Psychiatric disorders/anatomy (BS1 CH8)

Question 1

autonomic nervous system

Answer 1

controls involuntary responses in the body, including things like sweating, blushing, and pupil dilation, is divided into the sympathetic and parasympathetic systems.

Question 2

sympathetic nervous system

Answer 2

The sympathetic nervous system stimulates the body in the classic “fight or flight” response, mediated by hormones such as epinephrine and norepinephrine. If the body needs to get ready for action, it will dilate the pupils, raise the heart rate, and increase blood flow to skeletal muscles to prepare for sudden action.

Question 3

parasympathetic nervous system

Answer 3

By contrast, the parasympathetic nervous system is the “rest and digest” system that increases blood flow to the digestive system, slows the heart rate, constricts the pupils, and generally exerts actions opposite to those of the sympathetic nervous system. In turn, the autonomic nervous system is part of the peripheral nervous system, which describes the nervous system throughout the body and is distinguished from the central nervous system, which corresponds to the brain and spinal cord. The peripheral nervous system is also divided into the visceral nervous system, which modulates the digestive system, and the somatic nervous system, which connects to skeletal muscle to allow for voluntary movement.

Question 4

A group of patients have difficulty focusing on fixed objects when moving across the room or even rotating their heads. What structure is LEAST likely to be damaged in these individuals, based on their symptoms? A. Inferior colliculus B. Medial geniculate nucleus C. lateral geniculate nucleus D. Auditory cortex

Answer 4

B. Medial geniculate nucleus- no In the auditory pathway, the medial geniculate nucleus precedes the inferior colliculus. C.Lateral geniculate nucleus- no, The lateral geniculate nucleus is the point at which visual information enters the brain, part of thalamus. The patients’ troubles could stem from a deficiency of the visual system. D.Auditory cortex D is correct. The auditory cortex is responsible for processing sound information in the temporal lobe after it has passed through the medial geniculate nucleus. It is not mentioned that these patients have trouble perceiving sound. Note that some information is also sent to the inferior colliculus, which helps keep the eyes focused on singular points even when the head is rotating. This key part of the vestibulo-ocular reflex could easily be damaged in these people.

Question 5

What is one example of adaptation in relation to signal detection? A child living near a bread factory begins to associate the smell of bread with home. B. A resident who spends long hours in fluorescent lighting more frequently looks downwards. C. A man who resides above a bakery stops noticing the smell wafting from below. D. A teacher learns to pause his lecture when he hears the intercom speaker begin to crackle.

Answer 5

C is correct. While the bakery smells might be distracting at first, the man’s brain adapts, allowing him to focus on more relevant stimuli. A- wrong b/c this is not related to adaptation as much as it is to response bias. B- wrong b/c this is a physical habit formed from experience. It does not pertain to the resident’s altered perception of light. D- wrong b/c like B, this is a habit learned from experience and does not describe adaptation

Question 6

Huntington’s disease

Answer 6

Huntington’s disease is caused by an expanded CAG repeat in the gene that encodes the huntingtin protein on chromosome 4; this causes the progressive atrophy of brain structures. It is unrelated to dopamine.

Question 7

By blocking norepinephrine reuptake, duloxetine could cause which of the following side effects?

Answer 7

B is correct A.Increased frequency of urination Digestion is promoted by the parasympathetic (“rest and digest”) response, including increased urination/defecation. B. High blood pressure Blocking norepinephrine reuptake would potentiate its effects. Since norepinephrine is a mediator of the sympathetic nervous system response (commonly known as the fight-or-flight response), it may lead to side effects associated with sympathetic activation. High blood pressure, as a consequence of the fight-or-flight response, is a possible outcome.

