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z Clinical Sciences 2 > Topic 3 Neurological Conditions > Flashcards

Topic 3 Neurological Conditions Flashcards

1
Q

What are neurotransmitters?

A

Chemicals which allow the transmission of signals from one neuron to the next across synapses

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2
Q

What does dopamine do?

A

Critical for memory and motor skills

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3
Q

What does GABA do?

A

Mood modulator - When transmitters are too low these neurons can become excited leading to anxiety and irritability

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4
Q

What does glutamate do?

A

Major mediator of excitatory signals

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5
Q

What does serotonin do?

A

Inhibitor - imbalance is related to depression and sleep disorders

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6
Q

What does ACH do?

A

Excitatory - critical for sleep, attentiveness

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7
Q

What does norepinephrine do?

A

Flight or fight response

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8
Q

What does epinephrine do?

A

Abnormal levels linked to sleep disorders/anxiety

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9
Q

What is neurotransmission?

A

process by which neurotransmitters are released by the axon terminal of a neuron, bind to and activate the receptors on the dendrites of another neuron

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10
Q

Steps of neurotransmission

A

1 - action potential arrives at the axon terminal.
2 - calcium channels open and calcium enters the axon terminal
3 - increase in calcium causes the synaptic vesicles to move to the presynaptic membrane.
4 - neurotransmitter is released using exocytosis.
5 - neurotransmitter diffuses across the synapse and binds with receptors on the postsynaptic neuron

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11
Q

Define delirium

A

Acute transient confusional state of altered LOC, hallucinations and restlessness

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12
Q

Onset of delirium

A

Rapid (2-3 days)

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13
Q

What are the symptoms of delirium?

A 
slurred speech
altered LOC
hallucinations
restlessness
tremor
distress
conversation incoherent
violent
inattentiveness
misperception and misinterpretation
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14
Q

What are the risk factors of delirium?

A 
older age
dementia
severe illness
alcoholism
co-morbidities
vision impairment
hearing impairment
history of delirium
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15
Q

What are the consequences of delirium?

A 
prolonged hospitalisation
functional decline
increased use of restraints
increased mortality
possible development of dementia within two years
need for long term nursing home care
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16
Q

Define dementia

A

Umbrella term for several diseases characterised by progressive cognitive impairment and brain dysfunction not caused by impaired LOC

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17
Q

Onset of dementia

A

Gradual

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18
Q

Symptoms of dementia

A

Loss of memory, intellect, rationality, social skills, physical functioning, orientation and language

Alterations in behaviour and normal functioning
Personality changes
Mood swings
Difficulty recognising family
Manner flat
Aggressive
Decline in ability to perform ADLS
Agnosia
Apraxia
Dysphasia
Expressive dysphasia
Receptive dysphasia
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19
Q

Define alzheimers

A

Devastating condition characterised by progressive memory loss, impaired thinking, neuropsychiatric symptoms, inability to perform routine ADLs and intellectual deterioration interfering with social or occupational function

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20
Q

Stages of alzheimers

A

Mild: apparent in hindsight. Apathetic, lose interest in hobbies, less willing to try new things and adapt, slower to grasp complex ideas

Moderate: problems are more apparent and disabling. Not able to live independently. Forgetful of current or recent events, become lost easily, forget names, neglectful of hygiene or eating

Severe: severely disabled and needs continuous care for all ADL

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21
Q

Risks of alzheimers

A 
Advancing age
Family history
Female
Head injury
Low education level
Production of apoE4
High levels of homocysteine
Low levels of folic acid
Oestrogen/progestin therapy
Sedentary lifestyle
Nicotine in cigarette smoke
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22
Q

Aetiology of alzheimers

A

Cortical atrophy causing loss of memories stored
Increase of glutamate & decrease of ACH
Tau protein introduced and forms neurotic plaques and neurofibrillary tangles

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23
Q

CM of alzheimers

A 
Memory loss 
Confusion
Disoriented
Impaired judgement
Personality changes
Decline in ADLS
Behaviours
Sundowners
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24
Q

Dx of alzheimers

A 
Eliminate other causes
Diagnosis based on history and clinical findings
MMSE
Biomarkers
CT
PET
MRI
Metabolic screening
Genetics
Alzheimer algorithm
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25
Q

Tx of alzheimers

A

Goal of treatment to improve symptoms, no known cure

Cholinesterase inhibitors – prevent the breakdown of ACH by acetylcholinesterase (donepezil, rivastigmine).
NMDA receptor agonist – modulates the effect of glutamate at the NMDA receptor (memantine).
Antipsychotics – for neuropsychiatric symptoms (risperidone, olanzapine).

