Clincal cases Flashcards

1
Q

what is fibromyalgia characterized as?

A

Disease characterized by widespread MSK pain.

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2
Q

what causes fibromyalgia?

A

deficit in the way the brain processes pain. CNS is affected . pain modulatior pathways are altered leading to hypersensitivity

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3
Q

who is most at risk of Fibromyalgia?

A
  • family history
  • women
  • middle aged
  • people of low socioeconomic classes
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4
Q

what are some risk factors associated to fibromyalgia?

A
  • psychiatric problems
  • traumatic physical or emotional event
  • bacterial or viral infection
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5
Q

what disease is characterized by the following symptoms?

diffuse, burning-like bilateral and axial pain, stiffness, sleep disturbances and headaches?

A

fibromyalgia

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6
Q

what are some of the secondary effects caused by fibromyalgia?

A
  • irritable bowel
  • chronic fatigue
  • fibrofog
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7
Q

what disease is diagnosed with 11/18 pain points and ongoing pain for the past 3 months?

A

fibromyalgia

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8
Q

what treatments can be used for fibromyalgia?

A
  • pain meds and muscle relaxants

- antidepressants and anti epileptic drugs

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9
Q

is there a cure for fibromyalgia?

A

no since the cause is unknown

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10
Q

what is the implication of a PT and OT on fibromyalgia?

A

PT: flexibility and strength
OT: ADLs with minimal stress on body

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11
Q

what are life changes that may help reduce pain in patients with fibromyalgia?

A

meditation, sleep, exercise, reduced caffeine, smoking an alcohol

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12
Q

what are the different types of strokes?

A
  • ischemic (thromboic and embolic) where a clot is formed

- hemorrhagic where a vessel breaks

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13
Q

what happens in the case of a stoke to the brain tissue?

A

lack of o2 and nutrients leads to its death

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14
Q

who is most at risk of stoke?

A

men
>55
indigenous, african & south asian

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15
Q

what are risk factors associated to stoke?

A
HTN
Smoking
WHR
sedentary
diabetic
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16
Q

what does FAST stand for?

A
primary signs of stoke
Face drooping
arm weakness
slurred speach
time
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17
Q

what are other signs associated with stoke?

A
  • weakness on one side of the body
  • blurred or double vision
  • headaches
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18
Q

what are some common impairments after stoke?

A

depression & mood changes
low energy
cognitive deficits
dysphagia

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19
Q

how is stoke diagnosed?

A

using CT/MRI to identify location and type

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20
Q

what are the common treatments for stoke?

A

ischemic: tissue plasminogen ~4.5H after stoke to break down the clot or surgical removal via stent clipping
hemorrhagic: reduce bleeding and BP by clipping, endovascular embolization and high beam radiation

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21
Q

what is often used after stoke to reduce spasticity?

A

balcofen or

FES

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22
Q

what is the role of PT/OT for stoke?

A

PT: recover motor losses, endurance, ROM & strength
OT: fine motor skills, adaptive techniques & technologies

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23
Q

what is affected by addiction?

A

mesolimbic dopamine pathway by increasing the [dopamine] in the synapses which induces the production of cAMP and increases CREB production.

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24
Q

what is the result on dopamine caused by addiction?

A

natural endogenous dopamine production is reduced and hence increases the body’s demand for with

