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Pathophysiology Flashcards

1
Q

What can cause haemorrhagic stroke?

A

Ruptured Aneurysm
Head Trauma (Generally Subarachnoid or Intracerebral)
Dissection - carotid

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2
Q

What are 3 forms of ischaemic stroke?

A

Cerebral Thrombosis
Cerebral Embolism - Thromboembolism, Fat Embolism, Air embolism
Lacunar stroke

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3
Q

What are some symptoms of stroke?

A 
Weakness/Paralysis or numbness on contralateral side
Vertigo/dizziness 
Headache 
Visual loss/blurred vision 
Faintness 
Confusion 
Speech problems 
Difficulty swallowing 
Cognitive problems 
Memory problems 
Consciousness alterations
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4
Q

What does FAST stand for in terms of stroke?

A

Facial weakness
Arm weakness
Speech problems
Time to call 999

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5
Q

What is the immediate stroke management plan?

A 
FAST 
Scan – ischaemic or haemorrhagic 
Blood Tests 
Clot-Busting (4.5hr window) or haemorrhage evacuation  
Chest X-rays, ECG, Ultrasound
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6
Q

Which scans are best for each type of stroke?

A

CT – fast, easy to spot haemorrhage

DWI – best for ischaemic damage

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7
Q

Describe thrombolysis use in stroke management

A

Intravenous (IV) rtPA (Alteplase) within a 4.5hr window
Often stroke onset time unknown
If large clot burden, IV tPA poor response
Intra-arterial (IA) thrombolysis possible
Interventional neuroradioradiolgy - Endovascular thromboaspiration, Microcatheters can directly reach the thrombus

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8
Q

In which arteries might clot burdens be large?

A

Terminal carotid/proximal MCA and basilar

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9
Q

What are the 4 main types of CNS syndromes/infarct?

A

TACS (TACI) – Total Anterior Circulation Syndrome (ACA, MCA)
PACS (PACI) – Partial Anterior Circulation Syndrome
LACS (LACI) – Lacunar Syndrome
POCS (POCI) – Posterior Circulation Syndrome

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10
Q

What symptoms occur with Total Anterior Circulation Infarct?

A 
Higher Dysfunctions 
Dysphasias 
Visuospatial problems 
Homonymous Hemianopia
Motor/Sensory Deficits
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11
Q

What symptoms will lacunar infarcts produce?

A

Focal changes
Pure Motor or Sensory or Sensorimotor loss
Ataxic Hemiparesis

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12
Q

What symptoms occur with posterior circulation infarct?

A

Cranial nerve palsy & contralateral motor/sensory deficit
Bilateral motor or sensory deficit
Cerebellar signs
Eye Movement deficits/isolated homonymous hemianopia

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13
Q

What are cerebellar signs?

A 
DANISH
Dysdiadokinesia & dysmetria (overshoot)
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
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14
Q

What are lacunar infarcts?

A

Small lesions – lake-like cavities, giving focal deficits
Common in brainstem regions and deep cerebral white matter
Occlusion of small vessels: Lenticulostriate, Thalamogeniculate
Brainstem perforating vessels

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15
Q

What are watershed infarcts?

A

Systemic hypotension causing infarct in areas of overlap of supply
Most common ACA-MCA infarct caused by occlusion of carotid artery
Man in a barrel- loss of trunk sensation/motor function and aphasia
MCA-PCA affects visual processing

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16
Q

Where are spinal watershed areas?

A

T4-T8 – watershed between radicular arteries (thoracic and great radicular artery)
L1 – watershed between Great radicular artery and ascending sacral arteries

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17
Q

What are main causes for adolescent strokes?

A 
Hereditary 
CHD/AHD 
Congenital Abnormalities
Trauma 
Infection 
Metabolic 
Neoplasia
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18
Q

What are transient ischaemic attacks?

A

Mini-Stroke, usually results from drop in perfusion, often: Carotid Artery Insufficiency, Vertebrobasilar Insufficiency
Symptoms same as Full Stroke
Amourosis fugax - loss of blood flow to retina
Severe symptoms for <30 mins
Full recovery within 24
Use it as a WARNING SIGN

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19
Q

How do you calculate the risk of stroke after a TIA?

