pt15 Flashcards

(50 cards)

1
Q

What key roles does the thalamus serve?

A

Relays sensory information to cortex, transmits cerebellar/basal nuclei signals to motor cortex, and maintains consciousness

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2
Q

What constitutes the limbic system, and what are its functions?

A

Cortical (limbic lobe) and subcortical (amygdala, hippocampus, some thalamic/hypothalamic nuclei) areas for emotion, behaviour, memory, olfaction, motivation

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3
Q

What are the roles of epinephrine (adrenaline) and norepinephrine?

A

Excitatory neurotransmitters/hormones in the sympathetic “fight-or-flight” stress response

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4
Q

What functions does dopamine perform?

A

Excitatory, inhibitory, and modulatory roles in reward, addiction, motivation, and motor control

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5
Q

What are serotonin’s primary roles?

A

Inhibitory neurotransmitter regulating mood, emotion, appetite, digestion; precursor to melatonin for sleep

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6
Q

What is GABA’s function in the CNS?

A

Primary inhibitory neurotransmitter; regulates anxiety, vision, motor control; low levels cause irritability and anxiety

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7
Q

What role does glutamate play?

A

Most abundant excitatory neurotransmitter; critical for cognitive functions, memory, and learning

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8
Q

What percentage of the population is affected by migraines globally, and how do they rank in years lived with disability?

A

About 15.2% globally; first cause of health loss in women and second overall in years lived with disability

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9
Q

What are the core symptoms of a migraine attack?

A

Moderate to severe headache plus reversible symptoms such as photophobia, phonophobia, cutaneous allodynia, nausea, vertigo, and dizziness

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10
Q

What is a migraine aura and in what proportion of cases does it occur?

A

Transient neurological symptoms (most commonly visual disturbances) lasting 5–60 min, occurring in ~30% of migraines

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11
Q

How can a single-gene mutation cause familial hemiplegic migraine?

A

Mutation in CACNA1A (voltage-dependent Ca²⁺-channel subunit) → cortical hyperexcitability → cortical spreading depression triggering aura

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12
Q

What defines polygenic migraine susceptibility?

A

Interaction of >180 SNPs each conferring low risk, many in genes expressed in vascular and neuronal tissues

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13
Q

What role does the trigeminovascular system play in migraine pathophysiology?

A

Activation releases vasoactive neuropeptides (e.g., CGRP, PACAP, NO) causing meningeal vasodilation, inflammation, and nociceptive signalling

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14
Q

What are the three classes of acute migraine treatments?

A
  • Triptans: 5-HT₁ agonists → vasoconstriction & nociception modulation
  • Ditans: neuronal 5-HT₁F agonists → inhibit trigeminal nociception without vasoconstriction
  • Neuromodulation: non-invasive electrical/magnetic brain stimulation
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15
Q

What types of intracranial haematomas can result from traumatic brain injury (TBI)?

A
  • Epidural: between skull & dura
  • Subdural: between dura & arachnoid
  • Intracerebral: within brain tissue
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16
Q

What are common acute and chronic symptoms of TBI?

A
  • Acute: loss of consciousness, headache, nausea/vomiting, seizures, blurred vision, fatigue
  • Chronic: depression, persistent fatigue, sleep disorders (hypersomnia/insomnia)
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17
Q

How is acute TBI managed, and what long-term rehabilitation may be required?

A
  • Acute: airway/oxygen, control bleeding (surgery), anticonvulsants, diuretics, medically induced coma
  • Rehab: physical, occupational, speech therapy, neuropsychological support
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18
Q

What mechanisms underlie spinal cord injury, and how is injury completeness classified?

A

Vertebral fracture/dislocation compresses/crushes cord → disrupts ascending/descending tracts;
* Complete: no function below lesion
* Incomplete: partial preservation of function

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19
Q

What are major complications of spinal cord injury and its core treatments?

A
  • Complications: chronic pain, respiratory infections, bladder/bowel dysfunction, fractures
  • Treatment: multidisciplinary rehab (physical/occupational therapy, counselling)
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20
Q

How do CNS tumours impair function, and what symptoms do they cause?

A

Mass effect → pressure on adjacent tissue;
* Brain: headaches, seizures, nausea/vomiting, cognitive & behavioural changes, focal deficits
* Spinal: pain, sensory/motor disturbances

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21
Q

What are the principal treatment modalities for CNS tumours?

A

Surgical resection, radiotherapy, chemotherapy (depending on tumour type and location)

22
Q

How is epilepsy defined and classified by seizure onset?

A

Chronic predisposition to recurrent unprovoked seizures;
* Focal: localized onset
* Generalized: bilateral hemispheric onset
* Unknown: onset unclear

23
Q

What are the six etiological categories of epilepsy?

A

Structural, metabolic, immune, infectious, genetic, and unknown causes

24
Q

What therapeutic options exist for epilepsy?