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26
Q

Aetiology of parkinson’s

A

Exact cause unknown, combination of genetics and environmental factors (exposure to toxins), head trauma, CVA. Degeneration of the basal nuclei. Pathology shows failure of neurons that secrete dopamine. Decreased dopamine results in excess of cholinergic activity

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27
Q

CM of parkinson’s

A 
Gradual, insidious onset. 
Tremor
Rigidity
Bradykinesia
Short shuffling gait
Dysarthria
Dysphagia
Depression
Stooped posture
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28
Q

Dx of parkinson’s

A 
No specific diagnostic tests. 
Based on history and clinical features. 
Two of the triad of symptoms of tremor, rigidity and bradykinesia present. 
SPECT
Olfactory testing.
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29
Q

Tx of parkinson’s

A 
No cure. 
Management of symptoms. 
Medications: Carpidopa/Levodopa, Bromocriptine, apomorphine, amantadine, domperidone. 
Group support
Education
Exercise
Nutrition
DBS
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30
Q

Aetiology of MS

A

A progressive degenerative autoimmune disease characterised by disseminated demyelination of the nerve fibres of the CNS. Unknown cause. Suggested that it is related to infections (viral), immunological and genetic factors. Inflammatory process leads to destruction of myelin forming cells. Permanent disability after 20yrs or more.

Activated T cells penetrate the blood brain barrier (normal) but then inflammatory response initiates and myelin sheath of axons of motor, sensory and autonomic nerves are phagocytosed, with first-stage lesions then second-stage demyelination. Periods of exacerbation, then remission. May be exacerbated by infection, trauma, pregnancy.

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31
Q

CM of MS

A

Insidious and gradual. Varying symptoms over years.

  • first signs -
    paraesthesia, optic disturbances, abnormal sensations in extremities, on one side of the face,
  • early signs -
    muscle weakness, vertigo, and other visual disturbances, such as nystagmus, muscle weakness, vertigo, fatigue, diplopia (double vision), and partial blindness.
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32
Q

Dx of MS

A

Based on history
CM and MRI to detect lesions
Spinal tap (CSF)
CT

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33
Q

Tx of MS

A

No cure, treat symptoms.
Therapy tailored to individual.
Medications: Interferon beta, mitoxantrone, corticosteroids

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34
Q

What is meningitis

A

Inflammation of the pia mater, the arachnoid and the CSF-filled subarachnoid space.

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35
Q

Types of meningitis

A

Acute purulent/BACTERIAL meningitis:

Acute lymphocytic / VIRAL meningitis:

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36
Q

Aetiology of bacterial meningitis

A

Most caused by Neisseria meningitidis (meningococcus) or Streptococcus pneumoniae. Organism gains entry through the upper respiratory tract or bloodstream into the CNS. Inflammatory response increases CSF and moderate increase in ICP.

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37
Q

Aetiology of viral meningitis

A

Most common causes are Herpes Simplex Virus, enterovirus, coxsackievirus, EBV, measles, mumps, & West Nile virus

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38
Q

CM of bacterial meningitis

A 
Fever
Chills
Tachycardia
Headache
N&V
Photophobia 
Nuchal rigidity
Non-blanching petechial or purpuric rash
Abdominal pains
Decreased LOC and coma
Seizures
Death
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39
Q

CM of viral meningitis

A 
Manifests similar to bacterial meningitis
Mild throbbing headache
Mild photophobia
Mild neck pain
Stiffness
Fever 
Malaise
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40
Q

