Brainscape's Knowledge GenomeTM

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


See full index

BIOL.PSY 105. 1001 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

4 major symptoms of Parkinson’s

A
  • Tremor: in hands, arms, legs, head, and jaw
  • Stiffness: of the limbs, trunk
  • Bradykinesia: slowed movement/ Brady: slow kinesia: motion/movement
  • Impaired balance and coordination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Parkinson’s non-motor deficits:

A
  • Impaired sleep
  • Fatigue
  • Depression
  • Memory difficulties
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

5 stages of progression in Parkinson’s:

A

1: tremor and movement symptoms on one side of the body, changes in facial expression, posture, and walking.
2- symptoms worsen and affect both sides of the body
3- slowness of movement, loss of balance, frequent falling
4- walker required, help with daily activities required
5- wheelchair, bedridden, hallucinations, delusions, nurse required

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

What typically causes death in Parkinson’s

A

Pneumonia or infection from falling or in the lungs

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

Risk factors in Parkinson’s

A

Genetics: 5-10% causes are early-onset <50 years old
Age: typically in older age but could happen at a young age
Sex: affects 50% more men than women.
Exposure to toxins

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

Parkinson’s: Parts of the basal ganglia

A
  • The striatum: caudate and the putamen
  • Subthalamic nucleus
  • Substantia nigra: release dopamine. Where the dopaminergic neurons are degenerating. Not producing or releasing dopamine causing a shortage.
  • Globus pallidus interior/ exterior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Direct pathway

A

Central cortex, striatum , globus pallidus internal, thalamus

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

Indirect pathway

A

Central cortex, striatum, Globus pallidus external, subthalamic nucleus, globus pallidus internal, thalamus

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

Braak’s hypothesis in Parkinson’s

A
  • hyposmia- loss of smell
  • Sleep disorder
  • Constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How L-dops, MAO/COMT, dopamine agonists work

A
  • L-dopa: converts into dopamine
  • MAO/COMT: prevents the breakdown of dopamine
  • Dopamine agonists: substitute for dopamine.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain what multiple, sclerosis and autoimmune refer to

A
  • multiple: affects various regions of optic nerve, brain, spinal cord
  • sclerosis: hardening or scarring from damaged myelin
  • autoimmune: antibodies produced against healthy tissues=inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Multiple sclerosis symptoms:

A
  • Double vision, partial or complete blindness
  • Dizziness
  • slurred speech
  • numbness or tingling in limbs
  • weakness or fatigue
  • tremor, spasms, stiffness, or paralysis
  • lack of coordination balance
  • bladder and bowel dysfunction
  • depression, memory/concentration loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Multiple sclerosis: 4 patterns of progression

A

-Clinical- isolated syndrome: single episode > 24 hours, 50% have lesions found on MRI and likely progress to RRMS
-relapsing-remitting (RRMS): 85%, new or increasing symptom attacks with partial or complete recovery
-Secondary-progressive(SPMS): steady progression/ worsening after 20+ years of RRMS
-Primary-progressive (PPMS): 10-15% steady
progression/worsening from symptom onset, shows up later in life (40’s-50’S), equal numbers of men and women.

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

Multiple sclerosis risk factors:

A
  • Regions of temperate climate
  • Northern European descent
  • More women than men
  • Onset usually mid-20s
  • Family history
  • Other autoimmune diseases( type 1diabetes, thyroid disease, IBD)
  • Epstein-Barr virus (mono)
  • smokers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is myelin, which cells make it ?

A

Produced by oligodendrocytes and is made up of glial cells

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

What is tolerance in relation to the thymus

A

Healthy tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Role of T-cells, B-cells

A
  • T-cells: secret cytokines to signal other cells

- B-cells: secrete antibodies against antigen

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

Apoptosis:

A

The death of cells, normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

APC’s:

A
  • Antigen-presenting cells

- dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Self-antigens:

A

Antigen that comes from yourself, can be a healthy tissues protein that is supposed tO be there but us causing an immune response, causing the T-cells to react to the wrong thing

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

BBB

A

Blood-Brain barrier: t-cells can re-enter the bloodstream and eventually gain access to the CNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Blood Cerebrospinal fluid barrier

A

BCSFB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Plaques, where they can occur in CNS? (3 general areas)

A
  • Optic nerve
  • Brain
  • Spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How Ocrevus work?

A

Immunoglobulin/antibody medication against B cells. Block them from releasing antibodies attacking against yourself antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Two defining groups of symptoms + examples in autism

A
  • Repetitive/ Stereotypes behaviors
  • Arm flapping
  • Rocking
  • Twirling
  • excessive interest in a particular topic
  • Social interaction/communication
  • Avoiding eye contact
  • Failing to respond to name
  • delayed, flat or awkward speech echolalia(repeating what you are saying)
  • Difficulty understanding body language, gestures, emotions
  • Only interacting with others to achieve goal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

risk factors for Autism

A
  • Included both genetic and environmental contributions
  • Over 100 genetic loci
  • Family history- 5 times as likely if parent or sibling has it
  • Sex- 4.5 boy to every 1 girl
  • Older parental age (>35 years)
  • Premature birth (<26 weeks), low birth weight, birth trauma with ischemia(lack of blood supply) or hypoxia (lack of oxygen, under oxygenated)
27
Q

Atypical brain development (too rapid then stunted and ages when each happens)

A
  • 2-4 years, larger head circumference and brain volume than typical
  • 6-8 years, arrested growth compared to typical
  • Volume becomes similar to typical by adolescence/adulthood, but opportunity for environment to shape brain may have been missed
28
Q

Lobes and structures affected by autism

A

Temporal and frontal lobes

29
Q

Language-processing - Typical vs. autism

A

Language is typically processed in the frontal temporal cortices of the left hemisphere vs in autistic children who show an increase in activity of these areas in the right hemisphere, contributing to language-processing deficits.

