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Pathophysiology > Class #7 > Flashcards

Class #7 Flashcards

1
Q

Define hypotonia

A
  • soft muscles on palpation
  • diminished deep tendon reflexes
  • diminished resistance to passive movement
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2
Q

If your patient has hypertonia, how will they present?

A

hyperexcitable strech reflex causes rigidity and spasticity

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3
Q

What is clonus?

A

Involuntary rhythmic muscular contractions and relaxations

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4
Q

A defect causing weakness in both arms or both legs is called….

A

diparesis/paraparesis

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5
Q

What is hemiparesis?

A

a defect causing weakness in right arm and right leg

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6
Q

The inability to move one leg is called…

A

monoparalysis or monoplegia

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7
Q

Weakness in all four limbs is called…

A

quadriparesis or tetraparesis

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8
Q

What is the difference between UPPER motor neuron damage and LOWER motor neuron damage?

A

UPPER damage causes weakness and loss of voluntary motion. Here, the spinal reflexes remain intact but cannot be modulated by the brain. This causes increased muscle tone, hyperreflexia/hypertonia and spasticity

LOWER damage means that neurons directly innervating muscles are affected.
If neurons are irritated:
–fasciculation (involuntary muscle contractions).
If neurons die:
–spinal reflexes lost
–flaccid paralysis
–muscle atrophy

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9
Q

What is muscle atrophy? What causes it?

A

Muscle atrophy is the breakdown of muscle, which happens as a result of disuse or denervation over time

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10
Q

Explain the pathophysiology of muscular dystrophy

A

Necrosis of skeletal muscle fibers and tissues means that contractile proteins (sarcoma) are not properly attached to the cytoskeleton of muscle cell, and fat and connective tissue replace it. This doesn’t effectively contract muscle cell

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11
Q

Does muscular dystrophy affect the nerves?

A

NO, only the muscles are affected

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12
Q

Compare Duchenne MD and Becker MD

A

Duchenne is the most common form of MD and is a recessive X-linked gene, which means it appears early in childhood. More common in boys, and females are usually asymptomatic if carrier or present very mild symptoms. Beker MD is much more mild, and progresses slower, and appears later in childhood.

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13
Q

What symptoms may make me suspicious that my baby has muscular dystrophy?

A
  • asymptomatic at birth
  • look normal until they start to walk
  • calf muscle hypertrophy due to accumulation of fat tissue
  • by 2-3yrs old, they develop abnormal posture, (gowers sign) fall a lot, have contractors, joint immobility and scoliosis
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14
Q

How will my teen patient with muscular dystrophy present to me?

A
  • wheelchair
  • incontinence
  • recurrent respiratory infections d/t weak cough causing accumulation of secretions
  • cardiomyopathy
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15
Q

What is Gower’s sign?

A

When kids tower themselves in a triangle and then use their hands to push on their legs to stand upright

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16
Q

How can physicians diagnose muscular dystrophy?

A
  • check out family history
  • observe voluntary movement for clues
  • elevated creatinine kinase (CK-MM), which specifically indicates muscle breakdown
  • muscle biopsy
  • Echo, ECG to indicate cardiomyopathy
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17
Q

What are the treatment options for muscular dystrophy?

A
  • maintain ambulation as long as possible to slow the progression of muscle loss
  • prevent deformities
  • promote deep breathing and coughing and use medications to prevent respiratory tract infections
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18
Q

What 3 things cause disorders of neuromuscular junction?

A
  1. Decreased acetylcholine release
  2. Decreased acetylcholine effects on muscle cell (d/t loss of receptors) (MYASTHENIA GRAVIS)
  3. Decreased acetylcholinesterase activity causes too much acetylcholine at neuromuscular junction, which also interferes with nerve impulses
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19
Q

What is acetylcholinesterase?

A

enzyme that degrades acetylcholine in synaptic space

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20
Q

Who is most likely to get myasthenia gravis?

A
  • young adult women or men over 50
  • placental transfer from mom (often spontaneously resolved)

*Thymus tumor of hyperplasia

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21
Q

Define Myasthenia Gravis

A

An autoimmune disorder that causes decreased motor response d/t loss of functional acetylcholine receptors in 3 ways:

  1. gradual destruction of receptors at NM junction
  2. Injury to postsynaptic muscle membrane
  3. receptor sites blocked by antibodies
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22
Q

If I have a patient with Myasthenia Gravis, how can I expect them to present?

