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MBBS - Year 2 > Vascular System & Stroke - Stroke Rehab > Flashcards

Vascular System & Stroke - Stroke Rehab Flashcards

1
Q

Subjective disability

A

Ill health with absence of objective disease

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2
Q

Subjective well-being

A

Feeling good but having severe objective disease

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3
Q

Common psychosocial impacts of illness in severe condn

A

Disruption to normal life
Demand of treatments and care
Uncertainty of future

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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)

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5
Q

Sequence of psychosocial impacts of illness

A

Disease/ disorder –> impairment/ symptoms –> limitations/ disability –> restrictions —> dependency –> affects well-being —> changes life-evaluation

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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

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7
Q

Assessing subjective experience

A

Health status (e.g symptoms)
QoL (e.g. happiness)
HQRL (e.g. meaning)
Functional status (e.g. limitations)

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8
Q

PROMS

A

Pt Reported Outcome Measures

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9
Q

Key domains of illness impact

A 
Perceived health (symptoms)
Physical functioning 
Occupational/ role functioning 
Social functioning 
Emotional functional 
Cognitive functioning
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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

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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

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12
Q

Causes of anxiety in illness

A

Outcomes/ results of illness/ treatment

Unknown procedures

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13
Q

What does anxiety in illness result in

A

Irrational beliefs and heightened awareness of symptoms

Alters perception, interpretation and recall

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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
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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

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16
Q

Haemostasis

A

Normal blood clotting

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17
Q

Thrombosis

A

Excessive blood clotting

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18
Q

Thrombophilia

A

Predisposition to blood clots

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19
Q

Fibrinolysis

A

Natural clot destruction

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20
Q

VTE

A

Venous thromboembolism

Incl DVT/ PE

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21
Q

Causes of clots

A

Virchow’s triad

Endothelial injury
Hypercoagulability
Stasis of blood flow

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22
Q

Types of clots

A

Red clots

White clots

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23
Q

Where are red clots found

A

Arteries (arterial)

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24
Q

Where are white clots found

A

Veins (venous)

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25
Q

Arterial thrombosis condns

A

Stroke
MI
PVD

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26
Q

Venous thrombosis condns

A

VTE

Thrombophlebitis

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27
Q

Risk factors for red clots

A 
Aging 
Cholesterol deposition 
HTN 
DM 
Smoking
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28
Q

Risk factors for white clots

A

Genetic - APLS
Malignancy
Immobility
Drugs

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29
Q

Red clot composition

A

Mainly platelets, minimum fibrin

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30
Q

White clot composition

A

Mainly fibrin, minimum platelets

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31
Q

What do anti platelet agents prevent

A

Platelet adhesion, activation and aggregation.

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32
Q

What do fibrinolytic agents increase

A

Conversion of plasminogen to plasmin

Plasmin degrades fibrin and breaks up thrombin

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33
Q

What do anti-fibrinolytic agents prevent

A

Conversion of plasminogen to plasmin

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34
Q

Main groups of blood thinners

A

Anticoagulants
Anti-platelets
Thrombolytics

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35
Q

Types of anticoagulants

A

Oral anti-coagulants

Parenteral anti-coagulants

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36
Q

What are anti-coagulants used for

A

Prevention of venous thrombus development or extension of thrombus in venous circulation

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37
Q

DOACs

A

Direct Oral Anti-Coagulants

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38
Q

Main DOACs

A

Apixaban
Dabigatran
Edoxaban
Rivaroxaban

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39
Q

Benefit of DOAC’s vs warfarin

A

No routine monitoring requirements

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40
Q

Indications for DOAC’s

A

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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41
Q

Reversal agent for dabigatran

A

Idarucizimab

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42
Q

Reversal agent for apixaban and rivaroxaban

A

Andexanet

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43
Q

Parenteral anti-coagulants

A 
Heparin 
LMWH 
Heparinoids
Hirudins 
Fondaparinux
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44
Q

When would heparin be used over LMWH

A

Those w/ high risk of bleeding - can terminate rapidly by stopping infusion

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45
Q

Uses of LMWH

A

Prevention and treatment of VTE

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46
Q

Examples of LMWH

A

Enoxaparin/ Dalteparin/ Tinzeoparin

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47
Q

Heparinoid

A

Danaparoid - used for prophylaxis for DVT in pts undergoing general or orthopaedic surgery