Question 8

level 1 disorders

Answer 8

anxiety disorders

depressive disorders

bipolar and related disorders

schizophrenia spectrum and other psychotic disorders

trauma and stressor related disorders

personality disorders

obsessive compulsive disorders

somatic symptom disorders

dissociaive disorders

Question 9

monoamine hypothesis

Answer 9

of depression predits that the underlying pathophysiological basis of depression is a depletion in the levels of serotonin, norepinephrine and/or dopamine in the CNS

Small molecule neurotransmitters: from chapter 6 BS1
* Amino acids: e.g., glutamate and GABA.
* Biogenic amines: e.g., dopamine, norepinephrine, and serotonin.
* Acetylcholine: binds both ionotropic and metabotropic receptors.

Norepinephrine: involved in arousal and motivation.

Dopamine: involved in reward processing and coordinating movement.

Serotonin: involved in regulating mood, appetite, and sleep.

Question 10

bipolar disorder I

Answer 10

mood swings and episodes tend towards manic phase, exgreme energh, insomnia, impuslivity and then manic follwoed by wings into typical depression

MANIC phase

• high energy
• high self esteem
• racing thoughts
• quick talking
• impuslive
• irratibl

Question 11

Bipolar II disorder

Answer 11

depressed phase

• low energy
• less intense manic episodes
• lack of cocnentraiton
• loss of interest
• helplessness
• sucidal thoughts

to be bipolar need to exhibit both phases, difference which is emphasized more, bipolar II depressd phase predominates
he main difference between bipolar I and II is the severity of symptoms. People with bipolar I disorder experience more severe highs (mania) and may not have depressive episodes. While people with bipolar II experience a less severe high (hypomania), their diagnosis includes depressive episodes.

BD-2 was characterized by more prominent and longer depressions with some hypomania and mixed-features but not mania and rarely psychosis. BD-2 subjects had higher socioeconomic and functional status but also high levels of long-term morbidity and suicidal risk. Accordingly, BD-2 is dissimilar to, but not necessarily less severe than BD-1, consistent with being distinct syndromes.

Question 12

schziophrenia disorder

Answer 12

delusions, hallucinations

disorganized speech and thoughts

life long condition, symptomsaren’t ncessarily more severe just lasts longe

may involve “negative” symptoms

involve a general detachment from objective reality

*delusions are a belief, like gov trying to control my mind; hallucaination involves sensory/perceptions could be visual or auditory not a belief its a sensory perception

Question 13

schziophrenia 2

Answer 13

positive symptoms: something they have, a behavior present in the patient that is not present in healthy ppl, for it to be a positive symptom we are saying ti is present*

1. psychotic beahviors not seen in healthy ppl
2. hallucinations, delusions, disorganized speech or beahvior

negative symptoms: something lacking or something they dont have* somthing expect to see but do not

1. disruptions to normal emotions and behaviors, absence of normal patterns
2. avolition (loss of motivation to do things) flattened affect, reduced speech/or interactions

cognitive symptoms:

1. thought patterns that make it hard to lead a normal life and cause emotional distress, like knowing you have hallucinations, emotional distress cause d by that can really affect daily life why so problematic and included as diagnosis on list of mental disorders
2. poor executive funcitoning, rouble focusing or paying attention, problems with working memory

what is going on: abonormalities in neurons and abnormally lwo activity in frontal cortex, makes sense with poor executive functioning, difficulty planning, reasoning making decisions all related to frontal lobe can be an indication of potentially of schizophrenia

2.

Question 14

Personality disorder clusters

A

Answer 14

milder version of schizophrenia* out of touch with reality

odd/eccentric: think midler versions of schizophrenia*

• paranoid PD manifests the paranoid tendencies
• Schizoid PD manifests the social withdrawal and flattened affect
• Schizotypal PD manifests milder hallucinations and delusions

Question 15

Cluster B personality disorder

Answer 15

dramatic/erratic: think of these as over-the-top or unstable, issues iwth interpersonal relationships

