Unit 4 Flashcards
(45 cards)
Schizophrenia
Psychopathological disorder characterized by emotional withdraw & flat effect (-), w/ hallucinations & delusions (+)
Schizophrenia symptomology
Flat effect -
Withdraw -
Hallucinations +
Delusions +
Abnormal behavior +
Cognitive impairment +
-Memory, attention, social perception
-Autism relates w/ social cues
Schizophrenia Prevalence
<1% of populations
-60% being M
Onset typically late adolescence /early adulthood
-Large # onset around 40 (usually F, if F, potentially menopause cause)
Schizophrenia & Genetics
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
SCZ & Environment
INC rates in urban areas
-INC stress, population, & hazards (lead, ect)
Working class
-Work environment hazards
Migrants
-INC stress, poverty, & nutritional issues
SCZ & Epigenetics
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!
SCZ Brain structure & function - Ventricles
Enlarged ventricles
-Loss of surrounding neurons
-DISC 1 (wiring & organize neurons) (tested in mice, hard to tell SCZ present)
SCZ Brain structure & function - HPC
Hippocampus
-Small
-DEC glutamatergic neurons
-Abnormal hpc cytoarchitecture
*neurons out of line
MAY explain cognitive deficits, as contributes to behavior, thought, & speech
SCZ brain structure & function - Frontal Cortex & Cortical Tissue
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+
SCZ Biochem & treatment
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
SCZ DA hypothesis
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
SCZ DA Hypothesis 2
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
SCZ Typical VS Atypical antipsychotics
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
SCZ Glutamate Hypothesis
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!
Pros & Cons of SCZ Meds
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!
Feeding Behavior
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!
Why we eat
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
DIGESTION & PANCREATIC HORMONES
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
Pancreatic Hormones
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
INSULIN & DIABETES
Type 1
-“Childhood”
-Disorder insulin production = No insulin, no GLC storage, RIP (kills) cells & neurons from too much GLC
-Give insulin
INSULIN & DIABETES 2
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
BIOLOGICAL INITIATION OF FEEDING 1/3
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
BIOLOGICAL INITIATION OF FEEDING 2 & 3 /3
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
BRAIN & HORMONES INTERACT IN FEEDING
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