A
  • Antiseizure meds (e.g., sodium valproate, levetiracetam)
  • Surgery for focal epilepsy
  • Neurostimulation: vagus nerve or deep brain stimulators
  • Ketogenic diet
25
What characterizes multiple sclerosis (MS) and its epidemiology?
Autoimmune neuroinflammatory disease → CNS demyelination & neurodegeneration; female > male 3:1
26
What are common presenting symptoms of MS?
Visual disturbances, gait/balance problems, bladder dysfunction, sensory changes (numbness/tingling), spasticity, cognitive impairment
27
What are the main disease-modifying treatments for MS?
* First line: T-cell targeted therapies (reduce cytokines, promote Tregs) * Subsequent: S1P modulators (sequester lymphocytes), monoclonal antibodies, steroids for relapses
28
What underlies narcolepsy, and how prevalent is it?
Loss of orexin (hypocretin) neurons → impaired wakefulness regulation; affects ~0.02–0.05% of population
29
What are the hallmarks of narcolepsy type 1 vs. type 2?
* Type 1: excessive daytime sleepiness, cataplexy, low CSF orexin * Type 2: daytime sleepiness, normal orexin, rare cataplexy
30
How is narcolepsy diagnosed?
* Polysomnography (PSG) to exclude other sleep disorders * Multiple Sleep Latency Test (MSLT): rapid sleep onset and SOREMPs * Epworth Sleepiness Scale
31
What treatments are used for narcolepsy?
* Stimulants: modafinil * SSRIs/SNRIs: suppress REM to reduce cataplexy * Sodium oxybate: GABA_B agonist for cataplexy
32
How is major depressive disorder defined and categorized?
Persistent sadness/loss of interest; DSM-5 subtypes include MDD, dysthymia, PMDD, and depression due to another medical condition
33
What risk factors predispose to late-onset depression?
Neurodegenerative diseases (AD, PD), stroke, MS, seizures, chronic pain, life stressors (bereavement, caregiver burden)
34
What neurotransmitter disturbances are implicated in depression?
Reduced CNS serotonin activity; also involves norepinephrine, dopamine, glutamate, and BDNF; vascular lesions may disrupt mood circuits
35
What DSM-5 criteria are used to diagnose major depression?
≥5 of 9 symptoms (including depressed mood or anhedonia) over 2 weeks, e.g., sleep/appetite changes, fatigue, suicidality
36
What are first- and second-line pharmacotherapies for depression?
* First line: SSRIs (citalopram, fluoxetine) * Second line/add-ons: SNRIs, atypicals (trazodone), TCAs (amitriptyline), MAOIs (with low-tyramine diet)
37
What are key psychotherapies for depression?
* CBT: modifies maladaptive thoughts/behaviours * IPT: targets interpersonal issues (grief, disputes) in time-limited sessions
38
What defines generalized anxiety disorder (GAD)?
Excessive worry ≥6 months, with restlessness, fatigue, concentration problems, irritability, muscle tension, and sleep disturbance
39
What risk factors contribute to GAD?
Childhood behavioral inhibition, early life stressors, family history, medical conditions (thyroid/cardio), caffeine excess
40
What are pharmacological and psychotherapeutic treatments for GAD?
* Pharmacology: SSRIs/SNRIs, benzodiazepines (GABA_A agonists) * Psychotherapy: CBT and other talking therapies
41
How is schizophrenia characterized, and what are its core symptoms?
Chronic psychotic disorder → positive symptoms (hallucinations, delusions), negative symptoms (anhedonia, social withdrawal), cognitive deficits
42
What pathophysiological mechanisms and treatments are involved in schizophrenia?
Genetic, environmental, neurotransmitter (↑ dopamine), neuroinflammation; treated with dopamine-blocking antipsychotics and CBT
43
What is dementia?
A syndrome of progressive decline in brain function causing cognitive impairment and reduced quality of life
44
How common is dementia worldwide and how is its prevalence expected to change?
Currently affects ~55 million people; projected to rise to 139 million by 2050
45
What are the most prevalent types of dementia?
Alzheimer’s disease (≈80 % of cases) and vascular dementia; also Lewy body and frontotemporal dementias
46
What are common symptoms of dementia?
Memory loss, reduced cognition, language/speech difficulties, personality and behavioural changes, sleep disturbance
47
What characterizes Alzheimer’s disease pathologically?
Extracellular β-amyloid plaques, intracellular phosphorylated tau tangles, neuroinflammation, and massive neuronal loss in hippocampus and cortex
48
How is Alzheimer’s disease diagnosed?
Multidisciplinary: medical history, cognitive tests (e.g., s-MMSE), amyloid-PET, CSF biomarkers (Aβ, tau); current methods are costly and invasive
49
Which plasma biomarkers are under investigation for Alzheimer’s?
Aβ₄₀/Aβ₄₂ ratio, p-tau₁₈₁ and p-tau₂₁₇, GFAP, and neurofilament light (NfL)
50
Why is p-tau₂₁₇ a valuable Alzheimer’s biomarker?
Predicts cognitive decline, stratifies patients by risk/severity, and monitors response to disease-modifying therapies