Unit 4 Flashcards

(45 cards)

1
Q

Schizophrenia

A

Psychopathological disorder characterized by emotional withdraw & flat effect (-), w/ hallucinations & delusions (+)

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2
Q

Schizophrenia symptomology

A

Flat effect -
Withdraw -
Hallucinations +
Delusions +
Abnormal behavior +
Cognitive impairment +
-Memory, attention, social perception
-Autism relates w/ social cues

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3
Q

Schizophrenia Prevalence

A

<1% of populations
-60% being M
Onset typically late adolescence /early adulthood
-Large # onset around 40 (usually F, if F, potentially menopause cause)

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4
Q

Schizophrenia & Genetics

A

Concordance Rates:
-50% MZ
-17% DZ

Genome Wide Asssocation Study (GWAS):
-Genes relating w/ DA (COMT, degrading enzyme), ST, & Glutamate
-Overlaps w/ genes implicated in bipolar & autism spectrum disorder (ASD)
-DISC 1 Gene disruption/disabled

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5
Q

SCZ & Environment

A

INC rates in urban areas
-INC stress, population, & hazards (lead, ect)

Working class
-Work environment hazards

Migrants
-INC stress, poverty, & nutritional issues

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6
Q

SCZ & Epigenetics

A

Offspring of older fathers & younger mothers
-Some studies disagree w/ father
-Young mom = INC disposition
-INC ASD risk w/ older mom & dad

Pregnancy difficulties
-Hemorrhaging & T2 diabetes in mom
-Viral infection
*INC viral enzyme in baby brain & CSF (cerebrospinal fluid)
*Jan-Apr baby (cold climates as well)

Low birth weight & small head circumference

Birth difficulties
-lack of O2/emergency C-section

CHICKEN & EGG, WHERE START? CORRELATION!

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7
Q

SCZ Brain structure & function - Ventricles

A

Enlarged ventricles
-Loss of surrounding neurons
-DISC 1 (wiring & organize neurons) (tested in mice, hard to tell SCZ present)

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8
Q

SCZ Brain structure & function - HPC

A

Hippocampus
-Small
-DEC glutamatergic neurons
-Abnormal hpc cytoarchitecture
*neurons out of line

MAY explain cognitive deficits, as contributes to behavior, thought, & speech

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9
Q

SCZ brain structure & function - Frontal Cortex & Cortical Tissue

A

Frontal Cortex
-Overactive
-@ rest during cognitive tasks
-May contribute to - symptoms
*Mood disturbances & social withdraw

Cortical tissue
-Over pruned during adolescence
-Too much lost gray matter from puberty+

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10
Q

SCZ Biochem & treatment

A

Marijuana use
-Worse symptoms
-MAY trigger onset in genetically predisposed ppl
*COMT

Ppl w/ SCZ have INC endogenous cannabinoids
-Attenuates stress response

THC activates receptors & anandimides

Ppl w/ SCZ have INC CB1 receptors
-Independent of marijuana use
-In CNS

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11
Q

SCZ DA hypothesis

A

Too much dopamine/DA receptors & synthesis
-May boost response to irrelevant stimuli
-INC cocaine use causes SCZ like symptoms

COMT may cause DA breakdown
-too many receptors
*Causes inability to may attentions (Causing abnormal behavior)
-Changes brain & neuron layout

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12
Q

SCZ DA Hypothesis 2

A

DA (D2) receptor antagonist revolutionized psychiatry
-Good treating + symptoms
-DA & ST
-Block DA receptor
*Side effects: Tardive dyskinesia (muscle control), pseudo-PD
*DA plays role in muscle movement & control

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13
Q

SCZ Typical VS Atypical antipsychotics

A

Typical:
Primarily block DA
-No work in 1/4 w/ SCZ

Atypical:
Greater ST receptor block/antagonism
Better treats - symptoms
Produces tardive dyskinesia
INC chance of weight gain

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14
Q

SCZ Glutamate Hypothesis

A

Glutamate (GLT) is everywhere
-DEC GLT receptors
-DEC glutamate n/t in those w/ SCZ w/ age (IDK???)
-PCP & Ketamine mimic psychotic symptoms
*NMDA receptor agonists
-Glutamate receptor (NMDA) agonist = DANGER!
*Too much = BAD!

