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A&P Lecture > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Hormones Influence…

A

metabolism, internal environment (water, temp, ions), reproduction, growth & development

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2
Q

How do hormones act on target cells

A
  1. Alter rate of enzymatic reactions/levels
  2. Control transport of ions or molecules across membrane
  3. Control gene expression and synthesis of proteins
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3
Q

4 Criteria for a hormone

A
  1. Secreted by a cell or group of cells
  2. Secreted into the blood
    Secretion is movement from inside cell to ECF
    Pheromone is hormone secreted outside the body
  3. Transported to a distance target
  4. Exert their effects at very low concentrations
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4
Q

Hormone binding

A

Target cell must have the right receptor to bind hormone.
Hormone-receptor binding initiates cellular mechanism of action (the hormone affect)
Hormone can act on one or multiple tissues (receptor dictate response)

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5
Q

Terminating hormone activity

A

Regulation is critical (limit duration of effect)
Hormones degraded by liver or kidneys

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6
Q

Half-life

A

Amount of time to reduce hormone concentration by half

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7
Q

Hormone Classification

A

~50
Source of production, what controls their release, chemical classes

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8
Q

Chemical classes of hormones

A

Peptide- derived from proteins
Steroid- derived from cholesterol (lipid)
Amine- derived from amino acids

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9
Q

Peptide hormone synthesis

A

Range from 3 amino acids to complex glycoproteins
1. Transcribed in nucleus then translated
2. Translation on ribosome results in preprohormone
3. Moves through ER and signal sequence is removed results in Prohormone that enters Golgi
4. Golgi packs prohormone into secretory vesicles and enzymes chop it into active hormone
5. Vesicles stored in cytoplasm until release signal is given

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10
Q

Peptide hormone characteristics

A

water soluble, dissolve easily in ECF, transported easily in blood but half-life is generally short

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11
Q

Cellular Mechanism of action of Peptide hormone

A

Lipophobic- unable to cross cell mem without help
Bind cell surface receptors to form complex
Most work through cAMP, others through tyrosine kinase
Rapid response once bound to the receptor

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12
Q

Steroid hormones characteristics and examples

A

Share common structure based on cholesterol
Production is limited to adrenal cortex (aldosterone, cortisol) and male/female gonads (estrogens, progesterone, testosterone) and placenta of pregnant women.
Long half life
Entry of hormone obeys mass action

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13
Q

Steroid hormone synthesis

A
  1. Produced by smooth ER
  2. Lipohilic cross membrane easily but needs carrier in the blood
    Carrier protects hormone from degradation
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14
Q

Albumin

A

Most abundant protein in blood, nonspecific carrier

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15
Q

Cellular Mechanism of action of Steroid hormones

A

Receptors in cytoplasm or nucleus; ultimate destination is nucleus to have a genomic effect, not a fast response

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16
Q

Amine Hormones

A

Created from tryptophan or tyrosine
Melatonin (tryptophan)
Catecholamines (tyrosine)
Thyroid (tyrosine)

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17
Q

Catecholamines

A

epinephrine, norepinephrine, dopamine
Behave like peptide

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18
Q

Thyroid hormones

A

behave like steroid hormones
regulate overall metabolism, temperature, and many functions

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19
Q

Release of hormones

A

Released as result of stimuli, continuously, or circadian rhythms
Reflex pathways regulate release (simple and complex endocrine, neuroendocrine)
Rely on feedback mechanisms

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20
Q

Simple Endocrine Reflex

A

1 integrating center; endocrine cell acts as both the sensor and the IC
Hormone is output and release is regulated by negative feedback `

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21
Q

Parathyroid Hormone (PTH)

A

parathyroid cell detects low calcium in blood, releases causes Ca release from bone, decreased Ca excretion in kidney, increase Ca absorption by intestine
when Ca levels rise, parathyroid gland stops PTH release

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22
Q

Insulin, simple endocrine control

A

Simple endocrine; release by pancreas controls blood glucose
Pancreatic beta cells detect high blood sugar, release insulin and cells take-up glucose, glucose levels return to normal

