midterms i guess idk cymbalta is frying my brain Flashcards
(185 cards)
1
Q
What does the permeability of the cell membrane depend on
A
molecular size, lipid solubility, and charge
2
Q
What can cross the membrane and what cannot
A
Gases can go across, polar molecules and ions need help of proteins
3
Q
The relative rate of simple diffusion is () to the gradient across the membrane
A
roughly proportional
4
Q
What type of transporter is a Na+ K+ pump? What does this type of transporter do
A
ATPase, it moves both molecules against their concentration gradients
5
Q
What is secondary active transport
A
When something is moved down concentration gradient and something else uses that energy to move up
6
Q
How are protein channels made and how do they filter
A
Made of 4-5 subunits that form a central pore. The physical properties determine the size and electric charge of things that can go through
7
Q
Where do ligand gated channels trigger events
A
at the membrane because they are on the membrane lol
8
Q
What part of voltage gated channels sense the potential difference across the membrane, and how does it work
A
The S4 segment acts as the voltage sensor. In the resting state (polarized), the inside of the membrane is negatively charged, attracting the positively charged S4 segment inward. Upon depolarization, the reduced negative charge inside the cell causes the S4 segment to move outward, triggering the opening of the channel.
9
Q
What usually mediates endocytosis and why?
A
Usually receptor mediated to capture proteins
10
Q
What are some reasons for exocytosis
A
Bulk transmembrane transport of molecules, such as neurotransmitters
11
Q
What are the two types of exocytosis? Explain how they work and in what instances are they used
A
Exocytosis 1, dubbed kiss and run, and 2, full exocytosis. For 1, the vesicle can disconnect many times before contents are emptied. Only part of the contents go into interstitial fluid, and it is used for low rates of signalling. For 2, it is used for high levels of signalling and membrane proteins.
12
Q
What creates a concentration gradient
A
enzyme ion pump, 3 Na+ are pumped out and 2 K+ are pumped in. Uses a shit ton of energy (1/3 of energy needs).
13
Q
Why is the resting potential of the membrane not the same as the estimated resting potential of Na/K inequality (-10mV)?
A
Because the membrane is more permeable to K+ than Na+ and because there’s like no K+ outside, the K+ pumped in all want to go out. So they go out, until its wayyyy too positive outside, then they stop. At this point, its -70 mV
14
Q
What does the Nernst equation describe and under what circumstances can you use it
A
It describes the balance between chemical force of diffusion and electrical force of repulsion (charges). You can only use it if there is only one ion species diffusing across the membrane
15
Q
You use the Nernst equation to find the equilibrium potential for K+. What does this value mean
A
Its what the membrane potential would be if there were only K+ ions in the cell. Or, its what K+ wants the membrane potential to be (but it doesn’t get what it wants because the other ions are there to fuck shit up lol)
16
Q
What is Eion
A
membrane potential that exactly opposes the concentration gradient (positive value)
17
Q
What are the membrane potentials of K+ and Na+, and why is the actual membrane potential closer to that of K+’s?
A
K+ is -90, Na+ is +60. Its closer to K because K is more permeable, and according to the Goldman Equation (basically more overpowered Nernst Equation), the permeability of an ion is proportional to the resting membrane potential
18
Q
Where are the Cl- ions concentrated and why
A
Outside the cell because theres a shit ton of big proteins and they are negative for some reason and the Cl-s are like fuck this shit im out. It’s not actively pumped out. They just don’t like being inside
19
Q
What is conductance
A
How easy stuff (e.g. Na+) goes through a protein channel in the membrane
20
Q
How is a Na+ channel opened
A
It is a voltage gated channel so the membrane needs to depolarize to -55, which then opens the activation gate. Shit ton of Na+ enters, and the cell depolarizes rapidly. Inactivation gate closes, then no more Na+. In order to remove the inactivation gate, you need the membrane potential to be lower than -55
21
Q
What do you need for an action potential
A
A shit ton of Na+ channels, so the membranes can depolarize
22
Q
What causes the repolarization part of an action potential
A
Na+ channels are now closed and K+ leaks out of the cell, hyperpolarizing it.
23
Q
When the membrane potential is positive, what force drives Na+ into the cell?
A
Concentration, not electrical forces. Electrical forces is only when the membrane potential is not positive
24
Q
Draw an action potential graph, labelling key points and explain
A
Check membrane 2 slide 24
25
What are the two types of refractory periods, explain them
Absolute and relative. Absolute is when none of the channels are reconfigured, relative is when some but not all are reconfigured, If you want to fire during relative refractory period, you need a stronger depolarization, and these action potentials will be of lower amplitude because the cell is EXTRA negative due to the K+ still leaving the cell.
