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CP2 > HCoLL > Flashcards

HCoLL Flashcards

1
Q

Lacunar Stroke (LACS) Symptoms

A

Pure motor - contralateral weakness of face, arm, leg

Pure sensory - contralateral numbness of face, arm, leg

Mixed - contralateral weakness and numbness

Ataxic hemiparesis - ipsilateral lower limb weakness and lack of coordination

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2
Q

Total Anterior Circulation Stroke (TACS) Symptoms

A

ALL THREE OF:

Unilateral weakness and/or sensory deficit

Homonymous Hemianopia

Higher cerebral dysfunction e.g. dysphagia, visuospatial problems

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3
Q

Partial Anterior Circulation Stroke (PACS) Symptoms

A

TWO OF:

Unilateral weakness and/or sensory deficit

Homonymous Hemianopia

Higher cerebral dysfunction e.g. dysphagia, visuospatial problems

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4
Q

Posterior Circulation Stroke (POCS) Symptoms

A

Cerebellum - ataxia, balance issues, nystagmus, vertigo

Occipital lobe - visual field defects e.g. homonymous hemianopia

Thalamus - sensory deficits

Brain Stem - cranial nerve palsy

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5
Q

Arterial supply to lower limb cortex area

A

Anterior Cerebral Artery

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6
Q

Arterial supply to upper limb and face cortex area

A

Middle Cerebral Artery

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7
Q

Lesions causing homonymous hemianopia

A

Lesion of left or right optic tract impacting both paths which travel within it

Infarct to middle cerebral artery

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8
Q

Amaurosis Fugax

A

Transient occlusion of the retinal artery causing temporary vision loss in one eye

Described as ‘curtain coming down’

Usually only lasts a few seconds and vision will return gradually over several minutes

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9
Q

Link between AF and stroke

A

Blood can pool in the atria leading to thrombus formation

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10
Q

Investigating Haemorrhagic Stroke

A

Non-contrast CT head
Clotting
FBC - is thrombocytopenia cause of bleed?
LFTs - is liver failure the source of bleed?
U&E’s - some stroke treatment contraindicated in renal failure
Toxicology - is this the cause of bleed?
LP if subarachnoid haemorrhage suspected

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11
Q

Treating haemorrhagic stroke

A

Supportive Care
BP control
Neurosurgery referral
Reversal of anticoagulant if applicable

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12
Q

Complications of haemorrhagic stroke

A

Seizure
Aspiration pneumonia
DVT/PE
Delirium

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13
Q

Investigating ischaemic stroke

A

Urgent non-contrast CT head BUT normal CT cannot rule out stroke

ECG to check for arrhythmias and ischaemia and to rule out concordant MI

Glucose - Hypo can mimic stroke and Hyper associated with intracerebral bleeding

U&E to exclude electrolyte disturbances as cause

Prothrombin time (PT) to exclude coagulopathy as cause

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14
Q

Treating ischaemic stroke

A

Presentation < 4.5 hours

  • Thrombolysis (e.g. Alteplase)
  • Supportive care
  • Antiplatelet therapy (aspirin or clopidogrel)
  • High intensity statin
  • Consider thromboectomy

Presentation > 4.5 hours OR thrombolysis contraindicated

  • Supportive care
  • Consider thromboectomy
  • Antiplatelet therapy (aspirin or clopidogrel)
  • High intensity statin
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15
Q

Complications from ischaemic stroke

A

Conversion to haemorrhagic stroke
DVT due to immobility
Reactions to thrombolysis
Aspiration pneumonia

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16
Q

Wernicke’s aphasia

A

Loss of ability to understand language

Fluent speech but makes little sense - ‘word salad’

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17
Q

Broca’s aphasia

A

Understands language but finds it very difficult to talk

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18
Q

Areas supplied by Middle Cerebral Artery (MCA)

A

Basal Ganglia
Frontal Lobe
Temporal Lobe
Parietal Lobe

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19
Q

Areas supplied by Anterior Cerebral Artery (ACA)

A

Frontal Lobe

Parietal Lobe

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20
Q

Areas supplied by Posterior Cerebral Artery (PCA)

