Lecture Exam 2 SLO's Flashcards

1
Q

Distinguish between chemical and electrical driving forces

A

Chemical~ rate of transport depends on the size of the concentration gradient; passive transport; outward or inward

Electrical~ affects charged particles only (ions); opposites attract, likes repel; inward or outward

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2
Q

List equilibrium potentials for Na+ and K+

A

Na+~ +60mV
K+~ -94mV

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3
Q

How does equilibrium potential determine the cell’s permeability to Na+ and K+?

A

~ value for the electrical and chemical driving forces to be the same magnitude so the same amount of ion enters and leaves

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4
Q

Define equilibrium potential

A

~ membrane potential at which the electrical driving force exactly opposes (balances) the chemical driving force; no net movement of the ion
-electrochemical gradient=0

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5
Q

Define membrane potential

A

~ a difference in electrical potential across the plasma membrane; sign of membrane potential is net charge inside the cell

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6
Q

Determine the direction of movement of a solute/ion based on electrochemical driving forces.

A

~ opposites attract and likes repel, moves from high to low concentration, so net flux determines direction of solute/ion
-moves more toward one direction if does not meet equilibrium potential

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7
Q

Identify the three general things that influence the rate at which a substance can be passively transported across a membrane.

A

~ magnitude of driving force, membrane surface area, membrane permeability

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8
Q

Distinguish between passive transport and active transport, recognize examples

A

Passive~ net flux is down the electrochemical gradient; simple diffusion, facilitated diffusion, and diffusion thru channels; has affinity for molecule on either side

Active~ net flux is up electrochemical gradient; primary and secondary active transport, utilizes ATP because going against gradient, has greater affinity for molecule on other side

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9
Q

Describe simple diffusion

A

~ spontaneous transport of molecules across the plasma membrane

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10
Q

Describe how magnitude of driving force impacts simple diffusion

A

~ magnitude of driving force decreases with time
- starts to slow down until equilibrium

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11
Q

Describe how membrane surface area impacts simple diffusion

A

~ huge surface area is physiologically significant on the inner mitochondrial membrane, intestines and alveoli, increased by microvilli and cristae
-more can cross

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12
Q

Describe how membrane permeability impacts simple diffusion as well as factors to consider

A

~high permeability= higher net flux and more stuff can cross
~low permeability= less can cross, low net flux
-lipid solubility (nonpolar passes easier)
- size and shape of molecule (too big, can’t cross)
- temperature
- membrane thickness (harder to pass when thicker)

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13
Q

Describe facilitated diffusion

A

~ requires a transmembrane protein, following a conformational change a molecule could be taken back across the membrane
- net flux depends on concentration gradient
-hinge mechanism for conformational change
- no preferential direction

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14
Q

What are the three factors impacting facilitated diffusion?

A

~ transport rate of individual carriers
~ magnitude of concentration gradient
~ number of carriers
-levels off because of saturation of carriers, carriers work as hard as they can, max out, increases in concentration gradient won’t help

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15
Q

Describe diffusion through channels

A

~ can be regulated to be open or closed; with conc gradient
-aquaporins and ion channels
-start out shut or open and signaled to do opposite action

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16
Q

Define active transport

A

~transmembrane protein (carriers) that use energy to drive molecules in a preferred direction

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17
Q

Identify the two general factors that influence the rate of active transport

A

~presence of a pump and electrochemical gradient

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18
Q

What is the steady state?

A

~ occurs when the concentration gradient offsets affinity; reduce the level on one side and bring molecules back

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19
Q

Identify four factors affecting the permeability of membranes to molecules that cross by simple diffusion

A

~ lipid solubility, size and shape of molecules, temperature and membrane thickness

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20
Q

How does lipid solubility affect membrane permeability?

A

~ non polar molecules pass easier through phospholipid bilayer (fat likes fat)

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21
Q

How does the size and shape of the molecule affect membrane permeability?

A

~ if the molecule is too big it cannot cross the membrane

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22
Q

How does temperature affect membrane permeability?

A

~low temperatures decrease fluidity of fatty acid tails and make the membrane less permeable

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23
Q

How does membrane thickness affect membrane permeability?

