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Topics in Medical Biosciences > Brain Diseases > Flashcards

Brain Diseases Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the positive and negative symptoms of Schizophrenia?

A

Positive symptoms: psychosis, hallucinations, delusions, paranoia
Negative symptoms:
social withdrawal, lack of motivation, cognitive and attention impairment

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2
Q

What does the treatment of Schizophrenia entail?

A
  • treatment with antipsychotic drugs
  • interfere with dopamine function
  • chlorpromazine blocks dopamine receptors
  • reserpine
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3
Q

How does the drug Reserpine work against schizophrenia?

A
  • lowering neurotransmitter levels
  • inhibitor of vesicular monoamine transporters (VMAT)
  • this block neurotransmitter recycling thus depleting levels of neurotransmitters
  • can cause low dopamine therefore causing Parkinsonism
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4
Q

How does the drug Chlorpromazine work against schizophrenia?

A
  • blocks dopamine receptors

- can cause low dopamine therefore causing Parkinsonism

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5
Q

What are the causes of schizophrenia?

A
  • reduced function of NMDAR
  • strong genetic contribution
  • may be a developmental disorder of brain organisation resulting in thinning of the prefrontal cortex. Due to excessive synaptic pruning.
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6
Q

How are mood disorders treated?

A

Manipulating monoamine neurotransmitter metabolism

  • MAO inhibitors
  • Neurotransmitter re-uptake inhibitors
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7
Q

How do antidepressants work?

A

Act by prolonging neurotransmitter action.

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8
Q

How do Iproniazid antidepressant function?

A

inhibiting MAO thus increasing neurotransmitter levels at synaptic cleft

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9
Q

How does Prozac antidepressant function?

A

blocks serotonin re-uptake

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10
Q

How do selective serotonin re-uptake inhibitors (SSRIs) antidepressant function?

A

increase serotonin levels

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11
Q

How are anxiety disorders treated?

A
  1. Anxiolytic drugs that enhance GABA transmissions
    - neurotransmitter for inhibiting synapses
    - used to use barbiturates to activate GABA but overdose is lethal so instead use benzodiazepine
  2. decrease glutamate concentration/ transmission
    - drugs that inhibit the glutamate pathway
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12
Q

How can you modulate GABAergic inhibition to treat anxiety disorders?

A

GABA receptors have 5 subunits, 2 α, 2 β and a γ. GABA binds between α and β and benzodiazepine binds between α and γ. When they both bind, this enables the GABA receptor to stay open for longer and Cl ions are able to come in and be inhibitory.

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13
Q

Define drug addiction.

A

“compulsive drug use despite long-term negative consequences, loss of self-control and propensity to relapse”

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14
Q

How does drug addiction happen?

A
  • addictive drugs hijack the brains reward system by increasing the concentration of dopamine in targets of VTA neurons (ventral tegmental area)
  • overall there will be more dopamine than usual
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15
Q

How does nicotine enhance dopamine production?

A

Activates ACh receptors to excite dopamine neurones

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16
Q

How does opium and cannabinoids enhance domaine production?

A
  • opium and cannabinoids inhibit the GABAergic neurons, causing disinhibition of dopamine neurons
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17
Q

How does cocaine enhance dopamine production?

A

Cocaine blocks the plasma membrane dopamine transporter and dopamine re-uptake

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18
Q

How does Ecstasy enhance dopamine production?

A

reverse the dopamine membrane transporter, causing vesicle-independent release of dopamine
- increase dopamine synthesis and prevent its degradation

19
Q

Why are drugs addictive?

A
  • if dopamine neurons signal a reward, the action that preceded the reward is reinforced through dopamine regulation of neural circuits
  • drugs hijacks the brains reward system
20
Q

What is epilepsy?

A

Disorder of neural network excitability

  • abnormal balance between the actions of excitatory and inhibitory neurones
  • dysfunction of synapses
  • chronic condition with recurrent seizures
21
Q

What can cause epilepsy?

A
  • head injury, infection, stroke, brain cancer, drug abuse
  • genetic predisposition (mutation in channels)
  • seizure predisposes to having future seizures
22
Q

What treatment can be given to people who suffer from epilepsy?

A
  • drugs that inactivate Na+ channels to reduce excitation
  • drugs that inhibit Ca2+ channels to reduce synaptic transmission
  • brain surgery
  • GABAa receptor agonists (benzodiazepine)
23
Q

What is autism?

