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PSY324 > week 12 > Flashcards

week 12 Flashcards

1
Q

what is a tumour?

A

Mass of cells
Growth is uncontrolled
No function
Benign or Malignant

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2
Q

what is the difference between Benign and Malignant tumours?

A 
Benign Tumours
Encapsulated
Not cancerous
Usually removable
Commonly do not reoccur
Do not spread or invade

Malignant Tumours
Cancerous
Invade or damage nearby tissues (infiltration)
Metastasize (cells break away and travel through blood or lymphatic system to form new tumours)

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3
Q

Is metastasis an easy process?

A

Movement of tumours to other parts of the body is called metastasis
A complex process, cancer cells break off primary tumours and move to new locations. Dangerous and often unsuccessful

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4
Q

What are some “challenges” that migrating cancer cells may face?

A

Some may die b/c they are unable to survive in the bloodstream
Others may die when they are squeezed through tight spaces
Others destroyed by immune system

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5
Q

how do tumours damage the brain?

A

Benign: Compression
- pushing up against brain tissue and stopping the flow of cerebral spinal fluid
Malignant: Infiltration (spread)

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6
Q

what are some symptoms of someone who might have a brain tumour?

A 
Severe headaches
Ataxic/stumbling gait
Nausea and vomiting
Lack of coordination
Unusual drowsiness
Weakness/loss of feeling in limbs
Change in personality or memory
Changes in speech
Change in vision
Seizures
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7
Q

what are the 2 types of brain tumours regarding were the tumour starts?

A

Primary(start in brain) vs. secondary(started in another part of the body and migrated to the brain)

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8
Q

What are 7 types of brain tumours?

A

Gliomas (glial cells)
Meningioma (cells of meninges- dura mater)
Pituitary adenoma (cells of pituitary)
Neurinoma (schwann or cranial nerve cells)
Angioma (blood vessel cells)
Pinealoma (pineal gland cells)
Metastatic carcinoma (varied primary tumor)

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9
Q

What are possible risk factors of brain tumours?

A 
Sex (3:2 male: female ratio) b/c bigger brain mass larger chance for glioma cancer
Exposure to high dose radiation
Genetic risk alleles (varied)
- E.g.: Von Hippel-Lindau Syndrome
Traumatic brain injury
Lower risk among those with asthma
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10
Q

does using a cellphone increase tumours?

A

Mobile subscription rates associated with death rates from brain cancer
Not associated with other cancers (breast, lung, stomach) or heart disease
Note: not causative

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11
Q

Does brain size matter with the possibility of brain tumours?

A

MRI scans among 124 patients (mostly Caucasian) with high-grade glioma and 995 controls
Increased intracranial volume of 100mL associated with 69% increase risk of developing high-grade glioma.
After adjusting for intracranial size, females at higher risk than males.

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12
Q

What is a Seizure and a Convulsion?

A

Seizure: period of sudden excessive activity of cerebral neurons
Convulsion: seizure of neurons of the motor system; uncontrollable wild movement of the muscles

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13
Q

What can a seizure cause?

A

Can cause brain damage - namely to hippocampus due to over excitation of neurons
Status epilepticus; single episode that causes a series of seizures without the ability to regain consciousness

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14
Q

do all seizures cause convulsions?

A

no, some seizures go unnoticed

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15
Q

what are treatments for seizures?

A

anticonvulsive drugs that increase inhibitory processes, ketogenic diet (high fat, low carb and protein diet), brain surgery (ablation)

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16
Q

What are possible causes of seizures?

A 
Injury (head trauma)
Stroke
Developmental abnormality (e.g. malformed blood vessels)
Tumor
Drugs that cause fever
Genetics (generalized seizures)
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17
Q

What are 2 types of seizures?

A

I. Generalized seizures (no local onset, widespread)
Tonic-clonic (grand mal)
Absence (petit mal)
Atonic (temporary paralysis)

II. Partial seizures (focused source)
Simple (change in consciousness)
Complex (loss of consciousness)

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18
Q

What is Grand Mal?