A

ABCD2
A — Age: > 60 years, 1 point
B — BP: >140/90 mmHg, 1 point
C — Clinical features: unilateral weakness, 2 points; speech problems but no weakness, 1 point
D — Duration of symptoms: ≥ 60 mins, 2 points; 10–59 mins, 1 point
D — Diabetes: 1 point
Score ≥4, high risk of stroke
2 TIAs in close succession – high risk (even if ABCD2 <3)
1:10 TIAs with no treatment will have full stroke within 1 year

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20
Q

What assessment score is used for stroke risk in a patient with AF?

A

CHADVASC scale if patient has AF

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21
Q

What members of the MDT could be required in post stroke management?

A 
Consultant physicians 
nurses 
physiotherapists 
occupational therapists 
speech and language therapists
clinical psychologists 
rehabilitation assistants 
social workers
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22
Q

What are mortality rates post stroke?

A

20% mortality within first month
10% mortality within year
Rest recover but ~50% have disability
Recurrence rate 30-43%

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23
Q

What is post stroke pain?

A

Thalamic pain Occurs 1 week- 6 months after stroke
Can occur anywhere in spinothalamic system
Generally occlusion of thalamo geniculate arteries
Symptom (referred to contralateral side): Burning pain with sharp components, Hyperalgesia & Allodynia, Treat as for neuropathic pain (Amitriptyline)

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24
Q

What is vascular dementia?

A

Many vascular CNS events, including stroke
Multi-infarct dementia - from many small TIA
Single-infarct dementia - related to large stroke
Lacunar infarct – variable depending on size
Biswanger’s dementia – multiple lacunar infarcts caused by
arteriosclerosis of subcortical vessels
Multi-infarct dementia linked to step-wise progression in cognitive decline
Lifestyle changes/BP can prevent
Early detection vital
Early signs: vascular cognitive impairment, Slow thought, Difficulties planning, Speech impairment, Mood and behaviour changes, often mistaken for depression

