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Clinical disorders > Clinical Disorders > Flashcards

Clinical Disorders Flashcards

1
Q

What are some of the risk factors of Parkinson’s disease?

A

Male sex
Antipsychotics
Genetics
Stroke
Old age

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2
Q

What three symptoms make up the general symptom of Parkinsonism?

A

Bradykinesia
Rigidity
Tremor

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3
Q

What symptoms are associated with Parkinson’s Disease?

A

Parkinsonism
Psychiatric/cognitive
Physical e.g. balance/dizziness

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4
Q

What are the two hypotheses for the development of Parkinson’s Disease?

A

Loss of dopamine in the basal ganglia

Lewy bodies blocking dopamine in the brain

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5
Q

What symptom, along with one of the following is needed for a Parkinson’s Disease diagnosis?
Tremor
Stiffness/rigidity
Balance issues/falls

A

Bradykinesia (slow movements)

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6
Q

What would functional imaging show, when scanning patients with Parkinson’s Disease?

A

Decreased dopamine uptake

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7
Q

What pharmacological treatment is available for Parkinson’s patients, and what does it do?

A

Dopamine agonists
e.g. Carbidopa and Levodopa

Also may be prescribed MAO-inhibitors (anti-depressants)

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8
Q

What non-pharmacological treatment may be offered to Parkinson’s patients?

A

Deep brain stimulation to control movements

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9
Q

What two areas might DBS be inserted into, in Parkinson’s patients?

A

Subthalamic nucleus or the globes pallidus interna

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10
Q

What symptoms might show, when a patient has a brain tumour?

A

Headache
Raised intercranial pressure
Eye problems
Seizures
Dizziness
Different presentation depending on where the tumour is

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11
Q

What might cause brain tumour symptoms?

A

Extra pressure, due to the mass

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12
Q

How are brain tumours graded?

A

1-4
1 - benign and cured easily
4 - malignant and not cured very easily

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13
Q

What is chemotherapy, and what risks are associated?

A

Kills the cancer cells

Can lead to hair loss, infection, etc…

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14
Q

What are immune checkpoint inhibitors in brain tumour management?

A

Allow T cells to kill the cancer cells

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15
Q

What do targeted therapies target, in brain tumour management?

A

Targets specific chemical in the tumour

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16
Q

What non-pharmacological approaches are used for the management of brain tumours?

A

Surgery to remove the tumour
Radiation to kill cancer cells
Radiation surgery

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17
Q

What risk factors are associated with the development of Alzheimer’s disease?

A

Age over 40
Social factors e.g. poorer education and social isolation
Hypertension
Diabetes

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18
Q

What three deficits are associated with Alzheimer’s disease?

A

Memory (episodic)
Visuospatial (disorientation)
Language (no fluidity in speech)

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19
Q

What two pathophysiological causes are associated with Alzheimer’s disease?

A

Amyloid plaques and Tau tangles

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20
Q

How can amyloid cause Alzheimer’s disease?

A

Overproduction of plaques building up in memory areas

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21
Q

How can tau cause Alzheimer’s disease?

A

Clumps of tau builds up in neurones

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22
Q

What pharmacological therapies are associated with Alzheimer’s?

A

Amyloid lowering therapy
Anti-tau therapies

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23
Q

What non-pharmacological management strategies are used in Alzheimer’s disease?

A

Supportive therapy and environmental controls

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24
Q

How does vascular dementia present?

A

Cognitive issues e.g. slowing and planning issues

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25
Q

What causes vascular dementia?

A

Blood flow reduction, potentially due to small vessel disease or stroke, etc…

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26
Q

How does frontotemporal dementia present?

A

Behaviour changes
Language issues
Cognitive problems
Physical and social isolation

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27
Q

What causes frontotemporal dementia?

A

Neurodegeneration of the temporal/frontal lobes, potentially due to tau build up
Genetics

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28
Q

What percentage of frontotemporal dementia is genetic?

A

30%

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29
Q

How does dementia with Lewy bodies present?

A

Fluctuations in symptoms e.g. memory and cognitive
Hallucinations
Motor symptoms e.g. parkinsonism

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30
Q

What causes Lewy body dementia?