A

Thalamus
Midbrain
Temporal Lobe
Occipital Lobe

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21
Q

Dysarthria

A

Motor disturbance of speech results in patients finding it difficult to communicate

Comprehension, reading and writing are not affected, this is purely a motor problem

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22
Q

Higher cortical dysfunction symptoms

A 
Dysphasia 
Dysphagia 
Dyspraxia 
Sensory Neglect 
Visual Neglect 
Agnosia 
Astereognosis (numbers drawn on hand)
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23
Q

Symptoms of delirium

A

According to DSM-IV all below must be present:

Disturbance in consciousness
Acute onset and fluctuating course
Cognitive changes
Can be attributed to a medical cause

Other symptoms include:
Hypoactive (most common) mixed, or hyperactive 
Reversal of sleep-wake cycle 
Delusions and hallucinations 
Emotional changes 
Motor changes
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24
Q

Investigations in delirium

A

Mental state exam

Cognitive assessments

Delirium screening tool such as confusion assessment method (CAM)

Assess hydration

Assess for infection as cause with urinalysis, FBC, CRP, CXR

Chemistry panel for metabolic disturbances (LFT’s, U&E’s, Glucose etc.)

Check drug levels in patients on lithium, digoxin or quinidine

Alcohol levels

ECG to rule out MI

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25
Q

Treating delirium

A

Correct underlying physical issues

Ensure patient has appropriate aids

Orientate patient to time, place and person consistently

Sleep hygiene

Remove catheters, cannulas etc. if it is safe to do so to reduce infection risk

Reduce noise

Reduce medication

Sedation (haloperidol, lorazepam etc) should only be used if patient is a risk to themselves or others.

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26
Q

Elements of abbreviated mental test score (AMT)

A 
Age
Time 
Address for recall
Year
Name of hospital
Recognition of 2 people
Date of Birth
Year of first world war
Name of current monarch
Count backwards 20-1

SCORE BELOW 8/10 IS ABNORMAL

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27
Q

Maximum doses of sedation in the elderly

A

Lorazepam - PO/IM 0.5-1mg MAX 3mg

Haloperidol - PO 0.5mg IM 1-2mg MAX 5mg

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28
Q

Functions of Parietal Lobe

A

Processing sensory information

Proprioception

Calculation

Construction

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29
Q

Functions of Frontal Lobe

A

Voluntary motor activity

Speaking

Personality

Logic

Behaviour

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30
Q

Functions of Temporal Lobe

A

Attention

Verbal and Visual memory

Learning

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31
Q

Pathophysiology of Alzheimer’s Dementia

A

Neuronal loss and atrophy in multiple areas of cerebral cortex and subcortical areas

Excess plaques of tau proteins (beta-amyloid)

Enlargement of ventricles

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32
Q

Pathophysiology of Vascular Dementia

A

Damage to brain due to vascular issues such as stroke and prolonged hypertension causing myelin damage

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33
Q

Pathophysiology of Lewy Body Dementia

A

Lewy bodies are abnormal protein structures in the brain which interfere with dopamine and acetylcholine

Occurs in substantia nigra of basal ganglia

Low dopamine uptake (can be identified by a DAT scan)

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34
Q

Genes offering mild protection against Alzheimer’s

A

APO-E2

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35
Q

Genes which increase the chance of developing Alzheimer’s

A

APO-E3 and APO-E4

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36
Q

Genes associated with the development of early onset Alzheimer’s

A

Amyloid Precursor Protein (Chromosome 21)

PSEN-1 (Chromosome 14)

PSEN-2 (Chromosome 1)

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37
Q

Core symptoms required for a dementia diagnosis

A

Decline in memory which may be most obvious when trying to learn new information

Decline in cognitive functions such as thinking, judgement, planning and organisation

Decline in emotional control which may present as aggression, apathy or lability

Symptoms present for 6 months

38
Q

Additional symptoms seen in Lewy body dementia (e.g. other than core dementia symptoms)

A 
Parkinsonism
Hallucinations 
REM sleep disorder
Neuroleptic sensitivity 
Other psychiatric disturbances
39
Q