26
You have your worst enemy strapped to a vivisection table, and you are about to inject a lethal injection you lawfully stole from a high security prison. What does the lethal injection do to your enemy's cells
It prevents the cells from producing an action potential by keeping it above 20 mV, and the Na+ will be permanently inactivated. So the lethal injection puts a ton of K+ in extracellular space so the resting potential is no longer negative. (wow imagine uoft telling us how to kill ourselves, its like they actually want some of us to die off to reduce the load on their facilities while still milking our money)
27
Why is there a hyperpolarization after the action potential
Because K+ is leaving the cell to repolarize, and they overshoot a little
28
What is impulse conduction
When an action potential passively spreads because of the local changes in membrane potential
29
Can unexcitable cells depolarize?
Yes, they can conduct passive currents but cannot generate action potentials because they don't have axons to carry the action potential elsewhere
30
What is a length constant for excitable cells
It measures how quickly a potential difference goes to zero as a function of distance. So, the bigger, the better (if you want the signal to send). It is the distance you can travel until the voltage drops to 37% of the original value.
31
How do you increase the length constant
Increase membrane resistance so you basically wrap duct tape around a pipe so you get less leakage. Increasing diameter so there is less internal resistance. However the best way is myelination
32
Express the length constant in terms of membrane an internal resistance
square root of membrane resistance over internal resistance
33
What are glial cells
cells that assist the nervous system, required for nutrition and increased membrane resistance. specialized glial cells form a myelin sheath.
34
What are the two types of specialized glial cells that myelinate?
Schwann cells that wrap all around a part of one axon. Oligodendrites streak out like octupus tentacles and wrap a bunch of axons separately
35
What is saltatory conduction
When action potentials jump from Nodes of Ranvier because they spread passively through myelinated regions. Only exposed membranes at nodes are excitable
36
What does one action potential at a node of ranvier do for the following nodes? Why is this helpful for not fucking up action potentials?
It brings the next 10 nodes to -55mV to generate action potentials. This is to prevent action potentials dying if a few nodes are poisoned.
37
What is a remak bundle
When a schwann cell surrounds a bunch of axons with only one layer, slightly insulating them
38
Why are refractory periods important
Because it prevents the action potential from going backwards, and makes it die out at the end of the cell.
39
What is a synapse
Association of a neuron with another neuron or muscle or gland
40
What is an electrical synapse and what cells are they present
At gap junctions bridged by connexins that allow small ions and depolarization to happen. There are no neurotransmitters. This is common in neurons and glial cells as well as cardio contractile muscles
41
How does exocytosis happen at the bouton
Ca++ is the ion that always triggers exocytosis. It is ingested when action potentials open the voltage channels for Ca++, and exocytosis happens. Some kiss and run, some full fusion. Vesicles are normally docked and ready to go
42
What are the chances of vesicle release at synapses
10-90%
43
What are the two different types of post synaptic receptors, explain the similarities and differences
The binding of neurotransmitter causes a change in shape of the receptor protein for both. A metabotropic receptor initiates a metabolic cascade to activate enzymes, and molecules that bind to it are considered neuromodulators. An ionotropic receptor directly opens channels, and molecules that bind to it are considered neurotransmitters
44
Binding of neurotransmitters to the post synaptic membrane for ionotropic receptors causes what
Excitatory or inhibitory post synaptic potentials, or respectively known as EPSPs and IPSPs. EPSPs happen when the ion channel caused by the ligand lets in positive ions, such as Na+ and K+, which depolarizes the membrane. IPSPs happen when the ion channel lets in Cl- or lets K+ out, which hyperpolarizes
45
What are the four common ionotropic ligands
Acetylcholine, Glutamate, GABA, Glycine
46
How does the metabotropic pathway work
Binding of the ligand activates an enzyme that is usually g protein coupled, this produces second messengers, which then activate other proteins. Until it phosphorylates a membrane protein.