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23
Q

Neuroendocrine reflexes

A

CNS in the IC, neurons make decisions
Insulin regulation CNS:
Food in intestine activates stretch receptor, receptor signals CNS, CNS signals pancreas to release insulin, cells take up glucose to return levels

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24
Q

Posterior Pituitary

A

Extension of nervous tissue, controls homeostatic functions
stores 2 neurohormones produced by hypothalamus
Vasopressin- regulate water balance (ADH)
Ocytocin- controls ejection of breast milk and uterine contractions
Released directly to bloodstream

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25
Q

Anterior pituitary

A

true endocrine gland, controls many homeostatic functions

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26
Q

Posterior pituitary process

A

Neurohormone is made and packaged in cell body of neuron in hypothalamus, vesicle transported down cell, vesicle stored in post. pituitary until released in blood

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27
Q

Anterior pituitary process

A

Neurons in hypothalamus synthesize trophic neurohormones release them into capillaries of portal system
Portal veins carry trophic neurohormones to ant. pituitary where they act on endocrine cells
Endocrine cells release peptide hormones into second set of capillaries for distribution to rest of body

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28
Q

Portal system

A

2 capillary beds, ensures trophic Neurohormones go directly to Ant. pit and not other part of body

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29
Q

Trophic Hormones

A

released by neurons of hypothalamus, specific to trigger release of certain ant. pit hormones
Released into portal system (control)
Tiny amount of trophic can control AP activity

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30
Q

Short loop negative feedback

A

The first or second hormone in the pathway provides feedback
(prolactin, GH, ACTH)
Pituitary gland pathways

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31
Q

Long loop negative feedback

A

Final hormone in pathway provides feedback
(cortisol, thyroid hormone)
Preferred form of feedback
Pituitary gland pathways

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32
Q

3 Types of hormone interactions

A

Synergism, Permissiveness, antagonism

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33
Q

Synergism

A

Two or more hormones interact with target and combination result is greater than each individually (additive effect, working together)

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34
Q

Permissiveness

A

One hormone cannot filly exert effects unless a second hormone is present; second hormone may or may not have biological action
ex: maturation of reproductive system (via steroid and gonadotropin hormones) only occurs if thyroid hormones are present.

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35
Q

Antagonism

A

When one hormone opposes the action of another hormone; result of 2 hormones competing for same receptor or two hormones acting on different receptors

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36
Q

3 basic patterns of endocrine pathology

A

excess, deficiency, abnormal responsiveness

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37
Q

Hypersecretion

A

Leads to exaggerated effects, can occur anywhere along the pathway
Causes: tumors, exogenous hormone treatment
Decreases trophic hormone release

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38
Q

Exogenous treatment

A

outside source, may lead to endocrine gland atrophy
Increases negative feedback which means less natural hormone –> atrophy

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39
Q

Hyposecretion

A

Too little of a hormone is secreted, can occur anywhere along the pathway, increases trophic hormone release
Cause: atrophy of a gland due to disease
Reduces negative feedback

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40
Q

Abnormal Responsiveness

A

Target tissue cannot respond properly to hormone
Can occur anywhere along pathway (typically within cell)
Causes: down regulation of hormone receptor, genetic mutation of hormone receptor, genetic mutation of signal molecule in pathway

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41
Q

Primary Pathology

A

Due to a problem with the last endocrine gland pathway (work through diagram)

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42
Q

Secondary Pathology

A

Due to a problem with the Anterior pituitary gland (work through diagram)

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43
Q

Tertiary Pathology

A

Due to a problem with the Hypothalamus; rare because hypothalamus is neural tissue and if neural tissue is messed up there will be a bigger fatal problem before an endocrine problem.
(work through diagram)

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44
Q

How does the nervous system demonstrate emergent properties

A

Consciousness, intelligence, and emotion can not be explained by the anatomy and properties of neurons

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45
Q

Central Nervous System

A

CNS; consists of brain and spinal cord

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46
Q

Peripheral Nervous System

A

PNS; consists of afferent and efferent neurons

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47
Q

Afferent Neuron

A

Carry information TO the CNS, sensory neurons (PNS)