A

~ harder to pass of thicker

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24
Q

Compare the movement of molecules through carriers to channels

A

Channels~ require ATP for active transport and have a greater affinity for a molecule on one side

Carriers~ passive transport, do not possess greater affinity for either side of membrane

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25
Q

Define primary active transport

A

~ ATP is used directly, pumps act as carrier and enzyme whose function is ATP hydrolysis (ATPase)

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26
Q

Define secondary active transport

A

~ powered by the electrochemical gradient created during primary active transport

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27
Q

Describe the Na/K ion pump

A

~primary active transport
~ Na enters the pump, pump is phosphorylated by ATP and undergoes a conformational change- flips open on ECF side to release Na into the ECF, pump is dephosphorylated, undergoes another conformational change, K binds and is released into the ICF

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28
Q

Describe sodium linked glucose transport

A

~secondary active transport
~ K concentration increases inside the cell, Na concentration decreases inside the cell, concentration gradient is created by primary active transport, Na would deplete without secondary active transport so, Na is replenished and helps glucose into the cell by cotransport

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29
Q

Describe sodium proton exchange

A

~ secondary active transport (counter)
~ Na concentration decreases, K concentration increases, Na is brought back in and exchanges a H proton for it; by countertransport, leak channels (always open) allow Na/K back in and out depending on the direction of the electrochemical gradient

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30
Q

Define osmosis

A

~passive flow of water across the membrane, unaffected by membrane potential, has an affect on cell volume

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31
Q

Define osmolarity

A

~ total solute particle concentration of a solution

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32
Q

Define an iso-osmotic solution

A

~ two solutions with equal osmolarity; [solute]=[H2O]

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33
Q

Define a hyperosmotic solution

A

~ a solution whose osmolarity is higher than another; [solute] > [H2O]

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34
Q

Define a hypo-osmotic solution

A

~ solution whose osmolarity is lower than another; [solute] < [H2O]

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35
Q

Describe osmotic pressure

A

~ water is moving up an osmotic pressure gradient; follows solute movement from low to high concentrations; indirect measure of solute concentration

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36
Q

Define tonicity

A

~ concentration of impermeant solutes in ECF ONLY relative to ICF

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37
Q

Describe an isotonic solution

A

~ equal concentrations of impermeant solutes ONLY in ECF relative to ICF

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38
Q

Describe a hypotonic solution

A

~ less impermeant solute outside compared to inside; water flows in and cell swells

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39
Q

Describe a hypertonic solution

A

~ more impermeant solute outside compared to inside; water flows out and cell shrinks

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40
Q

Explain how water moves across membranes using the concepts of osmolarity and tonicity

A

~ water flow follows the movement of molecules
~ molecules flow passively from high concentration to low and water flows up concentration gradient

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41
Q

Describe excessive sweating

A

~ excessive sweating can increase the osmolarity of the plasma and cause cells to shrink
-sweat out ions and salts from rbcs into plasma, increasing total osmolarity and increasing tonicity of plasma (ECF) so water flows out of cells and cells shrink

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42
Q

Describe water intoxification

A

~ hyperhydration can expose cells to decreased plasma osmolarity and swelling
-increase water concentration inside the cells, water follows higher concentration of ions inside cells and cells swell and burst

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43
Q

Describe diabetes mellitus

A

~ glucose permeates the membrane relatively well via facilitated diffusion, insulin-dependent glucose carriers are impaired or absent in diabetes making glucose impermeant to cells
-this increases the tonicity of the plasma causing cells to shrink and become damaged (increase of glucose in plasma- ECF- so hypertonic and water flows out and cell shrinks

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44
Q

Define endocytosis

A

~molecules in ECF brought into the cell via formation of an endosome
-phagocytosis
-pinocytosis
-receptor mediated

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45
Q

Define exocytosis

A

~ molecules are packaged into secretory vesicles inside the cell and released into ECF; replenishes pinched off phospholipids from endocytosis

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46
Q

Describe phagocytosis

A

~ engulfing and bringing in larger materials; membrane creates pseudopods that go up around fuse together and pinch off brining in material
-phagosome (endosome)
-can also bring in materials to degrade by fusing with a phagolysosome which releases digestive enzymes