47
What are the three 2nd messengers for metabotropic pathways
cAMP, cGMP, and lnP3s
48
explain how the b-adrenoreceptor works, what is the ligand, what type of pathway does it go through
It is a metabotropic pathway, the ligand is noadrenaline, which activates adenyl cyclase via g-protein alteration, and that phosphorylates the membrane Ca++ channel, increasing Ca++ influx. This is an EPSP
49
What are ligands for metabotropic receptors
ACh, peptides, catecholamines (noadrenaline and dopamine), serotonin, purines (ATP, adenosine), gases (NO, CO)
50
What parts of a neuron are not excitable and where PSPs occur
Dendrites and cell body
51
What is the trigger zone
The nearest excitable membrane at the beginning of the axon
52
How do post synaptic potentials (PSPs) travel
Through passive conduction
53
What are the two types of PSP summation
Spatial summation, when 10-30 PSPs at different synapses add up. Temporal summation is when there are only a few active synapses but they generate EPSPs at a high frequency and the summed potentials reach the threshold
54
Draw spatial summation and temporal summation as a function of membrane potential (mV) and time.
Check answers in membrane 04 pages 24-25
55
Where are IPSPs located and why are they there
They are between EPSPs and the trigger zone, so they can shunt the signals. It's like casting counterspell in BG3 but instead of casting it whereever the fuck you want, you need to be positioned between the enemy and their target.
56
How does the IPSP shunt the signals provided by the EPSPs (how does your neuron cast counterspell, esentially)
It opens the Cl- channel, which has a resting membrane potential around -70mV. This does nothing at resting membrane potential, but when the membrane is depolarized, it clamps the membrane potential back down to resting, inhibiting the signal
57
Which are more common, IPSPs and EPSPs
IPSPs. Imagine if you had no inhibition. that would be very bad. you would drink vodka almost every day and lick your self harm scars until your tongue pushed past your epidermis and you would think of strade all the same
58
How do spike trains form for action potentials. What does this tell the brain
You have refractory periods, and hyperpolarization. The Na+ channels reconfigure because the cell is too polarized (it is voltage gated). The voltage gated K+ channels also close when membrane is repolarized. With all the right things closed, the membrane can go through diffusion back to resting MP, and fire again considering the EPSP still persists. This spike train tells the brain it is a big signal
59
What is a receptor potential, does it depolarize or hyperpolarize
a change in membrane potential when an external sensory que is recieved. This generally causes depolarization, except for photoreceptors
60
Where are sensory receptor proteins, and how do they work
they are in the cell membrane like the receptor proteins for post synaptic potentials (PSPs). They can either directly open ion channels or activate an enzyme with g-protein coupling, producing a secondary messenger, and amplifying the signal (like in a metabotropic pathway)
61
What is a PSP
post synaptic potential
62
Where are olfactory neurons located
At the olfactory epithelium, high in the nasal cavity
63
Write out the pathway for olfactory neuron signalling
Specific receptor proteins bind to specific odorants, g-protein is activated, adenyl cyclase activated, secondary messenger (cAMP) released, cAMP bind to ion channels, allow Na+ and Ca++ through, depolarizing the membrane
64
What are the two types of sensory cell transmission
1. action potential generated at a branch point. the receptor potential will need to be summed at the branch point for an action potential 2. no AP produced, the depolarizing current goes through the membrane and causes influx of Ca++ which triggers exocytosis (vescicle release)
65
How does the taste receptor signal
Influx of Ca++, the depolarizing current reaches the other end of the cell, and vescicles are released.
66
What is adaptation for membrane potentials
When the membrane potential is not sustained even though the stimulus is present
67
What are the two types of membrane potential adaptations
Slow, where the receptor potential (i.e. depolarization) is sustained throughout the stimulus, but declines slightly. It is interested in the magnitude of stimulus. Rapidly adapting is where the receptor potential is zero when the stimulus is constant. It is kind of like a f'(x) of the stimulus. It only cares when there is a change in magnitude. It can be positive and negative
68
What is habituation
When repeated stimuli get weaker and weaker responses over time. This depends on the cell, some exhibit this a lot, others do not
69
If a stimulus is very strong, what will happen? What concept explains this
Coding of stimulus intensity. It says that receptor potential varies depending on stimulus strength. Strong stimuli cause greater receptor depolarization, and more neurotransmitter is released or the action potentials are at a higher frequency.
70
How do higher threshold sensory neurons help with coding of stimulus intensity
It allows the neurons to bypass the refractory period, and can sense sensations stronger than refractory periods allow
71
What is the labelled line strategy and why is it bad
A way of coding for modality in neurons. One pathway is for a specific stimuli quality and nothing else, it is bad because there are too many qualities to code for.
72
How do neurons code for modality
Population code, different receptors pick up on different signals, the stimuli is coded for by the ratio of activity across different receptors
73
What is a receptive field
the spatial area of which a neuron responds to, i.e. the area where you can activate a neuron. each sensory neuron has a different receptive field. for skin, it can be 1-2 cm across, for fingertips, 1mm
74
Why do you need a blood brain barrier
To avoid changing concentration gradients, because if there is permanent depolarization, then Na+ will be closed permanently and no more action potentials.