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25
Which patients are susceptible to sub dural haemorrhages?
Elderly and alcoholic | Due to neural shrinkage, bridging veins are under increased tension
26
What is a likely cause of a sub arachnoid haemorrhage?
Bleed here is from cerebral artery aneurysm
27
What can a meningioma lead to?
Can produce focal symptoms from cortical or cranial nerve compression Raised ICP may cause multiple deficits, headache or loss of consciousness
28
What are the two layers of the dura mater?
Periosteal layer | Meningeal layer
29
Why can Periorbital infection spread from the orbit to the meninges?
Dura and subarachnoid space extend through the optic canal to the posterior of the orbit
30
Which artery runs past the pterion and is therefore at risk of rupture with a skull fracture?
Middle meningeal - extradural haemorrhage
31
What is a risk with an extradural haematoma?
Lucid period - patient will regain consciousness, seem fine and then suddenly collapse when pressure builds up
32
What innervates dura in the posterior cranial fossa? | And what clinical significance does this have?
Cervical spinal nerves | Compression of cervical nerves in neck can cause referred pain headache in occipital lobe
33
What carries sensory info from the meninges?
``` Trigeminal nerve (CN V) - Innervates a large amount of dura including the tenotoria CN V Also innervates face, sinuses and teeth – referred pain headaches possible ```
34
What feature allows rapid drainage of dural venous sinuses?
Valveless and endothelial lined
35
Where does the sigmoid sinus drain into?
Through jugular foramen | Into internal jugular vein
36
What drains the scalp?
Emissary veins through cranial bones to superior sagittal sinus
37
Where do periorbital veins drain?
Cavernous sinus. Form a route for orbital/nasal region infection spread
38
What is the Glasgow outcome score?
1. Dead 2. Vegetative state (sleep/wake cycle but not sentient) 3. Severely Disabled (conscious but dependent) 4. Moderately disabled (independent but disabled) 5. Good recovery (may have minor sequelae)
39
What is diffuse axonal injury?
Trauma causes axon to twist and tear | Result is permanent death of the neuron
40
What are cardinal features of raised ICP?
Nausea Papilloedema Headache
41
What is the Monro-Kellie doctrine?
v.intracranial (constant) = v.brain + v.CSF+ v.blood + v.mass lesion
42
When should ICP be treated?
When above 20mmHg
43
What cranial perfusion pressure should be maintained?
Above 65mmHg
44
What is cerebral perfusion pressure?
CPP = MAP - ICP
45
What are Neurocritical care principles?
``` Free water (as dextrose solutions) NOT administered. Decrease plasma osmolality so increase water content of brain tissue Elevated blood sugar levels associated with worsening of neurologic injury after cerebral ischaemia. Ischaemic brain metabolises glucose to lactic acid, lowering tissue pH, exacerbating ischaemic injury Hypertonic solutions and osmotic diuretics (mannitol) - low molecular weight, osmotically active particles may leak into the cerebral interstitium, Mannitol - no effect in reducing brain water content ```
46
What Mental sequelae may exist in patients post head trauma?
personality disorders, memory disorders, reduced reasoning power, apathy, lack of drive, temper tantrums, family disruption
47
What is the most common neurological disorder?
Epilepsy
48
What are the main categories of epilepsy?
Partial and generalised
49
Which form of epilepsy has no loss of consciousness or post-ictal confusion and its symptoms depend on focal site?
Simple partial seizure
50
What symptoms might occur from a simple partial temporal seizure?
Aura-smell/taste, déjà vu, jamais vu, emotional changes, Oral automatisms, gestures eg dystonic or fidgetting
51
What symptoms might occur from a simple partial parietal seizure?
Sensory Nausea, choking, sinking sensations Illusions of body distortion
52
What symptoms might occur from a simple partial frontal seizure?
Brief, frequent, cluster, mainly motor, often bilateral eg kicking, cycling, violent, bizarre. Head version often from sleep
53
What symptoms might occur from a simple partial occipital seizure?
Visual hallucinations – simple or complex (shapes to scenes) Vision may black out Visuo-spatial distortions Head turning, headache, nausea
54
What are complex partial seizures?
Altered consciousness, but may seem fully aware Symptoms: automatisms (chewing, swallowing, repeated displacement behaviour) Prior to onset may experience senseof déjà vu/jamais vu, perceptual changes, auras Generally temporal lobe in origin, can progress to generalised May have some post-ictal confusion
55
What is a Partial with Secondary Generalised seizure?