A 
A Generalized seizure, 
Most severe
Convulsions
Warning symptoms: mood changes, aura
Loss of consciousness
2 phases: tonic(muscles are contracting arms stretched out) and clonic (trembling of muscles the jerky movements, the convulsions)
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19
Q

What is an Absence Seizure?

A

Common in children (4-12yrs).
Stare off into space for brief moments, blinking eyes.
10-20 sec duration
Unaware of surroundings, touch, and sound.
Sudden with no warning.
Labeled as inattentive and unmotivated in school.

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20
Q

what is a stroke?

A

lack of distribution of oxygen of blood flow to the brain

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21
Q

What are 2 types of strokes?

A

Hemorrhagic strokes (20%)
Rupture of cerebral blood vessels cause bleeding in the brain
Due to malformed vessel or weakened vessel from HTN
Pressure on brain tissue
Intracerebral & Subarachnoid

Obstructive/Ischemic strokes (80%)
Plugging of blood vessels that prevents flow of blood to the brain
Via thrombus (blood clot) or embolus (piece of broken material)
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22
Q

what are Intracerebral & Subarachnoid ( subtypes of Hemorrhagic strokes)?

A

Intracerebral: bleeding that occurs in the brain tissue and usually this is because of small arteries associated with high blood pressure
Subarachnoid: blood vessels on the surface of the brain rupture and bleed into the space between the brain of the school, due to anyersum

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23
Q

What are symptoms of strokes?

A

Numbness or weakness, especially on one side of body
Sudden trouble speaking or understanding speech
Sudden trouble seeing
Sudden trouble walking or maintaining balance, dizziness

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24
Q

What are some treatments for strokes?

A

Medication
anti-hypertensives (e.g. beta-blockers)
Anticoagulant (e.g. coumadin)
Clot dissolving drugs (tPA, DSPA)

Surgery
malformed blood vessel
Carotid endarterectomy
Arterial stent in obstructed carotid artery
Physical therapy and Lifestyle changes
25
Q

What are developmental disorders due to?

A

Exposure to chemicals/toxins in utero
Inherited Metabolic Disorders
Genetic mutation

26
Q

What happens to the baby if the mother contracts Rubella (German Measles) while the baby is in utero?

A

Congenital rubella syndrome; range of incurable illnesses, classic triad; sensorineural deafness, eye abnormalities congenital heart disease

27
Q

What happens to the baby if the mother drink alcohol while the baby is in utero?

A

Fetal alcohol syndrome; smaller eyes, thin upper lip

Impairment: Stunted neurodevelopment, low IQ, LD, poor interpersonal skills, impaired sight and hearing

28
Q

what is Phenylketonuria (PKU), a Inherited Metabolic Disorder?

A

Phenylketonuria (PKU)
Lack of enzyme that converts phenylalanine (phe) into tyrosine
Impedes myelinization of neurons in CNS
Severe cognitive impairment if not diagnosed immediately after birth
Low phe diet & Kuvan (aka:sapropterin)
- phenylalanine-free medical formula and carefully measured amounts of fruits, vegetables, bread, pasta, and cereal

29
Q

What is the Tay-Sachs disease?

A

Both parents need to be carrying the gene
Eastern European Jewish descent
Recessive gene on chrom 15
Metabolic “storage” problem - lysosomes
Swelling of brain @ ~ 4 months of age
Exaggerated startle, listlessness, irritability, spasticity, seizures, delayed mental and social skills, neurodegeneration, early mortality (~5 years)

30
Q

what is Down Syndrome?

A

Extra copy of chromosome 21 (Trisomy 21)
Brain 10% lighter, simpler convolutions, smaller frontal lobes; degeneration after age 30 (inflammation and beta amyloid).
Delayed mental and social development
Impulsive behavior, poor judgment, short attention span, slow learning, early dementia

31
Q

What is the Degeneration of neurons due to?

A 
Transmissible Spongiform Encephalopathies (TSE)
Parkinson’s Disease
Huntington’s Disease
Alzheimer’s Disease
Amyotrophic Lateral Sclerosis (ALS)
Multiple Sclerosis (MS)
32
Q

What are the treatments for developmental disorders?