75
Where is the BBB not present
At the hypothalamus and pituitary gland, to allow release of hormones. And around the circumventricular organs around the 3rd ventricle so neurons can sense specific chemicals. Basically, where you need to interact with the endocrine system or need to be sensitive to metabolites in plasma
76
From the outermost to the innermost, list the menings of the brain
Dura mater, a tough sac containing the brain and spinal cord. Arachnoid membrane, delicate tissue like a web, empty parts filled with cerebrospinal fluid. There are blood vessels and capillaries to the brain tissue in arachnoid membrane. Pia mater, right on top of the brain tethered to the arachnoid membrane
77
What is the differerence between the lining of general endothelial cells and brain endothelial cells
Brain endothelial cells don't have fenestrations (gaps) that allow molecules through to maintain BBB
78
What are ventricles? How are they connected
The thing that allows you to make fun of people who call your brain empty. Because technically, it is empty (somewhat). Are symmetrical, and lateral ventricles are big and look like a satanic ram's horns if you look at them from the front. Lateral ventricles empty into 3rd ventricle in the middle under the cerebral hemisphere, and the 3rd ventricle uses the aqueduct of sylvius to go to the 4th, which has a central canal going to the spinal cord
79
How does cerebrospinal fluid drain from the brain and spinal cord
1/2 of it goes through the arachnoid villi (a little pouch stickin into the venus system) into venus system, and the rest goes to veins
80
How is cerebrospinal fluid made
From plasma by the choroid plexus, which lines the 3rd, 4th and lateral ventricles. The choroid plexus are made of epithelial cells connected by tight junctions, and makes cerebrospinal fluid continuously. Some are produced by capillaries inside the brain.
81
How does the osmolarity of common ions of cerebrospinal fluid compare with that of blood
Same [Na+] as blood, greatly reduced [K+], [Ca++], [Mg++] (it also is less viscous than blood. fuck this shit i was going to make a very unfunny joke about how brainfucking is before family because that cerebrospinalussy is thicker than blood but thats scientifically inaccurate fuck that shit dead dove fics are going to land me in jail one day HAHAHAHHAHA AIM GOING INSANE
82
How much cerebrospinal fluid in the cranium and spine
140 for cranium, most is in subarachnoid space. 75 ml for spine. THIS IS WHY IM ALWAYS SO PISSED WHEN PEOPLE DRILL INTO SKULLS IN FANFICTIONS AND THERE. IS. NO. FUCKING. LIQUID. ITS SUPPOSED TO BE WET AND DISGUSTING!!!! AND YOU'RE WRITING IT LIKE A DRY TRANSPHOBE KAREN'S PUSSY??? WHAT HAPPENED TO CREATIVE LIBERTIES WHAT HAPPENED TO LITERATURE??????
83
What are astrocytes, why are they important
cells that provide a bridge between neurons and blood vessels by putting their feet (????) around capillaries. They are important because they are effective at glycolysis and produce lactate, which is used for ATP production in neurons. They can also remove excess neurotransmitters
84
How do astrocytes regulate local blood flow
They are positioned between blood vessels and neurons, so when neurons release glutamate, it triggers Ca++ release within astrocytes, which release PGE2 at the end, and that causes vasodilation (increases blood flow)
85
What is a set point for homeostasis
a optimum value for a certain value
86
What are the types of responses organisms can make when they need to maintain homeostasis
1. cellular (such as a blood vessel contracting)
2. tissue/organ (blood flow decreases)
3. systemic (organism as a whole)
87
Cortisol levels is an example of what in homeostasis? (think circadian rhythms)
Oscillation around a setpoint, it changes based on your circadian rhythms. Remember they made you make jarate and analyzed that shit? It's because they needed an average of your daily cortisol levels
88
Between negative feedback and positive feedback, which maintains homeostasis? How do both work
Negative feedback has a stimulus that stops the initial stimulus to avoid getting the same response over and over. It maintains homeostasis. Positive feedbackk reinforces reinforces the response and makes you get further and further from the set point
89
How do you locally maintain homeostasis
Gap junctions (small ions move through these, which connect adjacent cells), contact-dependent (membrane protein binds to membrane protein), autocrine (molecules move through interstitial fluid, acting on the secreting cell), and paracrine (diffuse to adjacent cells)
90
How do you communicate long distance
Using hormones (to control enzymatic reactions, transport of ions/molecules, gene expression). And using the nervous system (neurotransmitters and neurohormones, which are chemicals released into the blood)
91
What are simple and complex reflexes
Simple uses only one of endocrine or nervous, complex uses both. Complex can have many integrating centers but only has one response
92
List the speed, nature of signal, specificity, duration of action, and coding for stimulus intensity for neural reflexes
The specificity is high, it targets few cells. The signal usually goes by electrical signal and neurotransmitter, occasionally by gap junction. It is very fast, usually lasts short, and signals are the same in strength. Frequency tells strength
93
List the speed, nature of signal, specificity, duration of action, and coding for stimulus intensity for neural reflexes
The specificity is low, and it depends on which cells have the corresponding receptor. The signal goes by blood stream, and is slower. Responses last longer, and different amount has different responses
94
What is the difference between exocrine and endocrine
Exocrine is released on pores, or in a duct, like sweat and digestive enzymes. Endocrine is in blood
95
Where are hormones made, and how do you stop the production
can be made in different places in the body (think primary and secondary endocrine organs), and you need to stop the synthesis (you can't just expect it to stop on its own).
