Vascular System & Stroke - Stroke Rehab Flashcards
(171 cards)
1
Q
Subjective disability
A
Ill health with absence of objective disease
2
Q
Subjective well-being
A
Feeling good but having severe objective disease
3
Q
Common psychosocial impacts of illness in severe condn
A
Disruption to normal life
Demand of treatments and care
Uncertainty of future
4
Q
What do impacts of illness and their consequences depend on
A
Nature of condn (e.g. severity, course, symptoms)
Individual (e.g. age, expectations, coping)
Social factors (e.g. support, resources)
5
Q
Sequence of psychosocial impacts of illness
A
Disease/ disorder –> impairment/ symptoms –> limitations/ disability –> restrictions —> dependency –> affects well-being —> changes life-evaluation
6
Q
Impacts of acute vs chronic illness
A
Acute illness causes fear, uncertainty but pt can enter ‘sick role’
Chronic illness comes with challenge of continuing obligations of normal life and managing illness but w/ new limitations
7
Q
Assessing subjective experience
A
Health status (e.g symptoms)
QoL (e.g. happiness)
HQRL (e.g. meaning)
Functional status (e.g. limitations)
8
Q
PROMS
A
Pt Reported Outcome Measures
9
Q
Key domains of illness impact
A
Perceived health (symptoms) Physical functioning Occupational/ role functioning Social functioning Emotional functional Cognitive functioning
10
Q
Clinical reasons for measuring psychosocial impact
A
Screening for hidden problems
Identifying & prioritising problems
Communication
Identifying preferences, shared decision-making
Monitoring change/ response
Aid in treatment & resource allocation decisions
11
Q
Emotional impacts of illness
A
Many c/c illness cormobid w/ depression creating further worsening of health (e.g. angina, arthritis, asthma, diabetes)
Severe, sudden physical condns can also trigger anger, anxiety, depression
12
Q
Causes of anxiety in illness
A
Outcomes/ results of illness/ treatment
Unknown procedures
13
Q
What does anxiety in illness result in
A
Irrational beliefs and heightened awareness of symptoms
Alters perception, interpretation and recall
14
Q
Depression definition
A
An effective (mood) disorder characterised by feeling sadness and general withdrawal from those around us Associated w/ suicide, poor adherence and poor motivation
15
Q
Why do we treat emotional impacts of illness
A
Physical and mental health aren’t separate
Increases survival, decreases risk of complications, increases QoL, poor treatment outcome and decreases cost of care
16
Q
Haemostasis
A
Normal blood clotting
17
Q
Thrombosis
A
Excessive blood clotting
18
Q
Thrombophilia
A
Predisposition to blood clots
19
Q
Fibrinolysis
A
Natural clot destruction
20
Q
VTE
A
Venous thromboembolism
Incl DVT/ PE
21
Q
Causes of clots
A
Virchow’s triad
Endothelial injury
Hypercoagulability
Stasis of blood flow
22
Q
Types of clots
A
Red clots
White clots
23
Q
Where are red clots found
A
Arteries (arterial)
24
Q
Where are white clots found
A
Veins (venous)
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Arterial thrombosis condns
Stroke
MI
PVD
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Venous thrombosis condns
VTE
| Thrombophlebitis
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Risk factors for red clots
```
Aging
Cholesterol deposition
HTN
DM
Smoking
```
28
Risk factors for white clots
Genetic - APLS
Malignancy
Immobility
Drugs
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Red clot composition
Mainly platelets, minimum fibrin
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White clot composition
Mainly fibrin, minimum platelets
31
What do anti platelet agents prevent
Platelet adhesion, activation and aggregation.