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25
what cortical organs are involved in addiction?
amygdala hippocampus cortex
26
who is most at risk of addiction? of intoxication?
addiciton: men intoxication: women
27
what are the common risk factors associated to addiciton?
``` poor familial status peer pressure easy access to drugs impulsive personality mental health issue abuse ```
28
what are signs and symptoms often associated to addiction?
craving tolerance nelect of responsibilities development of mental illnesses
29
what are the common symptoms associated to withdrawal?
``` sweating vomiting and nausea increased HR irritability hallucinations ```
30
what are the common treatments used for addiciton?
self help groups as they are empowering medications to help prevent withdrawl CBT
31
what is alzheimer?
neurogenerative disease which causes cortical cell death
32
what causes alzheimer?
- development of amyloid plate which disrupt synaptic communication, and increase cell death and excitotoxicity - neurofibrillary tangles which impede communication
33
what NTs seem to be decreased in Alzheimer?
NE ACh serotonin
34
what part of the brain shows atrophy in Alzheimer
medial temporal lobe and hippocampus
35
what causes Alzheimer?
unknown cause
36
what are the risk factors associated to Alzheimer
- genetic (APOE 4 or trisomy 21 gene) - environmental - lifestyle
37
who is most at risk of Alzheimer
women > 60 african americans, causians , and hispanics
38
what symptoms are associated with mild AD?
short term memory loss
39
what symptoms are associated with moderate AD?
``` short term memory loss inappropriate behavior redundancy apraxias damage to cortical areas involved in reasoning, conciousness, language and information processing ```
40
what symptoms are associated with severe AD?
``` brain atrophy communciation impairments dysphagia seizures gait abnormalities bladder and bowel impairments ```
41
how can Alzheimer be diagnosed?
no explicit test | use medical history, imaging techniques, lab tests and neurological exams
42
what medication can be given to treat Alzheimer?
-cholinesterase inhibitor which allows to maintain ACh and thus increase communication between cells anti-psychotic drugs
43
how can PT OT help patients with Alzheimer?
-improve gait and balance and promote PA and cognitive health educate patient and caregiver on AD and help with communication strategies
44
what is Parkinsons disease?
neurological motor disorder that is due to the loss of dopaminergic neurons in the substancia nigra
45
what is the role of lewy body formation in PD?
Believed to prevent neuronal functionning
46
when is PD generally diagnosed?
~60-65 years old
47
what is the greatest risk factor associated to PD?
age
48
who is most at risk of PD?
men | western countries
49
what are some risk factors associated to PD?
genetics | environmental (pesticides)
50
what is the effect of coffee and cigarets on PD?
recuces risk, considered to be negative risk factors
51
what disease are the following symptoms associated with? - tremors - rigitidy - bradykinesia - dysphagia, incontinence/cosntripation - dementia - depression - day time sleepiness
-parkinson disease
52
what are the most common treatments for pd?
- Levodopa which increases Dopamine availibility - deep brain stimulation which inhibits the inhiitory pathway by inhibiting the STN and allows to take smaller medications
53
what is paranoid schizophrenia?
mental disorder characterized by debilitating symptoms such as hallucinations, dellusions and constant suspiciousness
54
what is the cause of schizophrenia?
assumed to be caused by environmental and genetic factors which alter brain
55
what NT appear to be in excess in schizoprenia?
dopamine
56
what are risk factors associated with schizophrenia?
- positve family history - drug abuse - pregnancy complicaitons - low family income - childhood trauma - social isolation - living in rural area
57
who is more at risk of schizophrenia?
men and women are at equal risk, but men seem to show symptoms at a younger age 18-30 years old
58
how is schizophrenia diagnosed?
-2 symptoms have been consistently present for the past 6 months (delusion, hallucinations, disorganized speech and behavior, negative symptoms) CT/MRI: enlarged lateral and 3rd ventricle, loss of grey matter and smaller frontal and temporal lobes -psychosocial evaluation urine and blood tests
59
what are some positive symptoms associated to schizophrenia?
