Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pre-Med 2022-2023 > BMC L8 > Flashcards

BMC L8 Flashcards

1
Q

PaNuclues

A

Cluster of neurones in brain

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

Ganglion

A

Cluster of neurones in spinal cord

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

Plexus

A

Many ganglion connected together

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

Name 6 neurogenative diseases

A

SHAPE CJD

Schizophrenia
Huntingsdon Disease
Alzheimers disease
Parkinson’s disease
Epilepsy
CJD

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

What is AD?

A

Alzheimer’s disease:

Slow, progressive, neurodegenerative disorder

Most common form of dementia

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

State 2 causes of AD

A
  1. Intracellular accumulation of tau proteins as NFTs, neurofibrillary tangibles
  2. Extracellular amyloid plaques
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

State the symptoms of AD

A
  1. Short term memory loss, easily missed, not diagnosed
  2. Long term memory loss, confusion, loss of language, irritability, agression
  3. Loss of bodily function
  4. Death, usually 7 years after diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

AD diagram - brain of patient

A

Pay attention to:

Cortex (sulci) - shrinks
Hippocampus - shrinks - memory, spatial navigation, consolidation of info
Ventricles - expand
White matter - shrinks

In general, brain shrunken

Perirhinal cortex shrinks - memory, navigation
Entorhinal cortex shrinks - Object perception, memory

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

How do we distinguish Familial / Genetic AD

A
  1. Early onset <65
  2. Autosomal dominant
  3. Loss of bodily function, loss of memory, progressive aphasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does the cholinergic hypothesis of AD postulate?

A

Oldest theory, postulates loss of ACh as cause

Basis of current drug therapies

Drugs which combat ACh loss not effective

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

Explain the Amyloid hypothesis of AD

A

“Extracellular accumulation of beta amyloid plaques/deposits”

  1. Proteolysis of APP (amyloid precursor protein, unknown function, found in synapses) leads to formation of beta amyloid deposits
  2. Beta amyloid deposits accumulate as extra cellular plaques
  3. This is neurotoxic - toxic to surrounding neurones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why are Downsyndrome patients likely to develop AD by age of 40?

A

Amyloid hypothesis of AD.

APP gene - chromosome 21
Downsyndrome patient - trisomy chromosome 21

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

How is APOE4 a risk factor of AD?

A

Apolipoprotein

Risk factor
Isoform of APP
Breaks down beta amyloid plaques

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

What is the role of tau protein?

A

Tau protein binds to microtubules and stabilises them and helps them assemble

The tau protein is phosphorylated by kinase. It then forms Tau-P. Tau-P is what binds to the microtubules and stabilises them

Tau-p is dephosphorylised by phosphatase, forming tau, so it then dissociates from microtubules causing them to diassemble

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

Explain the tau hypothesis

A

Tauopathis, abnormal phosphorylation - Hyperphosphorylation - tau phosphorylates into helical paired filaments forming NFTs

NFTs (neurofibrillary tangles) are toxic to surrounding neurones

NFTs formed in the cell early (intracellular)
NFTs formed out cell later (extracellular)

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

Why may the tau hypothesis be unreliable?

A

Because the evidence contradicts whether tau-p binds or dissociates from microtubules

17
Q

How can we detect AD?

A

PET scan of brain

Iluminates Tau Protein and Amyloid Plaques

Different pattern for Tau protein

Tau protein - usually found in hippocampus

18
Q

Explain the noradrenergic hypothesis of AD

A

Loss of noradrenergic neurones in locus coerulus - OCCURS IN BOTH, AD, PD

Leads to symptoms of AD

Locus coeuruleus innervates hippocampus, spinal cord, cerebellum

19
Q

How can AD lead to psychiatric depression and psychosis?

A

Noradrenergic hypothesis:

Loss of noradrenergic neurones, therefore, loss of noradrenaline.

20
Q

What is Parkinson’s Disease?

A

Slow, progressive, neurodegenerative disease

  1. Loss of cells in substania nigra - diminishing of substantia nigra
  2. Less dopamine produced
  3. Increased output from basal nuclei
  4. Reduced activity of thalamus
  5. Reduced output of cerebral cortex
  6. Hypokinetic disorder
21
Q

What is the substantia nigra? Describe its location and function.

