Exam 3 Flashcards
1
Q
Hormones Influence…
A
metabolism, internal environment (water, temp, ions), reproduction, growth & development
2
Q
How do hormones act on target cells
A
- Alter rate of enzymatic reactions/levels
- Control transport of ions or molecules across membrane
- Control gene expression and synthesis of proteins
3
Q
4 Criteria for a hormone
A
- Secreted by a cell or group of cells
- Secreted into the blood
Secretion is movement from inside cell to ECF
Pheromone is hormone secreted outside the body - Transported to a distance target
- Exert their effects at very low concentrations
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)
5
Q
Terminating hormone activity
A
Regulation is critical (limit duration of effect)
Hormones degraded by liver or kidneys
6
Q
Half-life
A
Amount of time to reduce hormone concentration by half
7
Q
Hormone Classification
A
~50
Source of production, what controls their release, chemical classes
8
Q
Chemical classes of hormones
A
Peptide- derived from proteins
Steroid- derived from cholesterol (lipid)
Amine- derived from amino acids
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
10
Q
Peptide hormone characteristics
A
water soluble, dissolve easily in ECF, transported easily in blood but half-life is generally short
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
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
13
Q
Steroid hormone synthesis
A
- Produced by smooth ER
- Lipohilic cross membrane easily but needs carrier in the blood
Carrier protects hormone from degradation
14
Q
Albumin
A
Most abundant protein in blood, nonspecific carrier
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
16
Q
Amine Hormones
A
Created from tryptophan or tyrosine
Melatonin (tryptophan)
Catecholamines (tyrosine)
Thyroid (tyrosine)
17
Q
Catecholamines
A
epinephrine, norepinephrine, dopamine
Behave like peptide
18
Q
Thyroid hormones
A
behave like steroid hormones
regulate overall metabolism, temperature, and many functions
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
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 `
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
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
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
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
25
Anterior pituitary
true endocrine gland, controls many homeostatic functions
26
Posterior pituitary process
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
27
Anterior pituitary process
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
28
Portal system
2 capillary beds, ensures trophic Neurohormones go directly to Ant. pit and not other part of body
29
Trophic Hormones
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
30
Short loop negative feedback
The first or second hormone in the pathway provides feedback
(prolactin, GH, ACTH)
Pituitary gland pathways
31
Long loop negative feedback
Final hormone in pathway provides feedback
(cortisol, thyroid hormone)
Preferred form of feedback
Pituitary gland pathways
32
3 Types of hormone interactions
Synergism, Permissiveness, antagonism
33
Synergism
Two or more hormones interact with target and combination result is greater than each individually (additive effect, working together)
34
Permissiveness
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.
35
Antagonism
When one hormone opposes the action of another hormone; result of 2 hormones competing for same receptor or two hormones acting on different receptors
36
3 basic patterns of endocrine pathology
excess, deficiency, abnormal responsiveness
37
Hypersecretion
Leads to exaggerated effects, can occur anywhere along the pathway
Causes: tumors, exogenous hormone treatment
Decreases trophic hormone release
38
Exogenous treatment
outside source, may lead to endocrine gland atrophy
Increases negative feedback which means less natural hormone --> atrophy
39
Hyposecretion
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
40
Abnormal Responsiveness
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
41
Primary Pathology
Due to a problem with the last endocrine gland pathway (work through diagram)
42
Secondary Pathology
Due to a problem with the Anterior pituitary gland (work through diagram)
43
Tertiary Pathology
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)
44
How does the nervous system demonstrate emergent properties
Consciousness, intelligence, and emotion can not be explained by the anatomy and properties of neurons
45
Central Nervous System
CNS; consists of brain and spinal cord
46
Peripheral Nervous System
PNS; consists of afferent and efferent neurons
47
Afferent Neuron
Carry information TO the CNS, sensory neurons (PNS)
48
Efferent Neuron
Carry information AWAY from the CNS, Motor/movement neurons (PNS)
49
Somatic Motor Neurons
Controls skeletal muscles
50
Autonomic Motor Neurons
Controls cardiac and smooth muscle, exocrine glands, some endocrine glands, some adipose
51
Enteric Nervous system
Part of digestive tract, controlled by autonomic nervous system, and capable of autonomous action
52
Basic cell types of the nervous system
Neurons- basic signaling units
Glial Cells- support cells
53
Neuron
A functional unit of the nervous system, act as an IC, unique shape with long extensions
54
Classification of a Neuron
Structure- how many processes originate from cell body
Function-sensory, interneurons or efferent
55
Can you label the parts of a neuron??