Dx of bacterial meningitis

A 
H&P
Blood cultures
CT scan
Lumbar puncture (CSF)
Sputum & nasopharyngeal specimens for culture
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41
Q

Dx of viral meningitis

A 
H&P, Blood H&P
Blood cultures
CT scan
Lumbar puncture (CSF)
Sputum & nasopharyngeal specimens for culture, CT scan, lumbar puncture (CSF), sputum & nasopharyngeal specimens for culture
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42
Q

Tx of bacterial meningitis

A

Analgesia
IV fluids
Antibiotics - rifampicin, ciprofloxacin, ceftriaxone, corticosteroids

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43
Q

Tx of viral meningitis

A

Usually self-limiting and symptomatic treatment only

HSV type 2 requires antiviral drug treatment: acyclovir

44
Q

What is encephalitis

A

Acute inflammation of the parenchyma of the brain. Serious, sometimes fatal disease.

45
Q

Aetiology of encephalitis

A

Epidemic which are transmitted by ticks or mosquitoes

Non-epidemic which occurs as a complication of measles, chicken-pox or mumps

46
Q

CM of encephalitis

A 
Non-specific
Fever
Headache
N&V
Confusion
Lethargy
Disorientation
Seizures
Focal paralysis
Delirium
Cushing’s triad (hypertension, bradycardia, irregular breathing)
Coma
47
Q

Dx of encephalitis

A 
H&P
CT
EEG
MRI
PET
IgM antibodies to virus in serum or CSF
48
Q

Tx of encephalitis

A

Patients usually require intensive care
Measures to control intracranial pressure and ventilation
Encephalitis due to HSV or varicella zoster virus treated with antiviral, acyclovir

49
Q

Outline focal brain injury

A

Force of impact causes contusions. Results from compression of skull at point of impact and rebound effect. Impact against object or within skull.

50
Q

Outline diffuse brain injury

A

Result from shaking effect caused by high levels of acceleration or deceleration. Produces strains and distortions within the brain. Can cause irreparable cognitive impairment

51
Q

Outline hypoxic brain injury

A

Deprivation of oxygen with maintained blood flow

52
Q

Outline excitotoxic brain injury

A

During prolonged ischemia excess glutamate is outside cell causing ion channels to remain open and over exciting brain cells. Higher energy and oxygen consumption drives uncontrolled opening of other channels. Excessive influx of Na into cells draws water in to cells. Na/Ca pump fails due to ATP deficiency, ↑Ca in cells causes auto digestion from activated enzymes. Anaerobic metabolism with glycogen instead of glucose. Death of cerebral cells in the micro neurones responsible for higher order brain function.

53
Q

Outline intracranial pressure

A

When CPP slows and ICP increases brain tissue experiences severe hypoxia, if ICP is not evenly distributed throughout the cranial vault compartments the brain tissue moves to a compartment of lesser pressure (herniation).

54
Q

Outline cerebral oedema

A

Increase in brain tissue volume due to abnormal fluid accumulation. Occurs after brain insult: trauma, infection, haemorrhage, tumour, ischaemia, infarct or hypoxia. CM vary: little early compensation, as ICP increases: headache, nausea and vomiting, decreased LOC, coma, pupillary changes.

55
Q

Outline ischaemic brain injury

A

Reduced or interrupted blood flow

56
Q

What is ischaemia

A

Situation of reduced or interrupted blood flow

57
Q

Types of ischaemia

A

Focal Ischaemia

Global Ischaemia

58
Q

What is focal ischaemia

A

Only a region of the brain is under-perfused
Collateral circulation provides blood flow to the borders of the focal ischaemic region
Maintains a low level of metabolic activity, preserving membrane integrity.
Interruption of glucose delivery results in depletion of ATP & increased lactic acid production

59
Q

What is global ischaemia

A

Cardiac arrest is global and causes loss of glutamate and Na K pump
Blood flow to entire brain is compromised and is inadequate to meet the metabolic needs of the entire brain
Unconsciousness occurs within seconds when severe
If cerebral circulation restored immediately, consciousness is regained quickly.