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48
Q

Efferent Neuron

A

Carry information AWAY from the CNS, Motor/movement neurons (PNS)

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49
Q

Somatic Motor Neurons

A

Controls skeletal muscles

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50
Q

Autonomic Motor Neurons

A

Controls cardiac and smooth muscle, exocrine glands, some endocrine glands, some adipose

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51
Q

Enteric Nervous system

A

Part of digestive tract, controlled by autonomic nervous system, and capable of autonomous action

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52
Q

Basic cell types of the nervous system

A

Neurons- basic signaling units
Glial Cells- support cells

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53
Q

Neuron

A

A functional unit of the nervous system, act as an IC, unique shape with long extensions

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54
Q

Classification of a Neuron

A

Structure- how many processes originate from cell body
Function-sensory, interneurons or efferent

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55
Q

Can you label the parts of a neuron??

A

Go do it on the diagram biotch

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56
Q

Synapse

A

The region where an axon terminal of the presynaptic cell communicates with its postsynaptic target cell. Electrical signal converted to chemical

57
Q

Axon terminal

A

enlarged ending of axon, usually releases a chemical

58
Q

Nerves

A

When the AXONS of many neurons are bundled together

59
Q

Mixed nerves

A

carry afferent and efferent information

60
Q

Sensory Nerves

A

Carry afferent info only

61
Q

Motor nerves

A

Carry efferent info only

62
Q

Cell body

A

nucleus and organelles, act as control center for neuron

63
Q

Dendrites

A

thin branched structure that receives incoming info

64
Q

Axons

A

most nerves have single structure that transmits outgoing electrical signal
Hillock- axon origin
Terminal- contains mitochondria and membrane-bound vesicles with chemicals

65
Q

Ependymal cells

A

Glial, CNS
Creates barriers between compartments like the blood brain barrier, source of neural stem cells

66
Q

Astrocytes

A

Glial, CNS
Source of neural stem cells, takes up extra K+, water, & neurotransmitters, secretes neurotrophic factors, helps form blood-brain barrier, provide substrates for ATP production

67
Q

Microgilia

A

Glial, CNS
act as scavengers, clean the environment (vacuum)

68
Q

Oligodendrocytes

A

Glial, CNS
Form myelin sheaths (insulate)

69
Q

Schwann Cells

A

Glial, PNS
Form myelin sheaths (insulate) secrete neurotrophic factors

70
Q

Satellite cells

A

Glial, PNS
Support cell bodies/keep them happy

71
Q

Myelin

A

Concentric layers of phospholipid membrane, provides insulation around axons so electrical can move faster, small gaps along axon
Increase myelin = increase speed of electrical signal

72
Q

Nodes of Ranvier

A

tiny gaps between myelin sheath where axon is exposed to ECF

73
Q

Membrane potential

A

Separation of electrical charge across cell membrane, influenced by uneven distribution of ions between cell and ECF and the different membrane permeability to those ions
Around -70 mV

74
Q

Nernst Equation

A

Tells us the membrane potential of a cell if that cell was permeable to only that individual ion

75
Q

Goldman-Hodgkin-Katz (GHK)

A

equation calculates the membrane potential that results form the IONS that can cross the cell membrane (rather than just one ion in Nernst)

76
Q

Vm depolarizes

A

Vm increases, more positive
Entry of + ion
Exit of - ion

77
Q

Vm hyperpolarizes

A

Vm decreases, more negative
Entry of - ion
Exit of + ion

78
Q

Ion concentration levels inside the cell

A

K+ high
Na+, Cl- low

79
Q

Ion concentration levels outside the cell

A

Na+, Cl- high
K+ low

80
Q

Mechanically gated channels

A

Open in response to forces such as pressure

81
Q

Chemically gated channels

A

Open when the right ligand binds

82
Q

Voltage gated channels

A

respond to changes in cell’s membrane potential

83
Q

Current

A

The more channels that open, the faster the ions can flow in/out which creates current