A

Lewy bodies build up in the brain cells

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31
Q

What symptoms are shown in delirium?

A

Cognitive problems
Hallucinations (auditory)
Physical issues
Social withdrawal and lack of cooperation

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32
Q

What are the two types of delirium?

A

Hypo and hyperactive delirium

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33
Q

What risk factors are associated with delirium?

A

Old age, neurocognitive deficit, ICU, psychosocial drugs

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34
Q

What 5 criteria are needed for a diagnosis of delirium?

A

Disturbed attention or awareness
Rapid development
Cognitive disturbance
No better explanation
Evidence of a general medical condition

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35
Q

What may cause encephalopathy?

A

Illness, vitamin B1 deficiency, or hepatic insufficiency

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36
Q

What risk factors are associated with Huntington’s disease?

A

Ages 35-45
Genetics

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37
Q

What symptoms are shown in Huntington’s disease?

A

Movement issues
Cognitive issues
Emotional issues
Metabolic issues e.g. weight loss and speech problems

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38
Q

What two things cause Huntington’s disease?

A

Genetics
Neurodegeneration

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39
Q

What mode of inheritance is Huntington’s disease?

A

Autosomal dominant

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40
Q

How many CAG repeats are needed for Huntington’s disease to be present?

A

Over 40 CAG repeats

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41
Q

What area is particularly impacted by neurodegeneration in Huntington’s disease?

A

The striatum

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42
Q

What two investigations can be done to diagnose Huntington’s disease?

A

CAG repeat testing
Imaging showing striatal atrophy

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43
Q

In Huntington’s disease management, what is Tetravebazine’s mechanism of action?

A

Inhibits dopamine 2, serotonin and norepinephrine

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44
Q

What non-pharmacological management can be used to treat Huntington’s disease?

A

Physiotherapy
Occupational therapy
Social support
Cognitive and behavioural support

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45
Q

What risk factors may lead to stroke?

A

Hypertension, smoking, diabetes, lifestyle, old age

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46
Q

What symptoms can a cortical stroke lead to?

A

Cognitive problems

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47
Q

What symptoms can a sub-cortical stroke lead to?

A

Patient is alert, but paralysed

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48
Q

What symptoms can a brainstem stroke lead to?

A

Unsteady, complications e.g. locked in syndrome, quadriplegic

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49
Q

What is the cause of an ischemic stroke?

A

Blocked artery, leading to reduced blood flow and oxygen to the brain

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50
Q

What four things may lead to blocked arteries, causing an ischemic stroke?

A

Atheroma
Thrombosis
Embolism
Heart attack

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51
Q

What is an embolism?

A

Clot breaks off and blocks another area

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52
Q

What is atheroma?

A

Fatty material build up in the arteries

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53
Q

What causes a brain haemorrhage?

A

Vessels rupture, leading to a brain blood, due to high blood pressure

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54
Q

Where would an intracerebral haemorrhage be?

A

Bleeding in or around the brain

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55
Q

Where would a subarachnoid haemorrhage be?

A

Bleeding in the space around the brain

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56
Q

How can a cerebral vein lead to a haemorrhage?

A

Blocked vein leads to back pressure and no blood flow, may also lead to seeping

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57
Q

What causes an aneurysm?

A

High blood pressure means vessels burst

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58
Q

What are the two types of aneurysm?

A

Fistula and cavanova

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59
Q

What is a fistula aneurysm?

A

When blood goes from high to low pressure

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60
Q

What is a cavanova aneurysm?

A

Vessel seep slightly

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61
Q

What is a lacunar syndrome?

A

Small subcortical lesion caused by a blocked artery

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62
Q

What may cause lacunar syndromes?

A

Small vessel disease
Stroke
Ataxia
Pure motor
Dyatheria clumsy hand syndrome

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63
Q

What three things might cause a cardiogenic stroke?

A

Heart doesn’t beat properly
Patent foramen ovale (hole in heart doesn’t close and clot travels to other side of the heart)
Myocardial infarction (heart attack leads to decreased blood flow)

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64
Q

What three tests are used in the investigation of stroke?