32
What do fibrinolytic agents increase
Conversion of plasminogen to plasmin
| Plasmin degrades fibrin and breaks up thrombin
33
What do anti-fibrinolytic agents prevent
Conversion of plasminogen to plasmin
34
Main groups of blood thinners
Anticoagulants
Anti-platelets
Thrombolytics
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Types of anticoagulants
Oral anti-coagulants
| Parenteral anti-coagulants
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What are anti-coagulants used for
Prevention of venous thrombus development or extension of thrombus in venous circulation
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DOACs
Direct Oral Anti-Coagulants
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Main DOACs
Apixaban
Dabigatran
Edoxaban
Rivaroxaban
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Benefit of DOAC's vs warfarin
No routine monitoring requirements
40
Indications for DOAC's
Stroke prevention if AF pt
| All except edoxaban can be used for VTE prophylaxis after elective hip or knee replacement suregry
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Reversal agent for dabigatran
Idarucizimab
42
Reversal agent for apixaban and rivaroxaban
Andexanet
43
Parenteral anti-coagulants
```
Heparin
LMWH
Heparinoids
Hirudins
Fondaparinux
```
44
When would heparin be used over LMWH
Those w/ high risk of bleeding - can terminate rapidly by stopping infusion
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Uses of LMWH
Prevention and treatment of VTE
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Examples of LMWH
Enoxaparin/ Dalteparin/ Tinzeoparin
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Heparinoid
Danaparoid - used for prophylaxis for DVT in pts undergoing general or orthopaedic surgery
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Example of a hirudin
Bivalirudin - direct thrombin inhibitor
| Can also be used to treat NSTEMI
49
Types of oral anti-coagulants
DOACs/ NOACs
| Vit k antagonists - warfarin, acenocoumarol
50
Direct Xa inhibitors
Rivaroxaban
Apixaban
Edoxaban
51
Direct thrombin inhibitors
Dabigtran
| Bivalirudin
52
Fondaparinux
Synthetic pentasacharide
| Inhibits factor X
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Examples of anti-platelet agents
Aspirin
Clopidogrel, Prasgrel, Ticraglor
Dipyridamole
54
Examples of fibrinolytics/ thrombolytics
Steptokinase
Alteplaste
Retreplaste
Tenectoplase
55
Antidote for heparin and LMWH
Protamine sulphate
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How long does warfarin take to have an effect
48 - 72 Hrs
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What must be monitored with warfarin
INR
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INR
International Normalised Ratio
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Normal INR
1
Higher the INR, thinner the blood
INR of 2 = takes blood 2x as long to clot
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Warfarin reversal
Vit K - main agent
FFP
Spp clotting factor
61
Aspirin MOA
Irreversibly inactivates COX -1 and alters balance between TXA2 and PGI2
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Clopidogrel MOA
Inhibits ADP induced aggregation
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Typical drugs given after arterial thrombosis
```
Fibrinolytic (alteplase) given acutely
Aspirin 300mg stat 2/52
Clopidogrel 75mg OD
Statins initiated within 48 hrs regardless of serum [Cholesterol]
DOAC's for AF pts
```
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When should alteplase be given after a stroke
Within 4.5 hrs of onset
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What type of anti-hypertensive should be used following a stroke
Beta-blockers
66
When can drugs be given for an ischaemic stroke
After excluding ICH stroke
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Advantages of thrombolytics
Improved long term outcomes i.e., function and independence
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Disadvantage of thrombolytics
Small window of use, for stroke require CT first
Risk of ICH (1%)
No H/O trauma/ surgery/ Haem stroke/ dental procedure
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When to use DOACs w/ caution
If ClCr < 30ml/min (dabigatran)
If ClCr < 15ml/ min (apixaban, rivaroxaban, edoxaban)
Depending on age and wt
70
TXA2
Thromboxane A2
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PGI2
Prostacyclin
72
Clinical use of aspirin
Acute treatment of ACS and stroke
2' prevention of arterial thrombosis after cardio/cerebrovascular events
Prevention of pre-ecclampsia
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Adverse effects of aspirin
GI bleeding
Bronchospasm