84
Q

Properties of graded potential

A

can be hyper or depolarization
Occurs at dendrites or cell body
Utilize mechanical, voltage, and chemically gated channels
Size is proportional to strength of signal (how many ions are flowing)
Decrease in strength as they move away from origin (Varied strength)
GP determine if AP is initiated

85
Q

When do GP occur

A

When chemical signals from other neurons open/close chemically gated ion channels

86
Q

Subthreshold event

A

No AP, determined by the SUM of graded potentials arriving at the trigger zone (axon hillock)

87
Q

Suprathreshold event

A

AP down axon (-55 mV), determined by the SUM of graded potentials arriving at the trigger zone (axon hillock)

88
Q

Properties of Action Potentials

A

Occur at trigger zone and travel through axon
only use voltage gated channels (K+ and Na+ only)
Only depolarizing
do NOT lose strength as they travel (all or none response)

89
Q

AP along the axon

A

Not one single AP, instead a series of channel openings like a domino effect

90
Q

Rising phase of AP

A

due to increased permeability to Na+.
Voltage-gated Na channel opens and Na rushes into cell [K+ channel is open but slow] (depolarizing)
Peaks at +30mV where Na channels close and K channel opens

91
Q

Falling Phase of AP

A

Increase K+ permeability (channels already open), K+ rushes out (hyperpolarizing)
at -70 mV K+ stays open and Vm keeps falling- undershoot
K+ retention and Na+ leak bring Vm back to - 70 mV

92
Q

Voltage Gated Na+ at -70 mV

A

Activation gate closed
Inactivation gate open
No flow of Na+

93
Q

Voltage Gated Na+ at -55 mV

A

Activation gate opens
Inactivation gate still open
Na flows into cell

94
Q

Voltage Gated Na+ at +30 mV

A

Activation gate remains open
Inactivation gate closes
No Na+ flow

95
Q

Voltage Gated Na+ during falling phase

A

Both gates reset to their original positions
Activation gate is closed
Inactivation gate is open
No flow of Na+

96
Q

Why does the voltage gated Na+ channel have 2 gates?

A

More control over flow of Na+ and thus control over depolarization

97
Q

Absolute Refractory period

A

Time for Na channels to reset to original position
Rising phase and most of falling phase
NO additional APs can be sent
Prevents backwards AP

98
Q

Relative Refractory period

A

Some of the Na channels are reset and K channels open
Vm is moving from -80 to -70 mV
An extra stronG Gp could trigger another AP

99
Q

Why is a larger stimulation needed to generate another AP during the relative refractory period?

A

B/c at that point the Vm is in the undershoot period (less than -70 mV) so you need a larger signal to get to the -55 mV threshold

100
Q

Conduction of AP down the axon

A

Travels long distances
Axon enriched with Na and K channels
Faster along myelinated axons
Movement is saltatory conduction (domino effect)
Chemicals/drugs can interfere with conduction

101
Q

What causes the domino effect?

A

The Na flow into the cell depolarizes the next section of the membrane. Channels down the axon remain closed until apart of the active section. (Diagram slide 43)

102
Q

What returns Na and K to their “correct” place?

A

Na/K pump

103
Q

Myelin increasing conduction

A

Myelin prevents Na from leaking out of the cell as it moves down the axon. Channels are concentrated in the nodes and Na moves down the axon depolarizing the next section (Diagram slide 44)

104
Q

Presynaptic cell

A

Axon terminal, releases chemical or electrical signal

105
Q

Postsynaptic cell membrane

A

Doesn’t have to be a neuron, could be muscle, glands, etc.
Have receptors for chemicals or gap junctions for electrical.