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47
Q

Describe pinocytosis

A

~ bring in molecules dissolved in ECF; no pseudopods, membrane creates a pit and molecules flow in and pinch off- endosome

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48
Q

Describe receptor mediated endocytosis

A

~ requires a receptor protein; line up of clathrin proteins creates a coated pit and pinches off into cell

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49
Q

Explain in general terms how the polarity of epithelial cells allows them to absorb and secrete materials

A

~ apical membrane actively transports Na into cells along with glucose by cotransport, glucose accumulates and exits via facilitated diffusion at the basolateral membrane
~ active pumping of solute across membrane followed by passive water movement (osmosis)

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50
Q

Describe cystic fibrosis

A

~ buildup of mucus that increases chances of respiratory infections
~ cystic fibrosis patients’ protein can’t pump Cl- out to attract Na+ out , so no H2O movement and H2O cannot loosen up mucus so pathogens stay in the mucus

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51
Q

Describe transcytosis

A

~ across cell; move material across the cell by a vesicle
-endocytosis-> exocytosis
-how you digest a pill in the small intestine

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52
Q

What are the three major functional classes of chemical messengers?

A

~ paracrines/autocrines, neurotransmitters, and hormones

53
Q

Define paracrines

A

~ reach target cells via simple diffusion, act locally

54
Q

Define autocrines

A

~ act on cell that secreted them

55
Q

Define neurotransmitters

A

~ synaptic signaling, synapse-specific, released by neurons

56
Q

Define hormones

A

~ released from glands…mostly, exception of neurohormones, all cells exposed, only cells with receptors are affected, travel thru bloodstream

57
Q

Describe the basic structure and function of amino acid messengers.

A

~glutamate, aspartate, glycine, GABA
~hydrophilic, receptors on plasma membrane
~ synthesized within neurons, not from food
~ synthesized in cytosol of neurons
~packaged into vesicles in the same cell and stored until exocytosed

58
Q

Describe the basic structure and function of amine messengers.

A

~ lipophobic;contains an amine group NH2
~ catecholamines: dopamine (neurotransmitter), norepinephrine (neurotransmitter) and epinephrine (hormone)
~ serotonin (neurotransmitter), histamine (paracrine), thyroid hormones (only amine that is lipophilic)
~ receptors on plasma membrane
~ derived from amino acid, except thyroid hormone synthesized in cytosol, packaged in vesicles until exocytosed

59
Q

Describe catecholamine synthesis.

A

cytosol:
1. derived from tyrosine
2. made into L-dopa
3. dopamine
vesicle:
4. enzymatic reaction-> norepinephrine
5. release norepinephrine into the cytosol into epinephrine

60
Q

Describe the basic structure and function of peptide/protein messengers.

A

~ most chemical messengers are polypeptides (peptide is < 50 amino acids and protein is > 50 amino acids)
~ hydrophilic, receptors on plasma membrane
~ synthesis same as any protein, proteolytic enzymes in Golgi or vesicles create final product

61
Q

Describe the basic structure and function of steroid messengers

A

~ derived from cholesterol
~ always function as hormones and travel through bloodstream
~ lipophilic
~ receptors in cytosol, few exceptions on membrane
~ synthesized in smooth ER or mitochondrion because the membrane is permeant and cannot be stored in cells which secrete them (dissolve in fat)
~ cholesterol:
testosterone -> estradiol
progesterone
->cortisol/aldosterone

62
Q

Describe the basic structure and function of eicosanoid messengers.

A

~ lipids, paracrines
~ mostly derived from arachidonic acids (fatty acid)
~ lipophilic, receptors in cytosol
~ membrane phospholipid-> phospholipase A2 removes fatty acid from membrane and turns into arachidonic acid which can take the cyclooxygenase pathway or lipoxygenase pathway

63
Q

What are the products of the cyclooxygenase pathway of eicosanoid synthesis

A

~ prostaglandins, prostacyclins, thromboxanes

64
Q

What is the product of the lipoxygenase pathway of eicosanoid synthesis

A

~ leukotrienes

65
Q

Describe transport of hydrophilic messengers

A

~ chemical messenger dissolves in blood which is primarily water and acts as a hormone because its traveling through the blood and endocrine cell

