Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MSK > Nero WK 6 > Flashcards

Nero WK 6 Flashcards

(51 cards)

Start Studying
1
Q

Describe the basic structure and function of the components of the limbic system

A

Hippocampus - memory and spatial nav

Olfactory bulb - interprets smell

Hypothalamus - regulates drive: hunger, thirst, sleep

Amygdala - emotion: fear and aggression

Thalamus - relay station

Fornix - connects the hippocampus to other parts

Mamillary Bodies - spatial memory, memory consolidation

Limbic Lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Limbic Lobe components

A

Cingulate gyrus - emotional regulation, DM and pain processing
Parahippocampal gyrus - memory encoding and retrieval
Medial orbitofrontal gyri - DM, social behaviour
Uncus - olfactory and memory processing
Temporal poles - semantic memory
Anterior insular cortex - emotion and empathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Papez Circuit in memory

A

Hippocampal formation –> Via Fornix –> Mamillary Bodies –> via mammillothalamic tract –> Ant. Thalamus –> Int. Capsual –> Via cingulum –> cingulate gyrus –> parahippocampal formation (entorhinal cortex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Anatomy of the fornix

A

Fimbra –> from hippocampal formation
Crura –> legs
Body –> midline
Columns –> anterior and downward curves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Location of Amygdala and function

A

Basolateral nuclei = multimodal sensory input
Cortiomedial nuclei = related to hunger (drives hypothalamus)
Central nucleus = ANs control and emotional response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Learning v Memory

A

learning = acquisition of knowledge or skill leading to changes in behaviour/ attitudes and capabilities

Memory = retention and recall of learnt info or experiances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

3 stage memory model

A

sensory = brief retention of sensory info (Ionic, echoic, Hapatic (touch))
Working (Short term) = temporary storage and manipulation of info
Long term = Encoding and storage of information for later retrieval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Declarative v Nondeclarative memory

A

Declarative = conscious recollection
Nondeclarative = implicit memory expressed through performance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is long term memory formed

forgetting

A

Encoding = turning sensory info into STM
Storage = retention of encoded memory over time
Retrieval = accessing and bringing stored info back into conscious awareness

Forgetting
- Encoding or Retrieval failure
- Interference = when newer memories disrupt retrieval of older memories

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

contributors for enhancing memory

A

Elaboration
Visual imagery
Dual coding
Motivation
Spaced repetition
interleaving
Testing effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Effects of sleep on learning

A

Slow-wave sleep facilitates the consolidation of new memory encoding in the hippocampus
- Allow gradual redistribution to LTM
- integration of new memories with old
- Increase retention and consolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

types of Aphasias

A

draw diagram and explain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define executive function

A

The PFC higher-order cognitive processing:
working memory = STM
Inhibitory control = stop inappropriate response
Cognitive flexibility = shift thinking or behavior for changing demands
Fluency = smooth production of ideas, words or actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Deficits in executive function presents as

A

-Frontotemporal Dementia
- Orbitofrontal = emotion instability, impulsiveness, restlessness
- Dorsomedial = action and apathy, lack of concern, akinesia
PD
Tumour
Cerebro VD
TBI
Psychiatric conditons (ADHD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Criteria for MDD dianosis

A

5 or more for more than 2 weeks
1. Depressive mood
2. Diminished interest in activities

+
Weight loss
sleep changes
fatigue
feelings of worthlessness
low conc
recurrent suicidal thoughts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

explane
Disruptive Mood Dysregulation
Disorder

Major Depressive Disorder

Persistent Depressive Disorder

Premenstrual Dysphoric Disorder

A
  1. Childhood-onset disorder characterised by severe temper outbursts
    and persistent irritability.
  2. Mental health condition characterised by persistent feelings of sadness,
    hopelessness, and loss of interest in activities.
  3. Chronic mood disorder characterised by long-lasting depressive
    symptoms, including low self-esteem and impaired functioning.
  4. Severe form of premenstrual syndrome characterised by mood swings,
    irritability, and physical symptoms.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Aetiology of MDD (Genes x Environment)

A

1 degree relative x3
genetic 35% (polygenetic)
Childhood adversity x2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pathophysiology of MDD
Monoamine hypothesis

A
  • Low serotonin levels and norepinephrine –> depressive symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pathophysiology of MDD
Dysfunctional HPA axis activity

A
  • High Cortisol levels and increased CRH
  • Release of ACTH
  • acts on adrenal cortex to release cortisol
    NEGATIVE FEEDBACK LOOP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Brain Connectivity during MDD
Hyper and Hypo cennectivity

A

Hypoconnectivity –> Reduced functional or structural connectivity between brain regions.