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48
Q

Example of a hirudin

A

Bivalirudin - direct thrombin inhibitor

Can also be used to treat NSTEMI

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49
Q

Types of oral anti-coagulants

A

DOACs/ NOACs

Vit k antagonists - warfarin, acenocoumarol

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50
Q

Direct Xa inhibitors

A

Rivaroxaban
Apixaban
Edoxaban

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51
Q

Direct thrombin inhibitors

A

Dabigtran

Bivalirudin

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52
Q

Fondaparinux

A

Synthetic pentasacharide

Inhibits factor X

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53
Q

Examples of anti-platelet agents

A

Aspirin
Clopidogrel, Prasgrel, Ticraglor
Dipyridamole

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54
Q

Examples of fibrinolytics/ thrombolytics

A

Steptokinase
Alteplaste
Retreplaste
Tenectoplase

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55
Q

Antidote for heparin and LMWH

A

Protamine sulphate

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56
Q

How long does warfarin take to have an effect

A

48 - 72 Hrs

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57
Q

What must be monitored with warfarin

A

INR

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58
Q

INR

A

International Normalised Ratio

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59
Q

Normal INR

A

1
Higher the INR, thinner the blood
INR of 2 = takes blood 2x as long to clot

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60
Q

Warfarin reversal

A

Vit K - main agent
FFP
Spp clotting factor

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61
Q

Aspirin MOA

A

Irreversibly inactivates COX -1 and alters balance between TXA2 and PGI2

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62
Q

Clopidogrel MOA

A

Inhibits ADP induced aggregation

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63
Q

Typical drugs given after arterial thrombosis

A 
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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64
Q

When should alteplase be given after a stroke

A

Within 4.5 hrs of onset

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65
Q

What type of anti-hypertensive should be used following a stroke

A

Beta-blockers

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66
Q

When can drugs be given for an ischaemic stroke

A

After excluding ICH stroke

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67
Q

Advantages of thrombolytics

A

Improved long term outcomes i.e., function and independence

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68
Q

Disadvantage of thrombolytics

A

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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69
Q

When to use DOACs w/ caution

A

If ClCr < 30ml/min (dabigatran)
If ClCr < 15ml/ min (apixaban, rivaroxaban, edoxaban)
Depending on age and wt

70
Q

TXA2

A

Thromboxane A2

71
Q

PGI2

A

Prostacyclin

72
Q

Clinical use of aspirin

A

Acute treatment of ACS and stroke
2’ prevention of arterial thrombosis after cardio/cerebrovascular events
Prevention of pre-ecclampsia

73
Q

Adverse effects of aspirin

A

GI bleeding
Bronchospasm

Toxic doses cause respiratory alkalosis followed by acidosis

74
Q

Heparin MOA

A

Accelerates action of anti thrombin - inactivates factors Xa and thrombin (IIa)
Also effects IXa, XIa, XIIa

75
Q

Heparin administration

A

S/c or IV infusion

76
Q

Clinical use of heparin

A

Treat DVT/ PE
Unstable angina
Acute peripheral arterial occlusion

77
Q

Adverse effects for heparin

A

Bleeding - main effect
Thrombocytopenia
Hypersensitivity reactions
Osteoporosis

78
Q

Administration of clopidogrel, prasugrel, ticagrelor

A

Given orally, loading dose first then OD

79
Q

Clinical use of clopidogrel, prasugrel, ticagrelor

A

Prevention and treatment of MI and other vascular events

Often given with aspirin (increases effects)

80
Q

Adverse effects of clopidogrel, prasugrel, ticagrelor

A 
Bleeding 
GIT discomfort 
Rashes 
Neutrepenia - rarely 
Ticagrelor can cause dyspnoea
81
Q

Administration of fibrinolytics

A

Iv injection or infusion

82
Q

Clinical use of fibrinolytics

A

MI
A/c ischaemic stroke and other arterial thrombosis
Severe cases of DVT/ PE

83
Q

Adverse effects of fibrinolytics

A

Bleeding - most important
Reperfusion dysrhythmias
Nausea and vomiting
Hypersensitivity reactions

84
Q

LMWH MOA

A

Accelerates action of antithrombin increasing its inactivation of factor Xa

85
Q

LMWH administration

A

S/c injection

86
Q

Clinical use of LMWH

A

Prevent VTE

Treat DVT/ PE, MI, unstable angina

87
Q

Adverse effects of LMWH

A

Bleeding - main effect

Less likely than heparin to cause thrombocytopenia, hypersensitivity reactions, osteoporosis

88
Q

Warfarin MOA

A

Vit K antognist

Prevents carboxylation of factors II, VII, IX and X

89
Q

Functional assessment done by PTs

A

Baseline mobility, ROM, muscle power, sensation, balance

90
Q

Stroke management done by PTs

A

Resp (tracheostomy)
Early mobilisation and promoting neurological recovery
tone and spasticity management
Discharge planning
Preventing complication - aspiration pneumonia

91
Q

Hierarchy of cognition

A

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)