Simple partial seizure, patient conscious and aware progressing to generalised (Grand-Mal) when activity reaches thalamus Temporal foci often associated with auras and hallucination Frontal foci ‘motor seizures’, stiffness/jerking in limbs Parietal foci ‘sensory seizures’, tingling/warmth on ipsi side Occipital foci generally preceded by visual hallucinations light/colour
56
Which seizure type is characterised by tonic and clonic phases?
Generalised Tonic-Clonic (Grand-Mal)
57
What occurs in a tonic phase of a seizure?
whole body stiffness, breathing may stop (cyanosis), loss of bladder control
58
What is a post ictal period?
unconsciousness, muscle relaxation, slow regain of consciousness, confusion, sleepy, headaches and aching limbs, no recall of episode
59
What are the two forms of status epilepticus?
Convulsive - grand mal | Non convulsive - petit mal
60
Describe a convulsive status epilepticus seizure
``` Prolonged seizure state Whole brain involved Ictal period of > 5 mins Repeated seizures with no recovery between (>30 mins) Medical Emergency ```
61
What is a non convulsive status epilepticus seizure?
long-lasting, absence or focal-type seizures
62
What is an absence seizure?
Part of the generalised seizure spectrum Rare in adults, generally starts between 6-12 yrs Girls > Boys Symptoms: seem to ‘switch-off’ but cannot be alerted or woken up Responds well to anti-epileptics
63
What is NEAD?
Non-epileptic attack disorder, no physical reason or changes in brain activity, but has similar symptoms. Also known as psychogenic non-epileptic seizures. Bite tip of tongue, not sides as seen in grand mal
64
What is an EEG recording?
Activity patterns of populations of neurons by recording changes in gross current flow Levels of synchrony between neurons causes changes in patterns, if fire together give larger amplitude oscillations Patterns of synchrony cause rhythms
65
What are the 5 rhythms seen on an EEG?
Alpha – 8-13Hz Mainly occipital, quiet, eyes shut, meditation Beta >14Hz Parietal and frontal, activity and tension, sleep spindles Gamma – 40Hz binding, learning and memory Theta – 4-7Hz Parietal and temporal, alertness, L&M Delta <3.5 Hz Cortical, deep sleep, coma
66
What 4 things can cause changes in neuronal excitability and lead to epileptic activity?
Reduction in GABA Increase in Ach transmission Increase in Na+ transmission Decrease in K+ transmission
67
What are first line Treatments for Partial Seizures and Partial with Secondary Generalised seizures?
``` Carbamazepine Lamotrigine Oxcarbazepine Sodium valproate Levetiracetam ```
68
What are Second Line (adjuncts) treatments for partial seizures?
Clobazam, gabapentin, topiramate
69
What are first line treatments for grand mal seizures?
Sodium valproate Lamotrigine Carbamazepine Oxcarbazepine
70
What are first line treatments for petit mal seizures?
Ethosuximide | Sodium Valproate
71
What treatments are given in an emergency situation for convulsive status epilepticus?
Commence i.v. Lorazepam (repeated after 10 mins) After 25 mins: phenytoin sodium, fosphenytoin, or phenobarbital sodium After 45 mins: Anaesthetize with thiopental, midazolam or non-barbiturate anaesthetic (propofol) Buccal Midazolam/Rectal diazepam (if resus facilities not available)
72
What treatments are suitable for NEAD?
Remove any AEDs in use Antidepressants Psychotherapy
73
What is Antiepileptic Hypersensitivity Syndrome? And what do you do about it?
Starts 1-8 weeks from treatment initiation Initial signs: Fever, rash, swollen lymph nodes Severe signs: Blood, liver kidney and respiratory abnormailites, Vasculitis and organ failure Withdraw drug immediately Topical steroids and antihistamines for rash Systemic corticosteroids? Beware of rebound seizure activity
74
What are the generalised mechanisms of action of anti epileptic drugs?
``` Sodium Channel Blocker Calcium Channel Blocker GABA modulation GABA mimetics Most are dirty drugs so have multiple actions ```
75
How do Na channel blockers work as anti epileptic drugs?
Primarily targeted for voltage-dependent Na+ channels | Only block channels in inactivated state to reduce electrical activity by extending refractory period
76
Which antiepileptic drugs have Na channel blocker activity?
Phenytoin Carbamazepine Lamotrigine Sodium Valproate
77
What are side effects of Na channel blocking AEDs?
``` CNS effects, cognitive impairment, visual impairment Peripheral neuropathy Skin problems Gum hyperplasia Anaemia and other blood disorders Osteomalacia Teratogenicity ```
78
In what ways can AEDs affect GABA activity?
``` Enhance activation of GABA-A mediated channels Action at co-agonist sites Inhibition of GABA breakdown Inhibition of GABA uptake GABA mimetics ```
79
How do benzodiazepines work as AEDs?