96
How are hormones identified
Remove the gland and see what happens >:)
Replace extract from the gland
Give extra glands (NOTE: THIS FLASHCARD CAN AND WILL BE INTEGRATED INTO THAT MORALLY GRAY LESBIAN ORIGINAL STORY I'M PLANNING ABOUT STOCKHOLM SYNDROME, TORTURE, AND PHARMACOLOGY)
Purify extract and test in biological assay
97
What are the two types of hormones (hydro??)
Hydrophilic, which dissolve in plasma, and cannot cross membranes because they aren't lipid soluble. Examples include peptide hormones, protein hormones, and catacholamines. It is exocytosed and produced in advance then stored. Hydrophobic, which is the opposite. Examples include steroid and thyroid hormones (think about your mom to remember this. Your mom is homophobic and has thyroid problems, and has used steroids during menopause.) It is produced on demand and allowed to diffuse across membranes. In blood, it is bound to carrier proteins
98
What are the three types of hormones
Peptide/protein (3 or more amino acids), steroid (derived from cholesterol [OH THATS WHY THOSE STEROID CREAMS SMELL LIKE THE CHOLESTEROL THAT CAME WITH MY FACE CASTING KIT]), amine (derived from single amino acids)
99
Which of the three types of hormones are hydrophobic
Steroid. The rest are hydrophilic
100
How common are peptide/protein hormones? When is it made, how is it synthesized, how is stored, when is it exocytosed, how is the half life?
Most proteins are peptide/protein. It is made on demand, synthesized like secreted proteins because it is exocytosed. It is stored in vesicles, has a short half life in plasma. It binds to membrane receptors
101
What is the precursor for a peptide/protein hormone
Prohormone, which has a precursor that is preprohormone. The signal sequence is cut off, turning it into prohormone, which is then cut into active hormone and peptide fragments
102
How many peptide/protein hormones can a preprohormone make
Several copies of the same hormone, or more than one type of hormone, it depends on specific proteolytic processing enzymes
103
For steroid hormones: When is it made, how is it synthesized, how is stored, when is it exocytosed, how is the half life?
It is made on demand, synthesized from cholesterol, it is not stored in vesicles, and diffuse into target cells or endocytosed. It has a long half life, and can bind to carrier proteins for an even longer half life
104
How do you know which steroid hormones are made
It depends on which enzymes are present in the cell
105
What are amine hormones synthesized from
Tryptophan (melatonin, behaves like peptides or steroids), and tyrosine (catacolamines and thyroid hormones)
106
What is melatonin
Darkness hormone (wait does this mean in baldurs gate if sharrans cast darkness, you should also have a slight chance to fall asleep?), secreted at night, made in pineal gland. Has diverse effects
107
Where are catacholamines synthesized, what are some examples
Synthesized in adrenal medulla, some examples are dopamine and adrenaline
108
What senses stimuli for hormone release
Endocrine cells, they sense metabolites, hormones, neurohormones, neurotransmitters
109
How do stimuli trigger hormone release
They act through intracellular pathways to change the membrane potential, increase free cytosolic Ca++, change enzymatic activity, increase the transport of hormone substrates into the cell, alter transcription of genes encoding for hormones or enzymes needed for hormone synthesis. Promote survival, and sometimes growth of endocrine cell
110
How do hypothalamic and anterior pituitary hormones regulate other hormones
Hypothalamus activates anterior pituitary, which then stops the hypothalamus. Peripheral endocrine gland is activated by the anterior pituitary
111
What are the types of hormone interactions
Synergistic (1+2>3), permissive (mom says its my turn on the xbox), and antagonistic (strade putting a shock collar on mc to prevent them from leaving the house lmfao)
112
How do hormones signal
Hormone binds to receptor, changes the conformation and activity of receptor, starts intracellular signalling pathway, causes protein synthesis or modifies already existing target proteins
113
What characteristics do receptors share
Large proteins with families of similar ones, can have multiple receptors for one ligand and more than one ligand for one receptor, there is a variable number in cells, can be activated and inhibited, present in membrane, cytoplasm, and nucleus. Obviously, they are saturatable because once you run out of receptors, more ligand is useless.
