, Bone disease, Osteoporosis, Bone cancer
fractures
104
Classification of fractures
* Type
* Location
* Pattern
105
preliminary dx of osteoporosis?
-2.5 or lower on the DEXA scan
106
Recommendations for Vit D and calcium intake in people with Osteoporosis
1500 mg every day calcium
400-800 iu vitamin D every day
107
Classification: Type
Classified as open or closed
108
Location
refers to the long bones: ie: humerus, femer
109
pattern
refers to the direction and characteristics of the fracture
110
fracture physiology response
* 1st 30 minutes “Local shock”: Absence of neural function
* After 30 minutes: Pain and muscle contraction returns. Muscle spasms may cause overriding of fractured bone.
111
fracture stages of healing
* hematoma formation
* cellular proliferation
* callus formation
* ossification
* remodeling
112
* Deformity or shortening of extremity
* Crepitus
* Ecchymosis
* Edema
* Impaired sensation or Numbness
* Loss of motor function
* Loss of pulse distal to fracture
* Pain
\* clinical manifestations of?
fracture assessment
113
* Application of pulling force to a body part to provide reduction, alignment, and immobilization
* Types: Skeletal, Skin, Buck’s , Pelvic, Balanced suspension
FracturesTraction
114
* Also called Straight or Buck’s Traction
* Use tape, boots, splints
* Purpose: Reduce a fracture, Decrease muscle spasms
* Weight application: 5-10 pounds
* Duration: 48-72 hours
fractures: skin traction
115
type of traction?
skin traction
116
* Pins or wires inserted into bones
* Purpose: Align bones and joints – “pull” on bones
* Weight Application: 5-45 pounds
* Duration: long term
skeletal traction
117
type of traction?
skeletal traction
118
* Body part is suspended in desired position using splints, ropes, and weights
* Purpose: Improve mobility while maintaining fracture alignment
* Duration: Long term
* Weight application: varies
Balanced suspension
119
type of traction?
balanced suspension
120
type of device?
external fixator
121
pin care
* use sterile normal saline and qtip with first pressure to circle pin site and clean around it to prevent the skin from growing up the pin (2-4 times a day)
* sometimes paint around them with betadine or apply an antimicrobial
122
4 fracture complications
Fat embolism
Compartment syndrome
Avascular necrosis
Infection / Osteomyelitis
123
* Fat globules lodge in pulmonary or peripheral circulation
* Long bone fractures
* Occurs within first 4 days
* patho:Impaired gas exchange
Impaired cerebral circulation
fractures: fat embolism syndrome
124
first clinical manifestation with fat embolism syndrome
subtle changes in behavior and orientation
125
other clinical manifestations of fat embolism syndrome
Seizures, focal neurologic deficits
Respiratory depression and respiratory failure
Decrease in oxygenation
Petechial rash
Substernal chest pain, dyspnea, tachypnea
Low grade fever
126
1. Increased pressure within one or more compartments causes massive compromise of circulation to the area
2. _Results in_: increased circulation to muscles & nerves. Tissue hypoxia with cellular acidosis. Tissue death with loss of limb. Pain NOT relieved by pain meds
fracture compartment syndrome
127
Increased pressure within a fascial compartment of the lower extremities or the forearm.
↓
Compression of nerves and blood vessels
↓
Nerve damage, loss of motor function and tissue ischemia
compartment syndrome patho
128
Early signs of compartment syndrome (2)
* Pain
* Normal or decreased peripheral pulse
129
late compartment syndrom s/s (5)
* Cyanosis
* Paresthesia
* Paresis / loss of motor fx
* Severe pain
* Renal failure (myoglobin release
130
* An interruption in the blood supply to the bony tissue
* Results in death of bone
* Assessment: Pain, Decreased sensation
Fracture: Avascular necrosis
131
* Acute or chronic infection of bone & soft tissue
* Usually bacterial
* Commonly caused by Staphylococcus aureus
osteomyelitis
132
Inflammation with recruitment of phagocytes
↓
Release of O2 free radicals and proteolytic enzymes
↓
Pus formation which impairs blood flow
↓
Ischemic necrosis of bone
osteomyelitis patho
133
* Local/systemic infection
* Severe bone pain unrelieved with meds, aggravated with movement
* Fever, chills, restlessness, malaise
* Warmth at infection site, localized pain/ redness over the bone/ possible wound drainage
* Elevated WBCs, erythrocyte sedimentation rate, and C-reactive protein
assessment for osteomyelitis
134
TENS
-apply electrodes to skin, apply electrical impulse to nerve endings in the stump to get rid of phantom pain
135
* AKA Degenerative Joint Disease (DJD)
* A metabolic disorder of the articular cartilage and subchondral bone of diarthrodial (synovial) joints.