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15
Q

Pros & Cons of SCZ Meds

A

PROS:
No straight jackets & sedatives
Patients involved in activities
Patients can leave hospitals (complicated)

CONS:
Changed roles of psychiatrists (not just prescribing meds)
INC non-compliance outside hospital (no want take meds)
-Leads to homelessness, jail, or prison (New asylums)
*Lack of proper treatment, keeping them jailed
*More likely to try to commit suicide

THERE IS NO MAGIC FIX!

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16
Q

Feeding Behavior

A

Homeostasis- Internal equilibrium
-We eat because we NEED to!

Regulatory systems (hormones & neurons) defend our set points
-Temp- 98.6F
-Fluid lvls (Vasopressin - BP)
-Body weight & Glucose lvls in blood
*Those on show gained weight after leaving show from not keeping diet

We can make new set points!

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17
Q

Why we eat

A

Nutrients needed for energy
Satisfaction of eating
-Dorsal striatum (food thought, planning, & eating movement)
-NAc (Nucleus accumbens) & Orbital Frontal Glucoreceptors (OFC)
*Control eating motivation & reward

Complex cultural & psychological
-Overwhelm regulatory systems
-May lead to eating disorders

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18
Q

DIGESTION & PANCREATIC HORMONES

A

Digestion- fats, proteins, carbs metabolized into usable chemicals in stomach
-ST: Glucose (GLC) stored as glycogen in liver/muscle cells & neurons
*GLC needs maintained at certain lvl

-LT: Excess fat stored in adipose tissue
*Use fat when GLC lvls low

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19
Q

Pancreatic Hormones

A

GLC regulation (sugar & energy regulation)
1) Insulin moves GLC
-GLC signal pancreas, beta cells release insulin
-Insulin stores GLC in liver & muscle cells as glycogen
-INC ST storage

2) Glucagon: Glycogen to GLC
-Useable for energy
-Still ST

20
Q

INSULIN & DIABETES

A

Type 1
-“Childhood”
-Disorder insulin production = No insulin, no GLC storage, RIP (kills) cells & neurons from too much GLC
-Give insulin

21
Q

INSULIN & DIABETES 2

A

Type 2
-Adult onset
-Cell receptors don’t recognize insulin/produce energy
-Treat w/ metaphormin, INC receptor sensitivity
-Lifestyle changes needed, obesity risk factor
-Lvls of GLC INC for longer

22
Q

BIOLOGICAL INITIATION OF FEEDING 1/3

A

1) Low GLC & fat lvls
Glucoreceptors (in liver) talk w/ feeding initiation center of HPC
-Glucoreceptors → GLC lvls travel vegus nerve, INC feeding
-INC GLC = INC insulin released to store/utilize

23
Q

BIOLOGICAL INITIATION OF FEEDING 2 & 3 /3

A

2) Insulin
If low, DEC GLC = INC appetite
Small INC of insulin = DEC appetite
*If too much GLC = hypoglycemia

3) Those w/ T2 diabetes untreated have INC GLC lvls but always hungry from low insulin

24
Q

BRAIN & HORMONES INTERACT IN FEEDING

A

Ventromedial Hypothalamus (VMH)- Stops eating
-Lesions here = over eating & obesity (FAT RAT)
-Is our satiety area