A

NIH stroke score
Modified Rankin score
Imaging

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65
Q

What pharmacological management is used for the treatment of stroke?

A

Thrombosis (alteplase)

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66
Q

How does thrombosis work?

A

Dissolves blood clots and prevents new clots, plasminogen to plasmin

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67
Q

When is the use of thrombosis suitable?

A

Up to 9 hours after the stroke
Strokes with a small core and large perfusion lesion

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68
Q

What is an MR tissue clock in stroke investigation?

A

If the stroke is seen on diffusion, but not FLAIR or T2 MRI, the stroke happened under 4 hours before

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69
Q

What is the main drug used for thrombolysis in stroke management?

A

Alteplase

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70
Q

What is a thrombectomy in stroke management?

A

Catheter is used to pull the clot out from the groin

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71
Q

When is thromobectomy suitable for stroke management?

A

When the stroke happened up to 24 hours before, with a small/medium core, and a large perfusion area

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72
Q

What symptoms are show in coma patients?

A

Unresponsiveness and unarousableness

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73
Q

When symptoms are show when a patient is in a vegetative state?

A

Wakefulness, but no awareness

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74
Q

What symptoms are show when a patient is in a minimally conscious state?

A

Very altered consciousness, some awareness, and some interaction with the environment

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75
Q

What might cause altered levels of consciousness?

A

Sleep wake cycle nuclei damage
Reticular activating system damage
The cortex damage

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76
Q

On the JFK coma recovery scale, what score suggests a patient is in a minimally conscious state?

A

A score of above 10

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77
Q

What does the Wessex head injury scale measure?

A

Responsiveness and interaction with the environment providing a scale outcome of different sensory modalities

78
Q

What three responses does the Glasgow coma score measure?

A

Eye opening
Verbal
Motor

79
Q

What score is the worst on the Glasgow coma scale?

A

A score of 3

80
Q

What is imaging used to find in patients with a disorder of consciousness

A

Regional changes in blood flow and metabolism
Rule out seizures and look for a sleep wake cycle

81
Q

What is a mild TBI defined as on the mayo criteria?

A

Unconsciousness for 0-30 mins
Anterograde amnesia
GCS 13-15

82
Q

What is a moderate TBI defined as on the mayo criteria?

A

Unconscious for 30mins to 24 hours, GCS of 9-12

83
Q

What is a severe TBI defined as on the mayo criteria?

A

Unconscious for over 24 hours, GCS of 9 or under

84
Q

What is a symptomatic TBI?

A

Shows some symptoms of a TBI e.g. visual issues and confusion

85
Q

What two urgent assessments are needed when treating a TBI?

A

Check for swelling
Check for intercranial haemorrhage

86
Q

When would you need to do a head CT on a TBI patient?

A

If they lost consciousness, are old, have vomited more than once, have had seizures or lost sensorium

87
Q

If a TBI patient doesn’t need a head CT, high GCS, and no focal neurology, how long should they be observed for?

A

6-8 hours

88
Q

What two non-pharmacological treatments are used for TBI management?

A

Craniotomy or Burr holes

89
Q

How can a craniotomy treat a TBI?

A

Sucks out the haematoma/blood

90
Q

How can burr holes treat a TBI?

A

Small holes are made in the skull to relieve pressure

91
Q

What are the signs of raised inter cranial pressure?

A

Headache
Nausea/vomiting
Vision issues
Cushing reflex

92
Q

What is the Cushing reflex?

A

A sign of raised inter cranial pressure
High blood pressure
Decreased respiration
Bradycardia

93
Q

What theory suggests that raised pressure in the skull is due to one of the contents of there brain pushing into an area?

A

Monroe-Kellie doctrine

94
Q

What might cause an intraparenchymal haemorrhage?

A

Hypertension or tumour

95
Q

What symptoms may be caused by an intraparenchymal haemorrhage?

A

Headache
Nausea/vomiting
Reduced conscious level
Agitation

96
Q

What symptoms are shown when a patient has a subarachnoid haemorrhage?

A

Sudden onset of a ‘thunderclap headache’
Meningism (nausea, photophobia)
Reduced consciousness
3rd/6th nerve palsy
Vasospasm

97
Q

What type of brain injury might cause a subarachnoid haemorrhage?