Toxic doses cause respiratory alkalosis followed by acidosis
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Heparin MOA
Accelerates action of anti thrombin - inactivates factors Xa and thrombin (IIa)
Also effects IXa, XIa, XIIa
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Heparin administration
S/c or IV infusion
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Clinical use of heparin
Treat DVT/ PE
Unstable angina
Acute peripheral arterial occlusion
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Adverse effects for heparin
Bleeding - main effect
Thrombocytopenia
Hypersensitivity reactions
Osteoporosis
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Administration of clopidogrel, prasugrel, ticagrelor
Given orally, loading dose first then OD
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Clinical use of clopidogrel, prasugrel, ticagrelor
Prevention and treatment of MI and other vascular events
| Often given with aspirin (increases effects)
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Adverse effects of clopidogrel, prasugrel, ticagrelor
```
Bleeding
GIT discomfort
Rashes
Neutrepenia - rarely
Ticagrelor can cause dyspnoea
```
81
Administration of fibrinolytics
Iv injection or infusion
82
Clinical use of fibrinolytics
MI
A/c ischaemic stroke and other arterial thrombosis
Severe cases of DVT/ PE
83
Adverse effects of fibrinolytics
Bleeding - most important
Reperfusion dysrhythmias
Nausea and vomiting
Hypersensitivity reactions
84
LMWH MOA
Accelerates action of antithrombin increasing its inactivation of factor Xa
85
LMWH administration
S/c injection
86
Clinical use of LMWH
Prevent VTE
| Treat DVT/ PE, MI, unstable angina
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Adverse effects of LMWH
Bleeding - main effect
| Less likely than heparin to cause thrombocytopenia, hypersensitivity reactions, osteoporosis
88
Warfarin MOA
Vit K antognist
| Prevents carboxylation of factors II, VII, IX and X
89
Functional assessment done by PTs
Baseline mobility, ROM, muscle power, sensation, balance
90
Stroke management done by PTs
Resp (tracheostomy)
Early mobilisation and promoting neurological recovery
tone and spasticity management
Discharge planning
Preventing complication - aspiration pneumonia
91
Hierarchy of cognition
If the lower levels are impaired, a person will not be able to achieve the higher levels
Sensory (bottom) --> Attention --> perception --> memory ---> praxis --> executive (top)
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Executive function - cognition
Ability to make choices, set goals, plan and organise a task
93
Acute complications post stroke
```
HTN
PE
Complications w/ nutrition and feeding
Aspiration pneumonia
Malignant MCA syndrome
```
94
Shoulder subluxation due to stroke
Consequence of weakness of shoulder girdle
| Wt of upper limb drags on shoulder capsule and ligaments
95
Management of shoulder subluxation due to stroke
Good moving and handling
Positioning
Analgesia
Orthotics
96
Spasticity
Condn in which there is an abnormal increase in muscle tone or stiffness of muscle, which might interfere w/ movement, speech, or be associated with discomfort or pain
97
Management of spasticity
```
Eliminating aggravating factors
Antispasmodics/ Botulinum toxin
Analgesia
Splinting and casting
Positioning and casting
Positioning in bed and chair
Passive stretches
```
98
Exacerbating factors of spasticity
```
Incontinence
Constipation
Pain
Pressure sores
Infection
General discomfort
```
99
Considerations for d/c planning
Is the pt able to raise an alarm in emergencies
How will the pt get in/out of a bed/ chair/ toilet
Can they manage stairs
Independently prepare modified meals
Initiate and remember to do ADL
Returning to driving or arranging transportation
100
What do statins reduce
Cholesterol
| Triglyceride levels
101
Surgical treatment for ICH
Removal of haemotoma to relieve ICP
102
Treatment for ICH strokes
Pts should be given rapid bp lowering drugs (IV)
| Pts taking anti-coagulants should have it reversed
103
What needs to be prescribed alongside DOACs and Asp/ Clop
PPi in those over 60 and/or a hx of dyspepsia
104
What kind of stroke is usually seen in younger pts
Haemorrhagic
Usually presents with sudden, severe headache due to increased ICP
105
Communication disorders after stroke
Aphasia
Dysarthria
Apraxia of Speech
Dysphonia
106
Aphasia
An acquired communication disorder that impairs a person's ability to process lang, but does not affect intelligence
107
When does aphasia occur
When there is damage to the area of the brain responsible for lang (Broca's and Wernicke's) - located in left hemisphere for majority of pts
108
Approximately how many pts will have a degree of aphasia following a stroke