66
Q

Describe transport of lipophilic messengers

A

~ hormone that does not like water, would clump together in blood without proteins, enters the blood and binds to carrier proteins but not all i.e free hormones bind to a receptor reversibly

67
Q

Compare and contrast signal transduction mechanisms for lipophilic and lipophobic messengers

A

lipophilic:
~ can cross membrane via simple diffusion and bind to the receptor slow effects because of changes in protein synthesis, newly synthesized proteins stay in target cell after messenger is gone so effects persist for long time, receptors usually in cytosol or nucleus of target cells

lipophobic:
~cannot permeate membrane so receptors are on the plasma membrane of the target cell; channel linked receptors, enzyme linked receptors and g protein linked receptors

68
Q

What are the factors affecting receptor binding

A

~ messenger concentration (increase until saturation)
~ receptor concentration (more receptors= more binding, up regulation and down regulation)
~ receptor affinity (high affinity reach saturation sooner)

69
Q

Differentiate between up regulation and down regulation

A

UP:
~ increase the number of receptors relative to normal conditions due to chronically low messenger concentration

DOWN:
~ decrease number of receptors relative to normal conditions due to chronically high messenger concentration

  • with constant binding the body must adapt to prevent an over sensitized body
70
Q

Differentiate between agonists and antagonists

A

Agonist:
~ ligand causes cell response with binding

Antagonist:
~ ligand prevents cell response with binding, competes with agonist molecule for the binding site

71
Q

Describe channel linked receptors

A

~ will ONLY cause a channel to OPEN; also called ligand gated channels, fast response because of immediate movement
- transmembrane protein acts as both the receptor and channel
- messenger binds, signals channel to open and allow ion movement by electrochemical driving force, alters the cell’s electrical properties
- can also interact with intracellular proteins for varied responses, effects occur quickly, but binding is brief so the effects are short lived
ex: Ca carries a positive charge so alters the electrical properties of the cell, forms Ca-calmodulin, protein kinase is activated, phosphorylation of the protein, altered structure and function via covalent regulation

72
Q

Describe enzyme linked receptors

A

~ fast response
~receptor and enzyme in one protein, tyrosine kinase is most common
- once chemical messenger binds, activates tyrosine kinase (phosphorylate protein with tyrosine amino acid), covalent regulation

73
Q

Describe G protein linked receptors

A

~ slow response, signaled to open or closed; regulated by G proteins
~ G protein linked channel is separate from protein (complex protein in quaternary structure found loosely anchored to the outside surface)
- G protein activated by GDP binding, swapped for GTP and alpha subunit dissociates and slides under until reaching channel, tells the channel to open, allows flow of ions

74
Q

G protein linked enzymes

A

~alpha subunit slides to enzyme instead, can activate or inhibit protein (Gs or Gi)
-cAMP
- cGMP
-DAG
-TP3
-Calcium

75
Q

Compare and contrast communication mediated through the nervous and endocrine systems

A

Nervous:
~ fast but short lived responses typically impacting ion channels
~ electrical communication along neuron itself and chemical communication between synapses
~secretory cell neurons, target cells neuron muscle or gland, neurotransmitters, receptors on postsynaptic target cell, immediate effect, brief duration

Endocrine:
~ typically impacts protein synthesis or acts on G protein linked receptors, slower effect but longer lasting
~ secretory cell endocrine cell, target cells most cell types in body, hormones, through bloodstream, receptors on target cells throughout body, delayed effect, long duration

76
Q

Describe signal amplification using the cAMP example

A

~ start with one messenger binding to the receptor, activates many G proteins which go to the enzymes and pump out the second messenger molecules
ex: one messenger binds to one receptor, several G proteins are activated, each G protein activates an adenylate cyclase, each adenylate cyclase generates hundreds of cAMP molecules, each cAMP activates a protein kinase A which phosphorylates proteins

77
Q

Describe the role of the pineal gland

A

Primary
- pineal gland~ secretes melatonin for sleep signals, located in the brain, impacted by working nightshift, blindness, living in Alaska with inconsistent sunlight and darkness