• antisocial PD is sociopathy, with no regard for right or wrong or other’s rights; think about adolescent, killing neighbor dog and feeling no remorse about it, no real remorse or empathy
• borderline PD is severe abandonment anxiety and emotional turbulence, brandon marshall exhbited and diagnosed it, very quick shift form love to hate, folks tend to be more prone to self harm, highly manuplative struggle to have good relationships
• Histronic PD is overdramatic attention seeking and emotional overreaction; see more in females, often manifests itself as seductive beahvior inappropriately so
• Narcissistic PD is inflated sense of self and lack of empathy, super self centered generally pretty out going but narcissist needs affirmation of other ppl, why they tend ot be pretty charismatic and outgoign wnat to have sense of self reinforced

* antisocial PD can be though of as conduct vs emotional regulation*

Question 16

Cluster C personality disorder

Answer 16

anxious/fearful: think of these as anxiety or OCD related, world has many risks and dangers response determines; patterns of extreme fear of anxiety

• avoidant PD presents as very extreme shyness and fear of rejection
• dependent PD presents as over-dependence on others to meet needs
• Obsessive-compulsive PD presents as a milder form of OCD

Question 17

somatic symptoms disorder

Answer 17

• excessive and/or medically unexplained symptoms
• commonly encountered in primary care

to the patient the suffering si real and causes a whole lot of distress when they cannot get a medical explanation to it, mental disorder is most causes symptoms are real; somatic again means related to the body

specific diagnoses: somatic symptom disorder, illness anxiety disorder, conversion disorder, factitious disorder

somatic- main distress physical, in body there is pain

illness anxiety- more like darwin stress is primarily psychological, the term that sort of used to be used is hypochondratic no its too vague so been broken down into different things that may be wrong, somatic symptoms may or may not be present but real distress may be psychological will i die from this illsness? conversion disorder actual cahnge ins ensory or motor function with no discernable cause, temproary blindness like when all parts of hte eye should function correctly nothing functionally wrong with the eye, or temporary paraylsis no one can explain why that is conversion disorder!

factitious disorder= munchasusen or munchausen by proxy*term doesnt apply in DSM 5 but how it is refered to the one where symptoms are either falsified where patient is actually falsifyign evidence of the symptoms or sometimes munchausen by proxy caregiver intentionally inflicting harm on child to get attention* lke feeding kid poison to get htemn sick to get all this attentio

Question 18

dissociative identiy disorder

Answer 18

-disruptions and/or discontinuities in core identity

-abnormal itnegration of consciousness, identity and emotion etc.

specific diagnoses:

dissocaitive identiy dsiorder

(dissoctaive amneisa- gap, period of time cannot remember often defense mechanism of brain shutting down becuase somethign was so traumatic)

depersonalization/ derelaization disorder

depersonalization= out of body, numb am I relaly even here? out of body experiment

derealization=(external world, dream like I am here i am not feeling lke I am fuzzy or numb but objects in external world feeling that way) environment feels dream like

the person knows this isnt accurate so its that awareness that causes the person to be so uncomfortable*

Question 19

personality disorders in general

Answer 19

maladaptive, inflexible behavior patterns

Question 20

neurodevelopment disorder

Answer 20

difficulty with social interactions

difficulty understanding emotions of others

natural inclinatin for rote, repetitive activities

= autism

what makes it a neurodevelopmental disorder* vs neurocognitive, its developmenbtal so manigests itself early in developmetn typically, usually hard ot reat, behaviorla therapy can be done to really help with these things

characterized by intellecutal disability it is a spectrum and there are a lot of really ridiculously intellgient ppl on that spectrum

• manifest early in development, early onset usually before grade school
• appear as deficits generally difficult ot treat

characterized by intellectual disbaility, communication orders; not often intellectual disability often communication disorder

ALSO ADHD* (motor restlessness, impusivlity, hard time concentrating, distractiability) other diagnoses less likely to be tested, intellectual disability and tourette’s syndomr

Question 21

alzheimer’s disease

Answer 21

these are 2 abnormal structures in the brain associated with Alzheimer’s disease:

1. amyloid plaques: clumps of proteins fragments that accumulate outside of cells
2. neurofibrillary tangles: clumps of altered proteins inside cells

its destruction and death of nerve cells that causes memory failure, personality changes, problems carrying out daily activities and other symptons of alzheimer’s disease

most pl develop some but those with A’s disease develop way more, specifically develop first in areas particualrly important for memory then expanding to other areas of the brain, older people in genreal will show some of thsi ppl with alzheimer’s will show far more

problematic becuase it inhibits/ play cirtical role in blocking communication among the nerve cells and really disrupting processes cells need to surive, root of problem is destruction adn death of nerve cells causing memory failure adn personality changes all these symptoms of althzimers its destruction of nerve cells, see impaird memory, then impared judgement, difficulty finding, progression can last anywhere from 2-20 years, average is 8 years for severe decline

Question 22

parkinson’s disorder

Answer 22

another neurocgonitive disorder like alzheimer’s

another role in whats going on in the brain

if alzheim’er is tyupically manifesting itself in problems with memory, the most characteristic symptom of parkinson’s is muscle control, someone shaking a lot** can certainly be an indication before parkinson’s its a problem with motor function and muscle control causing you to shake involutnarily! here again something at play in the brain seems to be assocaited with abnormally low doapime levels, that finding is enouraing in a way suggesting that maybe if that problem can be addressed maybe there is hope to move in the right direction to treat this, movement disorder is also caused by death of cells the death of cells generate dopamine*

• dopaminergic neurons in the substantia nigra of the basal ganglia die off, mkaing it harder to contorl movements, one on each side of mem,brane we see cells have been killed off here

-dopamine is involved in sending messages to areas of the brain that control coordination and movement- if we see reduction in dopamine levels will see parksinon, chronic and progression disorders like alzhemiers, not like one day you do not have parkinson’s and hte next day you do see gradual decline as conditions worsen, about 50-80% of parkinson’s patient eventually see some sort of dimentia as disease progresses starts out as motor function then majority of cases it manifests itself as some sort of dementia

• dopamine levels progressively drop, so symptoms gradually become more severe
• abnormal aggregates of proteins called Lewy bodies develop inside neurons

alzhimer’s what is the problem with muscle control

Lewy body dementia- almost reverse of parkinson’s earlier symptoms are congitive and the later syumptoms are motor funcitoning, with parksinson’s its motor function first

Question 23

what are the three physiological indicators of a mammal’s circadian rhtym

Answer 23

melatonin released by the pineal gland, body temperature, serum cortisol levels

as morning approaches body temperature rises, core body temperature reaches a high during the day and dips in early fternoon which is why we crash in mid afternoon its related to fluctations in body temp and serum cortisol, after an hour you wake up reaches a high then gradually dec during the day

when insomnia see opposite abnormally high at night when they should be low, any variation in the melation, cortisol can impact sleep

Question 24

sleep stages

Answer 24

• what is important* 3 and 4 most restorative sleep! this is where our blood pressure drops, breathing slows and muscle is relaxed, where tissue growth and repair is adn energy stored, v improtant to get to this stage, if never get that deep restorative sleep with sleep apena have an issue
• rem stage rapid eye movement when we dream about 25% of hte night we are dreaming, first rem stage occurs about 90 min after and occurs later on

Question 25

REM

Answer 25

rapid eye movement, burts of quick eye movement

about 25 % of night when dreams occur, occurs about 90 min after falling asleep then every 9 0minutes after, gets longer later on

in beginning not experiencing REM and then as we progress through teh night it will occur about every 90 min but each stretch will get longer and longer, dreaming is very important for psych repair, get phsyical repair in stage 3 and 4 but psych repair from dreaming

so when cut sleep short it will be problematic for us, body doesnt have time to repeat all phases needed for repair, memory consoldiation*