unhealthy cognitive and sensory processes that are in addition to what is expected in a healthy individual (these are in addition to healthy perceptions) such as Hallucinations, delusion
60
what are some negative symptoms associated to schizophrenia?
-avolition -decreased motivation neglect of personal hygiene -reduced eye contract -child-like behaviors
61
what are some cognitive deficits associated with schizophrenia?
speech memory and attention deficit
62
what is used to treat schizophrenia?
antipsychotic drugs can be good to restore dopamine balance (clozapine) --> multiple secondary effects
63
what is diabetic peripheral neuropathy
uncontrolled blood glucose levels which leads to nerve destruction in the PNS and narrows down the blood vessels thus increases susceptibiltiy to hypoxia, apoptosis and myelin degeneration.
64
what are the risk factors associated with DPN?
- type 2 diabetes - poor control of blood sugars - kidney damage - smokers due to narrowing and hardening of arteries
65
at what age does risk for DPN increase?
~60-80
66
what are the common symptoms associated with DPN?
feeling of numbness, tingling and pins/needles muscle weakness and low muscle tone dry and cracked feet due to inactive sweat glands
67
how can we diagnose for DPN?
- reduced amplitude of AP - slow sensory and motor nerve conduction velocity - lab tests for FBG and HB A1c - blisters and sores
68
how can DPN be prevented?
- diet changes - stop smoking - PA - proper footcare - regulation of BG levels
69
what medication can be used to reduce pain associated to DPN?
- antidepressant - anticonvulsants - opiods - topical cream capsaicin - transcutaneous nerve stimulation
70
what is GBS?
immune attack of the myelin sheaths on the peripheral nerve axons
71
what are the different types of GBS based on ?
based on the different part of the peripheral nerve that is involved
72
when is the actute phase of GBS reached? when is the peak?
lasts 4 weeks | peak is reached after 2 weeks
73
what happens during the second phase of GBS?
symptoms stabilize
74
does a GBS patient fully recover?
no
75
how many people are affected by GBS annually
100K
76
who is most at risk of GBS
males between 15-35 and 50-75 military personnel
77
whta is a common risk factor associated with GBS?
GIT or respiratory infection
78
what disease is the symptoms associated with? tingling and symetrical weakness in LL which progresses in UL. muscular weakness CN damage pain in the back, thighs, butt and shoulders VNS complications
GBS
79
how can GBS be diagnosed?
``` bilateral symptoms rapidity of symptom onset conduction velocity tendon reflex electromyography and ct/mri ```
80
how can GBS be treated
intravenous immunoglobulin treatment to provide healthy antibodies and plasmapharesis to clean out harmful antibodies from plasma
81
what medications are be prescribed to patients with GBS
pain meds and anticoagulants
82
what is the role of PT in GBS
pain help with strength and fatigue use of EMS, Heat packs and exercise
83
what is the cause of TBI?
exernal force to the head with penetrating and non-penetrating injury
84
what leads to a primary injury?
bruising, bleeding and tearing side the skull.
85
what is the secondary injury ?
inflammation, ICP reduced blood flow
86
what is the most common cause of TBI?
Falls, MVA, sports, violenece or assults
87
who is most
young adults between 15-24 MVA males and then >60 years old due to falls
88
what symptoms are associated to mild TBI?
``` vomiting dizziness lethargy memory loss brief loss of conciousness ```
89
what symptoms are associated to moderate/severe TBI?
``` visible trauma on neuroimagine extended loss of conciousness bleeding confusion lack of sleep ```
90
how can TBI be diagnosed?
CT/MRI/Xrays and EEGs | 15 point gasglow coma sclae
91
what are some long term complications associated with TBI?
physical and sensory impairments intellectual deficits communication deficits behavioural and emotional issues
92
how can TBI be treated?
emergency care medication including diuretics to decrease ICP, anti-siezure meds and coma inducing drugs surgery to remove blood clots, repair fractures and prevent further bleeding
93
how can PTOT help with TBI
-relearn motor skills help with ADLs movement patterns balance
94
what is huntington’s disease?
autosomal dominant disease that leads to hyperkinetic movements
95
what causes HD?
unknown cause but believed to be due to the breakdown and degeneration of nerve cells in the striatum
96
what changes may the patient of HD undergo?
