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
Treating delirium
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.
26
Elements of abbreviated mental test score (AMT)
``` 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
27
Maximum doses of sedation in the elderly
Lorazepam - PO/IM 0.5-1mg MAX 3mg Haloperidol - PO 0.5mg IM 1-2mg MAX 5mg
28
Functions of Parietal Lobe
Processing sensory information Proprioception Calculation Construction
29
Functions of Frontal Lobe
Voluntary motor activity Speaking Personality Logic Behaviour
30
Functions of Temporal Lobe
Attention Verbal and Visual memory Learning
31
Pathophysiology of Alzheimer's Dementia
Neuronal loss and atrophy in multiple areas of cerebral cortex and subcortical areas Excess plaques of tau proteins (beta-amyloid) Enlargement of ventricles
32
Pathophysiology of Vascular Dementia
Damage to brain due to vascular issues such as stroke and prolonged hypertension causing myelin damage
33
Pathophysiology of Lewy Body Dementia
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)
34
Genes offering mild protection against Alzheimer's
APO-E2
35
Genes which increase the chance of developing Alzheimer's
APO-E3 and APO-E4
36
Genes associated with the development of early onset Alzheimer's
Amyloid Precursor Protein (Chromosome 21) PSEN-1 (Chromosome 14) PSEN-2 (Chromosome 1)
37
Core symptoms required for a dementia diagnosis
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
Additional symptoms seen in Lewy body dementia (e.g. other than core dementia symptoms)
``` Parkinsonism Hallucinations REM sleep disorder Neuroleptic sensitivity Other psychiatric disturbances ```
39
Effects as a result of temporal lobe damage
Diminished attention Short term memory issues Trouble with speech production
40
Effects as a result of parietal lobe damage
Problems recognising people and/or objects Difficulty carrying out sequences of actions
41
Effects as a result of frontal lobe damage
Reduced inhibition Problems initiating or stopping actions Reduced ability of reasoning and abstract thought
42
AMT-4
Name Age DOB Current Location
43
Cognitive Assessments
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
Elements of confusion screen
``` 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
Medication groups for managing demential
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
Acetylcholinesterase Inhibitors
Rivastigmine Donepezil Galantamine
47
NMDA Receptor Antagonists
Memantine
48
4 A's of Dementia
Amnesia Aphasia Ataxia Agnosia
49
Risk factors for pressure ulcer development
``` Increased age Reduced mobility Paralysis Malnourishment Sensory impairment ```
50
Treatment of pressure ulcers
Pressure reducing aids and repositioning Cleansing and dressing with hydrocolloid dressing Analgesia Antimicrobial therapy Debridement Reconstruction
51
When to refer pressure ulcers to coroner
One or more stage 3/4 ulcer | Two or more stage 2 ulcers
52
Causes of osteoporosis
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
Risk factors for osteoporosis
``` Female sex Post menopause Maternal history of osteoporosis Previous fractures Vitamin D deficiency Hypogonadism Hyperthyroidism ```
54
Diagnosing osteoporosis
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
Osteoporosis treatment
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
Complications of osteoporosis
``` Fractures DVT Reduced mobility Chronic pain Treatment side effects ```
57
Potential causes of Parkinson's
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
Pathophysiology of Parkinsons
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
Symptoms of Parkinson's
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
Parkinsons Plus Syndromes
Progressive Supranuclear Palsy (PSP) Corticobasal Degeneration (CBD) Multi-System Atrophy (MSA)
61
Diagnosing Parkinsons
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
Treating Parkinson's Pharmacologically
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
Non-pharmacological treatment of Parkinson's
Counselling and Psychological therapies Education OT/Physiotherapy SALT
64
Side effects of Levodopa
``` Impulse control disorders Drowsiness Postural hypotension N&V Hallucinations Confusion Motor Symptoms such as dyskinesia ```
65
Side effects of Dopamine Agonists
``` Impulse control disorders Leg swelling and discolouration Hallucinations Confusion Drowsiness/day-time sleepiness Movement disorders less common than levodopa ```
66
Parkinson's Prognosis
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
Stress incontinence Vs Urge incontinence
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
Nervous control of continence
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
Bladder outlet obstruction
Any condition which leads to an obstruction of urine, causing the bladder to become overfull and leak
70
Muscles involved in continence
Detruser muscle of bladder Pelvic Floor (Levator Ani and coccygeus) Periurethral muscles
71
Causes of Incontinence
DIAPPERS ``` Delirium Infection (UTI) Atrophy of vagina Pharmacological side effects Psychiatric issues Excessive urine output Restricted mobility Stool impaction ```
72
Drugs which can cause incontinence
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
Investigating incontinence
``` Medication review – any anticholinergic drugs? Diuretics? Bloods – U&E’s, eGFR Urinalysis Post-void residual measurement Uroflowmetry Cough stress test ```
74
Pharmacological treatments of overactive bladder
Oxybutynin (anticholinergic) Intravaginal oestrogen Botox
75
Pharmacological treatments of stress incontinence
Duloxetine (SNRI) Pseudoephedrine
76
Treatments for bladder outlet obstruction as a result of BPH
Alpha blockers 5-alpha reductase inhibitors
77
Conservative management for incontinence
``` Fluid intake diary Cutting out alcohol, coffee etc. Weight loss Pelvic floor exercises Biofeedback ```
78
Two questions which comprise the 2 stage capacity test
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
What must someone be able to do to be deemed to have capacity
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
Advanced directive (ADRT)
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
5 Principles of Capacity
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
Antiemetics to avoid in Parkinson's
DO NOT use Metoclopramide or Prochlorperazine Safe to use Domperidon, Cyclizine and Ondansetron
83
Systems to investigate in falls
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
Investigations required after a fall
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
Drugs which can contribute to falls
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
Drugs which we become less sensitive to with age
Beta Blockers Beta Agonists Furosemide
87
Elements of pharmacokinetics
Absorption Distribution Metabolism Excretion
88
Pharmacokinetic changes in older age
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
Assessing pressure ulcers
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
Elements of comprehensive geriatric assessment (CGA)
``` Physical health Psychological health Social and environmental factors Mobility Functional status Medication review ```