Question 26

stage 1 sleep

Answer 26

eeg= theta waves

eog= slow rolling eye movements

emg= moderate activity

characteristics= Fleeting thoughts; non-REM sleep

Question 27

stage 2

Answer 27

eeg= sleep spindle, K complex

eog= no eye movement

emg= moderate activity

characteristics= increased relaxtion; decreased temp, heart rate, and respiration

Question 28

stage 3 and 4

Answer 28

eeg= delta waves

eog= no eye movement

emg= moderate activity

characteristics= heart and digestion slow; growth hormones secreted; deepest level of sleep

Question 29

REM 2

Answer 29

eeg= similar to beta waves but more jagged

eog= bursts of quick eye movements

emg= almost no activity, “paradoxical sleep”

characteristics= when dreams occur

Question 30

Where specifically does sensory info enter the spinal cord?

Answer 30

= dorsal horn

sensory neurons enter spinal cord, sending messages into the spianl cord and motor neurons project out ot hte spinal cord, incoming is sensory outgoing is motor. anatomically the input is the dorsal face of spinal cord and hte output part is the ventral** back is the dorsal part of your body, so the sensory neurons project into your spinal cord from the back, output comign from spinal cordbut heading toward your belly the ventral side**

SNESORY DORSAL SIDE

MOTOR OUT ON VENTRAL SIDE***

ventral side of your body is your belly**

Question 31

voluntary movement

Answer 31

primary motor cortex where motor commands originate

• when brain says I will initiate some kind of movement command comes down from some kind of area of frontal lobe called primary motor cortex
• then has to travel from tippy top of brain all the way down and out to the muscle supposed to carry out the command, so startign from the primary motor cortex, command has to travel down through brainstem and down along spinal cord then out from spinal cord to the actual muscle** all along teh way action potential, action potenial until it reaches htemusce supposed to contract*

Question 32

diagnosis

Maladaptive behavior =

Answer 32

Maladaptive behavior = criterion of abnormality

Question 33

biomedical model

Answer 33

Emphasizes the role of biological factors (genetic predispositions, abnormal brain development, altered brain structure and function) in causing psychiatric disorders.

Biomedical treatments: psychopharmacology, electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS), vagal nerve stimulation, deep brain stimulation.

Probably most relevant for schizophrenia and bipolar disorder.

Question 34

**biopsychosocial model

Answer 34

Emphasizes the role of psychological factors (e.g., low self-esteem, a tendency to ruminate on negative thoughts) and social factors (e.g., social isolation, poverty) in addition to biological factors.

Question 35

Panic disorder:

Answer 35

Panic disorder: transient episodes of intense anxiety (“feeling of impending doom”) often without any apparent cause and accompanied by physical symptoms (sweating, shortness of breath, mild chest pain).

A KIND OF anxiety disorder**

Question 36

Bipolar Disorder (card 3)

Answer 36

A combination of recurrent episodes of depression and mania, which is characterized by elevated mood, increased goal-oriented activity, decreased need for sleep, increased energy, grandiosity, and rapid speech.

Often complicated by psychosis = a break from reality involving auditory hallucinations or delusional thinking.

Can also occur in combination with hypomania, a milder form of mania.

Question 37

Schizophrenia

Answer 37

A severely disabling psychiatric disorder that arises most commonly in young adulthood and features a mix of positive and negative symptoms:

• Positive symptoms:* auditory hallucinations, delusional thinking (false beliefs, often paranoid), and disorganized behavior (dressing oddly, speaking unintelligibly, failing to maintain personal hygiene, etc.).
• Negative symptoms:* social withdrawal, loss of interest in pleasurable activities (anhedonia), cognitive deficits, flattened emotional expressions. avolition (loss of motivation to do things) so anhedonia is loss of interest or ability to enjoy pleasurable things

Neuroleptics = first-generation, anti-psychotic drugs:

Positive symptoms tend to respond to treatment, but negative symptoms often do not.