30
Q

Wernicke’s

A

In charge of understanding languages and is in temporal lobe

31
Q

Fusiform gyrus

A

located on the medial side of the temporal lobe, is less active in autistic children, which may contribute to facial and emotion-processing deficits.

32
Q

Cingulate gyrus

A

located on the medial side of each hemisphere, is involved in self-awareness, empathy, and response-inhibition, and also shows decreased activation in autistic children. In the limbic lobe/system

33
Q

Amygdala

A

situated deep within the temporal lobe, undergoes this atypical pattern of development, which may contribute to difficulties with socio-emotional processing and anxiety.

34
Q

Caudate

A

the production of stereotypical behaviors is fronto-striatal circuitry
involving the caudate nucleus, which also undergoes this atypical development pattern

35
Q

Purkinje cells: Where are they and how are they different in typical vs. an autistic brain?

A

Purkinje cells are located in the cerebellum. In autistic brains they are smaller and less densely packed, impairing language, imitation and attention processes.

36
Q

Dendrites, long and short-range connections in typical vs. autistic brain

A

Increase in short range connections but decrease in long range connections between cortical areas, these areas are not talking to each other and not being coordinated, not as much activity connecting them together.

37
Q

Describe the hypothesized role of glutamate and GABA and its relation to seizures in 30% of autistic cases.

A

Too much glutamate is creating too much citation and GABA is not creating enough inhibition, causing too much electrical activity leading to seizures.

38
Q

Two neuropeptides that regulate affiliative/bonding behaviors

A
  • oxytocin

- vasopressin

39
Q

How does Balovaptan work?

A

It is supposed to improve social interactions and communication by easing anxiety. It is a vasopressin antagonist.

40
Q

4 symptom domains in schizophrenia

A 
Postive:
Hallucinations
Delusions
Disorganized thoughts 
Affective: 
Depression 
Dysphoria 
Anxiety 
Suicidality 
Negative:
Blunted affect 
abolition 
anhedonia 
alogia
Asociality
Cognitive: 
Attention 
Learning 
Working memory 
Executive functioning
41
Q

Risk factors of schizophrenia

A
  • Advanced paternal age
  • Famine while in utero
  • Prenatal complications (preeclampsia)
  • obstetrical complications
  • Birth location (urban)
  • Birth season(early spring)
  • Migration
  • Cannabis use
42
Q

Gene location

A

Chromosome 22
right arm
22q 11.2 deletion

43
Q

What happens to brain volume, ventricles, temporal lobe, cortical gray matter, and gyrification

A
  • Brain volume: decreased
  • Ventricles: enlarged lateral and third ventricles
  • Temporal lobes: smaller medial
  • cortical gray matter: decreased
  • gyrification: altered
44
Q

Latent inhibition in typical vs. schizophrenia

A
  • prepulse inhibition in typical: they will be primed and the startled response will be less
  • in schizophrenia, no matter how much prepulse you give them they can’t regulate their responses and it will be the same.
45
Q

Dopamine role in schizophrenia:

A

Blocking receptors ameliorates symptoms

46
Q

Glutamate role in schizophrenia:

A

Blocking receptors exacerbates symptoms

47
Q

GABA role in schizophrenia:

A

is not activated when glutamate is blocked, doesn’t inhibit=disinhibition

48
Q

PV interneurons role in schizophrenia

A

regulate gamma oscillations, critical to working memory, and other cognitive functions impaired in schizophrenia. Alterations in gamma band activity are associated with multiple symptom domains

49
Q

4 dopaminergic pathways and functions

A
  • Meso-cortical: Cause some of the cognitive and negative symptoms
  • Miso-limbic: hyper function causes some of the positive symptoms
  • Nigro-striatal: negative side effects on the nitro-striatial pathway
  • Tubero-infundibular: negative side effects on the tubers-infundibular pathway.
50
Q

1st vs 2nd generation D2 antagonists

A
  • 1st generation: block d2 receptors, typical, chlorpromazine and haloperidol, high risk EPS
  • 2nd generations: blocks D2 and 5HT2A, atypical, clozapine, high risk metabolic issues
51
Q

Animal model used by Allen

A

a mouse

52
Q

Scientific question/ area of research for Allen

A

visual system/ approach behavior/ primary visual cortex

53
Q

behavior studied

A

pray detection and freezing or approaching

54
Q

Brain areas studied

A

superior colliculus (SC)

55
Q

Differences in behaviors and brain areas activated between subject age groups

A

Different ages:
Younger: approaching more
older: freezing more

56
Q

Human subjects in scurry

A

Early deaf people and normal hearing

57
Q

What happens to the auditory cortex in deaf people

A

it adapts and is used for other functions. Starts processing new information, visual, tactical, and other sensories

58
Q

ED

A

early deaf

59
Q

NH

A

normal/ healthy hearing

60
Q

AC

A

auditory cortex

61
Q

S1:

A

Primary somatosensory cortices

62
Q

S2:

A

secondary somatosensory cortices

63
Q

STS:

A

SUPERIOR TEMPORAL SULCUS

BIOL.PSY 105. 1001 (2 decks)

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