Lateral Hypothalamus- Makes hungry
-Lesions here = stop eating & weight loss

When these areas are lesioned, eventually a new set point is made

25
BRAIN & HORMONES INTERACT IN FEEDING pt 2
Arcuate Nucleus (AN)- Bunch of cell bodies & neurons -Receive signals about GLC lvls from insulin & other signals -Fat cell, leptin (hormone), released from adipose tissue *Generally inhibits feeding hormone *Those obese have leptin insensitivity, INC feeding
26
BRAIN & HORMONES INTERACT IN FEEDING pt 3
Gut hormones: ST energy -Stomach → Ghrelin → hungry -Intestines → PYY336 → stop eating *PYY336 low in obese ppl
27
Neurons in the AN
POMC Neurons- Inhibit appetite / = satiety NPY- Stimulates appetite / = hunger -Can inhibit POMC -Ghrelin activates, causing feeding
28
B&HIIF pt 4
Insulin & PYY336 inhibit feeding. They dot not activate POMC, they inhibit NPY, DEC appetite Leptin stimulates POMC while inhibiting NPY, DEC feeding Feeding is a balance of 2nd order neurons -Lateral Hypothalamic = Orexigenic = INC appetite -PVN (Para ventricular nucleus) = anorexigenic = DEC appetite NST (Nucleus of Solitary Tract) = integrate signal from gut & brain -Comes in from GI tract
29
Appetite Modulators
Orexin- Has receptors in hypothalamus ⇅ - STIMULATE feeding in animals Anandamide- Body's THC -CB1 (in brain) & CB2 receptors
30
Parkinson's Disease (PD) Def & symptoms
Tremors of hands & face at rest -Rigid walking -"mask like" appearance - no face muscle control -Apraxia - Difficulty engaging in effortful movement
31
PD Prevelance
1-2% of US ages 65&+ -Rare but not never in Y-A M x2.5 more than F to get -Possibly from working in hazardous environments
32
NEUROBIOLOGY OF PD
Genes Defect in genes that encode for -Alpha-synuclein *Found in synaptic buttons *Releases n/t (Not enough DP) -Parkin *Degrades unneeded proteins
33
PD NEUROBIOLOGY THEORY
Defects in either gene leading to accumulation of alpha-synuclein -Forms Lewy bodies, screwing up neurons *Mitochondria cannot power neuron, killing it
34
BRAIN AREA COMPROMISED
Midbrain! Degeneration of DA containing cells in substantia niagra Dopaminergic neurons project to striatum -DA to striatum controls voluntary movement
35
PD TREATMENT
-Agonist at DA receptors (No work well) -MAOIs (INC DA activity) -LDOPA *Precursor for DA *Can cross BBB (DA cannot) *Side effects: Tolerance, hallucinations, INC libido *Only treats symptoms, not cell death -DBS- Pacemaker stimulates striatum (axon terminal from substantia niagra) to release DA
36
Exercise and PD
Postmortem examinations reveal DA loss in the substantia nigra pars compacta (SNc), and the consequent loss of DA in the striatum in the brains of PD patients. -Exercise restores BDNF levels and has has neuroprotective effects against the neurotoxicity induced by 6-OHDA. -No BDNF = No TH -TH decrease in both SED group and SED + K252a group -When K252a added, all groups that received 6-OHDA showed decreases of TH levels. -intermittent treadmill exercise employed an increase of BDNF levels -Treadmill running at 5 days/week during 18 weeks DEC dopaminergic cell loss, INC dopamine and its transporter expression, and consequently improves balance and motor coordination -The intermittent exercise protocol could be more beneficial than continuous exercise, in addition to being closer to the exercise protocols undertaken in PD patients.
37
Exercise & PD pt 2
-TH in the CPu, and showed reduced motor symptoms -treadmill exercise = changes in BDNF lvls = activate TrkB-dependent mechanisms (related to survival of nigrostriatal dopaminergic neurons) -blockade BDNF–TrkB signaling = worsened neuroprotective effects of exercise after K252a injection -Physical activity INC serum BDNF, which cross the blood–brain barrier, and may decrease the PD risk
38
First-rank symptoms of SCZ
Auditory hallucinations Highly personalized delusions Changes in affect (emotion)
39
Supersensitivity Psychosis
Exaggerated “rebound” psychosis when antipsychotic meds are reduced, probably as a consequence of the up-regulation of receptors during drug treatment
40
Basal Metabolism
Use of energy for -Heat production -Maintenance of membrane potentials -All the other basic life-sustaining functions of the body.
41
Cephalic Phase of feeding
Triggered by sights, smells, and tastes that we have learned to associate with food
42
Digestive Phase of feeding
Food entering the digestive tract prompts an additional release of insulin
43
Absorptive Stage
As digested food is absorbed into the bloodstream, gluco-detectors detect the increase in circulating glucose and signal the pancreas to release still more insulin
44
Orexigenic Neurons VS Anorexigenic Neurons
Orexigenic neurons promote feeding behavior. Anorexigenic neurons inhibit feeding behavior.
45
Cholecystokinin (CCK)
Peptide hormone released by gut after ingestion of food high in protein and/or fat.