A

neurodevelopment disorder. Deficits in communication and reciprocal social interactions, reduced emotions and difficulty adapting behaviour to a changing environment
- reduced neural synchrony patterns

24
Q

What is the predominant cause of autism?

A

Genetic

- mutation in genes to do with synapse development and function

25
Q

What is fragile X syndrome?

A

neurodevelopment disorder. intellectual disability and autism spectrum disorder

  • affects boys
  • defect in FMR-1 gene
26
Q

What does the FMR-1 gene do?

A

gene involved in the regulation of translation

- produces FMRP that represses protein translation that is required for learning

27
Q

What happens during the onset of Alzheimers?

A

Loss of memory and disorientation
- affects the hippocampus
Microglia dysfunction can occur

28
Q

What are the pathological features of Alzheimers?

A

increase in Aβ-Amyloid plaque formation and neurofibrillary tangles in the hippocampus, amigdala and cortex

29
Q

How does Amyloid β formation take place?

A
  • precursor is APP (amyloid precursor protein)
  • Aβ-Amyloid is a product of the APP cleavage
  • cleavage occurs in two places, β-secretase and γ-secretase
  • α-secretase cleavage prevents the formation of Aβ-Amyloid
30
Q

What is familial Alzheimers cause by?

A

mutations in the amyloid precursor protein (APP) and Presenilin, increase β-Amyloid production
- down syndrome patients have an extra copy of APP and develop Alzheimer’s in the 40’s

31
Q

What is ApoE in terms of Alzheimers?

A

Found high number of patients with alzheimers have a link to ApoE

  • ApoE is a component of high-density lipoproteins involved in lipid transport and metabolism
  • AD patients have ApoE-ε4 allele instead of ε3.
32
Q

What usually clears up β-Amyloid plaque aggregates?

A

microglia

- through phagocytosis

33
Q

How can microglia dysfunction be negative to humans?

A
  • won’t clear up aggregates

- can inflame and lose track of what to clear out and start attacking healthy neurons

34
Q

What is the treatment for Alzheimers?

A

aim to reduce the amyloid plaques and neurofibrillary tangles
- drugs to reduce Aβ toxicity and increase clearance
- done by inhibiting γ-secretase
Biomarkers to detect Amyloid β deposits before symptoms are onset

35
Q

What is the general procedure from lab to clinic for drug to a disease?

A
  1. determine the pathogenic process to intervene
  2. use biochemical assays to identify a drug candidate
  3. optimise the candidate for affinity, activity, safety in vitro and in animal models
  4. test in human trials
    Phase 1 - safety
    Phase 2 - proof of concept
    Phase 3 - large patient population
36
Q

What happens during Parkinsons disease?

A
  • tremor, rigidity, problems walking

- death of dopaminergic neurones of the substantia nigra

37
Q

What is the pathology of Parkinsons Disease like?

A

Presence of Lewy bodies, which is α-synuclein aggregates, clog up function of neurons and interfere with normal function

38
Q

Is Parkinsons inherited?

A

There is no clear inheritance pattern, mostly sporadic

39
Q

Where does α-synuclein aggregation begin in Parkinsons?

A

Starts in the brainstem and substantia nigra, then spreads throughout cortex

  • defective proteostasis
  • behave like prions
  • loss of vesicle release
40
Q

What does α-synuclein accumulation cause in Parkinsons?

A

Blocks vesicle trafficking, protein clearance and degradation and build up causing oxidative stress
- the accumulation interferes with the priming of vesicles, decreasing the size of the releasable pool

41
Q

What other genes have seen to be involved with Parkinsons?

A

Pink1 - mitochondria-associated kinase
Parkin - Uq-proteasome system for protein degradation. Regulate mitochondrial function, movement along microtubules and removal of damaged mitochondria.
DNAJC6, GAK - endocytic pathways

42
Q

What is the treatment strategy for Parkinsons?

A 
Boost dopamine levels
- administer of L-Dopa
- dopamine neurons keep dying
Target the lysosome to increase lysosomal function
Deep brain stimulation
-  can alleviate symptoms
Cell Replacement Therapy
- transplantation of dopamine neurons into the brain
43
Q

What are the challenges of cell replacement therapy for Parkinson?

A
  • need Dopaminergic neurons in large amounts
  • no contamination from other cell types
  • immunosuppression
  • better to use stem cells to produce the dopaminergic neurons in vitro (iPSC’s)

Topics in Medical Biosciences (12 decks)

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