Act on GABAA receptor (γ subunit) to increase activity as co agonist Reduces neuronal transmission by enhancing inhibition
80
What is Flumazenil?
Benzo antagonist | Included in coma cocktails
81
What are barbiturates?
Work in same way as benzos but on the β-subunit of the GABAA receptor to increase activity Reduces neuronal transmission by enhancing inhibition Commonly used as anaesthetics/anxiolytics
82
What are Side Effects of BDZs and Barbs?
``` Short-term use only (< 12 weeks) Tolerance and dependency can develop Impaired motor coordination (↓muscle tone) Impaired cognitive performance Sedation Disturbed sleep patterns (↓SWS) Retrograde amnesia Withdrawal on termination ```
83
What is Tiagabine?
Act to inhibit GABA transporter so prevent its reuptake
84
What is Vigabatrin?
Act to inhibit GABA transaminase so prevent GABA breakdown
85
Which AEDs block calcium channels?
Ethosuximide (T-type Ca2+ blocker) | Gabapentin
86
What are some future AED targets?
Glutamate Antagonists Gap Junction inhibitors Steroids Broad spectrum drugs (e.g. Topiramate,Levetiracetam)
87
Which AED can be used to treat trigeminal neuralgia?
Carbamazepine
88
What AED and antidepressant combo can be used to treat neuropathic pain?
Gabapentin and Amitriptyline
89
What arteries make up the circle of Willis?
``` Anterior cerebral artery (ACA) Anterior communicating artery (AComm) Middle cerebral artery (MCA) Posterior cerebral artery (PCA) Posterior communicating artery (PComm) Basilar artery (BA) ```
90
Explain why a haemorrhage into the pons could cause a sudden and profound unconsciousness
Damage to reticular formation
91
Explain why performing a lumbar puncture in a patient with raised ICP might be disastrous
Coning
92
What are the signs of decerebrate rigidity?
Extension of arms and legs and medial rotation of arms
93
Describe herniation syndrome
Supratentorial swelling; uncus forced through opening in tentorium cerebelli; pressure on midbrain; rise in pressure in posterior fossa; coning of medulla and cerebellar tonsils in foramen magnum
94
What type of disorder is MS?
An autoimmune demyelinating disorder
95
In the CNS which cells are responsible for the production of the myelin sheathing around axons?
Oligodendrocytes
96
Diagnosis of MS is supported by lumbar puncture and CSF analysis. What is a common feature of CSF from MS patients?
The presence of oligoclonal bands is supportive of a diagnosis of MS. Oligoclonal bands indicate that a CNS immune response has been triggered; between 2 and 5 bands present suggests the presence of immunoglobulins (IgG)
97
One of the characteristic feature of early MS is optic neuritis. What is optic neuritis and why is the optic nerve susceptible to degeneration in MS?
Optic neuritis: inflammation of optic pathways visible on fundoscopy Optic nerve and tracts are actually developmental extensions of CNS, myelin coating is provided by oligodendroglial cells. When function is disrupted it can trigger inflammatory responses which results in optic neuritis
98
Besides the relapsing remitting type, what other forms of MS exist?
``` Primary progressive Secondary progressive Relapsing progressive Benign Spinal fomr Neuromyelitis optica (Devic disease) Marburg variant ```
99
How does benign MS differ from relapsing-remitting MS?
Benign MS marked by episodes of neurological deficit that return to normal in between. Relapsing remitting, early stages are characterised by a return to normal following episodes but as the disease progresses there is incomplete recovery and a gradual decline in function. Late in the disease this becomes more progressive in nature. No such decline is seen in benign MS
100
Which therapeutic drugs are available for MS?
Symptomatic only: muscle relaxants (baclofen, benzodiazepines); short term use of steroids (e.g. methylprednisolone) for reducing inflammatory responses during relapses and analgesics for pain Interferon-beta and glatiramer are licenced for the treatment of relapsing-remitting MS
101
What dietary supplement(s) are suggested to be beneficial to MS patients?
healthy, balanced diet Linoleic acid found in seed oils, nuts and seeds, certain supplements, including evening primrose oil Vitamin D
102
42 yo man admitted to ED suffering paralysis of lower limbs, severe pain in legs and dysphagia. Symptoms came on over 3 days, started out as tingling sensation in legs, weakness and unsteadiness. Two weeks prior - minor cold and tickly throat. Which demyelinating disorder could account for all of the patient’s symptoms?
Guillain barré syndrome
103
What are two main treatments available for Guillain-barré syndrome?
``` IV immunoglobulin (IVIg) plasma exchange (plasmapheresis) ```
104
What are the 2 types of stroke?
Haemorrhagic | Ischaemic

Block 3 AR (8 decks)

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