A

there are none

33
Q

What is TSE?

A

Contagious brain disease
Brain tissue characterized by sponge-like appearance/swiss cheese
Aggregate misfolded prion protein (prion)
When folded becomes pathological version, which is the prion
Familial (PRNP gene) or Sporadic

34
Q

What are 3 examples of TSE?

A

Bovine spongiform encephalopathy (BSE) aka Mad Cow
The cows in the UK were displaying a disease, and humans were developing it, by eating food that is contaminated by the infected cows. People were dying

Creutzfeldt-Jacob disease (most common)
Transmitter through infected spinal fluid, can happen during cross-contamination during surgery
Aggressive disorder, 90% of cases death will occur in 12 months, rapid dementia,visual abnormality, impairments in coordination, speech abnormalities
Sporadically, no infection or genetic reason that can detected

Fatal familial insomnia
Genetically caused, rare autosomal dominant inherited prion disease, only one copy from parent to have disease, mostly caused by the mutation to prion protein. Incurable, progressive state of insomnia -> hallucinations, confusion, state of dementia, 18montsh survival span

35
Q

What is proteopathy?

A

TSE caused by accumulation of misfolded prion protein
When prion protein changes shape, it becomes an abnormal protein = the prion.
Prion protein = protein in the CNS.
Abnormal form comes into contact with normal form and transforms the normal form into an abnormal form… Domino Effect

36
Q

What is the prion protein important for?

A

Increase PrPc ~ proliferation of neurons in hippocampus
Mutation of PrPc ~ developmental abnormalities and decreased proliferation
Introducing prion protein killing enzyme in neuron stops the neurodegenerative process of the prion
Aggregation of the prion leads to cell death

36
Q

What are negative(not displaying something normally) and positive (excessively displaying) symptoms of Parkinson’s Disease?

A

Negative symptoms:
Disorders of posture/righting/locomotion*
Akinesia*(loss of ability to move your muscles voluntarily)
Disturbances of speech

Positive symptoms:
Tremors at rest*
Muscular rigidity*
Involuntary movements

Two or more cardinal (*) need 2 or more of these symptoms to. be diagnosed with Parkinson’s

37
Q

What are non-motor features of Parkinsons disease?

A 
Loss of smell
Depression
Anxiety
Sleep disorder; fatigue
Constipation
Dementia
38
Q

What are mutations that occur within the genes in patients with Parkinson’s?

A

Mutation of gene on chromosome 4 (alpha-synuclein - toxic gain of function, dominant mutation)
or chromosome 6 (parkin - loss of function)
Degeneration of nigrostriatal (dopaminergic) system
Presence of Lewy bodies = abnormal circular structures in cytoplasm of DA neurons, associated with dementia like symptoms

39
Q

What is treatment used for Parkinson’s Disease?

A

Neurosurgery – stereotaxic procedures:
Implantation of fetal cells into caudate nucleus and putamen of basal ganglia
Implantation of neural stem cells
Destruction of internal division of the globus pallidus (GPi) via radiofrequency current
Deep brain stimulation of subthalamic nucleus which inhibits Gpi
Gene therapy to increase GABA in subthalamic nucleus

40
Q

In depth explain these two Steortaxic Procedures; Lesion the Gpi and Inhibit Subthalamic nucleus via lesion or deep brain stimulation.

A

Lesion the Gpi
We can remove the inhibitory activity enhancing the thalamus leading to motor movement

Inhibit Subthalamic nucleus via lesion or deep brain stimulation
Minimising the amount of activity of the Gpi which would minimise the amount to activity in the thalamus

41
Q

How does music help with treatment in Parkinson Disease?

A

Areas involved in rhythm perception: premotor and supplementary motor areas, cerebellum, putamen of basal ganglia.
Improvement in gait, limbs coordination, postural control and balance.
Some improvement for psychological wellbeing.

42
Q

What is the Criteria of Alzheimer’s?