A

Initially, muscle weakness in the periorbital muscles, like ptosis, and diplopia) and general fatigue, both of which will progress throughout the day.
As it progresses, she will exhibit respiratory muscle weakness, difficulty speaking, chewing, and swallowing, and weak limbs.

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23
Q

Why might my patient experience a Myasthenia Crisis?

A 
stress
infection
emotional upset
pregnancy
alcohol
cold
surgery
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24
Q

If I think I may be developing Myasthenia Gravis, what kind of diagnostic process can I expect to go through to confirm my suspicions?

A
  • general history/physical
  • acetylcholine receptor blood test (would show a rise in acetylcholine receptor antibodies)
  • electrophysiologic studies (would identify the stage of the disease process)
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25
Q

How can Myasthenia Gravis be treated?

A
  • corticosteroids to suppress the immune system in an attempt to rectify the autoimmune process
  • Thymectomy (if thymoma)
  • Plasmapheresis
  • IgG IV (immunoglobulin)
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26
Q

Explain Plasmapheresis

A

a procedure used to treat MG and GB and MS where blood is removed, blood and plasma are separated, red cells are returned to the patient, while specific antibodies are removed from plasma and replaced with immunoglobulins before it is returned to the body

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27
Q

What is carpal tunnel?

A

Pain, parenthesis and numbness in thumb, 1st, 2nd, 3rd and 4th fingers that is worse at night,.

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28
Q

What causes Carpal Tunnel?

A

compression of median nerve passing through carpal bones and ligaments. This happens from inflammation of tendons, synovial swelling, tumours, RA, DM, or repetitive flexion-extension movements

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29
Q

Which muscle atrophies in carpal tunnel?

A

abductor pollicus muscle

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30
Q

How is carpal tunnel diagnosed?

A
  1. Tinel sign, which is light percussion over the median nerve at wrist. If there is a tingling sensation into the palm, this diagnosis is positive
  2. Phalen Maneuver patient completely flexes their wrist for 1 minute. If they experience paresthesia in that time, the diagnosis is positive.
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31
Q

How is carpal tunnel treated?

A
  • anti-inflammatories
  • immobilization
  • surgery
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32
Q

What isGuillain-Barre syndrome? It has been linked to what other illnesses?

A

acute inflammatory demyelinating polyneuropathy

  • Campylobacter jejuni as influenza before onset
  • cytomegalovirus
  • epstein-barr virus
  • mycoplasma pneumoniae
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33
Q

What are the clinical manifestations of Guillain-Barre syndrome? Where might they have pain?

A

-Ascending symmetrical muscle weakness starting from the toes and moving upward to paralysis
-loss of tendon reflexes
*Respiratory involvement causes difficulty breathing
ANS– orthostatic hypotension, flushing, sweating, urinary retention

PAIN– shoulder, back, posterior thighs

34
Q

Do those with Guillain Barre’s syndrome exhibit muscle atrophy?

A

MINIMALLY

35
Q

How is Guillain-Barre’s syndrome treated? Is this treatment successful?

A

-ventilation to support respiratory function despite paralysis
-prevent complications
-plasmapheresis
IV IgG (Immunoglobulin)

*80%-90% have full recovery in 6-12 months. This virus lies dormant, so these patients must go see the doctor for all future illnesses ex the flu

36
Q

Name the 2 disorders of the cerebellum and basal ganglia

A

Tourette’s Syndrome

Parkinson’s Disease

37
Q

Define Choreiform movements

A

Jerking movements

38
Q

Define Athetoid movements

A

twisting movements

39
Q

If your patient has tourette’s syndrome and their chart reports ballismus movements, what should you look out for?

A

violent flinging movements

40
Q

What is Dystonia?

A

rigid movements associated with tourettes or parkinsons

41
Q

4 types of hyperkinesia

A

choreiform (jerks)
Athetoid (twisting)
Ballismus (violent flinging)
Dystonia (rigid)

42
Q

What is tourettes syndrome?

A

dysfunction in cortical and subcortical regions (thalamus, basal ganglia, frontal cortex) that causes physical and phonic tics

43
Q

If your patient exhibits Coprolalia, what can you expect?