78
Q

Describe the role of the thyroid and parathyroid glands

A

Primary
Thyroid:
- T3 and T4 regulate metabolism, growth and development; hyperthyroidism and hypothyroidism
-calcitonin decreases blood calcium levels
Parathyroid:
-parathyroid hormone (PTH) increases blood calcium levels

79
Q

Describe the role of the thymus gland

A

Primary
- secretes thymosin, regulates T lymphocytes, located on top of heart under sternum, immune function in babies in children
- shrinks in adulthood

80
Q

Describe the role of the adrenal glands

A

Primary
Cortex:
- secretes adrenocorticoids- steroid hormones
-mineralocorticoids- aldosterone, regulates Na reabsorption and K secretion in kidneys
-glucocorticoids- cortisol, regulates stress response, substrate metabolism and blood glucose levels
-sex hormones- only small amount

Medulla:
-chromaffin cells secrete catecholamines- 80% epinephrine and 20% norepinephrine

81
Q

Describe the role of the pancreas

A

Primary
~ located under stomach above small intestine
~ insulin to decrease blood glucose (beta cells), glucagon to increase blood glucose (alpha cells), somatostatin for digestion and absorption (delta cells)

82
Q

Describe the role of the gonads

A

Primary
~ testes in men, produce sperm, secrete androgens, testosterone and androstenedione
~ovum in females, produce oocytes, secrete estradiol and progesterone

83
Q

Describe the heart’s endocrine function

A

~ secretes ANP to affect Na handling in kidneys

84
Q

Describe the kidney’s endocrine function

A

~ secretes erythropoietin for RBC production in marrow

85
Q

Describe the liver’s endocrine function

A

~ secretes IGFs for bone and soft tissue growth

86
Q

Describe the GI Tracts endocrine function

A

~ secretes multiple hormones to regulate digestion

87
Q

Describe the skin, liver and kidneys’ endocrine function

A

~ secretes 1.25- dihydroxy vitamin D3 to promote calcium absorption

88
Q

Describe the links between the hypothalamus with the posterior pituitary lobe

A

posterior/neurohypophysis:
- made up of nervous tissue, secretes 2 neurohormones: oxytocin (supraoptic nucleus, letdown reflex and uterine contractions) and vasopressin (paraventricular nucleus, water conservation)
- neurosecretory cells (axons) from hypothalamus, through the infundibulum to posterior pituitary
-axon terminals release hormones into capillaries

89
Q

Describe the links between the hypothalamus with the anterior pituitary lobe

A

~ made up of glandular tissue that secretes tropic hormones in response to hypothalamic hormones
- neurosecretory cells do not extend; release tropic hormones into first capillary bed at base of hypothalamus, travel through hypothalamic portal vein to second capillary bed and exit through anterior pituitary signaling endocrine cells to release hormone into bloodstream ( in series bloodflow between hypothalamic portal vein and anterior pituitary)

90
Q

Describe the role of tropic hormones in regulating the release of other hormones

A

~ hypothalamic tropic hormones are neurohormones that activate or inhibit the release of tropic hormones from the anterior pituitary gland.

91
Q

Describe the feedback loop of TRH, TSH and thyroid hormone

A

~stimulatory
1. TRH in hypothalamus
2. travel thru hypothalamic portal vein into anterior pituitary gland
3. activate TSH, released into thyroid gland
4. thyroid gland secretes thyroid hormone

92
Q

Describe the feedback loop of CRH, ACTH and cortisol

A

~stimulatory
1. CRH released from hypothalamus
2. travels through hypothalamic portal vein into anterior pituitary gland
3. signals release of ACTH into adrenal cortex
4. secretes cortisol

93
Q

Describe the feedback loop of GHRH, GH and IGFs

A

~stimulatory
1. GHRH released by hypothalamus
2. travels through hypothalamic portal vein into anterior pituitary gland
3. signals release of growth hormone into liver and cells throughout the body
4. liver releases insulin like growth factors

94
Q

Differentiate between long loop and short loop negative feedback

A

long loop:
- signal hypothalamus to stop from last hormone or signal second hormone to stop

short loop:
-signal hypothalamus from second tropic hormone to stop

95
Q

Describe antagonism hormone interactions

A

~ effects are in opposition i.e insulin and glucagon

96
Q

Describe additive hormone interactions

A

~ net effect= sum of individual effects i.e A=2x, B=4x, A+B= 6x

97
Q

Describe synergistic hormone interactions

A

~ net effect> sum of individual effects i.e A=2x, B=4x, A+B= 10x

98
Q

Describe permissiveness hormone interactions

A

~ presence of one hormone is necessary for another to exert its effects

99
Q

Differentiate between primary vs secondary abnormal hormone secretion and hypersecretion vs hyposecretion

A

primary~ last hormone malfunctioning

secondary~ one of the tropic hormones malfunctioning

hypersecretion~ secreting too much

hyposecretion~ not secreting enough

100
Q

Define and describe what is meant by afferent and relate that to the direction of information flow relative to the brain and spinal cord

A

~ afferent= sensory, in the PNS which divides into the somatic senses, special senses and visceral senses
~ carries sensory information from peripheral to CNS as input

101
Q

Define and describe what is meant by efferent and relate that to the direction of information flow relative to the brain and spinal cord.

A

~ efferent=motor, in the PNS which divides into the somatic nervous system (skeletal muscles) and autonomic nervous system which has sympathetic (cardiac, smooth muscle and glands) and parasympathetic divisions (enteric nervous system)
~ carries motor information either voluntary or involuntary from CNS to periphery as output

102
Q

Define and describe what is meant by associational and relate that to the direction of information flow relative to the brain and spinal cord.

A

~ interneurons, found exclusively in CNS
~ relay information between neurons

103
Q

Describe the basic anatomy of a neuron.

A

Dendrites -> soma -> axon hillock -> axon -> axon terminals -> synaptic cleft -> postsynaptic neuron
-axons are tubular extensions of the soma, full of the same ICF and cytoskeletal elements, have typical organelles

104
Q

Compare the functions of each part of a neuron and describe the different types of ion channels located in each

A

Dendrites~ receive input; leak channels and ligand gated channels
Soma~ amino acid chemical messenger synthesis; leak channels, ligand gated channels
Axon hillock~ tapering of soma, generate action potentials; voltage gated Na and K channels
Axon~ transmit information; voltage gated Na and K channels
Axon terminals~ sending information to postsynaptic neuron in synaptic cleft; voltage gated Ca channels

105
Q

Describe the grouping of neurons in the CNS and the PNS

A

CNS:
-tracts~ group of axons traveling together in the CNS (white matter, not an organ)
-nucleus~ group of neuronal soma in CNS (grey matter)

PNS:
-nerve~ axons traveling together in PNS (organ)
- ganglion~ group of neuronal soma in PNS

106
Q

Describe the structure and function of myelin

A

CNS:
-oligodendrocytes have multiple processes that reach out and wrap around the axon to myelinate it in segments with nodes of ranvier in between where signal “jumps” between nodes

PNS:
-Schwann cells form myelin by folding itself continuously around axon in segments with nodes of ranvier between

*myelin functions to speed up electrical signals along axons

107
Q

Explain the roles of Na and K permeability (leak channels and pumps) in establishing the resting membrane potential

A

Chemical driving forces for Na and K (Na wants to move in, K wants to move out

Na/K pump (establishes chemical driving forces for Na and K, actively prevents abolishment of concentration gradient as Na and K move across the membrane)

Differences in permeability of the membrane to Na and K (leak channels for both Na and K but WAY more open to K channels- greater permeability)

108
Q

Describe the various properties of graded potentials including the direction of change in
potential, the magnitude of change, and temporal and spatial summation

A

~ small, decremental changes in membrane potential that occur when ion channels are signaled to open or close

~the change in membrane potential decreases as it moves away from the stimulation site

~ can be hyperpolarizing (more negative membrane potential, inhibitory graded potential, ISP)

~can be depolarizing (less negative membrane potential, excitatory graded potential, EPSP)

~temporal summation- stimulus occurs quicker in time

~spatial summation- occurs in 2 different sites over entire surface area, multiple signals from different areas on neuron i.e at the same time in different areas

~ typically one synapse is not sufficient to trigger an action potential, requires more than one type; summed at axon hillock

109
Q

Explain how and where graded potentials can trigger an action potential.