* Progressive degeneration of joints as a result of wear and tear
* Affects weight-bearing joints
Osteoarthritis
136
* Age
* May be inherited as an autosomal recessive trait
* Excessive weight
* Inactivity
* Too strenuous exercise can cause secondary
* Hormonal factors
* Trauma
risk factors for osteoarthritis
137
Mechanical Injury →
Chondrocyte response →
Cytokine release →
Release of proteolytic enzymes →
Erosion of bone & cartilage →
Progressive increase in micro fractures →
Decrease synovial fluid d/t degeneration of cartilage
osteoarthritis patho
138
* Aching that is worse with activity and relieved by rest.
* Crepitus with movement
* Joint enlargement
* May involve 1 joint or many
osteoarthritis clinical manifestations
139
* Joint pain with movement – no pain @ rest
* Joint stiffness after rest
* Crepitus
* Joint enlargement
* Heberden nodes or Bouchard nodes
* Unilateral joints affected
* Limited ROM
* Skeletal muscle atrophy
osteoarthritis assessment findings
140
* Tylenol
* NSAIDs
* Salicylates
* Corticosteroid injections
* Muscle relaxants
* Magnet therapy
* Warm moist compresses, shower
* Paraffin dips
* Rest / positioning
pain control methos for osteoarthritis
141
assessment and nursing care of hip dislocation
1. Assessment: Sudden severe pain
- Lump in the buttock
- Limb shortening
- External rotation
2. _Nursing Care_: No adduction
- No rotation of extremity
- No hip flexion
142
3 Hip precautions
* affected leg should not cross the center of the body
* hip should not bend more than 90 degrees
* affected leg should not turn inward
143
* Maintain drains (Hemovac, JP)
* Maintain ice to affected joint
* Begin CPM machine per MD order, usually 24 to 48 hrs post-op
* Elevate affected leg
* Avoid internal / external rotation
total knee replacement post-op nursing care
144
* Chronic, systemic, inflammatory autoimmune disease
* Characterized by remission & exacerbations
* Etiology: The definitive cause of RA is unknown. Evidence points to an immune reaction
Rheumatoid arthritis
145
* Persistent joint pain, even at rest
* Morning stiffness of joints \> 30 minutes to 1 hour
* Tenderness, swelling of joints with decreased ROM
* Joint deformities r/t instability
* Extraarticular s/s (Systemic) = fever, fatigue , weakness, anorexia, weight loss, splenomegaly, subcutaneous nodules
* subcutaneous nodules, swan neck
rheumatoid arthritis assessment
146
* Elevated erythrocyte sedimentation rate
* Positive C-reactive protein
* Positive antinuclear antibody test
* Normal or mild leukocytosis
* Anemia
* Positive Rheumatoid factor
* X-ray: Narrowing of joint space and erosion of articular surfaces
rheumatoid arthritis dx
147
* ASA and NSAIDs
* Corticosteroids
* Anti-rheumatic drugs
* Antimalarial agents Immunosuppressives
* Cytotoxic drugs
* Heat and Cold
* Complementary Therapies
pain control strategies for rheumatoid arthritis
148
* Crystal induce arthropathy
* _Primary_: Innate error in metabolism → hyperuricemia
* _Secondary_: Renal failure
* _Clinical manifestations_: Acute attacks, chronic inflammation, tophi
Gout, AKA Gouty arthritis
149
patho for?
gout patho
150
Gout dx?
Monosodium urate crystals in synovial fluid or tophi.
151
* Autoimmune inflammatory disease causing inflammation of joints and tissue with an unknown cause.
* Diagnosis of Exclusion: No definitive tests.
* No Cure
* Goals of Therapy: Control pain, preserve joint range of motion and function, minimize effect of inflammation such as joint deformity, and promote normal growth and development.
Juvenile Rheumatoid Arthritis (JRA)
152
New treatment for Juvenile Rheumatoid Arthritis (JRA)
ENBREL: tumor necrosis factor (TNF) blocker that blocks the action of TNF.