Go do it on the diagram biotch
56
Synapse
The region where an axon terminal of the presynaptic cell communicates with its postsynaptic target cell. Electrical signal converted to chemical
57
Axon terminal
enlarged ending of axon, usually releases a chemical
58
Nerves
When the AXONS of many neurons are bundled together
59
Mixed nerves
carry afferent and efferent information
60
Sensory Nerves
Carry afferent info only
61
Motor nerves
Carry efferent info only
62
Cell body
nucleus and organelles, act as control center for neuron
63
Dendrites
thin branched structure that receives incoming info
64
Axons
most nerves have single structure that transmits outgoing electrical signal
Hillock- axon origin
Terminal- contains mitochondria and membrane-bound vesicles with chemicals
65
Ependymal cells
Glial, CNS
Creates barriers between compartments like the blood brain barrier, source of neural stem cells
66
Astrocytes
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
Microgilia
Glial, CNS
act as scavengers, clean the environment (vacuum)
68
Oligodendrocytes
Glial, CNS
Form myelin sheaths (insulate)
69
Schwann Cells
Glial, PNS
Form myelin sheaths (insulate) secrete neurotrophic factors
70
Satellite cells
Glial, PNS
Support cell bodies/keep them happy
71
Myelin
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
Nodes of Ranvier
tiny gaps between myelin sheath where axon is exposed to ECF
73
Membrane potential
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
Nernst Equation
Tells us the membrane potential of a cell if that cell was permeable to only that individual ion
75
Goldman-Hodgkin-Katz (GHK)
equation calculates the membrane potential that results form the IONS that can cross the cell membrane (rather than just one ion in Nernst)
76
Vm depolarizes
Vm increases, more positive
Entry of + ion
Exit of - ion
77
Vm hyperpolarizes
Vm decreases, more negative
Entry of - ion
Exit of + ion
78
Ion concentration levels inside the cell
K+ high
Na+, Cl- low
79
Ion concentration levels outside the cell
Na+, Cl- high
K+ low
80
Mechanically gated channels
Open in response to forces such as pressure
81
Chemically gated channels
Open when the right ligand binds
82
Voltage gated channels
respond to changes in cell's membrane potential
83
Current
The more channels that open, the faster the ions can flow in/out which creates current
84
Properties of graded potential
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
When do GP occur
When chemical signals from other neurons open/close chemically gated ion channels
86
Subthreshold event
No AP, determined by the SUM of graded potentials arriving at the trigger zone (axon hillock)
87
Suprathreshold event
AP down axon (-55 mV), determined by the SUM of graded potentials arriving at the trigger zone (axon hillock)
88
Properties of Action Potentials
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
AP along the axon
Not one single AP, instead a series of channel openings like a domino effect
90
Rising phase of AP
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
Falling Phase of AP
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
Voltage Gated Na+ at -70 mV
Activation gate closed
Inactivation gate open
No flow of Na+
93
Voltage Gated Na+ at -55 mV
Activation gate opens
Inactivation gate still open
Na flows into cell
94
Voltage Gated Na+ at +30 mV
Activation gate remains open
Inactivation gate closes
No Na+ flow
95
Voltage Gated Na+ during falling phase
Both gates reset to their original positions
Activation gate is closed
Inactivation gate is open
No flow of Na+
96
Why does the voltage gated Na+ channel have 2 gates?
More control over flow of Na+ and thus control over depolarization
97
Absolute Refractory period
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
Relative Refractory period
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
Why is a larger stimulation needed to generate another AP during the relative refractory period?