Effects as a result of temporal lobe damage

A

Diminished attention

Short term memory issues

Trouble with speech production

40
Q

Effects as a result of parietal lobe damage

A

Problems recognising people and/or objects

Difficulty carrying out sequences of actions

41
Q

Effects as a result of frontal lobe damage

A

Reduced inhibition

Problems initiating or stopping actions

Reduced ability of reasoning and abstract thought

42
Q

AMT-4

A

Name
Age
DOB
Current Location

43
Q

Cognitive Assessments

A

AMT-4 - anything below 100% is abnormal

AMT - anything below 7/10 considered abnormal

MoCA (Montreal Cognitive Assessment) – score of 26/30 or above is normal

MMSE (Mini Mental State Exam) – scored out of 30, 20-24 suggests mild dementia, 13-19 suggests moderate dementia and < 12 suggests severe dementia

MINI ACE/ACE-R (Addenbrooke’s Cognitive Exam Mini/Revised)

44
Q

Elements of confusion screen

A 
FBC – anaemia, infection
U&E – hypo/hypernatremia 
LFT’s with ammonia - HE
Coagulation – intracranial bleeding 
TFT’s – hyperthyroidism 
Calcium – hypercalcaemia 
B12 and folate
Glucose 
Blood cultures
CXR if indicated 
CT Head if indicated
45
Q

Medication groups for managing demential

A

Acetylcholinesterase Inhibitors (mild to moderate)

NMDA Receptor Antagonists (severe OR AchEI contraindicated)

Antipsychotics (Do NOT use in LBD and Parkinson’s)

Drugs are NOT indicated in FTD

46
Q

Acetylcholinesterase Inhibitors

A

Rivastigmine

Donepezil

Galantamine

47
Q

NMDA Receptor Antagonists

A

Memantine

48
Q

4 A’s of Dementia

A

Amnesia
Aphasia
Ataxia
Agnosia

49
Q

Risk factors for pressure ulcer development

A 
Increased age
Reduced mobility 
Paralysis 
Malnourishment
Sensory impairment
50
Q

Treatment of pressure ulcers

A

Pressure reducing aids and repositioning
Cleansing and dressing with hydrocolloid dressing
Analgesia
Antimicrobial therapy
Debridement
Reconstruction

51
Q

When to refer pressure ulcers to coroner

A

One or more stage 3/4 ulcer

Two or more stage 2 ulcers

52
Q

Causes of osteoporosis

A

Loss of bone mass due to ageing

Loss of body mass index

Corticosteroid use

Aromatase inhibitor use in females

Androgen deprivation therapy in males

53
Q

Risk factors for osteoporosis

A 
Female sex 
Post menopause 
Maternal history of osteoporosis 
Previous fractures
Vitamin D deficiency 
Hypogonadism
Hyperthyroidism
54
Q

Diagnosing osteoporosis

A

DXA scan is gold standard:

  • DXA T-score of 2.5 or less = Osteoporosis
  • T-score 2.5 or less + fragility fracture = Severe
  • T-scores most predictive of hip fractures

Fracture Risk Assessment

Vitamin D

Bone profile (ALP, corrected calcium, albumin, protein)

Phosphate

Parathyroid Hormone

55
Q

Osteoporosis treatment

A

Bisphosphonate is first line treatment PLUS calcium and vitamin D supplements

Bisphosphonates include:
Alendronic acid
Ibandronic acic
Zolendrolic acid

Second Line: Denosumab (monoclonal antibody)

Third Line: Parathyroid Hormone Receptor Agonist

56
Q

Complications of osteoporosis

A 
Fractures
DVT
Reduced mobility 
Chronic pain 
Treatment side effects
57
Q

Potential causes of Parkinson’s

A

Toxins:

  • Pro-drug MPTP in production of synthetic opioid MPPP
  • Heavy metal poisoning
  • Pesticides
  • Contaminated water

Infection such as post-encephalitic Parkinsonism

Head injury

Genetics

58
Q

Pathophysiology of Parkinsons

A

Loss of dopamine producing cells in the substantia nigra of the basal ganglia

Build up of eosinophilic inclusions such as Lewy bodies and nitrates

Neuronal loss in brainstem, spinal cord, cortex and peripheral autonomic nervous system