A

Linked to basal ganglia via midbrain
Crescent shaped mass of cells
Sends neurones to tissues on both side of brain
Therefore, helps control coordination and movement

22
Q

Describe the structure and location of the basal ganglia.

A

Basal ganglia located in midbrain.

Consists of

-Striatum - Caudate nucleus + putamen
-Corpus striatum - Striatum + globus pallidus
-Subthalmic nucleus
-Substantia nigra - dopaminergic region

23
Q

Explain the Lewy Body theory of PD

A

Lewy bodies are round inclusions of polymerised alpha synuclein proteins found in the cytoplasms of neurones in the substantia nigra

alpha synuclein found at pre-synaptic terminals, function unknown, involved in synaptic vesicles

leads to rare genetically inherited form of PD

24
Q

Explain the Parkin theory of PD

A

Parkin - involved in degradation of proteins
Mutation to parkin leads to a more common genetically inherited form of PD
“Juvinile PD”
Autosomal recessive
Early onset (<45)

25
Q

Explain dopamine replacement therapy

A

Treatment for PD

  1. L-DOPA restores dopamine levels, restores the balance
  2. Dopamine cannot cross BBB
  3. L-DOPA can
  4. L-DOPA is a precursor of dopamine
  5. L-DOPA produced by body, converted into dopamine by DOPA Decarboxylase
  6. issue is loses its effectiveness over time
26
Q

What is Huntington’s Disease?

A

Mutation to single gene located in chromosome 4

Autosomal dominant

This gene codes for protein called huntingtin - found in cytoplasm of cells

Function is not clear, aids in regulation of gene expression

CURRENTLY NO EFFECTIVE TREATMENT

27
Q

State the symptoms of Huntington’s Disease

A

Chorea - hyperkinetcis, voluntary random movements

Dementia - declining cognitive ability due to other factors than age

Death 15-20 years after onset due to
-falls
-heart disease
-pneumonia

28
Q

State common symptoms of schizophrenia

A
  1. Language disorganisation - neologisms
  2. Delusions (thought of insertion, withdrawl)
  3. Absence of focus
  4. Hallucinations
  5. Agitation
29
Q

State the classification of schizophrenia symptoms

A

positive symptoms: not normally present
-hallucinations, delusions, inability to focus, language disorganised

negative symptoms - lack of elements which are usually present in one’s life including
-emotions
-pleasure
-motivation

30
Q

How can we distinguish schizophrenia on an MRI scan?

A

-Enlarged ventricles
-Shrunken hippocampus tissue

31
Q

State the causes of schizophrenia

A

Genetic - disruption to embronyic brain development
Environmental
Excess dopamine = increase in positive symptoms
Low dopamine = increase in negative symptoms

32
Q

State treatments for schizophrenia

A

Antipsychotics - drugs which surpress dopamine receptors. This reduces positives symptoms.

Psychotherapy

Social rehabilitation

Antidepressants to manage associated depression

33
Q

State historic / last resort treatments for schizophrenia

A

Prefrontal lobe lobotomy

Electroconvulsive therapy, now only applied to one cerebral hemisphere, with muscle relaxant to prevent broken bones

34
Q

Give an example of a general seizure

A

Absence seizures

35
Q

What causes general seizures

A

Rythmic activity from brain stem is relayed to large areas of cortex by thalamus

36
Q

What happens during an absence seizure?

A

Petit mal
MILD SEIZURE
Early childhood
Expression goes blank

37
Q

What happens during a tonic clonic seizure?

A

grand mal

Loss of consciousness
Loss of bowel control
Loss of bladder control
Severe biting of tongue
Broken bones due to intense muscle contractions

38
Q

What causes a partial seizure?

A

Cerebral cortex divided into columns
Each column = isolated / single processing unit
Has an inhibitory surround (GABAergic)

Failure of inhibitory surround of the columns (isolated processing units of cerebral cortex)

This leads to uncontrollable wave of excitation in cerebral cortex

Leads to partial seizure

39
Q

Describe treatments for epilepsy

A
  1. Vagus nerve stimulators placed under skin of chest to prevent brain electrical activity from becoming chaotic
  2. Ketogenic diet - low carb, high fat
  3. Anticonvulsive drugs
  4. Surgery - removal of seizure focus, last resort, for partial seizures
  5. Prevent exposure to stimuli triggers - flashing light

Pre-Med 2022-2023 (57 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions