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Psych Neuro 3313 > Final > Flashcards

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1
Q

Neurological Disorders

A

Any disorder of the body nervous system

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2
Q

Stroke

A

Loss of brain function due to lack of blood and O2

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3
Q

Stroke Risk Factors

A

Hypertention (high blood pressure)- 35-50% risk
Atrial Fibrillation - 5% risk
High Cholesterol
Diabetes mellitus

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4
Q

Stoke Symptoms

A

Hemiplegia- paralysis one side of body
Hemiparesis- weakness one side of body
Hemineglect- lack or awareness on one side of thebody
Dysphagia- Difficulty swallowing
Dysarthia- Diffucult speaking, facial weakness
Aphasia- Diffuculty speaking and understanding speech, damage to language centers

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5
Q

Two arteries to brain

A

Common Carodid Artery

Vertebral Artery

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6
Q

Types of Stroke

A

Ischemic- blood clot

Hemorrhagic- Blood leaks into brain tissue

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7
Q

Infarct

A

Occurs after 3 hours of damage, permanent damage due to lack of nutrients, o2 to brain

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8
Q

Penumbra

A

At risk healthy brain tissue near the Infarct.

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9
Q

Stroke Exitotoxicity

A
  1. Lack of blood
  2. Depolarization
  3. Too many action potentials
  4. opening of NMDA and glutamate receptors, Influx of CA and Zn
  5. Ca and Zn induce apoptosis.
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10
Q

Stroke Treatments

A
  1. Get rid of blood clot
  2. Reduce # of action potentials
  3. block glutamate receptors, Ca, Zn channels
  4. Rehabilitation
  5. Physical therapy, occupational therapy, speech therapy, psychological treatment
  6. IPSC stem cell therapy- replace dead neurons with new stem cells from skin
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11
Q

Head Injuries

A

TBI- Traumatic brain injuries- Most common from falls then car accidents

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12
Q

Concussions

A

Head injury from the blow to the head with out penetration.

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13
Q

Coup/ Countercoup

A

Coup is where the brain hits the skull and the countercoup is the rebounce hit to skull

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14
Q

Concussion Damage

A

bent, or torn brain tissue at the junction between the axon and soma

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15
Q

Brain Hematoma

A

Epidural- between bone and dura mater
Subdural- between dura mater and arachnoid
Intercerebral- within the brain hemoraggic

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16
Q

Dementia Pugilistica

A

Features of dementia cuased by repeated damage to brain

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17
Q

Dementia Pugilistica is the Accumulation of …

A

Tau Protien, start at frontal cortex and then to amygdala and hippocampus and respective symptoms

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18
Q

Dementia Pugilisitca

A

Loss of neurons, scarring of brain tissue, plaques, neurofibrillary tangles

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19
Q

Types of Tumors

A

Gliomas- of glial cells (50.4%)
Meningoimas - of meninges (20.8%)
Pituitary adenomas - of pituitary gland (15%)
Nerve sheath tumors - of myelin around nerves (8%)

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20
Q

Tumor Treatments

A

Surgery to remove
Radiotherapy to kill
No chemotherapy since it can’t cross the BBB

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21
Q

Epilepsy

A

Long-term epileptic seizures

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22
Q

Seizures

A

Abnormal excessive and synchronous neuronal activity

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23
Q

Types of seizures

A

Partial simple- Clear area of origin no loss of consciousness
Partial Complex- loss of consciousness
Generalized- no clear area, large area effected by seizure
-Grand Mal- violent convulsions
-petit mal- brief period of unconsciousness

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24
Q

Lack of inhibition in Epileptic seizures

A
  1. GABA neuron loss
  2. Miswiring
  3. Lose of GABA receptor
  4. Disinhibition
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25
Q

Seizure treamtent

A
  1. Gaba agonist

2. Surgery if due to structural issues (corpus callosumectomy)

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26
Q

Neurocysticercosis

A

Pork Tapeworm infection of brain

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27
Q

Neurocysticercosis symptoms

A

seizures
Increased intercranial pressure and hydrocephalus (CSF blocked)
Back pain if cysts are in spinal cord.

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28
Q

Treatment of parasite infections

A

Anti-seizure medicine
Anti-worm medicine
Surgery to remove cysts

Prevention: vaccine pigs, cook meat

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29
Q

Encephalitis

A

Acute inflammation of brain due to bacteria, virus, fungi

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30
Q

Encephalitis Symptoms

A

Headache, fever, confusion, drowsiness, fatigue,

Severe symptoms: seizures, tremors, memory issues

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31
Q

Encephalitis causes

A 
Rabies virus
Herpes simplex
Poliovirus
measles virus
West Nile Virus
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32
Q

Primary Encephalitis

A

Virus directly invades the CNS (ex west nile)

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33
Q

Secondary encephalitis

A

virus invades first other parts of the body then brain

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34
Q

Meningitis

A

Inflammation of meninges and spinal cord, caused by bacteria in CSF (Milky spinal tap)

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35
Q

Brain inflamation and swelling restricts blood flow leading to…

A

Damage and symptoms

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36
Q

Meningitis symptoms

A

Headache, stiff neck, fever, confusion, vomiting, inability to tolerate light or loud noises.

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37
Q

Transmissible Spongiform Encephalophaties (TSE)

A

Digs holes in brain, (spongiform) Ex. Prion Disease

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38
Q

Prion disease

A

Microscopic holes are seen in brain

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39
Q

Prion Symptoms

A

memory changes, personality changes,movement problems

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40
Q

Prions cause normal proteins of prion proteins to be misfolded

A

These cause apoptosis of neurons as misfolded prion proteins enter and burst neurons

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41
Q

Types of prion disease

A
  1. Mad Cow disease.

2. Creutzfeldt-Jakob Disease (CJD) - human nerological disorder that is incurable and fatal

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42
Q

CJD death and pathway to symptoms

A

Misfolded proteins enter neuron and then replicate then burst neuron to be released into brain.

5% genetic cause, acquired by eating cows with Mad cow dissease or scrappies with prion disease

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43
Q

Multiple sclerosis (MS)

A

autoimmune condition and inflammatory disease in which the myelin are damaged.

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44
Q

MS symptoms

A

vision problems, stiff muscles, numbness in arms and legs, bladder control loss, mental physical fatigue, mood changes,

45
Q

Secondary progressive MS (SPMS)

A

Follows RRMS, continuous increase of symptoms, no remission

46
Q

Relapsing-remitting MS (RRMS)

A

Most common, includes relapes folowed by remission but a gradual inclease in MS symptoms as each occur

47
Q

Primary progressive MS (PPMS)

A

Steady worsening of neurological functioning without distinct relapses

48
Q

Progressive- relapsing MS(PRMS)

A

Steady worsening with occasional attacks, relapses

49
Q

MS affects…

A

only the white matter, immune system attacks the myelin, leads to inflammation and lesions in brain

50
Q

Cause of MS

A

No clear cause, combination of genetic, and environmental,

51
Q

Ataxias

A

Problems moving

52
Q

Dementias

A

Problems thinking

53
Q

Alzheimer’s

A

Most common form of dementia, no cure

54
Q

Symptoms of Alzheimers

A

difficulty remembering, confusion, aggression, mood swings, language troubles, long term memory loss, withdraw

55
Q

Alzhermers Cause

A

Plaques of beta amyloid in grey matter of brain
Neurofibrillary tangles due to phosphorylation of Tua protein
Inflamation

56
Q

Familial form of AD

A

Dominant inheritance with onset before 65

Mutation of APP, Presenilin 1, presenilin 2 genes.

57
Q

Sporadic AD

A

Most forms of AD, caused by combination of genetic and environmental conditions.

58
Q

Genetic risk factor of AD

A

inheritance of e4 allele of the APOE gene

59
Q

Environmental risks AD

A

Head trauma, high cholesterol, high blood pressure

60
Q

3 hypothesis of AD

A
  1. AB plaques hypothesis: Plaques form first then disease cascades
  2. Cholinergic hypothesis of AD (inflammation first)- Low Acetylcholine= inflammation
  3. Tau hypothesis: Tau protein clumps up, leads to microtubules falling apart and forming tangles.
61
Q

AD prevention and treatment

A

Boost acetocholine levels, reduce glutamate exitotoxicity.

62
Q

Parkinsons

A

Degenerative disorder of dopamine-generating cells in substantia Nigra

63
Q

Parkinsons Lack of Dopamine

A

Lack of activation of Basal Gangila to inhibit motor signals leading to loss of muscle control (tremors)

64
Q

Parkinsons Treatment

A

Increase dopamine levels, MAO-B inhibitors to prevent degradation of dopamine.

Levodopa helps replace dopamine

65
Q

Huntington

A

Genetic disorder that affects muscle coordination and cognitive and psychiatric decline.

66
Q

Cause of Huntington

A

Genetic dominant mutation of Huntington (HTT) gene.

40+ repeat of CAG
36-39 may or may not be HTT effected
<35 will not be effected

67
Q

HTT gene interaction

A

Effects Transcription, cell signalling, Caspase Activity- protein involved in apoptosis.

68
Q

Huntington disease effects

A

Striatum degeneration, hippo campus, substantia nigra

69
Q

Huntington patients show…

A

general atrophy of cortical tissue, enlarged ventricles.

70
Q

Tetrabenazine

A

dopamine antagonist- reduce Chorea (sporatic movements)

71
Q

Gene silencing

A

reduce HTT effect

72
Q

Schizophrenia

A

Mental disorder characterized by a breakdown of thinking and emotional responses.

No sex bias, but men have a earlier onset (18-25)

73
Q

Schizophrenia Positive, Negative, Cognitive deficits

A

Positive- symptoms that should not be present (hallucinations, delusions)
Negative- symptoms that are a lack of character (reduced speech, lack of emotions, social withdrawal)
Cognitive deficits- Memory issues, attention issues, decision making issues

74
Q

Schizophrenia causes

A

Genetic and environmental causes (old damaged sperm, Cannabis comsumption before 18, stress, Prenatal mother has an infection, Hypoxia)

Genetic - Disc1…. lots of genes

75
Q

Brain strucutre in schizophrenia

A
  1. Enlarged Ventricles- lose of neurons in those areas.
  2. Hippocampal cells are disorganized leading to cognitive deficits. More disoriented the more severe the disorder.
  3. Lower frontal lobe activity- lower executive functioning.
  4. decreased acivity in lateralization of brain
  5. Loss of grey matter in adolescent brain
76
Q

Biochemistry of schizophrenia

A

Dopamine hypothesis: Too much dopamine leads to schizophrenia. Dopamine antagonists seem to help schizophrenia but only the positive symptoms not the negative symptoms

Glutamate hypothesis: Reduced glutamate activity leads to schizophrenia. Trying to develop drugs to boost Glutamate signaling.

77
Q

Atypical antipsychotics

A

improve the negative symptoms of Schz (Clozapine - serotonin agonist)

78
Q

Major Depressive disorder

A

Depression most of the day with lost of interest in normal activites DSM-V: at least 2 weeks everyday
Lifetime prevalence of 20-25%

79
Q

MDD causes

A

genetic: 5-HTT (Serotonin transporteer)- short allele= less transporter= reduced reuptake= depression? but Prozac reduces reuptake and seems to help depression

80
Q

Clock gene and SCN in depression

A

Circadian rhythm disturbance leads to depression

81
Q

Envioment for MDD

A

Very high Cortisol can lead to depression, stress

82
Q

MDD structural abnormalities

A

Decreased hippocampus volume, and orbitofrontal cortex, decreased activity of Anterior cingualte cortex - role in rational fucntions and reward anticipation, decision-making, increased amygdala- emotional and emotional memory.
Decreased left hemisphere and increased rt activity= more negative less happy

83
Q

Biochem of Depression

A

HPA axis is overactive, and there is irregular circadian rhythms of cortisol secretion. The negative feedback of HPA axis may be inhibited.