Hyperconnectivity –> Increased functional or structural connectivity between brain regions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Bipolar I, II
Cyclothymic Disorder
Substance-induced

Study These Flashcards
A
  1. classic. HIGH mania & depression
  2. LESS manic and SAME to HIGHER depression

Chronic mood disorder characterised by numerous periods of hypomanic
and depressive symptoms that do not meet the criteria for a major depressive
episode or hypomanic episode.

22
Q

Diagnostic criteria for Bipolae disorder

Study These Flashcards
A

AT LEAST ONE MANIC EPISODE
a. Elevated levels of irritable mood and high energy

b. At least 3 of the following
- Higher self esteem
- Less Sleep
- Racing Thoughts
- Distractibility
- More goal orientated

23
Q

Aetiology and Epidemiology

Study These Flashcards
A

Aetiology: GENETIC –> 85% genetic link
ENVIRONMENTAL lower age of onset, childhood adversity,

24
Q

Bipolar Disease Pathophysiology

Study These Flashcards
A

circuitry
depressive episode= DMN>SMN
NT
–> low relase of serotonin from pathe nuclei –> basal Ganglia & thalamus = mania

manic episode =
SMN > DMN
NT
–> low release of Dopamine from Substantia nigra –> basal and thalamus = depression

25
Describe the criteria that need to be met for a clinical diagnosis of generalised anxiety disorder.
Excessive anxiety and worry about many things most of the time for 6 MONTHS. The anxiety is associated with at least three of the following symptoms: - Restlessness Fatigue - Difficulty concentrating - Irritability - Muscle tension Sleep disturbances
26
Pathophysiology of GAD
Dysregulation of primary inhibitory NT in CNS (GABA) --> decreased inhibition of neural circuits --> heightened arousal and anxiety OVERACTIVE AMYGDOLA --> HPA --> HIGH CORTISOL Serotonin receptors low binding (5-HT1A) signalling disrupted
27
Describe the criteria that need to be met for a clinical diagnosis of schizophrenia.
POSITIVE = added NEGATIVE = lack of something COGNITIVE = working memory M>F, 15-20, Genetic <80%, Dopamine D2 receptor, Subunit of NMDA receptor F>M after menopause DIAGNOSIS 2 or more in a month - Delusions - Hallucinations - Disorganised Speech Functions must be below normal for 6 months
28
Pathophysiology of Schizophrenia – The Dopamine Hypothesis
hyperactivity of dopamine activity in the MESOLIMBIC pathway = Positive symptoms Hypoactivity of the MESOCORTICAL pathway = Negative symptoms
29
Pathophysiology of Schizophrenia – The Glutamate Hypothesis
Hypofunction of NMDA glutamate receptors mostly on GABAergic interneuroms = disconnection of excitatory pathway = subcortical Dysregulation = positive and negative symptoms
30
Pathophysiology of Schizophrenia – Neuroinflammation
Maternal infection and inflammatory processes impact neurodevelopment.
31
32
-- SSRI -- SNRI -- Tricyclic Typical TCA -- Mirtazapine Atypical TCA
SSRI = Blocks serotonin reuptake to increase serotonin levels. SNRI = Blocks the reuptake of serotonin and norepinephrine to increase their levels. Tricyclic = Blocks reuptake of serotonin and norepinephrine, and blocks histamine and alpha-adrenergic receptors. Mirazapine = Blocks presynaptic alpha-2 receptors to increase serotonin and norepinephrine release.
33
Describe the indications, contraindications, and side effects of benzodiazepines.
Indications - Anxiety, seizures, insomnia, alcohol withdrawal Contraindications resp depression, 1st trimester preg, history of substance abuse, severe liver failure Side effects sedation, dizziness, drowsiness, cognitive impairment, memory problems,
34
mechanism of action Benzodiazapines
Binds to GABAa receptors--> modulates increase activity of GABA --> increases inhibitory effect --> increases Cl- --> hypopolarisation --> increase firing threshold
35
Stages of motivation
Drive = Hunger; the person has a craving to consume a certain food. Behaviour = The person consumes the desired food. Reinforcement = The person’s appetite is suppressed; they are no longer hungry. Motivation = They then become motivated to eat in future when they are hungry.
36
Describe the mesolimbic pathway and its role in motivation.