A

Traumatic or non-traumatic head injury

98
Q

When investigating a subarachnoid haemorrhage, what will CSF fluid look like, if this is what the patient has suffered with?

A

Blood in the CSF
Yellow CSF after 12 hours (blood breakdown products)

99
Q

What might cause a subdural haemorrhage?

A

Ruptured bridging veins

100
Q

What might cause an epidural haemorrhage?

A

Ruptured meningeal artery

101
Q

What symptoms might show after diffuse axonal injury?

A

Coma/vegetive state
Agitation
Varied cognitive dysfunction

102
Q

What causes diffuse axonal injury?

A

Shearing injury due to an acceleration, deceleration insult

103
Q

What symptoms does post traumatic amnesia lead to?

A

Psychiatric problems
Disruption of normal conscious level
Disorientation
Anterograde amnesia

104
Q

What test is done on TBI patients to test if they have post-traumatic amnesia?

A

The Westmead scale

105
Q

What amplitude would a normal awake adult’s EEG show?

A

10-100

106
Q

Interictal epileptic discharges suggest what diagnosis?

A

Epilepsy

107
Q

What causes epileptic activity on an EEG?

A

Paroxysmal depolarising shift, leading to neurones firing in bursts of action potentials caused by a large shift of membrane potential

108
Q

How do generalised seizures show on an EEG?

A

Bilateral, symmetrical and synchronised, spike/polyspike-and-wave discharges

109
Q

What is bipolar EEG?

A

Localisation by phase reversal

110
Q

What is referential EEG?

A

Localisation by highest amplitude

111
Q

What is epileptogenesis?

A

Changes in brain regions, leading tissue to generate spontaneous seizures

112
Q

What main differences are there between an epileptic and syncope seizure?

A

Confused after an epileptic seizure
Syncope lasts seconds, not minuets
Sheldon questionnaire (below 1 = epilepsy, above 1 = syncope)

113
Q

What three things are needed for a diagnosis of epilepsy?

A

2 unprovoked seizures, 24 hours apart
Or, 1 seizure, but have had a stroke/EEG activity shows epilepsy changes
Or certain symptoms, leading to a syndromic diagnosis

114
Q

What is vagal nerve stimulation, as a treatment for epilepsy?

A

Stimulate the vagal nerve with electrical impulses to prevent irregular brain activity

115
Q

What causes syncope seizures?

A

Loss of blood/oxygen to the brain temporarily

116
Q

What are generalised convulsive status epilepticus?

A

Last over 30 mins
Or, continuous seizures for 30 mins or more, without regained consciousness between seizures

117
Q

What might cause generalised convulsive status epilepticus?

A

Fever (between 6 months and 6 years old)
Meningitis

118
Q

What pharmacological treatment is used to treat epilepsy?

A

Anticonvulsants e.g. sodium valporate

119
Q

What is the mechanism of action of sodium valporate?

A

Alters electrical activity by affecting ion channels/neurotransmission (GABA/glutamate)

120
Q

What should be given to stop a seizure that has lasted over 5 mins?

A

Benzodiazapines e.g. buccal midazolam to increase GABA

121
Q

What ages are susceptible to infective encephalitis?

A

Below 1 and about 65

122
Q

What symptoms might be caused by infective encephalitis?

A

Fever
Headache
Neck stiffness
Cognitive issues
Seizures

123
Q

What virus is most likely to cause encephalitis?

A

HSV (usually HSV 1)

124
Q

How does the HSV virus lead to encephalitis?

A

Migrates to either the trigeminal ganglia or the olfactory bulb, replicates again and stays latent until it reactivates and causes an acute infection of the brain

125
Q

If a patient has infective encephalitis, what would they lumbar puncture show?

A

Increased white blood cell count

126
Q

What pharmacological treatment is given to patients with infective encephalitis?

A

Antivirals e.g. acyclovir to prevent the spread of infection

127
Q

What symptoms can autoimmune encephalitis lead to?

A

Neuropsychiatric problems
Limbic issues

128
Q

What is a common symptom of LGI-1 encephalitis?