59
Q

Symptoms of Parkinson’s

A

CORE:

Upper body bradykinesia + at least one of:
Rigidity
Resting Tremor
Postural Instability

ADDITIONAL:

Masked facies
Hypophonia (quiet voice)
Hypokinetic Dysarthria (rigid oral and laryngeal muscles)
Shuffling gait
Stooped posture 
Gaze disorders
Depression
Dementia 
Constipation
60
Q

Parkinsons Plus Syndromes

A

Progressive Supranuclear Palsy (PSP)

Corticobasal Degeneration (CBD)

Multi-System Atrophy (MSA)

61
Q

Diagnosing Parkinsons

A

Clinical diagnosis which may be supported by investigations such as:

Functional neuroimaging (DAT, SPECT)
MRI Brain
Trial of a Dopaminergic Agent (e.g. Levodopa)
Urine copper to exclude Wilson’s in younger patients
Genetic testing

62
Q

Treating Parkinson’s Pharmacologically

A

MAO-B Inhibitor
Mild, early symptoms (e.g. Rasagaline, Selegiline)

Levodopa with Carbidopa
Most effective and preferred in older patients (>70) as dopamine agonists can cause hallucinations and postural drop

Dopamine Agonists
Preferred first line in younger patients due to the risk of dyskinesias from levodopa in this age group
Dopamine agonists include: Ropinerole, Prampipexole

COMT Inhibitors
Extend the therapeutic effects of levodopa if it begins to ‘wear off’

63
Q

Non-pharmacological treatment of Parkinson’s

A

Counselling and Psychological therapies
Education
OT/Physiotherapy
SALT

64
Q

Side effects of Levodopa

A 
Impulse control disorders 
Drowsiness
Postural hypotension 
N&V
Hallucinations 
Confusion 
Motor Symptoms such as dyskinesia
65
Q

Side effects of Dopamine Agonists

A 
Impulse control disorders 
Leg swelling and discolouration 
Hallucinations
Confusion
Drowsiness/day-time sleepiness 
Movement disorders less common than levodopa
66
Q

Parkinson’s Prognosis

A

Progressive condition
Unilateral symptoms will become bilateral
More rapid rate of progression associated with older age of onset, multiple co-morbidities and rigidity/hypokinesia as a presenting symptom

67
Q

Stress incontinence Vs Urge incontinence

A

Stress Incontinence – Involuntary leakage of urine due to increased abdominal pressure and weakness of the urinary outlet

Urge Incontinence – Involuntary leakage of urine with associated urgency, a failure of the bladder to store urine properly due to high pressure

68
Q

Nervous control of continence

A

Pudendal nerve provides somatic control of the urinary sphincter and arises from S2-S4

Hypogastric nerve provides sympathetic control and arises from T11-S2

Pontine micturition centre in brain

69
Q

Bladder outlet obstruction

A

Any condition which leads to an obstruction of urine, causing the bladder to become overfull and leak

70
Q

Muscles involved in continence

A

Detruser muscle of bladder
Pelvic Floor (Levator Ani and coccygeus)
Periurethral muscles

71
Q

Causes of Incontinence

A

DIAPPERS

Delirium 
Infection (UTI)
Atrophy of vagina 
Pharmacological side effects 
Psychiatric issues 
Excessive urine output 
Restricted mobility 
Stool impaction
72
Q

Drugs which can cause incontinence

A

Antipsychotics – anticholinergic effects such as urinary retention

Cholinesterase inhibitors – increase bladder contraction

Calcium channel blockers – decrease smooth muscle contractility

Opioids – constipation leading to overflow incontinence

ACE-I’s – cough worsens stress incontinence

Alpha blockers – relax bladder outlet and can worsen stress incontinence

Diuretics

Hypnotics

73
Q

Investigating incontinence

A 
Medication review – any anticholinergic drugs? Diuretics?
Bloods – U&E’s, eGFR
Urinalysis 
Post-void residual measurement
Uroflowmetry 
Cough stress test
74
Q