A

~ if a cell is depolarized to a certain level i.e threshold, an action potential will result which will carry electric signals down the entire axon
- all stimuli are summed at the axon hillock
- occur in the membranes of excitable cells in response to graded potentials that sum together and reach threshold; not decremental so can be propagated long distances without decrease in amplitude, doesn’t weaken along aAXON
- rapid DEPOLARIZATION of the cell momentarily which reverse the membrane potential i.e more positive inside than outside

110
Q

Explain the changes in ion permeability associated with each stage of an action potential

A
  1. depolarization~ rapid, Vm changes from -70 resting to +30 due to a sudden and dramatic increase in permeability to sodium, so Vm approaches sodium’s equilibrium potential of +60 with flow of sodium down its electrochemical gradient
  2. repolarization~ membrane potential returns to +30 then resting levels of -70, within 1 millisecond of the increase in sodium permeability, sodium channels close and potassium channels open to increase permeability , potassium then moves down its electrochemical gradient and beings Vm back to resting
  3. hyperpolarization~ potassium permeability remains elevated after reaching resting potential and therefore becomes even more negative approaching potassium’s equilibrium potential of -94 before going back up to resting
111
Q

Explain the difference between ligand gated and voltage gated ion channels in generating a graded potential or an action potential

A

voltage gated channels~ activation gates and inactivation gates (specific to sodium) open and close in response to changes in membrane potential, need both activation and inactivation gate to be open for influx of sodium

ligand gated~ open in response to binding of chemical messengers to receptor binding sites

112
Q

Explain the propagation of an action potential from the axon hillock to the terminal and compare in myelinated and unmyelinated axons

A

~ electrotonic propagation
-separation of charge in ICF and ECF, serves as force for current to move (axon hillock)
- current depolarizes adjacent region of membrane to threshold eliciting action potential
-depolarization of adjacent regions continues until action potential reaches axon terminal

~myelinated (saltatory conduction) “jumps” from nodes of ranvier to next node (much quicker); train makes less frequent stops; found in areas that require quick response
~unmyelinated slower, train makes more frequent stops, has to move from site to site along axon depolarizing regions

113
Q

Describe the refractory periods: what causes each type (relative vs absolute) and the physiological significance of each

A

~ recovery; cannot immediately generate a 2nd action potential; during and immediately after action potential the membrane is less excitable than at rest; AP’s cannot be summed because refractory period prevents overlap, not graded

Absolute~ no stimulus can generate a 2nd action potential, regardless of strength; spans depolarization and repolarization phases; rapid opening of sodium channels will be set into motion until conclusion and cannot be affected by a second stimulus, and during repolarization, channels are closed and cannot be opened; an AP cannot be generated until most of Na gates are back to resting state, which occurs at the end of repolarization where inactivation gates are opened but activation gates are closed but capable of opening again.

Relative~ a stimulus much stronger than normal is necessary to generate a 2nd AP early, a stimulus a little bit stronger than normal is necessary for an AP later; occurs immediately after absolute refractory period because more sodium inactivation gates are opened later; due to increase in potassium permeability that continues during hyperpolarization

114
Q

Describe the differences between chemical and electrical synapses

A

Chemical
- chemical messengers, neurotransmitters to communicate with neurons, muscles or glands; most common
-axodendritic, axosomatic, axoaxonic

Electrical
- gap junctions, electrical coupling of cells with similar function; less common

115
Q

Describe the communication between chemical synapses

A
  1. AP flows down axon to axon terminal
  2. Ca voltage gated channel opens, allowing influx of Ca
  3. influx of Ca signals synaptic vesicles to fuse with the membrane and release neurotransmitters into synaptic cleft
  4. Ca binds to appropriate receptor on post synaptic neuron
  5. elicits response in cell
    or
  6. neurotransmitter can be degraded by enzyme on both pre synaptic and post synaptic neurons
    or
  7. can use reuptake molecule to recycle parts of the neurotransmitter to be resynthesized
    or
  8. can be washed away into ISF and then blood and used in body
116
Q