personality, cognitive and motor impairments
97
what is the life expectancy of HD?
15-20 years after onset of HD?
98
what are the risk factors associated to HD?
-family incidence (genetics)
99
what is the average age of incidence for HD? from what region?
35-44 years old | western europeans
100
what are symptoms observed in early phases of HD?
Irritability Difficulty making memories, decisions and learning Involuntary jerky movements Gait impairment
101
what are symptoms observed in later phases of HD?
difficulties swallowing weight loss slurred speach extreme rigidity
102
what are some psychological symptoms of HD?
ocd depression mood changes
103
how can HD be diagnosed?
genetic testing | neurological exam
104
how can PTOT help with HD?
PT: improving strength, balance, gait, maintain respiratory functions, fall prevention techniques, imitating deterioration of ROM, posture OT: enhance safety in independence in doing ADLs, recommending equipment and modifications
105
how can a speech pathologist help a HD patient?
* Assesses dysphagia & communication * Provides eating techniques to prevent choking * Techniques for speech and communication problems
106
what medicine can be used for HD?
dopamine depleating agent
107
what is bacterial meningitis?
acute infection that causes swelling of the meninges and leads to apoptosis, increased ICP and arterial blockage
108
what is the most important risk factor for bacterial menigitis?
weakened immune system
109
who si most at risk for bacterial meningitis?
people wioth weaker immine system | sub-saharan africa
110
what is the incidence rate for bacterial meningitis?
went from 15 motnhs to 39 years old due to the introduction of conjugate vaccine
111
what are common symptoms of bacterial meningits
``` Neck stiffness Headaches Fever, nausea, vomiting Muscle and joint pain Difficulty concentrating Photophobia & hearing loss due to compression of cranial nerves irritability swelling of fontanelles and high pitched cries ```
112
what are some complications associated with bacterial meningitis?
``` lack of coordination weakness concentration deficits long term hearing loss behvaioral changes ```
113
how to diagnose bacteial meningitis?
Lumbar puncture Blood sample with gram stain Imaging to identify swelling or inflammation
114
treatment for bacterial meningitis?
- corticosteroids to reduce inflammation - antibiotics - intravenous fluids - o2 therapy
115
how cna PTOT help with bacterial meningitis?
PT: evaluate and monitor improvement/regressions in patient’s level of balance and coordination & ensure proper positioning to avoid bed sores and muscle contractures OT: proper environment for patient’s recovery & provide patient with adaptive techniques o Provide patient education about disease and possible complications
116
what is autonomic dysreflexia?
Over reactivity of the SNS due to loss of SNS inhibition which results in an acute episode of peripheral hypertension accompanied with bradycardia. This further results in peripheral vasoconstriction.
117
what can trigger autonomic dysreflexia?
noxious/non-noxious stimuli bladder distention/obstruction occluded catheter fecal impaction
118
what can be some complications of autonomic dysreflexia?
Cerebral hemorrhage Neurogenic pulmonary edema Coma Myocardial infarction
119
what is the common risk associated to autonomic dysreflexia?
- people with lesion above T6 - complete SCI - MS patients - return of sacral reflexes after spinal shock
120
what are the general symptoms associated with autonomic dysreflexia?
``` overexcitation PSNS above, SNS below leads to o Flushing of the face o Profuse sweating above the lesion o Pale, cold skin below the lesion o Blurred vision & dyspnea o Pounding headaches o Nasal congestions  vasodilation (above the lesion PSNS) o Nausea  PSNS vagal effect o Chills and increased spasms o Increased SBP BY >20% ```
121
how can autonomic disreflexia be treated?
-patient needs to sit up right -monitor BP -removal of noxious stimuli or cause of AD pharmacological meds (nifedipine) topical nitroglycerine ointment above the lesion
122
what is the role of PT/OT in autonomic dysreflexia?
be aware of the symptoms and how to respond to them during a session educate about ADLs and various emptying techniques
123
what is MJD
spinocerebellar ataxia type 3 which is an autosomal dominant neurodegenerative disease that arises due to ingreated CAG codon repetetions
124
what is the function of the ATXN gene?