A

“feces talk”, obscenities, swearing/cussing, no control over talk

44
Q

What is Parkinson’s Disease?

A

Progressive disorder of the basal ganglia and substantial nigra pathway that causes depletion of dopamine, resulting movement disorders

45
Q

What are some risk factors getting Parkinson’s Disease?

A
  • genetics
  • brain tumours, CVA, head trauma
  • post encephalitic syndrome
  • adverse effects from antipsychotic drugs that block dopamine receptors
  • toxins
  • carbon monoxide poisoning
46
Q

What is parkinsonism?

A

adverse effect of an antipsychotic drug that causes dopamine receptors to become blocked

47
Q

Early physical manifestations of Parkinsons Disease

A 
unilateral first, then bilateral
1. Tremor
     -occurs at rest, stops  
     with purposeful 
     movement/sleep
2. Rigidity
     -not smooth, with facial  
     masking and  
     infrequent blinking
3. Akinesia/bradykinesia
     -absence/slow  
     movements
4. Postural instability
     -impaired balance,   
     shuffling gait
48
Q

What are the LATE manifestations of Parkisons?

A
  • difficulty planning, starting or carrying out tasks
  • dementia
  • falls
  • limited voluntary facial movements
  • tongue, palate, throat muscles become rigid
  • slow speech, poor articulation
  • sleep disorders
  • unable to express emotions
49
Q

How does Parkinson’s affect the ANS?

A
  • lacrimation (crying)
  • sweating
  • dysphagia (difficulty swallowing)
  • orthostatic hypotension
  • constipation/incontinence
  • impotence
50
Q

If my patient has parkinsons, what are their treatment options?

A
  1. Non-pharmacologic (groups, education, exercise, nutrition)
  2. Pharmacologic
  3. . Surgical
51
Q

What if my patient with parkinsons is not responding to traditional treatments?

A

Botulinum toxin injections for dystonias

52
Q

Explain the 3 pharmacologic options to treat parkinson’s disease.

A
  1. Increase dopamine
    • levodopa
  2. Stimulate dopamine receptors
    • bromocriptine
    • pramipexole
    • amantadine
  3. Slow breakdown or reuptake of dopamine
    • selegiline
    • rasagiline
53
Q

What is a thalamotomy? Pallidotomy?

A

surgical treatment of Parkinsons disease where part of the thalamus or globes pallidus in basal ganglia destroyed with electrical stimulation
*one side only

54
Q

What occurs when the surgeon uses deep brain stimulations to treat Parkinsons?

A

implant electrodes into the sub thalamic nuclei or intern of globes pallidus. These electrical impulses block abnormal nerve activity that causes tremors

55
Q

What does ALS stand for? What is the other more common name for this disease?

A

Amyotrophic Lateral Sclerosis

Lou Gehrig Disease

56
Q

Define ALS

A

Amyotrophy- denervation or shrinkage of muscle fibers lead to atrophy

Lateral Sclerosis- scarring of lateral columns of white matter

57
Q

What is ALS?

A

a genetic mutation that causes a glutamate accumulation because Calcium channels open more than normal. This damages both the upper and lower neurons, which impairs voluntary movement.

58
Q

What are the 3 locations that motor neurons are affected in ALS?

A
  1. Anterior horn or spinal cord. This causes decreased neuron firing, which leads to irritation, weakness, denervation atrophy, hyperreflexia
  2. Motor nuclei of brain stem
  3. Cerebral cortex, which causes weakness, lack of motor control, stiffness and spasticity
59
Q

What 3 things does ALS NOT affect?

A
  • sensory system
  • intellect
  • ocular motility
60
Q

What are the early manifestations of ALS?

A
  • muscle cramps
  • weakness and atrophy of one extremity
  • generalized weakness
  • hyporeflexia
  • fasciculations (involuntary contractions)
  • impaired fine motor control
61
Q

What are the LATE manifestations of ALS?

A
  • limb/head weakness
  • weakness of palate, pharynx, and tongue causing dysphagia
  • weakness of neck, shoulders and respiratory muscles (aspiration)
  • Death
62
Q

How can ALS be treated?