Explain fast response at chemical synapses

A

~ receptor dual functions as a receptor and a channel
-channel closed without binding, neurotransmitter binds, opens channel and ion movement
-ionotropic receptor; ion movement changes Vm- any change in Vm is called post synaptic potential, magnitude depends on amount of neurotransmitters binding

117
Q

Explain direct coupling in chemical synapses

A

~requires G protein; receptor and ion channel are separate proteins
-neurotransmitter binds to receptor, activates G protein, alpha subunit slides and tells channel to open or close

118
Q

Explain 2nd messenger signal transduction in chemical synapses

A

~ G protein, instead of using ion channel, generates a 2nd messenger molecule
- neurotransmitter binds to receptor, activates G protein, alpha subunit slides to enzyme, enzyme produces 2nd messenger molecule to signal for open/close of channel

119
Q

Describe fast excitatory synapses

A

~ ligand gated channel opens immediately and has fast response; influx of Na ions, efflux of K ions; net ion movement depolarizes cell because more Na ions flow into the cell

120
Q

Describe slow excitatory synapses

A

~ closure of K ion channels acts to depolarize a cell by preventing cations from leaving the cell
- neurotransmitter binds to receptor, activates G protein, alpha subunit slides to bind with adenylate cyclase, ATP is dephosphorylated to cAMP, protein kinase A phosphorylates cAMP and adds P group to K ion channel, signals channel to close, previous K movement is stopped, causes depolarization

121
Q

Describe inhibitory synapses

A

~ neurotransmitter binds to receptor, signals to open, K pumped out of cell, moves Vm further from threshold, becoming more negative i.e hyperpolarization or stabilization to resting Vm
-K+ efflux or Cl- influx

122
Q

Describe the process of neural integration and the role of the axon hillock in the process

A

~ one synapse alone doesn’t determine (is insufficient) whether an AP will result
-an AP is triggered if Vm is depolarized to threshold at the axon hillock, summation is necessary (adding up signals occurring at axon hillock of postsynaptic neuron, if it meets threshold -> AP)

123
Q

Differentiate between divergence and convergence

A

Divergence
- presynaptic neuron has collateral branches that synapse with multiple different postsynaptic neurons; multiple paths from one presynaptic neuron

Convergence
-postsynaptic neuron synapses with multiple different presynaptic neurons coming together

124
Q

Explain temporal summation

A

~ ‘in time’, always reference ONE synapse producing multiple post synaptic potentials very quickly in time
-signals ‘piggy back’ off of one another which prevents membrane potential from returning to resting state; add up the 2 EPSPs and meet threshold-> fire a 2nd action potential

125
Q

Explain spatial summation

A

~ from different origins along postsynaptic neuron
-look at several synapses; 2 EPSPs fire close together-> AP, 1 EPSP and 1 IPSP fire together, cancels out (resting)

126
Q

Describe the flow of Frequency Coding

A

Greater frequency of APs along presynaptic axon->
more depolarization at axon terminal->
more voltage gated Ca channels open->
more neurotransmitters released->
more binding of ligand gated channels on postsynaptic neuron

127
Q

Explain presynaptic modulation at axoaxonic synapses

A

~ do not generate graded potentials, regulates amount of neurotransmitters that presynaptic neurons release
-axoaxonic neuron release neurotransmitter that binds to axon terminal of axodendritic neuron which allows more calcium channels to be opened and more neurotransmitters to be released, boosts signal and binding

128
Q

Describe synthesis, release and degradation of acetylcholine

A
  1. acetyl coA and choline undergo enzymatic reaction by CAT-> acetylcholine
  2. acetylcholine is packaged into synaptic vesicles and stored until exocytosis
  3. exocytosed into synaptic cleft
    4.binds to receptor on post synaptic neuron, opens allowing ion movement and alters Vm but binding is reversible
  4. can then be degraded by acetylcholinesterase which can be found on both pre and postsynaptic neurons
    or
  5. can be reuptake into presynaptic neuron or washed into ISF and blood
129
Q

Are cholinergic receptors faster in skeletal muscle or the CNS?

A

~skeletal muscle; allows 2 AChs to bind, ligand gated channel; CNS is G protein regulated so slow