FINAL EXAM: Unit 1 Flashcards

1
Q

what is osmotic equilibrium?

A

fluid concentration equal in ICF & ECF

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2
Q

what is chemical disequilibrium?

A

ECF high in Na+, Cl-, Ca2+
ICF high in K+, anions

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3
Q

what is electrical disequilibrium?

A

ECF positively charged
ICF negatively charged

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4
Q

what is osmosis?

A

movement of water across a MB
-in response to a gradient

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5
Q

what is osmolarity?

A

number of particles per liter
-looking at combined total of NP & P

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6
Q

what is isosmotic?

A

same number of particles

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7
Q

what is hyperosmotic?

A

ECF is higher (outside)

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8
Q

what is hypoosmotic?

A

ICF is higher (cell)

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9
Q

what is tonicity?

A

comparing solution to cell volume
-look only at NP solutes!!

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10
Q

what is hypotonic?

A

cell swells, gains H2O
-ICF high

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11
Q

what is hypertonic?

A

cell shrinks, loses H2O
-ECF high

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12
Q

what is isotonic?

A

no gain or loss of H2O

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13
Q

what are penetrating solutes?

A

UREA
-freely diffuse across MB
-no water movement

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14
Q

what are nonpenetrating solute?

A

NaCl, GLUCOSE
-trapped by the MB
-needs water to move it

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15
Q

when ICF NP is bigger than ECF NP, water moves ____

A

water move INTO cell
-direction goes towards the higher amount

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16
Q

what is a conductor?

A

ions move freely through
-water

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17
Q

what is an insulator?

A

ion movement stopped
-phospholipid bilayer

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18
Q

how does the Na+/K+ pump impact RMP?

A

3 Na+ OUT, 2 K+ IN
-makes ECF more positive, ICF more negative

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19
Q

how does the K+ leak channel impact RMP?

A

K+ OUT (tonic control)
-makes ECF more positive, ICF more negative

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20
Q

how do anions impact RMP?

A

makes ICF more negative

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21
Q

what does depolarization do to RMP?

A

makes ICF more positive
-opening Na+ channels, removing K+ leak channels

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22
Q

what does hyperpolarization do to RMP?

A

makes ICF more negative
-opening Cl- or K+ channels

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23
Q

what does repolarization do to RMP?

A

returns RMP back to ~70mV

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24
Q

what type of cell secretes insulin? what is the process of it?

A

beta cells when glucose is HIGH
-ATP -> close K+ channels -> open Ca2+ channels
-exocytosis (release) of insulin

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25
Q

what is the mOsm of the ICF?

A

always 300mOsm NP!!!

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26
Q

osmolarity ____ predict tonicity

A

does not predict

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27
Q

is the cell more permeable to K+ or Na+?

A

K+

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28
Q

what is the generic response to a stimulus?

A

stimulus -> sensor -> input -> int. center -> output -> target

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29
Q

what is homeostasis?

A

range
-when disrupted it compensates for change

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30
Q

what is negative feedback?

A

response opposes / decreases initial stimulus
-brings toward homeostasis

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31
Q

what is positive feedback?

A

response enhances / increases initial stimulus
-brings away from homeostasis

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32
Q

what is feedforward control?

A

starts response prior to stimulus (smell, sight)

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33
Q

what is circadian rhythm?

A

repeatable & predictable day & night cycles (temp)

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34
Q

what is acclimatization?

A

adapting to the environments (altitude)

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35
Q

what are three types of local communication?

A

gap junctions
contact-dependent signal
paracrine & autocrine

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36
Q

how do gap junctions work?

A

direct connection through cytoplasm
-connexion proteins close & open junction

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37
Q

how do contact-dependent signals work?

A

ligand & receptor

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38
Q

how do paracrines & autocrines work?

A

paracrine: release from cell
autocrine: release from itself

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39
Q

what are two ways of long-distance communication?

A

endocrine glands
neurons

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40
Q

how do endocrine glands work for communication?

A

secrete hormones into the blood

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41
Q

how do neurons work for communication?

A

secrete neurocrines
-NT, neuromodulator, neurohormone

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42
Q

what is the generic signal pathway?