106
Q

Neurocrines

A

The chemical signal secreted by neurons

107
Q

Neurotransmitters

A

Fast paracrines that act locally

108
Q

Neuromodulators

A

Slower paracrines that act locally

109
Q

Neurohormones

A

Hormones released by neurons into blood stream

110
Q

Types of neurocrine receptors

A

Chemically gated ion channels (neurotransmitters)- fast synaptic potentials and G-protein coupled receptors (neuromodulators)-slow synaptic potentials, long-term effect

111
Q

7 classes of neurocrines

A

Chemical, Amines, Amino acids, purines, Gases, lipids, peptides

112
Q

Acetylcholine (ACh)

A

Chemical Neurocrine
Receptor: Cholinergic
Nicotinic (ion channel)
Muscarinic (GPCR)

113
Q

Norepinephrine and Epinephrine

A

Amine Neurocrine, catacholamine
Receptor: Adrenergic (GPCR)

114
Q

Dopamine

A

Amine Neurocrine, catacholamine
Receptor: Dopamine (GPCR)

115
Q

Amino acid Neurocrine example

A

Glutamate

116
Q

Purine neurocrine example

A

Adenosine

117
Q

Gas Neurocrine example

A

Nitric oxide

118
Q

NT production and storage

A

Made in cell body or axon terminal, stored in vesicles until signal for release. The signal is the depolarization of axon terminal

119
Q

NT Release

A

Exocytosis, released into synaptic cleft
1. Axon terminal depolarized by action potential
2. depolarization opens Ca channels and Ca enters cell
3. Ca triggers exocytosis (Active transport)
4. NT diffuse across cleft and binds with receptors on postsynaptic cell
5. Binding initiates response

120
Q

Termination of NT

A
  1. Chemicals broken down by enzyme
  2. Chemicals taken up by nearby glial cells
  3. Chemicals diffuse away from synapse (into bloodstream)
121
Q

Factors that affect strength of stimuli

A

Duration of signal will increase NT release
Frequency of AP

122
Q

Divergence

A

One neuron branches and communicates with several other neurons

123
Q

Convergence

A

One neuron receives input from many other neurons

124
Q

Synaptic Plasticity

A

When the activity of synapses are altered
Facilitate or depress activity

125
Q

Slow synaptic potentials

A

Mediated by GPCRs
slightly longer to trigger intracellular response through 2nd messengers
responses last longer

126
Q

Fast synaptic potentials

A

Associated with opening of ion channels by NT binding, depolarizes or hyperpolarizes

127
Q

Excitatory Postsynaptic Potential (EPSP)

A

Depolarizes, makes it more likely cell will fire AP

128
Q

Inhibitory postsynaptic potential (IPSP

A

Hyperpolarizes, makes it less likely cell will fire AP

129
Q

Temporal Summation

A

If 2 subthreshold potentials arrive at trigger zone within short period of time, they may sum to threshold and initiate AP

130
Q

Spatial summation

A

Several axon terminals onto one neuron, all subthreshold but sum to initiate AP
Most neurons

131
Q

Global presynaptic inhibition

A

Excitatory and inhibitory presynaptic neurons fire, summed signal is below threshold, no AP

132
Q

Selective presynaptic inhibition

A

Excitatory neuron fires, AP is generated, Inhibitory neuron fires blocking NT release at ONE synapse (one presynaptic axon)

133
Q

Prolactin (PRL)

A

Release triggered by Hypothalamus releasing dopamine
Milk production

134
Q

Growth Hormone (GH)

A

Metabolism and growth
GHRH (Growth hormone releasing hormone) stimulates release of GH

135
Q

Thyroid-stimulating Hormone (TSH)

A

synthesis and secretion of T3 and T4
TRH (Thyroid releasing hormone) stimulates release of TSH

136
Q

Adrenocorticotrophic Hormone (ACTH)

A

synthesis and release of cortisol.
CRH released from hypothalamus triggeres ACTH release from ant. pituitary which triggers release of cortisol from adrenal cortex

137
Q

Follicle-stimulating Hormone (FHS)

A

Maturation of germ cells in both sexes
Release triggered by GnRH from hypothalamus, goes to endocrine cells of gonads

138
Q

Luteinizing Hormone (LH)

A

Secondary sex characteristics
Follicle growth in females
spermatogenesis in males
Released triggered by GnRH from hypothalamus and goes to endocrine glands of gonads

A&P Lecture (3 decks)

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