The mesolimbic pathway is a dopaminergic circuit that starts in the ventral tegmental area (VTA) --> projects to the limbic system (nucleus accumbens.) Influencing motivation, reinforcement, and addiction. Dopamine release in the nucleus accumbens strengthens behaviours linked to pleasure and reward, driving individuals to pursue rewarding experiences. Dysfunction in this pathway is associated with addiction, depression, and schizophrenia.
37
Reinforcement and Reward
Unpredicted reward more happy Predicted reward mehh Omission of predicted reward feels worse Positive prediction errors = up dopamine Negative prediction errors = reduced dopamine influence learning process and adjusts behaviour
38
list psychoactive drugs
stimulants = Caffeine, nicotine, amphetamine, cocaine Depressants = Alcohol, benzodiazepines, antiseizure medications Opioids = Morphine, heroine, codeine, fentanyl, methadone Hallucinogens = Psilocybin, LSD Mixed effect =Cannabis, MDMA, ketamine
39
Indirect Psychoactive Drugs Direct Psychoactive Drugs
Direct = direct effect of CNS Indirect = influence on the activity of NT
40
types of dementia
Vascular Degenerative Neoplastic Traumatic Hydrocephalus Toxic/nutritional Infective Prion diseases
41
AD signs and symptoms
memory loss confusion mood changes Anxiety Seizures Incontinence Increased Sleeping Aspiration Pneumonia weight loss
42
Describe the pathological hallmarks of AD (i.e., plaques and tangles).
Increased amyloid-b ( Ab) Accumulation of abnormal protein fragments in the brain, forming plaques. Neurofibrillary tangles Twisted fibres composed of hyperphosphorylated tau protein, disrupting neuronal function. Widespread neuron loss Progressive death of nerve cells throughout various regions of the brain, leading to cognitive decline in Alzheimer's disease.
43
draw AD Amyloid Precursor Protein (APP) image thing
44
Explain the cholinergic hypothesis of AD.
suggests that cognitive decline is caused by the degeneration of cholinergic neurons in the basal forebrain, leading to down (ACh) levels. Impairs memory and learning. Treatments like acetylcholinesterase inhibitors UP ACh levels by blocking its breakdown, helping improve cognitive function.
45
Cholinergic meds for AD
Donepezil = Block the breakdown of acetylcholine (cholinesterase inhibitor) Rivastigmine = Block the breakdown of acetylcholine (cholinesterase inhibitor) Galantamine = Cholinesterase inhibitor and positive allosteric modulation of nicotinic acetylcholine receptors.
46
Outline other forms of dementia including pathophysiology and key differentiating features.
Chronic brain damage . Dementia pugilistica . Chronic traumatic encephalopathy . Alpha-synuclein . Lewy body dementia . Frontotemporal lobar degeneration
47
Describe the clinical evaluation for dementia including radiological investigation.
family history, past medical, educational, cognitive complaints, behavioural complaints EXAMINATION orientation, memory, language, attention, Abstract Think, MMSE TESTS B12 level test Thyroid Function Test
48
treatment strategies for AD and mechanisms of action
Donepezil = Block the breakdown of acetylcholine (cholinesterase inhibitor) Rivastigmine = Block the breakdown of acetylcholine (cholinesterase inhibitor) Galantamine = Cholinesterase inhibitor and positive allosteric modulation of nicotinic acetylcholine receptors. Memantine = NMDA receptor antagonist; regulates glutamate activity in the brain.
49
Non pharma testment for AD
Cognitive stimulation Psychological intervention Exercise Occupational therapy Healthy diet
50
Clinical Features of Delirium
Perceptual disturbance Incoherent speech Sleep-wake disturbances Psychomotor changes Disorientation Acute/fluctuating Symptoms Clin testing
51
Common cause for Delirium
Drugs, dehydration, detox, deficiencies, discomfort Electrolyte, elimination bad, environment Lungs (HYPOXIA), liver, lack of sleep Infectionm iatrogentic event, infarction Restraints, restricted movements, renal failure Injury, intoxication, UTI, unfamiliar environment Metabolc

MSK (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions