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Mammalian Physiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Glial Cells

A

nonexcitable, speed conduction, insulate, absorb K+, provide nutrients, remove waste, digest dead cells, cell parts, aid migration, elaborate and move spinal fluid.

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2
Q

Action Potential

A

Changes in potential are a local event

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3
Q

Nerve Track

A

Multiple nerves getting activated at different action potentials

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4
Q

Saltatory Conduction

A

Action potential jumps between nodes of Ranvier across the myelinated sections of the nerve. Much faster than the non-myelinated nerves

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5
Q

Refractory Period

A

The resetting of the Na+ channel which keeps impulse going one way

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6
Q

Absolute Refractory Period

A

When no amount of added stimuli will cause an action potential to start

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7
Q

Relative Refractory Period

A

The further away from the initial stimulus, the less intense stimulation needed until threshold is again reached.

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8
Q

Orthograde

A

towards Axon terminal and uses kinesin

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9
Q

Retrograde

A

Towards the cell body and uses dynein

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10
Q

Graded Potential

A

Dependent membrane permeability changes to K, Na, Cl, HCO3, and Ca. Variable polarity and they are additive/summation. May be the result of a local ion permeability change.

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11
Q

Temperol Summation

A

The same stimulus adding on itself causing a graded potential

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12
Q

Spatial Summation

A

Two different types of stimulation that add together causing a graded potential

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13
Q

Electrical Synapsis

A

Proteins called conexons form pores between the cells, permit the movement of small molecular weight molecules and charges. (Gap Junction)

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14
Q

Chemical Synapsis

A

Neurotransmitter-receptor

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15
Q

Synaptic Transmission Combines

A

Action potential, synapse, Calcium Calmodulin, Exocytosis, Release Neurotransmitter, Receptor funtion, change membrane potential

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16
Q

Synapse

A

Anatomical specialized junction between two neurons where chemical transmission ocuurs

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17
Q

Synaptic Transmission

A

AP arrives at the presynaptic membrane ( synaptic or axon knob), Ca2+ channels open, cytosolic Ca2+ increases causing synaptic vesicles to move and fuse with cell membrane, neurotransmitter released into synaptic cleft, diffues/migrates to post synaptic receptor thus opening or closeing specific ion channels. CaATPase moves Ca out as AP dissipates. Net result…dep or hyper polarization

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18
Q

Neurotransmitter Fate

A
  1. Bind to receptor
  2. Enzymatic transformation
  3. Diffuse
  4. Active Reuptake
  5. Auto Receptor (on pre-synaptic membrane)
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19
Q

Calcium Signal

A

Action potential dependent, many AP and the Ca2+ channels will stay open, decrease AP frequency and the channels will close, Ca ATPase moves calcium out.

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20
Q

Neurotransmitter Goups

A
  1. Aceylcholine
  2. Monoamines
  3. Amino Acids
  4. Gases
  5. Peptides
  6. Purines
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21
Q

Aceylcholine (as neurotransmitter)

A

Binds to both nicotinic receptors and muscarinic receptors. They are completely separate.

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22
Q

Monoamines-Biogenic Amines (as nerotransmitter)

A

Includes Catacholamines, Serotonin (different receptor), and Hitamines. Use Apha-Andrenic receptors and beta-andrenic receptors which overlap often and use second messengers.

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23
Q

Catacholamines

A

Monoamine neurotransmitters that are derived from Tyrosine. L-DOPA, Dopamine, Norephinephrine, epinephrine.

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24
Q

Amino Acids (as neurotransmitters)

A

Glycine, GABA (gamma amino-butyric acid/valium) Glutamate, Aspartate.

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25
Q

Gasses (as neurotransmitter)

A

Nitric Oxide (NO), Carbon monoxide (CO)

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26
Q

Peptides (as neurotransmitters)

A

Enkephalons, endorphins, VIP, Insulin, Gastirn, ADH, GnRH,

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27
Q

EPSP

A

Excitatory Postsynaptic Potential when depolarizing occurs

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28
Q

IPSP

A

Inhibitory Postsynaptic Potentials when hyperpolarizing occurs (graded potential).

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29
Q

AP determined?

A

Depends of frequency and type of stimulation. More impulses more message.

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30
Q

AP Uniqueness

A

Thousands of connections means nothing is ever the same.

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31
Q

Convergent Synapses

A

Multiple dendrites feed into a single axon terminal and thus propagate to a single dendrite.

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32
Q

Divergent Synapses

A

A single dendrite has multiple axon terminals feeding into multiple dendrites.

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33
Q

Synaptic Delay

A

a time delay between the arrival of the AP at the synaptic terminal and membrane potential changes at the post synaptic membrane.

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34
Q

Choline acetyl transferase

A

Makes Ach in the presynaptic neuron.

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35
Q

Acetylcholine esterase

A

Breaks down Ach in the presynaptic neuron and in the synaptic cleft.

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36
Q

Monoamie Oxidase

A

Breaks down monoamine neurotransmitters in the synaptic cleft and presynaptic neuron.

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37
Q

Grey Matter

A

Interneron glial cells responsible for “reflex”. Efferent goes to muscle to flex of withdrawl from stimulus.

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38
Q

Cholinergic Nerve Pathways

A

Nerve pathways that use acetylcholine

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39
Q

Central Nervous Sysem

A

Brain and spinal cord. Center of thoughts, interpreter of environment, and origin of control over body.

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40
Q

Peripheral Nervous System

A

Connect the CNS to the limbs and organs. All the neurons not in CNS.

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41
Q

Afferent Division

A

Sensory Systems

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42
Q

Efferent Division

A

Motor Systems

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43
Q

Somatic

A

Voluntary nerve system associated with skeletal muscle.

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44
Q

Autonomic

A

Regulates functions of our internal organs and also may control some muscles within our body

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45
Q

Parasympathetic

A

Controls homeostasis and is responsible for the body’s “rest and digest” functions

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46
Q

Sympathetic

A

Controls body’s response to a perceived threat and is responsible for “fight of flight” response.

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47
Q

CNS Excitatory Neurotransmitters

A

Acetylcholine and norephinephrine

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48
Q

CNS Inhibitory Neurotransmitters

A

GABA, Seritonin, Endorphins, Dopamine

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49
Q

GABA

A

Valium is used as an antagonist

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50
Q

Seritonin

A

LSD is an antagonist

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51
Q

Endorphins

A

Heroin is an antagonist

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52
Q

Parkinson’s Disease

A

Caused by lack of dopamine and treated with L-DOPA

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53
Q

Schizophrenia

A

Caused by excess dopamine and treated with chloropromazine antagonist.

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54
Q

Depression

A

Calcium channel blockers as possible treatment.

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55
Q

Manic Depression

A

Problems may come from regulatory or ion balance. Can be treated with Lithium

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56
Q

Epilepsy

A

Caused by discharge of excitatory neurotransmitters and can be treated with dilation agonist for inhibitory nerves.

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57
Q

Hyperchondriasis

A

Nervous disorder caused by abnormally high numbers of ESPS

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58
Q

Tenanus

A

Nervous disorder caused by a toxin released from bracteria which causes ISPS’s to be elimiated. Results in muscle spasm/lock jaw.

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59
Q

Nerve Gas

A

Affects nervous system by inhibiting Acetylcholine esterase. Cannot feel but the excitatory impulses remain.

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60
Q

Cerebrum

A

Consciousness, motor control, speech, muscle movement, memory, personality.

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61
Q

Cerebellum

A

Integration center for skeletal muscle function and balance. May dampen inputs and predict.

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62
Q

Medulla

A

Control of respiration and cardiovascular control

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63
Q

Thalamus

A

Integration of sensory input to the cerebrum

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64
Q

Hypothalamus

A

Endocrine function, temperature regulation, feeding, emotions.

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65
Q

Blood-Brain Barrier

A

High-density cells that restrict passage of substances from the bloodstream

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66
Q

Choriod Plexus

A

Cerebrospinal fluid

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67
Q

Stimulus

A

Binding to a receptor photon activated chemical change, pressure change, membrane permeability change.

68
Q

The code for Magnitude

A

Is frequency and recruitment

69
Q

Stimulus Characteristics

A

Modality, Quality, Intensity, Location, and Duration. Magnitude is coded by frequency.

70
Q

Modality

A

Type of stimulus (light v. sound)

71
Q

Quality

A

Stimulus variability (color v. pitch)

72
Q

Intensity

A

Magnitude (bright v. loud)

73
Q

Location

A

Geographic where. Dual organs.

74
Q

Duration

A

Time interval. Affects accommodation.

75
Q

Somatic Nervous System

A

Excitatory through a single neuron and uses acetylcholine on skeletal muscles

76
Q

Sympathetic

A

Two neurons that use Ach and can affect smooth muscle, cardiac muscles, and glads. Terminal neurotransmitter is norephinephrine. Responds to action and stress involuntarily.

77
Q

Parasympathetic

A

Two neurons that use Ach and can affect smooth muscle, cardiac muscles, and glads. Can excite or inhibit to get involuntary rest/digestion.

78
Q

Sympathetic Vs. Parasympathetic

A

Dual innervation of each other. One is always opposite the other. Thus, bot can excite or inhibit.

79
Q

Hormone

A

A specialized chemical messenger secreted by an endocrine gland.

80
Q

Endocrine Glad

A

A group of cells that secretes a chemical messenger into the extracellular space and messenger enters the blood system to effect a target organ in another location. A DUCTLESS GLAD

81
Q

Exocrine Glad

A

A group of cells that secrete a product into a duct that leads to a specific space.

82
Q

Hormone Chemical Classes

A

Amines, Peptide, and Steroids

83
Q

Amines (as hormones)

A

Thyroxine/Triiodothyronine and epinephrine/norepinephrine

84
Q

Peptides (as hormones)

A

Prolactin, oxytocin, insulin, vassopressin (ADH), calcitonin.

85
Q

Steroids (as hormones)

A

Aldosterone, Cortisol, testosterone, estrogen

86
Q

Transport of Hormones in Blood

A

Prohormone or as bound hormones

87
Q

Prohormone

A

large peptide that are enzymatically cleaved to form the active hormone. SO it’s a precursor.

88
Q

Bound Hormone

A

a hormone that is not very water soluble (lipids, thyroxine) is bound and carried by plasma proteins forming a Hormone-Protein Complex.

89
Q

Glucocorticoids

A

Steroids that are synthesized from cholesterol that includes corticosterone and cortisol

90
Q

Mechanism of Action for Peptides and Monoamines

A

Lipid insoluble, binds to receptor on cell membrane, activates adenylate cyclase or calcium channels, increase second messenger, activate protein kinases (calmodulin), phosphorylate/activate cell enzymes, and stimulate cell function.

91
Q

Mechanism of Action for Steroids and Thyroid Hormone

A

Lipid soluble, enter cell, binds with specific receptor in cytoplasm, receptor-hormone complex goes into cell nucleus, bind to DNA-associated protein, trigger transcription, mRNA to ER, get new protein, change cell function.

92
Q

Hormone Interaction

A

Potentiation/permissiveness and Pharacological Effects

93
Q

Potentiation Example

A

Thyroid hormones have no response in adipose. Epinephrine causes a small amount of fatty acids released in adipose.
Thyroid hormones and epinephrine together in adipose cells cause a large amount of fatty acids to be released.

94
Q

Potentiation/permissiveness

A

With two hormones present, one will be responsible for the other hormone to exert a full effect.

95
Q

Pharmacological Effects of Excessive Hormone secretion

A

Good: Cortisol suppresses allergy and inflammation
Bad: Excessive growth hormone causes giantism or acromegaly with excessive steroid use

96
Q

Pharmacological Effects of Decreased Hormone Secretion

A

Lack of insulin causes diabetes and lack of growth hormone can delay growth.

97
Q

Factors that Cause Hormone Release

A

Neuronal, Hormonal, Ionic, Organic/Nutrient

98
Q

Neuronal Signal Causing Hormone Release

A

Nipple stimulation, hypothalamus, prolactin inhibitin hormone relase decreased or prolactin releaseing hormone increased.
Also, nip stim, hypo, post pit, oxytocin, mam gland, milk letdown

99
Q

Full Prolactin Example

A

Nipple stimulation, hypothalamus, dopamine release decreased (decrease prolactin inhibitin hornmone) anterior pituitary, prolactin released, mammary glands, stimulation milk production.

100
Q

Thyroid Hormone Releasing Pattern

A 
Hypothalamus
-Thyrotropin Releaseing Hormone
Anterior Pituitary
-Thyroid Stimulation Hormone*
Thyroid Gland
-Thyroxine or Triiodothyronin*
Target Cells
-Increase metabolism
*hormonally induced release
101
Q

T3

A

Triiodothyronin

102
Q

T4

A

Thyroxine

103
Q

TRP and TSP

A

Thyrotropin Releasing Hormone and Thyroid Simmulation Hormone are both peptide hormones.

104
Q

Ionic Release of Hormone

A

Increase plasma calcium, thyroid cells, secrete calcitonin, inhibit bone calcium release, decrease plasma calcium.

105
Q

Decrease in Plasma Calcium

A

Parathyroid glad, Parathyroid Hormone released into the circulatory system, osteocytes release calcium, increase in plasma calcium, decrease of initial stimulus.

106
Q

Organic Release of Hormone

A

Increase plasma glucose, pancreas beta cells, stimulation of insulin secretion, increase plasma insulin, decrease plasma glucose.
OR
Decrease plasma glucose, pancreatic alpha cell secrete glucagon, increase plasma glucose.

107
Q

Insulin Action

A

Maintains plasma glucose levels to 70-120mg% by stimulating glycolysis, CAC, protein anabolism, glycogen anabolism, and lipogenesis. Signals absorption state.

108
Q

Glucagon Action

A

Maintain plasma glucose levels to 70-120% by stimulating gluconeogenesis, protein catabolism, glycogen catabolism, fat breakdown/acetyl CoA. Released during starved state.

109
Q

Posterior Pituitary Hormones

A

Oxytocin and Vasopression (anti duretic hormone) via nerve tracts

110
Q

Anterior Pituitary Hormones

A

THS, GH, ACTH, FSH, Prolactin, LH

111
Q

Anterior Pituitary Linkage

A 
Hypothalamus
-Releasing Factor via portal system
Anterior Pituitary
-Trophic Hormone via blood
Endocrine Gland
-travel in blood
Hormone
112
Q

Thyroid Hormone Releasing Pattern

A 
Hypothalamus
-Thyrotropin Releasing Hormone
Anterior Pituitary
-Thyroid Stimulating Hormone
Thyroid Gland
-Thyroxine (T4) or Triiodothyronine (T3)
Target Cells
-Increase Metabolism
113
Q

Portal System

A

A circulation pattern that goes from one capillary bed to another without passing through the heart (hypothalamus to anterior pituitary)

114
Q

Glucocorticoids

A 
Stress and Circadian Brain input
Hypothalamus
-Corticotrophin Releasing Hormone
Anterior Pituitary
-Adrenal Corticotrophic Hormone
Adrenal Cortex
-Cortisol, corticosterone
Effector Cells in Liver (Metabolism Immune Response)
115
Q

CRH

A

Corticotrophin Releasing Hormone

116
Q

ACTH

A

Adrenal corticotrophic hormone

117
Q

Corticosterone in other Mammals

A

Change metabolism and influence immune system

118
Q

Adrenal Glands and Cortioctcoids

A

In males, this coritsol tissue can release testosterone

119
Q

Growth Hormone Promoters

A

Exercise, sleep, fasting, stress, low plasma glucose

120
Q

Growth Hormone

A 
Hypothalamus
-somatostatin(-) growth hormone releasing hormone (+)
Anterior Pituitary
-Growth Hormone
Liver
-Insulin-like Growth Hormone 1
Protein anabolism renewal and growth
121
Q

Prolactin

A 
Nipple Stimulation
Hypothalamus
-Prolactin Releasing Hormone (+) Dopamine/PIH (-)
Anterior Pituitary
-Prolactin
Mammary Glands
Stimulate milk production
122
Q

Puberty

A

Sexual maturation

123
Q

Adolescence

A

total change to an adult

124
Q

Sperm Production

A

Spermatogium, primary spermatocytes, secondary spermatocytes, spermatids in seminier tubuals, mature spermatizoa

125
Q

Sertoli Cells

A

Form “blood-testes” barrier, provide nutrients to the mature(ing) spermatozoa, and serve as an endocrine cell by releasing inhibin and are stimulated by FSH

126
Q

Interstitial Cells

A

Are endocrine cells which release testosterone and is stimulated by LH

127
Q

Male Endocrinology

A 
Hypothalamus
-Gonadotrophic Releasing Hormone
Anterior Pituitary
-Folical Stimulating Hormone
-Lutenizing Hormone 
Testes
-Testosterone(Interstitial Cells)
-Inhibin (Sertoli Cells)
128
Q

Effects of Testosterone

A

Promote spermatogenesis, induce differentiation and maintain function of amle accesory organs, induce and maintain secondary sex characteristics, stimulate protein anabolism and bone growth, maintain sex drive and aggressive behavior, negative feedback of LH secrestion

129
Q

Prostate Gland

A

Testosterone accessory glad that secretes prostate fluid which makes up sperm and also pushes sperm out

130
Q

Bulbourethral Gland

A

Testosterone accessory glad that provides fluid and nutrients

131
Q

Oovm Producation

A

Oogonia (46), Primary Oocytes (46), 23, Oovum (23) and some polar bodies.

132
Q

Female Endocrinology Phase 1

A 
Hypothalamus 
-Gonadotrophic Releasing hormone
Anterior Pituitary
-Follicle Stimulating Hormone
-Lutenizing Hormone
Ovaries
-Estrogen (Follicle/Granulosa Cell (-))
-Inhibin (Follicle (-))
133
Q

Female Endocrinology Phase 2

A 
Hypothalamus
-Gonadotrophic Releasing Hormone
Anterior Pituitary
-Follicle Stimulating Hormone
-Lutenizing Hormone
Ovaries
-Estrogen (Follice/Granulosa cells (+))
-Inhibin (Follicle (-))
134
Q

Female Endocrinology Phase 3

A 
Hypothalamus
-Gonadotrophic Releasing Hormone
Anterior Pituitary
-Follicle Stimulating Hormone
-Lutenizing Hormonw
Ovaries in the Corpus Luteum
-Estrogen and Progesterone (-)
-Inhibin (Follicle (-))
135
Q

Endometrium

A

The unterine lining. Growth stimulated by estrogen. Shed during menstration and where a embryo implants.

136
Q

Myometrium

A

Smooth muscle layer beneath endrometrium

137
Q

Mucus Secretion

A

Stimulated by estrogen; abundant and nonviscous. When high progesterone levels, become very viscous.

138
Q

Period Time Line

A

21-35 days on average
Phase 1: 0-8days
Phase 2: mid-follicular to ovulation
Phase 3: menstruation

139
Q

Corpus Luteum

A

“Yellow Body” made of old granuolas, it becomes a temporary hormone releasing organ

140
Q

No Fertilization

A

Progesterone and estrogen are reduced and prostaglandins mediate degradation of the corpus luteum

141
Q

Menstruation

A

Drop in estrogen and progesterone affect endometrium. Prostagladins are produced along with vasoconstriction reducing O2 and nutrients. Endometrium degenerates. Prostaglandins cause uterine smooth muscle to constrict. Vasodilation occurs and endometrium hemorrhages. Endometrium lost.