84
Q

Monoamine in MDD

A

Lack of Serotonin- anxious irritable
Lack of Noradrenaline- loss of energy and interest
Lack of Dopamine- lack of happiness and enjoyment in life

85
Q

SSRI

A

Help increase levels of serotonin in MDD patients

86
Q

ECT for MDD

A

Electroconculsive shock therapy
Electrodes are used to control eletical currents in patientes head, causes brief seizures and seems to be effective for severely depressed.

87
Q

Bipolar disorder

A

Mood disorder characterized by unusual shifts in mood, energy, activity, and drive

88
Q

Mania

A

excessive energy excitement, illusions of grandiosity

89
Q

Bipolar causes

A

High genetic relationship, high concordance rate with twins, some similar behaviors and genes with schizophrenia,

Enviromental causes: prenatal mother has depression, psychosis and especially bipolar disorder.
Messed up sleep-wake cycle can induce bipolar disorder and shifts between depression and mania

90
Q

Bipolar brain structure

A

Reduced hippocampal volume and elevated basal ganglia activity increased amygdala volume and activation. Overall increased activity in the BP brain

91
Q

Bipolar biochemestry

A

Too much Norepiniphrine= mania

Too little serotonin= depression

92
Q

Anxiety disorders

A

Difficulty regulating and controlling anxiety, with symptoms around excessive and irrational fear and dread.

93
Q

OCD

A
  • Intrusive thoughts that produce uneasiness, fear, worry

- Repetitive behavior to reduce associated anxiety

94
Q

OCD causes

A

Gene and enviromental (head trauma, seizures etc)

Brain strucutrue- under activation of area responsible for stopping habitual behaviors (lateral orbitofrontal cortex), abnormal connetions between basal ganglia and frontal cortex

95
Q

OCD biochem

A

low serotonin levels

96
Q

PTSD

A

Recurrent thoughts of traumas, that impair daily functioning.

97
Q

PTSD brain structure

A

Shrinkage of hippocampus, and porr negative feedback of HPA axis= more coritsol in system.
Overactivation of the amygdala

98
Q

PTSD treatments

A

Psychotherapies (exposure thereapy)
Antidepressants
GABA agonists

99
Q

Autism Spectrum Disorder

A

Neurodevelopmental disorder,
Difficulties in social interactions, verbal and nonverbal communcaiton and repetitive behavior

Sex biased, males more likely than girls.

100
Q

Autism Genetics

A

Strong genetic contribution to autisms

101
Q

Autism enviroment

A

Prenatal Sodium Valporate to control mother’s bipolar disorder- led to decreased migration of neurons of babies, big scandal

102
Q

Autism brian strucutre

A

Small head at birth then large increase during first few years of life. Lack of synaptic pruning, too much connections in brain. Smaller corpus callosum in autism

103
Q

Biochemistry of Autism

A

Too high glumate to GABA ratio. Too much excitation= social disorganizaiton.
Reduced activity in the serotonin transporer= low serotonin levels in the brain but high levels in the blood

104
Q

Autism Treatments

A

Early intervention therepy to teach social and cognitive language skills
SSRI
Antipsychotics to reduce aggression and act on dopamine system

105
Q

ADHD

A

problems with attention, hyperactivity, impulsivity. These must begin by age 6-12

106
Q

ADHD causes

A

genetic and enviromental (over 50% is genetic) the rest is prenatal smoking/alcohol/lead, premature and low birth rate

107
Q

ADHD Brian strucutre

A

Less total grey matter, and inpairments in prefrontal cortex- inattention and impusivity and impaiments in basal ganglia leads to hyperactivity.

108
Q

ADHD biochem

A

reduced level of dopamine, treat with ritalin- dopamine agonist (reuptake inhibitor)

109
Q

ADHD treatments

A

Diatary changes-food resptrictions, reduce inflamation foods
Psychotherepay- earlier the better, EEG feedback and behavior thereapies.
Medication- ritalin

Psych Neuro 3313 (1 decks)

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