pre exam 3 Flashcards

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1
Q

main indicators of type 1 vs type 2 diabetes

A

type 1

  • 10% of patients
  • occurs at early age
  • autoantibodies mean that they have less beta cells (don’t produce insulin)

type 2

  • 90% of patients
  • older onset; often relates to weight gain (linked to obeisity)
  • tissues become insulin resistant after too much use; receptors not sensitive to it
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2
Q

how does type 1 diabetes work?

A
  • people generate autoantibodies directed against Beta cells in pancreas
  • antibodies normally target foreign pathogens for removal by immune cells
  • autoantibodies thus “prune” Beta cells, reducing amount of insulin that can be produced
  • variable time course for tissue loss/diabetes onset depending on pruning of cells!
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3
Q

type 1 diabetes treatments

A
  • frequent monitoring of blood glucose
  • regimented eating schedule
  • insulin administration (injection or pump)
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4
Q

how does type 2 diabetes form?

A
  • related to weight gain/obesity
  • overuse of insulin over time leads to insulin resistance, receptors don’t send signal to cell when insulin binds
  • hyperlipidemia is another indicator
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5
Q

type 2 diabetes treatments

A
  • monitor blood glucose
  • treatments to increase insulin release
  • diet
  • exercise

*must lose fat to increase receptor sensitivity, diet and exercise very important!!

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6
Q

consequences of uncontrolled diabetes

A

CV disease, hyperlipidemia, decreased blood blow and neuropathy, oxidative cellular damage

  • chronic high blood sugar leads to increase in free radicals (atom with an unpaired valence electron)
  • antioxidants normally donate electrons to them, reducing reactivity
  • too many free radicals for antioxidants to help; they damage molecules by stealing their electrons
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7
Q

how do we get an indication of someone’s blood glucose level?

A
  • glycolated hemoglobin gives good indication of 3 months of glucose levels
  • accurate measure because it doesn’t take into account recent eating (levels constantly varying)
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8
Q

how does diabetes affect peeing?

A
  • high blood glucose causes high levels of kidney glucose
  • SGLT transporters, which normally move glucose out of fluid, become saturated by the high glucose levels (glucose stuck)
  • kidney collecting ducts still have high levels of glucose, resulting in water movement into the kidney via osmosis (higher urine volume)
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9
Q

can single-celled organisms learn?

A
  • evidence: smile molds habituate and cross quinine bridge (adversive taste) quicker each day to reach food
  • more cellular adaptability than learning–learning lasts over time (durable)
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10
Q

subdivisions of the nervous system

A

central nervous system (brain and spinal cord)

peripheral nervous system (nerves)

  • sensory input
  • motor output
    • somatic (voluntary)
    • autonomic (involuntary)
      • sympathetic (prepares for emergencies)
      • parasympathetic (controls during non-emergencies)
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11
Q

flow of signals in the nervous system

A

sensory input (sensory receptor in PNS) - central processing/integration (CNS) - motor output (effector in PNS)

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12
Q

how did we develop sensory and motor functions?

A
  • internal homeostatic mechanisms developed first (breathing, heart rate, hormones)
  • then external sensory and motor developed (vision, olfaction)
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13
Q

social brain hypothesis

A

human social organization in large groups is associated with our growth of the cortex

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14
Q

human cortex

A
  • neocortex differentiates human brain from other animals
  • took less than 4 million years to develop
  • result of evolutionary pressures for survival
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15
Q

how is information processed in the brain? what are the levels of structure?

A
  • processing is distributed across many parts of the brain
  • neurons are units of processing; they form circuits and networks to process info

structures:
neuron cell - local circuit - network of cells - brain function

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16
Q

flow of information in ascending sensory pathways

A
  • go from sense receptor to primary sensory cortex (in the parietal lobe)
  • 3 cells involved
17
Q

flow of information in descending motor pathways

A
  • go from primary motor cortex to lower motor neuron

- 2 cells

18
Q

what can we learn from the homunculus

A

homunculus: sensory and motor cortexes laid out to map what body parts they respond to/signal

takeaways: brain is topographically organized, and different amounts of brain are dedicated to particular parts of the body
* lots of sensory/motor brain tissue for face and hands (important functions like speaking and using hands for tasks)