Question 38

Negative symptoms of schziophrenia

Answer 38

Negative symptoms: social withdrawal, loss of interest in pleasurable activities (anhedonia), cognitive deficits, flattened emotional expressions.

Neuroleptics = first-generation, anti-psychotic drugs:

Positive symptoms tend to respond to treatment, but negative symptoms often do not.

think: subtraction of stuff like flattened emotional expressions

Question 39

somatoform disorders 2

Answer 39

A category of disorders in which patients suffer from various physical symptoms (pain, gastrointestinal problems, sexual dysfunction, weakness, etc) that have no known medical cause.

The symptoms can be neurological (conversion disorder) or occurring in multiple organ systems (somatization disorder). Conversion disorder is under somatoform disorder, just specific to neurological symptoms

In somatoform disorders, the patient’s suffering is real and they are not faking the symptoms.

Somatoform disorders are distinct from malingering, when a patient intentionally lies about symptoms to obtain some other benefit (often financial), and factitious disorders, when a patient intentionally fabricates symptoms without any apparent incentive and may be motivated by the desire to “play the sick role.”

patients suffering is real, not clear what is causing them

Question 40

somatoform disorders 4

Answer 40

Somatic physical symptoms that are actually real but psychological basis, hte specific symptoms here thinkign heart attack, heart palpatations, all a panic attack really describing a panic attack here which is a feature of panic disorder that is a panic disorder think question on practice test 3

For the somatoform disorder ex. someone is getting a divorce so they get stomache aches and migraines, but rooted in stress or difficut life events that kind of a thing* so not could connect the two things but hte best answer here is panic* classic panic attack they would tell you person experiencing some difficult life event or strugglign withs tress and then developed a physical symptom as a result*

Question 41

Dissociative disorders 2

Answer 41

A category of disorders in which patients suffer from episodic altered states of consciousness with no known neurological cause, usually related to a traumatic event.

May be an extreme form of normal coping: “I don’t want to think about this,” “I wish I were somewhere else right now,” “This must be a dream.”

Dissociative amnesia: temporary loss of episodic memory.

Dissociative fugue: temporary amnesia for one’s personal identity.

Dissociative identity disorder: a controversial diagnosis in which patients report that they have multiple identities with distinct personalities; formerly known as multiple personality disorder.

• Controversial because the diagnosis used to be extremely rare, but increased 10- to 100-fold since it was popularized in books and movies, raising concerns that doctors may be unintentionally leading suggestible patients to produce these reports or that some patients may be fabricating them.

Question 42

Schizophrenia - dopamine hypothesis

Answer 42

Genetics: highly heritable, ~20× increase in risk for schizophrenia with a diagnosis in one first-degree relative.

The dopamine hypothesis: asserts that schizophrenia is due to an excess of dopamine signaling, based on the serendipitous finding that dopamine antagonist medications are an effective treatment for some symptoms.

* It’s now recognized that glutamate signaling is also abnormal and that dopamine activity may actually be too high in some regions and too low in others → probably oversimplifies the biological causes.

Agonist: A chemical substance that binds to and activates certain receptors on cells, causing a biological response. Oxycodone, morphine, heroin, fentanyl, methadone, and endorphins are all examples of opioid receptor agonists.

Antagonist: A chemical substance that binds to and blocks the activation of certain receptors on cells, preventing a biological response. Naloxone is an example of an opioid receptor antagonist

Question 43

Schizophrenia as a neurodevelopmental disorder:

Answer 43

Schizophrenia as a neurodevelopmental disorder:

Genes that have been implicated in schizophrenia play a role in regulating brain development.

Many patients have some cognitive symptoms and other unusual behaviors as adolescents before they go on to develop schizophrenia.

Malnutrition and exposure to influenza and other infections during pregnancy may increase the risk of developing schizophrenia.

Question 44

brain abnormalities in schizoprenia

Answer 44

Increased volume of ventricles: may reflect abnormal neuronal migration.

Tissue loss in prefrontal cortex.

Ventricles= fluid filled cavities in brain, loss of filled tissue in the prefrontal cortex

Question 45

Depression and Bipolar disorders

Answer 45

Genetics: Adoption studies and twin studies show strong genetic component, especially for bipolar disorder (60% concordance in monozygotic twins).

Neurotransmitter imbalance: Most current antidepressants act by increasing the availability of serotonin, norepinephrine, and/or dopamine so depression may be related to insufficient activity in these transmitter systems.

Brain abnormalities in depression and bipolar disorder:

1. Increased activity in the subgenual cingulate cortex, which is linked to feelings of sadness; electrical inactivation of this region relieves depression.
2. Increased amygdala volumes in some patients with bipolar disorder.

Question 46

Alzheimer’s disease

Answer 46

Genetics: Risk is strongly linked to mutations in the genes for amyloid precursor protein, presinilin, and APOE4.

Pathology: Memory loss and other cognitive symptoms are thought to be caused by the accumulation in the hippocampus of amyloid protein aggregates known as neuritic plaques and neurofibrillary tangles within hippocampal neurons.

-amyloid plaques: clumps of proteins fragments that accumulate outside of cells
- neurofibrillary tangles: clumps of altered proteins inside cell

Treatment: Cholinesterase inhibitors—which increase acetylcholine availability—may be mildly effective for memory symptoms but do not slow the progression of the disease.

There is currently no cure or effective treatment.

**Protein tangles kill neurons and that is why they lose their memory in alxheimer’s disease!*

Question 47

Alzheimer’s disease 3:

]from chapter Chapter 5, Cognition II about memory]

Answer 47

Associated with the accumulation of amyloid plaques and neurofibrillary tangles in the hippocampus and frontal cortex.

Caused in part by genetic factors and increasingly common in old age.

Features anterograde amnesia and attention deficits initially; later includes retrograde amnesia and many other cognitive deficits.

Question 48

Korsakoff ’s syndrome:

[again from Ch5- Cognition II, about memory]

Answer 48

Associated with deterioration of mammillary bodies.

Caused by long-term thiamine deficiency/malnutrition, usually due to severe, chronic alcohol abuse. (Vit B)

Features dense anterograde and retrograde amnesia, as well as confabulation—a tendency to unintentionally fabricate memories or distort reality, usually in response to questioning.

• E.g., “Where did you leave your car keys?”… “Car keys? I don’t own a car.”

Question 49

Parkinson disease 2

Answer 49

Pathology: accumulation of alpha-synuclein proteins → degeneration of dopamine-secreting neurons in the substantia nigra (pars compacta), which projects to the basal ganglia.

Abnormal basal ganglia circuits in Parkinson’s: neurons in the basal ganglia normally inhibit unwanted movement, and dopamine normally acts to reduce this inhibition to enable a desired movement; loss of dopamine in Parkinson’s disease → increased inhibition → increased effort is required to initiate movements.

Treatment: Drugs that increase dopamine availability provide temporary relief for many of the Parkinson’s motor symptoms.

Question 50

Problem with drugs that give dopamine…

Answer 50

-this protein accumulates and kills neurons normally producing dopamine, those neurons are really important to normal movement, so ppl with parkinson’s have tremors and movement problems so to some extent their siutuation can be improved becuase can take synthetic dopaimine in drugs and that can replace the dopamine so caused by neurons that make dopamine, so to some extent the dopamine can be replaced but only up to a point*

-Problem with dopamine drugs is that is giving ppl too much dopamine like parkinson’s patients it can make them hallucinate** which connects back to schzioprenia which is too much dopamine* so with parkinson you want more but not too much

Question 51

Stem cell therapy

Answer 51

Experimental approach to regenerating neurons in the CNS.

Normally, neurogenesis no longer occurs in most regions of the brain in adulthood →

Therefore, neurodegenerative diseases are challenging to treat because neurons that are lost cannot be replaced.