60
Q

CM of ischaemia

A

Acidosis (no removal of wastes)

61
Q

Three components which occupy the cranial vault

A

Blood (10%)
Brain tissue (80%)
CSF (10%)

62
Q

Normal ICP

A

5-15 mmHg

63
Q

CM of raised ICP

A 
Headache
Nausea
Vomiting
Increased blood pressure
Decreased mental abilities
Confusionabout time, then location and people as the pressure worsens
Double vision
Unresponsive pupils 
Shallow breathing
Seizures
Loss of consciousness
Coma
64
Q

Dx of raised ICP

A

Assess BP and pupils
Lumbar puncture
CT
MRI

65
Q

Tx of raised ICP

A

Frusemide
Acetazolamide
Mannitol

66
Q

What is the Monro-Kellie Hypothesis

A

Relationship between Blood, Brain & CSF.

When small increase in one occur, the other two must reduce sufficiently to maintain stable ICP.

67
Q

What is cerebral oedema

A

Increase in the fluid content of the brain.

68
Q

Types of cerebral oedema

A

Vasogenic
Cytotoxic
Ischemic
Interstitial

69
Q

What is vasogenic cerebral oedema

A

Caused by increased permeability of the capillary endothelium (BBB) of the brain after injury

70
Q

What is cytotoxic cerebral oedema

A

Toxic factors directly affect the cellular elements of the brain parenchyma, causing failure of the active transport systems (cells loose potassium, gain sodium and water = swell). Common causes are hypoxic and ischaemic injury

71
Q

What is ischemic cerebral oedema

A

Follows cerebral infarction (stroke). Components of both Vasogenic & Cytotxic oedema. Initially confined to the intracellular compartment, then brain cells necrose and release lysosomes = autodigestion. BBB permeability increases = oedema

72
Q

What is interstitial cerebral oedema

A

Most often with non-communicating hydrocephalus. Oedema caused by CSF shifting into extracellular spaces. Fluid volume increases, compresses white matter, causes rapid disappearance of myelin lipids.

73
Q

CM of cerebral oedema

A 
Headache
Neck painor stiffness
Nauseaorvomiting
Dizziness
Irregular breathing
Vision lossor changes
Memory loss
Inability to walk
Difficulty speaking
Stupor
Seizures
Loss of consciousness
74
Q

Dx of cerebral oedema

A 
Head and neck exam
Neurologic exam
CT
MRI
Blood tests
75
Q

Tx of cerebral oedema

A

Treat the cause

Localised swelling: dexamethasone.

Osmotic diuretics useful for acute vasogenic and cytotoxic oedema

76
Q

What is hydrocephalus

A

Various conditions characterised by excess fluid in the cranial vault or sub-arachnoid space.

77
Q

Types of hydrocephalus

A

Communicating: Impaired absorption of CSF within sub-arachnoid space. More often in adults.

Non-Communicating: Obstruction of CSF flow between ventricles. More often in children.

78
Q

CM of hydrocephalus

A
  • Acute Hydrocephalus - Rapidly increasing ICP
    Coma.
- Normal P hydrocephalus -
Memory and cognitive decline
Unsteady, broad-based gait
Falls
Apathy
Inattentiveness
Indifference
Urinary incontinence
79
Q

Dx of hydrocephalus

A

H&P
CT
MRI

80
Q

Tx of hydrocephalus

A

Surgical - surgery of cysts, tumours, haematomas, bypass; Ventriculo-peritoneal (VP) Shunt, Ventriculo-atrial (VA) Shunt.

Diuretics for normal pressure hydrocephalus.

81
Q

What is epilepsy

A

Disorder in which nerve cell activity in the brain is disturbed causing seizures. Recurrent without underlying correctable cause

82
Q

What is a seizure

A

Sudden, transient alteration of brain function caused by an abrupt explosive, disorderly discharge of cerebral neurons

83
Q

Types of seizures

A 
Partial/Focal Seizures
Myoclonic
Tonic-Clonic
Tonic
Atonic
84
Q

What is a partial/focal seizure

A

Only portion of the brain. Most common. Subtle, confusional conscious state

85
Q

What is a myoclonic seizure

A

Brief muscle jerks usually involving one or a group of muscles. No LOC, may fall or drop item

86
Q

What is a tonic clonic seizure

A

LOC, body stiffens (tonic) rapidly followed by jerking limbs (clonic). Lasts 2-3mins. Accompanied by confusion, lethargy after convulsions cease.