142
Q

Dysmenorrhea

A

Menstural cramps caused by prostagladins stimulating smooth muscle of the uterus to constrict.

143
Q

Endometriosis

A

Some endometrium goes into abdomine by exiting through the Fallopian tubes. Can then grow there.

144
Q

Low Plasma Estrogen

A

Hypothalamus secrets less GnRH so less FSH and LH (negative feedback)

145
Q

High Plasma Estrogen

A

Hypothalamus secretes more GnRH so there’s more FSH and LH (positive feedback)

146
Q

High Plasma Estrogen and Progesterone

A

Inhibits GnRH so less FSH and LH are released

147
Q

Inhibin

A

A peptide that inhibits FSH

148
Q

Effects of Estrogen

A

Increase growth of ovaries and follicles, growth and maintenance of reproductive tract (motility-uterine tubes, uterus, preps endometrium for progesterone), Simulate secondary sexual characteristic growth, vascular effects, feeds back on hypothalamus and pituitary, regulation of fluid, stimulates prolactin secretion inhibits prolactin milk inducing actions.

149
Q

Effects of Progesterone

A

Simulated secretions of endometrial glands and growth of myometrium during pregnancy, decreases motility of uterine tubes and uterus, stimulate breast growth, inhibit milk producing effect of prolactin, negative feedback on hypothalamus and anterior pituitary.

150
Q

Effects of Prostaglandins

A

In the ovary it interferes with function of corpus luteum

151
Q

Prostaglandin Effect on Endometrium

A

Without fertilization will constrict blood vessels for menstruation onset. With fertilization will change circulatory patter to facilitate implantation.

152
Q

Prostaglandin Effect of Myometrium

A

Increase smooth muscle contration. Helps menstruation and also starts up parturition.

153
Q

Menopause

A

Occurs around ages 40-50 and the ovaries cease functioning so estrogen levels progressively decrease. Can lead to bone demineralization/osteoperosis

154
Q

Erection

A

Parasympathetic nervous system and NO (ED medication works through NO pathway to dilate arteries)

155
Q

Orgasm

A

Linked to sympathetic nervous system

156
Q

Capacitation

A

The acidic environment on the vagina cause sperm to do this. Necessary to be able to fertilize egg.

157
Q

Fertilization Progression

A

Sperm and egg together form a zygote with 46 chromosomes. Travel down uterine tube for 3-4 days while dividing. Goes to Uterus. Implants after about 7 days.

158
Q

Trophoblast Cells

A

Starts on contact and as they grow they release chorionic gonadotrophin

159
Q

Chorionic Gonadotropin

A

Maintains the corpus luteum while the placenta is forming blood-placenta barrier. First peak excreted in urine and what is detected on pregnancy tests.

160
Q

Cervical Glads

A

During development they produce a thick mucas to create a barrier

161
Q

Placenta

A

Age dependent and lasts 9-10 months. Responsible for nutrient and waste exchange.

162
Q

Fetal hemoglobin

A

Has a higher affinity for oxygen but the production to “adult” hemoglobin starts almost immediately after birth.

163
Q

Parturition

A

Cortisol signal from fetus, estrogen and progesterone drop, mucus plug lost, chorioamnion is ruptured, uterine contractions, relaxin (peptide) dissolved pelvic cartilage, dialation of cervix, dropping of fetus to birth canal.

164
Q

Vernix

A

White film child is covered with when it first comes out

165
Q

Maconium

A

First bowel movement. If too soon sign of fetal distress

166
Q

Colostrum

A

The first milk. Switches to milk with water, lactose, fal, lg, and proteins

167
Q

Placenta after Birth

A

Myometrium contracts into size of softball, squishing the placenta with it.

Mammalian Physiology (6 decks)

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