114
Is the modification of existing proteins or synthesis of target proteins faster
Modification of existing proteins is faster
115
What are intracellular receptors
Receptors that bind lipid soluble hormones and can be in the cytoplasm or nucleus. They alter gene transcription
116
What are the types of plasma membrane receptors
g-protein coupled receptors (open ion channels or alter enzyme activity on the cytosolic side, activated when bound to GTP). Receptor-enzyme receptors, receptor channels and integrin receptors
117
What receptors do peptide hormones bind to
Surface receptors, cell activity regulated with secondary messengers
118
What receptors do steroid hormones bind to
Internal receptors, usually in the nucleus. It penetrates the plasma membrane, and takes hours or days to show effect due to time needed for protein synthesis
119
What is a hormone response element
A specific DNA sequence regulated by hormones, such as steroid hormones. Can be activated or repressed
120
How do g-protein coupled receptors work
Cytoplasmic tail is linked to the G protein. The g-protein coupled receptor adenyl cyclase-cAMP system is the signal tranduction pathway for many protein hormones. some use lipid second messengers
121
How do secondary messengers like cAMP amplify cell responses
by having one kinase phosphorylate many proteins, basically a small amount of ligand for a bigger effect
122
What are the three types of G proteins and what do they do
Gs activates adenyl cyclase, gq activates phospholipase c, releasing a lot of Ca++, and Gai inactivates adenyl cyclase
123
What does fight or flight responses do to the body
Liver releases glucose and fat releases fatty acids for energy. Heart has muscle contraction, skeletal and blood vessels have less vasoconstriction, so they dilate, allowing you to run. Intestine, skin and kidney have vasoconstriction.
124
What do alpha and beta receptors for adrenaline differ in
Alpha is on intestinal blood vessels, and binding causes constriction. Beta is on skeletal and blood vessels and binding causes dilation.
125
Epinephrine and noepinephrine bind to a lot of stuff. How do you know what effect it will have
It depends on the diferent receptors and the signal cascade of affected cell
126
How is cell signalling modulated
Hormone degradation, removing or increasing the number of receptors, desensitizing the receptors, breaking down second messengers, biological effect reduces hormone secretion
127
A ligand binds to a membrane receptor. You want to endocytose the ligand, how do you do so while also recycling the membrane receptor?
Receptor-ligand goes to clathrin coated pit, is endocytosed as it loses the clathrin coat. Receptors and ligands separate in an endosome, transport vescicles bring the receptors to the membrane while the ligand go to lysosome or golgi
128
Why is calcium important for normal physiology
Intracellular signalling, hormone secretion, blood clotting, neural excitability, muscle contraction, building and maintaining bone
129
Where does calcium come from, where does it go
It comes from diet, goes into extracellular fluid. Some goes into extracellular matrix (bone) and 0.9% into cells. It is excreted via urine in the kidneys
130
Where is most of the calcium
It is mostly in bones in the form of hydroxyapatite. A small amount is ionized and readily exchangable.
131
What are the three types of cells that form and maintain bones
Osteoblasts, which form bone by creating calcium phosphate complexes, osteoclasts, which destroy bone by secreting protease enzymes at low pH, and osteocytes that maintain bone (previously osteoblasts that got surrounded by bone)
132
Describe an osteoclast and how it eats away at hone
It is multinucleated and between bone and blood capilaries. It secretes HCl which eats at bone, and uses carbonic anhydride to make H+ which goes into the HCl and HCO3- which goes back into the blood
133
How long does it take to destroy bone and how long does it take to reform
3 weeks to destroy and 3 months to reform
134
What are RANK, RANKL, and osteoprotegrin
RANK is on osteoclast precursors, and is the activator of nuclear factor kappa b. RANKL is on osteoblasts, and is the RANK ligand. Osteoprotegrin, or OPG, secreted by osteoblasts block the RANK and RANKL interaction. Osteoblasts and osteoclast precursors form osteoclasts when bound by RANK and RANKL
135
What 3 hormones control plasma Ca2+ levels, where do they act
Parathyroid hormone (PTH), Calcitriol, and calcitonin. They act on the bones, kidneys, and digestive tract.