87
Q

What is a tonic seizure

A

Increase in muscle tone and stiffening of body. Injury if fall

88
Q

What is an atonic seizure

A

Loss of muscle tone, fall. No LOC, rapid recovery

89
Q

Aetiology of seizures

A

Cerebral lesions, biochemical disorders, cerebral trauma, fever, drug or alcohol abuse, infection, postnatal trauma, congenital malformations

90
Q

Dx of seizures

A 
H&P
Lab/blood tests
Urine
CT
MRI
CSF
EEG
91
Q

Tx of seizures

A

Correcting the cause
Counselling

Anti-epileptic medications: phenytoin, carbamazepine, valproic acid or valproate, benzodiazepines, oxcarbazepine, gabapentin

92
Q

What is a stroke

A

Damage to the brain from interruption of its blood supply.

93
Q

Types of strokes

A

Ischaemic

Hemorrhagic

94
Q

What is an ischaemic stroke

A

Thrombotic and embolic stroke. Arterial occlusions caused by thrombi formed in arteries supplying the brain or in intracranial vessels. Include TIAs and Lacunar Infarcts. 80% of strokes

95
Q

What is a hemorrhagic stroke

A

Intracerebral or subarachnoid haemorrhage. Ruptured blood vessel in the brain

96
Q

CM of ischaemic stroke

A 
Hemiparesis
Hemianopia (blindness in 1 eye)
Weakness 
Unilateral numbness
Language disturbance (aphasia)
Slurred speech (dysarthria)
Sudden unexplained imbalance or ataxia
97
Q

CM of hemorrhagic stroke

A 
Headache
N&V
Unilateral weakness
Numbness
Tingling
Speech and visual disturbances
Motor deficits
LOC due to raised ICP
98
Q

Dx of ischaemic stroke

A 
H&P
CT scan
MRI
Angiography
Lumbar puncture
99
Q

Dx of hemorrhagic stroke

A 
H&P
CT scan
MRI
Angiography
Lumbar puncture
100
Q

Tx of ischaemic stroke

A

Supportive
Maintain cerebral perfusion
Thrombolysis

Anticoagulants: warfarin, heparin, tPA thrombolytic drugs

101
Q

Tx of hemorrhagic stroke

A

Supportive
Control ICP
Prevent ischemia and hypoxia.

Diuretics: frusemide, mannitol
Anti-hypertensives.

102
Q

Risks of stroke

A 
Increasing age
Sex
Race
Family history
Hypertension
Smoking
Poorly controlled diabetes (atherosclerosis)
Carotid stenosis
Sickle cell disease
Hyperlipidaemia
Atrial fibrillation
103
Q

What is brain trauma

A

Traumatic insult to the brain possibly producing physical, intellectual, emotional, social and vocational changes

104
Q

Types of brain trauma

A

Open trauma: Causes primarily focal injuries

Closed trauma: Causes haematoma and focal (local) or diffuse (general) brain injuries

105
Q

Types of diffuse brain injury

A

mild concussion: immediate but temporary CM. Confusions (1-7mins), amnesia, headache. No LOC

classical concussion: LOC up to 6hrs, reflexes fail. Breathing ceases, low HR and BP then stabilise. Amnesia, confusional state (hrs – days), head pain, nausea, fatigue, attention and memory deficits, mood changes.

diffuse axonal injuries: Prolonged traumatic coma (>6hrs)
Mild: Post-traumatic coma 6-24hrs, residual deficits
Moderate: Widespread physiological impairment, prolonged coma (>24hrs) incomplete recovery.
Severe: Brainstem contusion

z Clinical Sciences 2 (5 decks)

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