92
Q

Executive function - cognition

A

Ability to make choices, set goals, plan and organise a task

93
Q

Acute complications post stroke

A 
HTN 
PE 
Complications w/ nutrition and feeding 
Aspiration pneumonia 
Malignant MCA syndrome
94
Q

Shoulder subluxation due to stroke

A

Consequence of weakness of shoulder girdle

Wt of upper limb drags on shoulder capsule and ligaments

95
Q

Management of shoulder subluxation due to stroke

A

Good moving and handling
Positioning
Analgesia
Orthotics

96
Q

Spasticity

A

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
Q

Management of spasticity

A 
Eliminating aggravating factors 
Antispasmodics/ Botulinum toxin 
Analgesia 
Splinting and casting 
Positioning and casting 
Positioning in bed and chair 
Passive stretches
98
Q

Exacerbating factors of spasticity

A 
Incontinence
Constipation 
Pain 
Pressure sores 
Infection 
General discomfort
99
Q

Considerations for d/c planning

A

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
Q

What do statins reduce

A

Cholesterol

Triglyceride levels

101
Q

Surgical treatment for ICH

A

Removal of haemotoma to relieve ICP

102
Q

Treatment for ICH strokes

A

Pts should be given rapid bp lowering drugs (IV)

Pts taking anti-coagulants should have it reversed

103
Q

What needs to be prescribed alongside DOACs and Asp/ Clop

A

PPi in those over 60 and/or a hx of dyspepsia

104
Q

What kind of stroke is usually seen in younger pts

A

Haemorrhagic

Usually presents with sudden, severe headache due to increased ICP

105
Q

Communication disorders after stroke

A

Aphasia
Dysarthria
Apraxia of Speech
Dysphonia

106
Q

Aphasia

A

An acquired communication disorder that impairs a person’s ability to process lang, but does not affect intelligence

107
Q

When does aphasia occur

A

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
Q

Approximately how many pts will have a degree of aphasia following a stroke

A

Around 1/3

109
Q

Types of aphasia

A

Different names depending on what areas of communication are affected

Expressive aphasia
Receptive aphasia
Acquired dysgraphia
Acquired dyslexia

110
Q

Expressive aphasia

A

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
Q

Receptive aphasia

A

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
Q

Acquired dysgraphia

A

Affects writing

113
Q

Acquired dyslexia - aphasia

A

Affects reading

114
Q

Strategies to help communication w/ aphasic pts

A

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
Q

Dysarthria

A

A speech disorder due to muscle weakness or incoordination

Motor issue

116
Q

How does speech sound with dysarthria

A

Can be slurred/ unclear

Can sound quiet or monotone

117
Q

Anarthria

A

Total loss of motor ability that enables speech

118
Q

When is anarthria seen in

A

Brainstem strokes - as well as ‘Locked-In Syndrome’

119
Q

What is Apraxia of Speech also known as

A

Verbal dyspraxia

120
Q

AOS

A

An oral motor speech disorder - pathways between motor cortex and facial muscles have been disrupted resulting in limited and difficult speech ability

121
Q

How may a pt with AOS present

A

With dysfluencies, inconsistent speech errors and repetitive muscle movement

122
Q

What are pts with AOS good at

A

‘Automatic speech’ - yawning, counting, swearing etc

123
Q

What does pure AOS mean

A

Language is fully intact - comprehension is good and there are word finding difficulties

124
Q

Dysphonia

A

Weakness (infl) in the laryngeal muscles resulting in reduced or no movement in one vocal cord

125
Q

What do pts with dysphonia sound like

A

Their voices sound rough/ strained/ hoarse - abnormalities of pitch, loudness, quality and variability
Some also completely lose their voice

126
Q

Communication and the MDT

A 
OT 
PT 
Nursing team 
Medical team 
Pharmacy 
Stroke research team 
Safeguarding team 
Continuing healthcare/ social work d/c team
127
Q

Dysphagia

A

Term for swallowing difficulties

128
Q

Most common causes of dysphagia

A

Stroke
Brain injury
Other neurological disorders

129
Q

What can dysphagia affect

A

Ability to eat and drink safely, can cause food and drink to enter airway –> choking, chest infections (aspiration pneumonia)

130
Q

Stages of normal swallow

A

Pre-oral
Oral
Pharyngeal
Oesphageal

131
Q

What can happen when swallowing goes wrong

A 
Aspiration 
Silent aspiration 
Malnutrition/ dehydration 
Missing key meds 
Impacts on pleasure and socialisation
132
Q

Clinical assessment of swallowing

A

Videofluroscopy aka modified Barium Swallow

Fibreoptic Endoscopic Evaluation of Swallowing (FEES)

133
Q

Alternative methods of feeding

A

NG tube/ bridle NGT
PEG/ RIG
Risk feeding

134
Q

Main types of drug receptors

A

Ligand-gated (ion channels)
G protein coupled receptors
Kinase linked receptors
Nuclear receptors