A

Memory impairment to learn or recall information
Plus one or more of the following
Aphasia (language)
Apraxia (motor movement)
Agnosia (naming)
Executive function (planning, organizing, sequencing)

43
Q

What is Mild Cognitive Impairments seen as, and does it automatically result in having Alzheimer’s?

A

Mild Cognitive Impairment (MCI) commonly seen as precursor to Alzheimers
Only 50% of ppl with MCI end up having Alzheimer’s

44
Q

What are 2 Hallmarks of Alzheimers Disease?

A

Senile plaques (beta-amyloid)
Proteopathy of Abeta protein
similar to prion disease
misfolding of Abeta leads to development of senile plaques

Neurofibrillary tangles (tau)
Tauopathy: molecular structure of tau is changed (hyperphosphorylated) and form abnormal protein filaments.

*diagnose only made post-mortem

45
Q

What is Pittsburgh Compound B (PiB)?

A

Positron Emission Tomography (PET)
Imaging technology
Record brain activity
Injection of radioactive tracer - one kind of tracer–> PiB
- Which Measure metabolic activity, pick up images of beta amyloid plaques in neural tissue
PET can also be used to image beta amyloid plaques in neural tissue

46
Q

Do people with Alzheimer’s have smaller hippocampus’?

A

yes, when compared to a healthy brain

47
Q

In terms of transmission in the brain, how does Alzheimers effect transmission?

A

Cholinergic changes in AD
Depletion of acetylcholine (ACh)
Decline in choline acetyltransferase (ChAT)
Low levels of cholinergic neurons and it’s receptors
Treatment: acetylcholinesterase inhibitors & NMDA receptor blockers

48
Q

What are risk factors of Alzheimers?

A 
Depression
Head injury
Education (Reserve Theory)
- high levels of education less chance of alzehimers 
Lifestyle (nutrition, exercise, stress, smoking)
Inflammation
Genetics
APP (amyloid precursor protein)
PS1 and PS2 (presenilin)
APOE e4 (Apolipoprotein)
49
Q

Which APOPE genotype is correlated in Alzehimers?

A

APOE e4

more APOE the higher the levels of amyloids

50
Q

How and when is Huntington’s Disease developed?

A

Inherited gene mutation of dominant gene on chromosome 4 (Huntingtin (htt) gene - toxic gain function)
Aggregation of misfolded htt protein in neurons (proteopathy)
Degeneration of cortex and basal ganglia (i.e., striatum) neurons and GABA projections to motor areas
Onset in 30s or 40s

51
Q

what are symptoms of Huntington disease?

A

Uncontrollable, jerky limb movements (Choria)
Cognitive impairment
Psychiatric illness

52
Q

What is Amyotrophic Lateral Sclerosis?

A

A motor neuron disease

Attacks spinal cord and cranial nerve motor neurons

53
Q

What are symptoms of Amyotrophic Lateral Sclerosis?

A 
rapidly progressive weakness
muscle atrophy
Spasticity - paralysis
Motor speech problems
dysphagia (swallowing)
respiratory compromise
5% frontotemporal dementia
54
Q

Is ALS hereditary or sporadic? And what happens with the proteins in patients with ALS?

A

10% hereditary; 90% sporadic

SOD1 gene on chromosome 21
Aggregation of misfolded proteins
toxic gain of the protein
Increases extracellular glutamate - excitotoxicity of motor neurons

55
Q

How can you treat ALS?

A

Riluzole – (pills) based on reducing glutamate excitotoxicity
Edaravone – (intravenous infusion) based on reducing free radicals

56
Q

What is Multiple Sclerosis (MS) And when does it normally develop?

A 
Autoimmune demyelinating disease
Interruption of signal via action potentials
Onset: late twenties or thirties
Interuteral viral theory
 own body is attacking it's self
57
Q

What are symptoms of MS?

A

Muscle weakness
Numbness
Tremor
Ataxia

58
Q

What are some treatments of MS?

A

focus on inflammation

Interferon beta
- Anti-inflammatory
Glatiramer acetate
-stimulates anti-inflammatory chemicals that suppress immune activity

PSY324 (11 decks)

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