regulation of transcription of certain aa and removing damaged excess proteins thus mutations leads to degeneration and cell death
125
what areas of the brain are affected by MJD?
BS, basal ganglia, SC, peripheral nerve, cerebellar cortex
126
what is the most prominent subtype of MJD?
type 2
127
what are the subtypes of MJD classified as?
- age of onset (1 being the youngest) - rate of onset (1= fastest_ - length of polyq tract (1= longest)
128
what are the risk factors associated to MJD?
- family onset (anticipation leads to worsening conditions) - portuguese descent - males
129
what illness is characterized by dystonia, spasticity, ataxia and decreased cerebellar functions as disease progresses?
MJD
130
what is amyotrophy? what disease is it a symptom of?
MJD | loss of feeling and hypoalgesia
131
how can MJD be diagnosed?
genetic testing symptom recognition imaging (pontocerebellar atrophy and enlargemnt of 4th ventricle)
132
what can be used to treat MJD?
levodopa to treat stiffness, slurred speech antispasmodic meds like balcofen modafinil to reduce day time sleepiness prism glasses to help with blurred vision since eye surgery only provides temporary results due to muscle degeneration
133
how are PTOT involed in MJD?
improve independence and gait strategies or mobility aids
134
what is whiplash caused by?
Caused by traumatic acceleration-deceleration mechanism which affects the neck and results in a cervical strain/sprain due to Rapid hyperextension or hyperflexion which results in Intense sheering force that can compress the joint capsules
135
what is the major cause of whiplash?
MVA and falls
136
why are females more at risk of whiplash?
due to lesser neck musculature
137
who is more at risk of whiplash in a MVA?
passenger
138
what country has the highest incidence rate for whiplash?
europe
139
how to diagnose whiplash?
understand the mechanism of injury and imaging techniques
140
what symptoms are associeated to whiplash?
``` • Neck and shoulder pain Decreases ROM of the neck Arm pain and weakness, jaw pain, back pain Cognitive symptoms including o Fatigue o Dizziness o Visual disturbances o Tetanus (noise in ear) ```
141
what are persistent symptoms of whiplash?
headaches | stiff neck and pain
142
what are some psychological symptoms associated to whiplash?
``` anger frustration stress PTSD sleep disturbances ```
143
how can whiplash be treated?
antidepressant drugs to relieve neuropathic pain lidocain injections to numb certain areas antiinflammatory drugs msucle relaxants surgery in cases of persistant pain
144
how can PTOT help with whiplash?
pain management, restor ROM and return to ADLs | promote healthy life habits including PA, modifications to ADLs to reduce pain
145
what is spastic cerebral palsy?
damage to the developing brain leading to motor deficits. can be acquires or congenital
146
what causes spastic hemiplegia?
unilateral lesion of the brain which Tends to affect the MCA
147
what is affected by spastic quadriplegia?
cavities that communicate with lateral ventricles diffuse cortical atrophy hydrocephalus
148
greatest prevalence for spastic cerebral palsy is seen in who?
preterm babies males low socio economic classes
149
what are the risk factors of SCP?
-menstrual cycle -previous pregnancy loss -thyroid or epilepsy disorders congenital malformations bleeding in 3rd trimester interuterine growth retardation treatment for thyroid, estrogen and progesterone premature baby asphyxia infection
150
what are symptoms associated with SCP?
``` stiff jerk movements muscle weakness decreased ROM movement and coordination problems fine motor stuggles hearing impairmeents delays in speech intellectual disabilities urinary incontinence ```
151
when do symptoms of SCP generally appear?
during infancy and preschool year due to development impairments
152
what impairment can be observed in spastic displegia?
muscle stiffness primarily in legs
153
what impairment can be observed in spastic hemiplegia?
asymmetrical gait
154
what impairment can be observed in spastic quadriplegia?
four limbs, trunk and face are affected | Co-occurring disorders including epilepsy
155
how can SCP be treated?
botox surgical interventions to alter the length of spastic tendons to restore balance and avoid excessive pulliung on the bone rhizotomy: cut nerve roots with excessive activity to reduce spasticity
156
how can PTOT help in SPC?
Aim to improve motor development, prevent MSK complications | Correct abnormal patterns of movements