19
Q

autonomic control in the brain

A
  • multicellularity demands some type of autonomic control
  • areas important for autonomic control: hypothalamus, spinal cord, medulla, pons, pituitary
  • damage to medulla/pons can be lethal (they control breathing and heart rate)
20
Q

autonomic functions of the hypothalamus

A

sleep/wake cycle, circadian rhythm, thermal regulation, hunger/thirst

21
Q

cell types in the brain

A
  • neurons and glial cells (astrocytes, oligodendrocytes, microglia)
  • 200 billion cells, each with up to 10k connections
  • glial cells may outnumber neurons
22
Q

astrocytes

A
  • biggest contributor to shaping neuron activity
  • couple neurons to blood vessels; can increase blood flow according to neuron’s metabolic demand
  • regulate amount of neurotransmitter between cells (can remove NT)
23
Q

oligodendrocytes

A
  • myelinate neurons in the CNS
  • myelin insulates the axon, allowing for faster conduction and processing
  • more myelin in the neocortex–newer development for faster processing because of increase in # of neuron cells
24
Q

microglia

A
  • immune-like role
  • find, mark, and eat pathogens and dead cells
  • clean up cellular debris after injury
25
Q

parts of a neuron and transmission of signal

A
  • dendrites (input)
  • soma (integration)
  • axon hillock/initial segment (signal generation)
  • axon (conduct)
  • synapse (output)

input - integration - conduction - output

26
Q

benefits of studying model organisms’ nervous systems

A
  • easier to study organisms with 10,000 neurons compared to 100 billion
  • more similarities than differences; help explain human conditions
27
Q

how can we observe electrical signaling?

A
  • scope inserted inside neuron cell to measure electrical current
  • dye can also be used
  • special microscopes allow us to observe dye movement
28
Q

how do electrical signals transfer between neurons? (general)

A
  • electrical signals turned into chemical signals
  • neurotransmitters (chemical messengers) are released and bind to ligand-gated ion channels on the dendrite
  • influx of ions cause charges to be sent to axon initial segment, where action potentials begin (high density of ion channels there, they open if the threshold potential is reached)
29
Q

how do electrical charges flow through a neuron?

A
  • charges enter via ions in channels

- current diffuses passively through dendrites and cell body to axon initial segment (like dye spreading out)

30
Q

dye metaphor for charge potentials

A

+ charges depolarize the cell and increase action potential generation (excitatory); like blue dye
- charges hyperpolarize the cell and decrease action potential generation (inhibitory); like red dye

***charges summate to create a net charge (some form of purple)

31
Q

cell potential termonology

A
  • polarization: separation of charge (inside of cells more - than outside)
  • depolarization: cell moving towards more + potentials
  • hyperpolarization: cell moving towards more - potentials
  • repolarization: restoring resting membrane potential (always negative)
32
Q

importance of summation of potentials

A
  • small potentials constantly being received at different areas of the dendrite
  • charges summate to form an overall net charge at axon initial segment
  • if net excitatory potential causes cell to depolarize to -55mV, an action potential is reached
33
Q

variables important for coding of info in the brain

A
  • frequency and pattern of action potentials is important for coding information in the brain
  • Dr. Erlichmann observed cells involved in breathing in small organisms (many less neurons)–burst of action potentials were required for breathing
34
Q

importance of membrane potential

A
  • inside of cells is negative relative to the outside, but difference in charge occurs only at the membrane
  • makes the cell like a small battery; potential energy powers membrane transport processes
  • membrane potential kept by Na+/K+ pumps
35
Q

neurotransmitter release and binding

A
  • action potential moves towards axon terminal, opening voltage gated Ca channels
  • Ca causes fusion of vesicles to membrane and release of neurotransmitters into synapse
  • ligand-gated ion channels open when neurotransmitters bind, allowing charges into postsynaptic cell
36
Q

types of ion channels in the dendrite

A
  • Na+ channels depolarize the cell, cause excitatory potentials (common)
  • Chloride channels hyperpolarize the cell, cause inhibitory potentials
37
Q

graph/numbers of action potentials

A
  • resting potential at -70mV
  • Na+ in causes the cell to depolarize
  • action potential reached if cell hits threshold potential of -55mV (can result from summation of potentials)
  • K+ out causes the cell to repolarize
  • excess K+ out may cause cell to hyperpolarize
  • cell then goes back to resting potential at -70mV