A

Faciobrachial dystonic seizures

129
Q

What are common symptoms of NMDA encephalitis?

A

Hallucinations, delusions, and flu symptoms

130
Q

What is paraneoplastic encephalitis?

A

Antibodies causing encephalitis, due to T cells attacking cancer, leading to neuronal loss/prevention of signalling

131
Q

How does the breakdown of LGI-1 lead to encephalitis?

A

Antibodies break the connection between ADAM22 and ADAM23 molecules

132
Q

How does the breakdown of NMDA receptors lead to encephalitis?

A

Leads to irregular signalling between the pre and post synaptic neurones

133
Q

How do corticoid steroids treat autoimmune encephalitis?

A

Anti-inflammatories that bind to and reduce glucocorticoid

134
Q

What is plasma exchange?

A

Purified plasma is taken from donors and transferred into autoimmune patients

135
Q

What is intravenous immunoglobin?

A

A patient’s own blood is taken and purified and transferred back into themselves

136
Q

What symptoms may be caused by guillian-barre syndrome?

A

Progressive weakness of the arms or legs
Loss of reflexes

137
Q

What causes autoimmune neuropathies?

A

Antibodies bind to myeline and injure the nerves, causing weakness

138
Q

What is conduction block usually caused by?

A

Disruption to the myeline sheath

139
Q

What causes vasculitis neuropathy?

A

Inflammatory destruction of nerve blood vessels

140
Q

What symptoms can vasculitis neuropathy lead to?

A

Motor and sensory pain and progressive weakness

141
Q

How does myasthenia gravis present?

A

Weakness and fatigue of muscles
Visual issues
Slurred speech and swallowing problems
Fluctuating symptoms throughout the day

142
Q

What causes myasthenia gravis?

A

B cell mediated antibodies attack the acetylcholine receptor or cancer

143
Q

What symptoms does Lambert-Eaton lead to?

A

Weakness of proximal muscles
Autonomic symptoms
Absent tendon reflexes

144
Q

What causes Lambert-Eaton?

A

Antibodies attack voltage gated calcium channels at the neuromuscular junction or cancer

145
Q

What pharmacological treatment is given to patients with Lambert-Eaton, and what does it do?

A

Amifampridine to increase the release of acetylcholine at nerve endings

146
Q

What are the risk factors of multiple sclerosis?

A

Female sex, age 20-40, family history, northern latitude

147
Q

What symptoms does multiple sclerosis lead to?

A

Dysfunction, fatigue, numbness, balance issues, relapses, progression

148
Q

What causes multiple sclerosis?

A

Inflammation leading to loss of nerve cells (T and B cells)

149
Q

What does gadolinium enhancement show in multiple sclerosis patients?

A

Identifies blood brain barrier disturbance

150
Q

What does the McDonald criteria state is needed for a multiple sclerosis diagnosis?

A

1 year of disease progression
plus either, DIS in the brain, spinal cord, or positive CSF

151
Q

How many oligological bands are present in multiple sclerosis patient’s CSF?

A

Two or more

152
Q

What do beta-interferons do for multiple sclerosis?

A

Prevent T cells, and reduce inflammation by binding to interferon alpha/beta receptor 1

153
Q

What can cause neuropathic pain?

A

Lesion of the somatosensory system, neurological disorders, diabetes, chemo

154
Q

What is the visual analogue scale?

A

Measures pain intensity

155
Q

What is the main investigation for neuropathic pain?

A

History and examination

156
Q

What is the brief pain inventory?

A

Measures how much pain interferes with everyday life

157
Q

What pharmacological treatments can be used for the management of neuropathic pain?

A

Amitriptyline, duloxetine, gabapentin or pregabalin

158
Q

What are the risk factors for migraine?

A

Female sex
Obesity
Family history
Stressful life events

159
Q

What symptoms might be caused by migraine?

A

Headache (throbbing)
Nausea
Movement aggravated
Aura
Pre or post-dromal phases

160
Q

What causes trigeminal nerve pain?

A

Inflammation of the trigeminal nerve leads to the innovation of large vessels and meninges in the brain
leads to the release of peptides and non painful stimuli appearing painful

161
Q

What is the cause of aura in a migraine?