A
  1. signal molecule, 1st messenger (ligand, extracellular signal)
  2. recep. protein, transducer (receptor, converts extra to intra)
  3. intracell signal molecule, 2nd messenger (activates pathway)
  4. target proteins (modifies, phosphorylation)
  5. response
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43
Q

describe lipophilic / hydrophobic signal molecules

A

lipid loving, water fearing
-diffuses easily into cell
-binds intracellular receptor
-alters gene expression
-SLOW

44
Q

describe lipophobic / hydrophilic signal molecules

A

lipid fearing, water loving
-binds receptor on surface of cell
-RAPID

45
Q

what are the four types of signal pathways?

A

receptor / ion channels
GPCR
receptor enzymes
integrin receptor

46
Q

how does the receptor / ion channel work?

A

ligand binds receptor
-opens/closes ion channel
-depolarization or hyperpolarization
-RAPID
-EX: muscle contraction

47
Q

how does the cAMP pathway work? (GPCR)

A
  1. ligand binds GPCR
  2. G-protein activates
  3. adenyly cyclase activates
  4. increases cAMP
  5. activates protein kinase A
  6. phosphorylation cascade
48
Q

how does the phospholipase C pathway work? (GPCR)

A
  1. ligand binds GPCR
  2. activates PLC
  3. activates DAG & IP3
  4. DAG activates protein kinase C
  5. IP3 releases Ca2+ stores
49
Q

how does the receptor enzyme work?

A

two parts
-receptor region (extracellular
-enzymatic region (intracelluar)

50
Q

how does the tyrosine kinase pathway work? (receptor enzyme)

A
  1. ligand binds extracellular region
  2. activates intracellular region
  3. activates tyrosine kinase
  4. phosphorylation cascade
51
Q

how does the integrin receptor work?

A

-receptor spreads across entire MB
-connects to cytoskeleton through an anchor protein
-extracellular matrix interacts with intracellular components
-antibodies, clotting factors

52
Q

how does nitric oxide (NO) modify signal pathways?

A

smooth muscle relaxation
-vasodilation
-neuromodulator
-LOCAL, SHORT ACTING

53
Q

how does carbon monoxide (CO) modify signal pathways?

A

vasodilation

54
Q

how does hydrogen sulfide (H2S) modify signal pathways?

A

vasodilator

55
Q

how do eicasanoids modify signal pathways?

A

lipid soluble

56
Q

how are eicasanoids synthesized?

A

PLA2 -> arachidonic acid -> leukotrines & prostanoids

57
Q

what are the effects of leukotrines & prostanoids?

A

leukotrines: asthma, allergy
prostanoids: inflammation, pain, NSAIDs inhibit them

58
Q

what is an agonist?

A

bind same receptor, mimic same response
-creates competition

59
Q

what is an antagonist?

A

bind receptor, blocks activity of ligand

60
Q

what does down-regulation do?

A

decreases number of receptors, decreases response

61
Q

what does desensitization do?

A

chemically modify receptor
-decreases response QUICKER

62
Q

what does up-regulation do?

A

increase number of receptors, increases response

63
Q

what are three ways to terminate a signal?

A

enzyme destroys ligand
neighbor cells uptake signal
down-regulation

64
Q

what is the difference between central and peripheral receptors?

A

central: brain, special senses
peripheral: everything else

65
Q

what is the difference between simple and complex reflex pathways?

A

simple: 1 integrating center, FAST
complex: multiple integrating centers, SLOW

66
Q

what is are differences b/w neural and endocrine reflex pathways?

A

neural: specific, electrical & chemical, FAST, short duration, increase frequency (identical in strength)

endocrine: nonspecific, chemical, SLOW, long duration, increase amount, endocrine cell is the [sensor, input, integration center]

67
Q

what are afferent neurons in a reflex pathway?

A

send signal to integrating centers

68
Q

what are efferent neurons in a reflex pathway?

A

send signal to targets

69
Q

describe the neural reflex pathway?

A

receptor
afferent neuron
NS
efferent neuron
muscle, gland, fat
contraction, secretion, metabolism

70
Q

describe the neuroendocrine reflex?

A

receptor
afferent neuron
NS
efferent neuron
blood
enzymatic rxns, transport, cell proteins

71
Q

describe the endocrine reflex?

A

endocrine system
hormone blood
enzymatic rxns, transport, cell proteins

72
Q

what are pheromones?

A

secreted into external environment

73
Q

what are cytokines?

A

made on demand, not stored

74
Q

what is a candidate hormone?