136
Where is parathroid hormone released, what is its purpose, and what stimulus cues its release
It is released from the parathyroid glands, increases plasma Ca++ concentration, and the stimulus is reasonably low blood Ca++. They are very sensitive to extracellular calcium concentration
137
What senses blood Ca++ levels
a receptor on the plasma membrane. If there is enough calcium, there are many ways for it to stop PTH, such as increasing the amount of vitamin D
138
How does PTH increase blood Ca++
Acts directly on the bones and kidney. Gets Ca++ out of bone so there is less bone, reabsorbs Ca2+ at the distal tubule in kidneys. It increases cAMP in osteoblasts, which decreases OPG and increases RANKL, meaning more osteoclasts
139
What organs are needed for calcitriol synthesis. How is it related to vitamin D3
skin, liver, and kidney. Vitamin D3 goes though several enzymatic steps to make calcitriol
140
What does calcitriol do to calcium
Targets intestine, bone, and kidney to increase serum concentration. Increases Ca++ intake from small intestine, renal Ca++ reabsorption and mobilization from bone
141
What is vitamin d3 hormone also called
calcitriol
142
How is blood phosphate controlled
PTH increases calcium release from bone, decreases phosphate reabsorption from kidney. It sacrifices phosphate. Calcitriol increases phosphate absorption by intestine and reabsorption by kidney
143
How are PTH and calcitriol released
PTH is released in bursts and calcitriol is in the body every day
144
Where is calcitonin secreted, what is it triggered by, what type of hormone
It is secreted by C cells of the thyroid gland, it is a peptide hormone with release triggered by high plasma Ca++. C cells can sense Ca++ levels.
145
What does calcitonin do
Protects the skeleton from losing too much Ca++ during pregnancy and lactation. Reduces osteoclast activity, stimulates osteoblasts, inhibits calcium reabsorption by kidneys
146
What happens when you have too much calcium
Groans (constipation), Moans (fatigue, lethargy, depression), bones (bone pain), stones (kidney stones) and overtones (confusion, weakness)
147
What happens when you have too little calcium
CATS: convulsions, arrhythmias, tetany, spasms, seizures, and stridor
148
How is water distributed in the body
2/3 intracellular fluid, 1/3 extracellular fluid. 75% of extracellular is interstitial, 25% is plasma
149
What are the average daily water gains and loses, where does it come and go
Gain is from food and drink, loss is from urine, skin, lungs, feces. Skin and lungs lose most of the water, 0.9 L/day. You gain and lose 2.5 liters per day, a little of which is from metabolic production
150
What does excessive water loss do
make you confused, have chest pain, low blood pressure, no urine (think about what happened when you cosplayed ghost in 40 degree celsius weather. you thought spiderman was kakyoin, felt dizzy, did not piss in like 6 hours)
151
What does too much water do
difficulties in breathing and walking
152
What part of the kidneys filters blood to make pee, how do you know total solute excreted (i.e. how much do you piss out)
Nephrons filter it. The amount you piss out is amount filtered (entering tubule) - amount reabsorbed + amount excreted (comes back into tubule from blood)
153
What does the nephron/kidney do
Excreting waste, regulating blood volume, controlling electrolytes and blood pH, making vitamin D
154
What does vasopressin (ADH) do, where is it made, what stimulates its release
It is synthesized in the hypothalamus and secreted from posterior pituitary. Increases water absorption in the kidneys, conserves body water, maintains fluid homeostasis, increases blood volume and blood pressure. It does this by regulating permeability of cells in kidney (increased permeability means increased reabsorption and low urine output). Low blood pressure causes vasopressin release, which is detected by the walls of the atria of the heart, and arteries. Plasma osmolarity is the strongest stimulus to facilitate vasopressin release
155
How does vasopressin make water in pee go to blood
By putting aquaporins on the side of the membrane facing the collecting duct lumen.