A

A depressed wave of cortical activity over the cortex

162
Q

What defines episodic and chronic migraines?

A

Episodic - fewer than 15 days of attacks a month
Chronic - headaches for 15 days or more a month

163
Q

What pharmacological treatment can be used for the management of migraines?

A

Triptins to prevent nociceptive neurotransmission

164
Q

What non-pharmacological treatments are suggested for patients with migraines?

A

Lifestyle e.g. good sleep, exercise, and stress reduction
Botox

165
Q

How do TAC headaches present?

A

One sided headaches
Red eyes, sweating, pain around the eyes
Pain doesn’t spread

166
Q

How do tension type headaches present?

A

Pressing pain
Bilateral

167
Q

How do cluster headaches present?

A

Severe unilateral pain
Restlessness
Pain in bouts or clusters

168
Q

How do paroxysmal hemicranias present?

A

Sudden onset
Unilateral attacks

169
Q

What symptoms might inter cranial pressure disorder lead to?

A

Headache (worse in the morning)
Aggravated by coughing or sneezing
Visual issues
Pulsatile tinnitus

170
Q

What might cause inter cranial pressure disorder?

A

Raised inter cranial pressure

171
Q

What would be shown on an MRI in a patient with raised inter cranial pressure disorder?

A

Sagging or a collection of subdural haemorrhage

172
Q

What non-pharmacological management might be given to patients with inter cranial pressure disorder?

A

Surgery to drain CSF
Weight loss

173
Q

What makes functional seizures different to epileptic seizures?

A

Last longer
Seizure changes as you observe it
Asynchronous movements
Pelvic thrusting
Head movements
Able to recall/responsive afterwards

174
Q

How do functional seizures show on EEG?

A

Don’t have epileptic activity

175
Q

What are the biopsychosocial causes of FND?

A

Biological - illness, disease, hyper mobility, physical event
Psychological issues
Social neglect

176
Q

How does predictive processing lead to FND?

A

Bottom up processing is overridden by background knowledge, so symptoms dampen when attention is redirected

177
Q

What treatment is offered to patients with FND?

A

Botox for jerking movements
MDC
Physio
CBT

178
Q

What is the DSM-5 criteria for depression?

A

Depressive mood
5 or more symptoms
Most of the day, everyday for 2 weeks or more
Impaired functioning

179
Q

What is psychotic depression?

A

Distortion of reality and delsuions/hallucinations

180
Q

What might cause mania?

A

Genetics
Immune dysregulation
White matter abnormalities
Limbic network damage
Neurotransmitter signal changes

181
Q

What defines bipolar disorders 1 and 2?

A

BP1 - at least 1 manic episode
BP2 - hypomania and depression

182
Q

What is cyclothymic disorder?

A

Continuous mood disorder for over 2 years, but not severe enough to be depression or BP

183
Q

What defines primary and secondary psychosis?

A

Primary - schizophrenia and mood disorders
Secondary - developmental, degenerative, and acquired conditions

184
Q

What is the cause of positive and negative symptoms in schizophrenia?

A

Positive - excess of dopamine
Negative - shortage of dopamine

185
Q

How do tricyclic acids work?

A

Block the reuptake of serotonin, norepinephrine, and dopamine

186
Q

What symptoms might be caused by myotonic dystrophy?

A

Foot drop, weak grip, cognition, frontal balding, high testosterone, cataracts

187
Q

What causes myotonic dystrophy?

A

Genetics (CGT repeats)

188
Q

What is the genetic inheritance of Duchenne’s?

A

X-linked

189
Q

What three things might cause neuropathies?

A

Hereditory
Metabolism/toxins
Autoimmune

190
Q

What symptoms are caused by motor neurone disease?

A

Bulbar, limb, respiratory, cognitive, progression, upper and lower motor dysfunction

191
Q

What three things might cause motor neurone disease?

A

Genetics
Glutamate
Neuroinflammation

192
Q

What is the Goldcoast criteria for motor neurone disease?

A

Progressive
Upper and lower motor neurone involvement (or 2 lower regions)
Exclusion of other disorders

Clinical disorders (2 decks)

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