Pharmacological treatments of overactive bladder

A

Oxybutynin (anticholinergic)

Intravaginal oestrogen

Botox

75
Q

Pharmacological treatments of stress incontinence

A

Duloxetine (SNRI)

Pseudoephedrine

76
Q

Treatments for bladder outlet obstruction as a result of BPH

A

Alpha blockers

5-alpha reductase inhibitors

77
Q

Conservative management for incontinence

A 
Fluid intake diary 
Cutting out alcohol, coffee etc. 
Weight loss 
Pelvic floor exercises 
Biofeedback
78
Q

Two questions which comprise the 2 stage capacity test

A

Stage 1 – Is the person unable to make a particular decision?

Stage 2 – Is the inability to make a decision caused by an impairment of or disturbed functioning of their brain?

79
Q

What must someone be able to do to be deemed to have capacity

A

Understand information given to them

Retain that information long enough to be able to make the decision

Weigh up the information available to make the decision

Communicate their decision by talking, sign language, blinking etc.

80
Q

Advanced directive (ADRT)

A

Documentation which states your healthcare wishes to be followed in an event where you are unable to communicate these decisions (e.g. unconscious)

Can cover a variety of interventions and situations such as CPR, antibiotics, escalation to HDU/ITU and so on.

ADRT can be ignored if a patient is detained under the mental health act

81
Q

5 Principles of Capacity

A

Capacity is assumed until proved otherwise

People should be helped to be able to make their own decision (e.g. visual aids, interpreter, correct any medical issues which may be hindering)

People are allowed to make unwise decisions

If a person lacks capacity then decisions should be made which are in their best interests

The least restrictive option should always be chosen

82
Q

Antiemetics to avoid in Parkinson’s

A

DO NOT use Metoclopramide or Prochlorperazine

Safe to use Domperidon, Cyclizine and Ondansetron

83
Q

Systems to investigate in falls

A

Vestibular (e.g. meniere’s, infections, ototoxicity)

Visual (e.g. retinopathy, cataracts, reduced field of vision)

Brain (e.g. dementia, parkinson’s, cerebrovascular disease)

Proprioception (e.g. sensory neuropathy, joint replacements)

Cardiovascular (e.g. postural hypotension, AF)

MSK (e.g. pain, myopathy, nerve problems)

84
Q

Investigations required after a fall

A

Lying/Standing BP (ALL patients)

ECG (ALL patients)

TILT tests may be done in some cases

Bone health - Vit D, calcium, phosphate, parathyroid hormone, protein, albumin, ALP, DEXA scan

Coagulation screen

Medication review

85
Q

Drugs which can contribute to falls

A

Antihypertensives (hypotension)

Beta Blockers (Reduced HR, BP, cerebral perfusion)

Diuretics (increased urination at night, dehydration)

Nitrates (redice cerebral perfusion)

Steroids (muscle weakness)

Antihistamines (drowsiness)

Benzos (drowsiness)

Neuroleptics (drowsiness, induce parkinsonism’s)

Tricyclic Antidepressants (low BP, confusion)

86
Q

Drugs which we become less sensitive to with age

A

Beta Blockers

Beta Agonists

Furosemide

87
Q

Elements of pharmacokinetics

A

Absorption

Distribution

Metabolism

Excretion

88
Q

Pharmacokinetic changes in older age

A

Increased/decreased body fat and decreased water impact the DISTRIBUTION of fat and water soluble drugs

Reduction of album impacts protein bound drug DISTRIBUTION

Changes in size and function of liver impact hepatic METABOLISM

Decreased eGFR impacts renal EXCRETION

89
Q

Assessing pressure ulcers

A

Waterlow score for ulcer risk

Swab and culture if infection suspected

Nutritional review

Bloods for infection, nutrition, general health - FBC, U&E, CRP, ESR, albumin, iron

Tests for osteomyelitis - MRI, bone biopsy

Skin biopsy if malignancy suspected

90
Q

Elements of comprehensive geriatric assessment (CGA)

A 
Physical health
Psychological health 
Social and environmental factors 
Mobility 
Functional status 
Medication review

CP2 (7 decks)

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