A

appears to look / act like a hormone but isn’t

75
Q

describe peptide hormone synthesis

A

preprohormone -> prohormone (R. ER) -> secretory vesicle

76
Q

describe transport of peptide hormones (solubility, receptor)

A

lipophobic / hydrophilic
-no transport protein
-surface receptors
-FAST

77
Q

describe synthesis of steroid hormones

A

cholesterol -> secreted on demand -> simple diffusion
-SMOOTH ER

78
Q

describe transport of steroid hormones (solubility, receptor)

A

lipophilic / hydrophobic
-transport protein
-intracellular receptors
-SLOW

79
Q

what are the two types of amine hormones?

A

catecholamines (NE, E, dopamine, melatonin)
thyroid hormone

80
Q

describe the synthesis of catecholamines

A

tyrosine -> secretory vesicle

81
Q

describe transport of catecholamines hormones (solubility, receptor)

A

lipophobic / hydrophilic
-no transport protein
-surface receptor
-FAST

82
Q

describe synthesis of thyroid hormone

A

tyrosine + iodine -> stored in colloid

83
Q

describe transport of thyroid hormones (solubility, receptor)

A

lipophilic / hydrophobic
-transport protein
-intracellular signal
-SLOW

84
Q

what is a synergistic hormone interaction?

A

effect of hormones is greater than the sum

85
Q

what is a permissiveness hormone interaction?

A

hormone isn’t active until the other hormone is present

86
Q

what is a antagonistic hormone interaction?

A

hormone effects oppose eachother

87
Q

what are trophic hormones? name the 5 major ones from the anterior pituitary

A

controls secretion of other hormones
-GH, ACTH, TSH, FSH, LH

88
Q

what is the portal system in the brain?

A

hypothalamus & anterior pituitary

89
Q

what is a long-loop feedback pathway?

A

terminal hormones inhibits hypothalamus & anterior pituitary

90
Q

what is a short-loop feedback pathway?

A

anterior pituitary inhibits hypothalamus

91
Q

what is the thyroid hormone feedback pathway? (check image in notes for full info)

A

TRH -> TSH -> T3 & T4 (thyroid gland)

92
Q

what is the cortisol feedback pathway? (check image in notes for full info)

A

CRH -> ACTH -> cortisol (adrenal cortex)

93
Q

what is the growth hormone pathway? (check image in notes for full info)

A

GHRH & GHIH/somatostatin -> GH -> IGFs (liver, other)

94
Q

pineal gland hormones, targets, and effects

A

[melatonin]
-> brain -> circadian rhythm

95
Q

hypothalamus hormones, targets, and effects

A

[DA, TRH, GHIH, CRH, GnRH, GHRH]
-> ant. pit. -> alter channels

96
Q

posterior pituitary hormones, targets, and effects

A

[oxytocin, vasopressin/ADH]
-> breasts, kidney -> milk ejection, water reabsorption

97
Q

anterior pituitary hormones, targets, and effects

A

[prolactin] -> breast -> milk production
[GH] -> liver -> growth
[ACTH] -> adrenal cortex -> cortisol release
[TSH] -> thyroid gland -> TH release
[FSH, LH] -> gonads -> egg/sperm release

98
Q

thyroid gland hormones, targets, and effects

A

[T3, T4, calcitonin]
-> bone, many -> Ca2+ levels, metabolism

99
Q

parathyroid hormone hormones, targets, and effects

A

[PTH]
-> bone, kidney -> plasma Ca2+

100
Q

pancreas hormones, targets, and effects

A

[insulin, glucagon, somatostatin]
-> many -> metabolism of glucose

101
Q

adrenal cortex hormones, targets, and effects

A

[aldosterone, cortisol, androgens]
-> kidney, many -> Na+/K+ balance, stress, sex

102
Q

testes hormones, targets, and effects

A

[androgens, inhibin]
-> many, anterior pit -> sperm production, inhibit FSH

103
Q

ovaries hormones, targets, and effects

A

[estrogen, progesterone, inhibin, relaxin]
-> many, ant. pit., uterus -> egg production, inhibit FSH, relax muscles

104
Q

what is the difference between hypersecretion and hyposecretion?

A

hyper: too much hormone
hypo: not enough hormone

105
Q

what is primary endocrine pathology?

A

last gland is defective
-HYPO: high TRH & TSH, low T3 & T4
-HYPER: low TSH & TSH, high T3 & T4.

106
Q

what is secondary endocrine pathology?

A

second gland is defective
-HYPO: high TRH, low TSH, T3 & T4
-HYPER: low TRH, high TSH, T3 & T4

107
Q

what is tertiary endocrine pathology?

A

first gland is defective (rare)
-all hormones either high or low