Stem cells are immature cells that have the potential to differentiate into any cell type—including neurons—so they could potentially be harnessed to replace lost neurons in neurodegenerative diseases like Alzheimer’s and Parkinson’s.

Types of stem cells:

1. Totipotent: can differentiate into any cell type, including extraembryonic placental cells, and therefore, they can form a complete new organism.
2. Pluripotent: can differentiate into almost any cell type, including neurons and all three embryonic germ layers.
3. Unipotent/multipotent: can differentiate into only one cell type or a family of closely related cell types but they are self-renewing.

Question 52

source of stem cells

Answer 52

1. Embryonic stem cells: derived from embryos that were fertilized in vitro—usually at clinics treating infertility—and were donated for research purposes. IN VITRO= IN A LAB
2. Adult stem cells: Found in some adult tissues (e.g., skin, digestive system), they normally serve to regenerate and repair damaged or aging tissue.
3. Induced pluripotent stem cells: These are adult cells that have been genetically modified to behave like embryonic stem cells by inducing them to express genes and growth factors that are critical for pluripotency.

Nobel Prize: to John Gurdon and Shinya Yamanaka “for the discovery that mature cells can be reprogrammed to become pluripotent.”

Induced pluripotency is extremely promising because it provides a source of stem cells for research and clinical treatment that avoids the ethical pitfalls of embryonic stem cells.

Question 53

Challenges to developing stem cell treatments for neurodegenerative disease:

Answer 53

1. Stem cell growth must be controlled to generate the correct cell type in the appropriate numbers.
2. Stem cells must be transplanted to the correct target and be able to survive within the host tissue.
3. Stem cells must generate appropriate neuronal subtypes, which in turn must be induced to integrate into adult circuits within the host.

_MUCH EASIER to target one area then integrate new brain cells all over the place**_

embryonic stem cells are bad and basically not used a lto anymore becuase htey have uncontrolled growth and that is the magic word that causes cancer, both protoncogenes and tumor suppressor genes are gone so uncontrollable growht in cell cycle easily leads to cancer and why embryonic stem cells are not good

skin stem cells and digestive system/ adult stem cells do not produce a huge
different range of cell types much much more sepcialized versus embryonic stem cells can produce any kind of cell in the body, much more versatile, but other issues if put an embryonic stem cell into someone’s body high probability get cancer. so do not want cells that good at dividing and becomming anythign floatign around

Question 54

Small molecule neurotransmitters:

from chapter 6 BS1

Answer 54

Small molecule neurotransmitters:
* Amino acids: e.g., glutamate and GABA.
* Biogenic amines: e.g., dopamine, norepinephrine, and serotonin.
* Acetylcholine: binds both ionotropic and metabotropic receptors.

Chemicals that are synthesized in the cell body neuron, stored in the presynaptic terminal, released into the synapse to modulate activity in the postsynaptic neuron, and cleared from the synapse by specific mechanisms.

Question 55

Neuroactive peptide neurotransmitters:
from Ch6 BS1

Answer 55

Neuroactive peptide neurotransmitters: These are proteins that act as neurotransmitters.
* Some examples include opioids and various hormones (vasopressin, oxytocin, insulin, etc.).

Chemicals that are synthesized in the neuron, stored in the presynaptic terminal, released into the synapse to modulate activity in the postsynaptic neuron, and cleared from the synapse by specific mechanisms.

Question 56

Functions for some neurotransmitters:

BS1 Ch6

Answer 56

• Glutamate: the principal excitatory neurotransmitter in the CNS; uses NMDA receptors (as well as other types of receptors).
• GABA: the principal inhibitory neurotransmitter in the CNS.
  means= Gamma-aminobutyric acid
• Norepinephrine: involved in arousal and motivation.
• Dopamine: involved in reward processing and coordinating movement.
• Serotonin: involved in regulating mood, appetite, and sleep.
• Acetylcholine: involved in learning and memory, sleep, arousal, and control of skeletal muscles.