156
What controls aldosterone synthesis
Negative feedback, high concentration of K+ in plasma, and angiotensin II (renin angiotensin pathway). High osmolarity of extracellular fluid inhibits synthesis
156
Where is aldosterone synthesized, what is its use? What type of hormone
It is made in the adrenal cortex, it regulates sodium and therefore water. It is a steroid hormone made in the zona glomerulosa in charge of Na+ reabsorption to maintain water, K+ secretion, and acts on the distal tube and collecting duct.
157
What is the half life of aldosterone
15 minutes
158
How does aldosterone increase blood Na+ and decrease blood K+
By preventing degradation of apical Na+ channel, increasing expression of Na+ and K+ channels and Na+/K+ atp pump. Channels face lumen of distal nephron (pee)
159
What do renal juxtaglomerular cells do when blood pressure falls
Secrete renin
160
What does angiotensin 2 do
Increase vasopressin, stimulate thirst. It is a potent vasoconstrictor (reduces blood flow) and increases proximal tubule Na+ retention
161
What causes activation of the renin-angiotensin-aldosterone pathway
Low blood pressure
162
What are the natriuretic peptides
ANP BNP CNP
163
What makes catecholamine release from the adrenal medulla. What does the adrenal medulla mostly release
spinal cord sends a sympathetic neuron which releases acetylcholine. The adrenal medulla mostly releases epinephrine
164
What does epinephrine do
liver releases glucose, fat releases fatty acid, heart contracts faster so you get the rush of energy, intestines have muscle relaxation because why do you need to digest food when you are dying??? Kidney has arteriole constriction and muscle has arteriole contraction for alpha receptors and relaxation for beta receptors. Brain increases in alertness, bronchodilation happens to let more oxygen into your system so you don't die lol
165
How does an epi pen counter the symptoms of anaphylactic shock
by promoting bronchodilation, vasoconstriction in the intestines, skin, and kidneys, and by promoting vasodilation in skeletal and cardiac muscles (to calm your tits)
166
List the hormones made from cortisol (they are steroid hormones since they are made from cortisol) in the adrenal cortex
Progesterone, corticosterone, cortisol, aldosterone, DHEA, androstenedione, estrone, testosterone, estradiol, di-hydrotestosterone
167
What are the physiological roles for androgens, how potent is it, what facilitates its production
androgens have less than 20% activity of testosterone (fuck) but can be converted to more potent androgens and estrogens in peripheral tissues. ACTH (adrenocorticotropic hormone) increases androgen production. For children, it facilitates male prenatal development, pubic hair, body odor, skin oiliness, and acne at the onset of puberty. For women, it maintains pubic and auxiliary hair, is the source of estrogens after menopause. For men, it does nothing (LUCKY FUCKERS)
168
What does the adrenal cortex secrete
Steroid hormones, aldosterone, glucocortoids, sex hormones
169
What is the main glucocortoid
Cortisol
170
What metabolic effects does cortisol have
promotes gluconeogenesis, breakdown of skeletal muscle proteins (that's why you get weaker), enhances lipolysis, supresses the immune system
171
How is cortisol regulated
With negative feedback loops, that block ACTH, its precursor, and CRH, the precursor of ACTH
172
What is addison's disease, what are the symptoms
a disease where immune cells destroy themselves, sometimes due to infection. this causes a hyposecretion of adrenal hormones, and can affect different layers of the adrenal gland. symptoms include hypotension and hypoglycemia
173
Where is ACTH made
anterior pituitary
174
What does the adrenal medulla secrete
catecholamines
175
What does the adrenal cortex secrete
Mineralocorticoids (aldosterone) in the zona glomerulosa, glucocorticoids (cortisol) in the zona fasciculata, and sex hormones (androgens) in the recularis.
176
What is cushings syndrome
Cortisol excess. It causes tumors and can be from cortisol therapy. Symptoms are hyperglycemia, muscle breakdown, lipolysis but buildup of fat on the trunk and face, increased appetite, mood elevation followed by depression, difficulty with learning and memory.
177
when are voltage gated channels closed, how are they opened
normally inside the cell is negative, so s4 is dragged inward. s4 goes outward when inside not so negative
178
list order of adrenal gland from outside to inside
adrenal medulla, adrenal cortex (zona glomerulosa, zona fasiculata, zona reticularis)
179
zona glomerulosa releases
aldosterone
180
zona fasiculata releases
cortisol
181
zona reticularis releases
sex hormones
182
ANP
made when atria walls of the heart sense stretch. decrease blood volume, blood pressure, aldosterone, vasopressin, increase K+ reabsorption
183
BNP
secreted in ventricles (from myocardial cells)
184
CNP
secreted from brain, pituitary, kidneys