Around 1/3
109
Types of aphasia
Different names depending on what areas of communication are affected
Expressive aphasia
Receptive aphasia
Acquired dysgraphia
Acquired dyslexia
110
Expressive aphasia
Affects pts speaking - Broca’s area
Varies in severity from being completely unable to speak to occasion difficulties finding target word
Might get stuck on words
May be able to use drawings/ writing/ symbols
111
Receptive aphasia
Affects auditory comprehension - Wernicke’s area
Irrelevant answers to q's
Usually able to recognise & use social phrases
Unlikely to realise they have receptive difficulties
112
Acquired dysgraphia
Affects writing
113
Acquired dyslexia - aphasia
Affects reading
114
Strategies to help communication w/ aphasic pts
Minimise or eliminate background noise where possible
Make sure you have their attention
Encourage all modes of communication
Try not to patronise but simplify sentence structure
115
Dysarthria
A speech disorder due to muscle weakness or incoordination
| Motor issue
116
How does speech sound with dysarthria
Can be slurred/ unclear
| Can sound quiet or monotone
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Anarthria
Total loss of motor ability that enables speech
118
When is anarthria seen in
Brainstem strokes - as well as 'Locked-In Syndrome'
119
What is Apraxia of Speech also known as
Verbal dyspraxia
120
AOS
An oral motor speech disorder - pathways between motor cortex and facial muscles have been disrupted resulting in limited and difficult speech ability
121
How may a pt with AOS present
With dysfluencies, inconsistent speech errors and repetitive muscle movement
122
What are pts with AOS good at
'Automatic speech' - yawning, counting, swearing etc
123
What does pure AOS mean
Language is fully intact - comprehension is good and there are word finding difficulties
124
Dysphonia
Weakness (infl) in the laryngeal muscles resulting in reduced or no movement in one vocal cord
125
What do pts with dysphonia sound like
Their voices sound rough/ strained/ hoarse - abnormalities of pitch, loudness, quality and variability
Some also completely lose their voice
126
Communication and the MDT
```
OT
PT
Nursing team
Medical team
Pharmacy
Stroke research team
Safeguarding team
Continuing healthcare/ social work d/c team
```
127
Dysphagia
Term for swallowing difficulties
128
Most common causes of dysphagia
Stroke
Brain injury
Other neurological disorders
129
What can dysphagia affect
Ability to eat and drink safely, can cause food and drink to enter airway --> choking, chest infections (aspiration pneumonia)
130
Stages of normal swallow
Pre-oral
Oral
Pharyngeal
Oesphageal
131
What can happen when swallowing goes wrong
```
Aspiration
Silent aspiration
Malnutrition/ dehydration
Missing key meds
Impacts on pleasure and socialisation
```
132
Clinical assessment of swallowing
Videofluroscopy aka modified Barium Swallow
| Fibreoptic Endoscopic Evaluation of Swallowing (FEES)
133
Alternative methods of feeding
NG tube/ bridle NGT
PEG/ RIG
Risk feeding
134
Main types of drug receptors
Ligand-gated (ion channels)
G protein coupled receptors
Kinase linked receptors
Nuclear receptors
135
Ligand - gated ion channels (ionotropic receptors)
Receptor is linked to the ion channel
Activation (agonist) = influx of ions
Time scale - milliseconds
136
G protein coupled receptors
G protein coupled receptors on cell membrane surface, once activated signal second messengers linked to enzymes or ion channel
Time scale - seconds
137
Kinase-linked receptors
Receptors linked to enzyme
Binding site for larger molecules like ligands (growth factors, cytokines)
Gene transcription --> protein synthesis
Time scale - hrs
138
Nuclear receptors
Receptors that are linked to gene transcription
| Cause proteins synthesised to take cellular effect
139
Examples of ligand-gated ion channels receptors
Nicotinic acid and Ach
140
Examples of G protein-coupled receptors
Opiate receptors & morphine
141
Examples of kinase-linked receptors
Tyrosine kinase and growth factors
142
Examples of nuclear receptors
Corticosteroids, thyroid, hormone (oestrogen)
143
Agonist
Drug that binds to receptor and elicits a repsonse
144
Antagonist
Drug that binds to receptor site and doesn't elicit a response/ block agonist from working
145
Example of antagonist
Naloxone (reverses the effect of morphine) - has no effect if given to pts that aren't taking opiates
146
Partial agonist
Drug that binds to receptor site and elicits a partial response (even with full receptor capacity)
147
Types of antagonist
Competitive
| Non-competitive
148
Competitive antagonists
Will compete for same receptor, can be overcome if we increase conc of the agonist, displacing it.