135
Q

Ligand - gated ion channels (ionotropic receptors)

A

Receptor is linked to the ion channel
Activation (agonist) = influx of ions
Time scale - milliseconds

136
Q

G protein coupled receptors

A

G protein coupled receptors on cell membrane surface, once activated signal second messengers linked to enzymes or ion channel
Time scale - seconds

137
Q

Kinase-linked receptors

A

Receptors linked to enzyme
Binding site for larger molecules like ligands (growth factors, cytokines)
Gene transcription –> protein synthesis
Time scale - hrs

138
Q

Nuclear receptors

A

Receptors that are linked to gene transcription

Cause proteins synthesised to take cellular effect

139
Q

Examples of ligand-gated ion channels receptors

A

Nicotinic acid and Ach

140
Q

Examples of G protein-coupled receptors

A

Opiate receptors & morphine

141
Q

Examples of kinase-linked receptors

A

Tyrosine kinase and growth factors

142
Q

Examples of nuclear receptors

A

Corticosteroids, thyroid, hormone (oestrogen)

143
Q

Agonist

A

Drug that binds to receptor and elicits a repsonse

144
Q

Antagonist

A

Drug that binds to receptor site and doesn’t elicit a response/ block agonist from working

145
Q

Example of antagonist

A

Naloxone (reverses the effect of morphine) - has no effect if given to pts that aren’t taking opiates

146
Q

Partial agonist

A

Drug that binds to receptor site and elicits a partial response (even with full receptor capacity)

147
Q

Types of antagonist

A

Competitive

Non-competitive

148
Q

Competitive antagonists

A

Will compete for same receptor, can be overcome if we increase conc of the agonist, displacing it.

149
Q

Non-competitive antagonists

A

Will not compete, often these agents cannot be displaced as they bind irreversibly

150
Q

Selectivity

A

Tendency of a drug to affect a spp receptor

151
Q

Receptor changes over time

A 
Desensitisation 
Tolerance 
Up-regulation 
Down-regulation 
Exacerbation
152
Q

Desensitisation - receptors

A

When receptors become less receptive to frequent doses of the same drug over a short period of time, which can lead to tolerance

153
Q

Tolerance - receptors

A

Requiring a bigger dose for the same response e.g. opioids, transdermal nitrates

154
Q

Up-regulation - receptors

A

Prolonged use of an antagonist, receptors up-regulate to minimise effect of antagonism.
Example – atenolol

155
Q

Down-regulation - receptors

A

Prolonged use of an agonist, receptors down-regulate and minimises receptor affinity to minimise effect of antagonism

156
Q

Exacerbation - receptors

A

Body has adapted itself to the exogenous agent. Removing it can exacerbate the condn you are trying to treat

157
Q

What does therapy optimisation involve

A

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
Q

Where is the Therapeutic Index found

A

Between ED50 and TD50

159
Q

When do we need to monitor drug levels

A 
Overdose 
Poor clinical response 
Suspected toxicity 
Rule out poor compliance 
Drug interactions 
Non-linear kinetics
160
Q

Types of adverse drug reactions

A

Type A reactions (pharmalogical)

Type B reactions (idiosyncratic)

161
Q

Type A ADR

A

Predictable
Dose dependent
Readily reversible (reducing dose/ withdrawing)
Common (80% of all reported ADRs)

162
Q

Type B ADR

A

Non-predictable

163
Q

What do doses adjust according to

A 
Wt 
Renal function 
Liver function 
Body surface area (BSA)
Nomograms
164
Q

When is drug monitoring less important

A

Predictable pharmacokinetics
Broad therapeutic range
Less individual variation
Minimal/ transient side effect profile

165
Q

Depression as a stroke complication

A

Anterior circulation strokes can cause changes in personality & emotion
Stroke is a life-changing event so can be psychological change

166
Q

Treating depression as a result of stroke

A

Mood screening
SSRIs, if not effective then nortriptyline
Psychotherapy

167
Q

Why should nutrition be treated after a stroke

A

Dehydration and malnutrition can lead to an increase in infections, cellular dysfunction and death if persistent

168
Q

How can we prevent inadequate nutrition after a stroke

A 
Dysphagia assessments 
NG tube as short term solution 
PEG feed if persisting >4 weeks 
Diet modification 
Rehab exercises - tongue strengthening exercises
169
Q

Pressure sores

A

Injuries to the skin and underlying tissue, caused by prolonged pressure on the skin

170
Q

Why should pressure sores be treated

A

If left untreated, can lead to infections such as cellulitis, OM and sepsis which can be life-threatening

171
Q

How can we prevent/ treat pressure sores

A

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

MBBS - Year 2 (20 decks)

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