A
  1. Riluzole– decreases glutamate accumulation and slows progression
  2. support ADLs
  3. Nutrition
  4. Counselling
63
Q

Explain the pathophysiology of Multiple Sclerosis

LOOK THIS UP

A

inflammation and destruction of myelin sheath of the white matter in the brain, spinal cord and optic nerve. Over time, hard, sharp-edged plaques replace the myelin sheath, and these plaques lack oligodendrocytes.

  1. sequential development of small inflammatory lesions
  2. Lesions extend and consolidate and scarring occurs on the nerve fibers
64
Q

If you have a patient with MS, how might they present?

A

unpredictable and dependent on location/extent

  • paresthesia (numbness, tingling, burning)
  • sexual/bladder dysfunction
  • fatigue, speech disturbances
  • MOOD SWINGS
  • optic nerve abnormalities (diplopia, gaze paralysis, nystagmus)
  • FATIGUE WITH DEPRESSION*
65
Q

What is Lhermitte sign?

A

when you flex the neck you feel a shock-like response down the back/legs

66
Q

4 “tracts” of MS manifestations

A

corticobulbar (speech/swallowing)
corticospinal (muscle strength)
cerebellar (gait, coordination)
spinocerebrellar (balance)

67
Q

What are the 4 types of MS?

A
  1. relapsing-remitting with acute worsening episodes but stable between
  2. secondary progressive-gradual worsening with episodes of improvement, previously had relapse-remittent
  3. Primary progression- continuous deterioration
  4. Progressive relapsing- gradual but with superimposed relapses
68
Q

How can MS be diagnosed?

A
  • evidence of CNS lesions occurring in different parts at least 3 months apart
  • MRI shows lesions (CT can be normal)
  • CSF- elevated IgG, elevated lymphocytes
69
Q

How can MS be treated?

A
  • manage symptoms
  • heathy lifestyles
  • physio
  • corticosteroids
  • adrenocorticotropic hormone (ACTH)
  • plasmapheresis
  • interferon to enhance immune system
  • glatiramer acetate to decoy T-cell response
  • Mitroxantrone to suppress leukocytes
70
Q

What happens if someone has a C4 injury?

A

tertraplegia

71
Q

What happens if someone has a T6 injury?

A

Paraplegia

72
Q

What happens if someone has a L1 injury?

A

paraplegia

73
Q

What is spinal cord shock?

A

complete loss of motor, sensory, reflex and autonomic function BELOW the level of the injury. This can include muscles, bowels, bladder and vasomotor tone. May recover in hours/days.

74
Q

What is central cord syndrome?

A

incomplete loss of motor power and sensation in the abdomen and chest (thoracic area)

75
Q

What is anterior cord syndrome?

A

damage to the area of the spinal cord that causes loss of motor power, pain and temperature sensation with preservation of position, vibration and touch sense from the nipples down

76
Q

What is Brown-Sequard Syndrome?

A

damage to only one side of the spinal cord that causes

  1. loss of pain and temperature sensation on the OPPOSITE side of the damage
  2. Loss of voluntary motor control on the SAME side as the damage
77
Q

What is conus Medullaris syndrome caused by? how does it present?

A

damage/compression to the conus medullaris

  • low back pain
  • bilateral sciatica
  • flacid bowel/bladder
  • sexual dysfunction
  • motor/sensory loss to legs/feet
78
Q

Name 3 Primary spinal cord injuries

A
  • gray matter hemorrhages
  • white matter edematous
  • necrosis of neural tissue
79
Q

Name 4 secondary spinal cord injuries

A

neurons and white matter damage caused by:

  • blood vessel damage
  • decreased vasomotor tone
  • local release of vasospastic substances
  • enzyme release from damaged cells
80
Q

How do health care professionals manage spinal cord injuries?

A
  • reduce neurological deficit and limit additional loss
  • immobilization, traction
  • decompression
  • surgery (to stabilize internally in order to enable early ambulation)
81
Q

What is autonomic dysreflexia?

A

an acute clinical syndrome that occurs as a complication of a spinal cord injury ABOVE T6. It results in vasospasm hypertension, bradycardia, diaphoresis and headache

82
Q

What can trigger autonomic dysreflexia?

A
  • pain
  • full bladder
  • bladder spasm
  • dressing change
  • uterine contraction
  • ejactulation
  • wrinkled sheets

Pathophysiology (10 decks)

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