149
Non-competitive antagonists
Will not compete, often these agents cannot be displaced as they bind irreversibly
150
Selectivity
Tendency of a drug to affect a spp receptor
151
Receptor changes over time
```
Desensitisation
Tolerance
Up-regulation
Down-regulation
Exacerbation
```
152
Desensitisation - receptors
When receptors become less receptive to frequent doses of the same drug over a short period of time, which can lead to tolerance
153
Tolerance - receptors
Requiring a bigger dose for the same response e.g. opioids, transdermal nitrates
154
Up-regulation - receptors
Prolonged use of an antagonist, receptors up-regulate to minimise effect of antagonism.
Example – atenolol
155
Down-regulation - receptors
Prolonged use of an agonist, receptors down-regulate and minimises receptor affinity to minimise effect of antagonism
156
Exacerbation - receptors
Body has adapted itself to the exogenous agent. Removing it can exacerbate the condn you are trying to treat
157
What does therapy optimisation involve
Ensuring optimal therapeutic effects over adverse effects
Looking at If its not working, side-effects or not needed anymore
Fine tuning dose for Narrow Therapeutic drugs
158
Where is the Therapeutic Index found
Between ED50 and TD50
159
When do we need to monitor drug levels
```
Overdose
Poor clinical response
Suspected toxicity
Rule out poor compliance
Drug interactions
Non-linear kinetics
```
160
Types of adverse drug reactions
Type A reactions (pharmalogical)
| Type B reactions (idiosyncratic)
161
Type A ADR
Predictable
Dose dependent
Readily reversible (reducing dose/ withdrawing)
Common (80% of all reported ADRs)
162
Type B ADR
Non-predictable
163
What do doses adjust according to
```
Wt
Renal function
Liver function
Body surface area (BSA)
Nomograms
```
164
When is drug monitoring less important
Predictable pharmacokinetics
Broad therapeutic range
Less individual variation
Minimal/ transient side effect profile
165
Depression as a stroke complication
Anterior circulation strokes can cause changes in personality & emotion
Stroke is a life-changing event so can be psychological change
166
Treating depression as a result of stroke
Mood screening
SSRIs, if not effective then nortriptyline
Psychotherapy
167
Why should nutrition be treated after a stroke
Dehydration and malnutrition can lead to an increase in infections, cellular dysfunction and death if persistent
168
How can we prevent inadequate nutrition after a stroke
```
Dysphagia assessments
NG tube as short term solution
PEG feed if persisting >4 weeks
Diet modification
Rehab exercises - tongue strengthening exercises
```
169
Pressure sores
Injuries to the skin and underlying tissue, caused by prolonged pressure on the skin
170
Why should pressure sores be treated
If left untreated, can lead to infections such as cellulitis, OM and sepsis which can be life-threatening
171
How can we prevent/ treat pressure sores
Encourage early mobilisation (such as turning)
Monitor pressure areas
Wound care such as cleaning and applying dressings
Ensuring adequate nutrition
Using a pressure-relieving mattress