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
Conduction of AP down the axon
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
What causes the domino effect?
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
What returns Na and K to their "correct" place?
Na/K pump
103
Myelin increasing conduction
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
Presynaptic cell
Axon terminal, releases chemical or electrical signal
105
Postsynaptic cell membrane
Doesn't have to be a neuron, could be muscle, glands, etc.
Have receptors for chemicals or gap junctions for electrical.
106
Neurocrines
The chemical signal secreted by neurons
107
Neurotransmitters
Fast paracrines that act locally
108
Neuromodulators
Slower paracrines that act locally
109
Neurohormones
Hormones released by neurons into blood stream
110
Types of neurocrine receptors
Chemically gated ion channels (neurotransmitters)- fast synaptic potentials and G-protein coupled receptors (neuromodulators)-slow synaptic potentials, long-term effect
111
7 classes of neurocrines
Chemical, Amines, Amino acids, purines, Gases, lipids, peptides
112
Acetylcholine (ACh)
Chemical Neurocrine
Receptor: Cholinergic
Nicotinic (ion channel)
Muscarinic (GPCR)
113
Norepinephrine and Epinephrine
Amine Neurocrine, catacholamine
Receptor: Adrenergic (GPCR)
114
Dopamine
Amine Neurocrine, catacholamine
Receptor: Dopamine (GPCR)
115
Amino acid Neurocrine example
Glutamate
116
Purine neurocrine example
Adenosine
117
Gas Neurocrine example
Nitric oxide
118
NT production and storage
Made in cell body or axon terminal, stored in vesicles until signal for release. The signal is the depolarization of axon terminal
119
NT Release
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
Termination of NT
1. Chemicals broken down by enzyme
2. Chemicals taken up by nearby glial cells
3. Chemicals diffuse away from synapse (into bloodstream)
121
Factors that affect strength of stimuli
Duration of signal will increase NT release
Frequency of AP
122
Divergence
One neuron branches and communicates with several other neurons
123
Convergence
One neuron receives input from many other neurons
124
Synaptic Plasticity
When the activity of synapses are altered
Facilitate or depress activity
125
Slow synaptic potentials
Mediated by GPCRs
slightly longer to trigger intracellular response through 2nd messengers
responses last longer
126
Fast synaptic potentials
Associated with opening of ion channels by NT binding, depolarizes or hyperpolarizes
127
Excitatory Postsynaptic Potential (EPSP)
Depolarizes, makes it more likely cell will fire AP
128
Inhibitory postsynaptic potential (IPSP
Hyperpolarizes, makes it less likely cell will fire AP
129
Temporal Summation
If 2 subthreshold potentials arrive at trigger zone within short period of time, they may sum to threshold and initiate AP
130
Spatial summation
Several axon terminals onto one neuron, all subthreshold but sum to initiate AP
Most neurons
131
Global presynaptic inhibition
Excitatory and inhibitory presynaptic neurons fire, summed signal is below threshold, no AP
132
Selective presynaptic inhibition
Excitatory neuron fires, AP is generated, Inhibitory neuron fires blocking NT release at ONE synapse (one presynaptic axon)
133
Prolactin (PRL)
Release triggered by Hypothalamus releasing dopamine
Milk production
134
Growth Hormone (GH)
Metabolism and growth
GHRH (Growth hormone releasing hormone) stimulates release of GH
135
Thyroid-stimulating Hormone (TSH)
synthesis and secretion of T3 and T4
TRH (Thyroid releasing hormone) stimulates release of TSH
136
Adrenocorticotrophic Hormone (ACTH)
synthesis and release of cortisol.
CRH released from hypothalamus triggeres ACTH release from ant. pituitary which triggers release of cortisol from adrenal cortex
137
Follicle-stimulating Hormone (FHS)
Maturation of germ cells in both sexes
Release triggered by GnRH from hypothalamus, goes to endocrine cells of gonads
138
Luteinizing Hormone (LH)
Secondary sex characteristics
Follicle growth in females
spermatogenesis in males
Released triggered by GnRH from hypothalamus and goes to endocrine glands of gonads
