Physiology-Midterm Flashcards
Physiology
Study of function of the body
Set point
Normal level that is supposed to be in the body
Sensor
Detects if there is a change or not
Afferent pathway
Pathway from the sensor to the integrating center
Integrating center
Decides how to respond to change
Efferent pathway
Pathway from the integrating center to the effectors
Effectors
Does the change that the integrating center told
Homeostasis
Maintains constancy in the body
Negative feedback
Something has changed and want to bring it back to normal. Follows homeostasis
Positive feedback
A change has happened and the change is going to continue. Doesn’t follow homeostasis and if doesn’t stop, can lead to detrimental effects. Stops through negative feedback or termination
Neural communication
Fast, localized, and between neurons and neurons or neurons to cells. Have neurotransmitters
Chemical communication
Slow and not localized. Chemicals include hormones, messengers, and modulators. Hormones can either be a neurocrine or endocrine
Paracrine
Cell secretes a chemical that influences other cells around it
Autocrine
Cell secretes a chemical that acts on itself
Intracellular fluid
Makes up 40% of total body weight. All cells are put into one group because of their similar plasma compositions
Extracellular fluid
Makes up 20% of total body weight. Divided into interstitial, plasma, and transcellular fluid
Transcellular fluid
Found in the synovial joins, cerebrospinal fluid, inocular regions of the eye, peritoneal, and pericardial
Interstitial fluid
Fluid surrounding the cell
Plasma
Fluid portion of blood
Capillary wall
Divides the interstitial and plasma
Donnan effect
Proteins (negative charged) in the plasma attracts positive ions from the interstitial fluid, making the concentration of positive ions slightly higher in the plasma
Osmolarity
Molarity x #of particles
Molarity
Moles/L of solution
Osmosis
Diffusing of water through a semipermeable membrane
Osmotic pressure
Pressure needed to force water to stay in its place when there is a concentration difference
Van’t Hoff’s equation
Pi= CRT
According to Van’t Hoff, 1 mOsm/L exerts a pressure of…
19.3 mmHg
Non-carrier mediated transport
No use of carrier proteins
Carrier-mediated transport
Use of carrier proteins
Simple diffusion
Diffusion across the cell membrane
Facilitated diffusion
Transport with the help of carrier proteins. Has specificity, competition, and saturation
Active transport
Moving against the concentration gradient so needs energy to do it
Primary active transport
ATP binding site on the protein as well as binding site of the molecules to be transported.
Example: Na/K pump, H+ pump, Ca
Secondary active transport
Using concentration gradient different established in primary transport, molecule will diffuse into the cell and this energy will help another molecule to move against its concentration gradient
Example: glucose moving in with the help of sodium
Tertiary active transport
Molecule moves against its concentration gradient based on concentration difference established in secondary active transport
Example: peptides transporting due to concentration gradient of H which was helped by Na/K pump
Capillary pressure
Goes out of the plasma into the interstitial fluid
Interstitial fluid pressure
If positive, goes towards plasma and if negative, goes towards interstitial fluid
Plasma colloid osmotic pressure
Goes inside the plasma. This pressure is greater than the interstitial fluid colloid osmotic pressure
Interstitial fluid colloid osmotic pressure
Goes into the interstitial fluid
Lymphatic system
Extra fluid that is filtered into the interstitial fluid is returned to the circulation by the lymphatic
Intracellular edema
Rare. Caused by depletion of nutrients and depression of the metabolic system
Extracellular edema
Common. Caused by abnormal leakage of fluid from plasma and failure of lymphatic to return extra fluid to circulation
Leakage of fluid into interstitial
- Leaky capillary
- Low plasma colloid osmotic pressure
- Increase in capillary pressure
Failure of lymphatics
- High ISF proteins cause increase interstitial colloid osmotic pressure
- Blocking of the lymphatic system
Protection against edema
- Lymphatics ability to increase 10-50 times
- Low compliance of interstitum
- Removal of ISFs from interstitial and go to lymphatics
Vesicular transport
- Rough ER synthesizes proteins that goes to the Golgi
- Smooth ER synthesizes lipids
- Golgi modifies by adding polysaccharides to make the protein active, and sorts and packages them in vesicles
- Proteins are exocytosed out of the cell
Exocytosis mechanism
- Nucleation:V-SNAP on vesicle attached to SNAP25 and t-snare and forms a loose complex
- Zippering: V-SNARE brings the vehicle closer to it
- Fusion pore opening: with influx of Ca, vehicle leaves the cell
- Regeneration: NSF and SNAPs dissolve the tight complex by hydrolation of ATP
- Budding: vesicle can now be used for endocytosis
Endocytosis mechanism
- Clathrin in membrane brings the material in forming a coated pit
- Actin and myosin constrict the neck
- Dynamin cuts it off and can now go inside the cell
Transcytosis
Movement between cell layers. Cell just needs to move it from one place to the other
Ex: IgG antibodies in mother, milk in mammary glands
Clathrin
Used for endocytosis and exocytsois of protein from Golgi to plamsa membrane
COPI
Reterograde protein. Moves between retrograde stacks of the Golgi. Moves from the Golgi to the ER
COPII
Anteroretrograde. Moves from ER to Golgi
Signal peptidase
Makes sure that the N terminus part goes through the lumen first
Translocans
Makes sure hydrophobic part stays in the channel and is in the correct orientation
Ion channels
Help in transporting charges and polar molecules across the hydrophobic cell membrane. Have a selectivity filter within their pore that helps to select the correct ion to go through.
Transport through their electrochemical potential
Structure of ion channels
Mace of alpha subunits that come together to form alpha helical polypeptide segments.
4 different structures:
- Homo-oligomers
- Hetero-oligomers
- Motifs
- Subunit + auxiliary subunit (beta or gamma subunit)
Selectivity of ion channels
- Size
- Nature of amino acid lining it (this is mostly used since some molecules are very similar to each other in size)
Leak channels
Non-gated channels that are open all the time. This determines the permeability of a molecule to the membrane
Gated channels
Channels that open due to a stimulus.
3 types:
- Voltage
- Ligand
- Mechanical
Voltage gated channels
Open due to change in voltage difference in a cell.
At rest, the inactivation is open while the activation gate is closed. When there is a change in voltage, positive amino acids that were close to the inner part of the cell move out and the activation gate will be open. When membrane voltage changes, it will go back to rest.
However, if the activation gate stays open for a very long time, the inactivation gate will close (refractory). Inactivation gate can only open when the membrane is back to res5
Lidocaine or bupivacaine
Anesthetic that when administered will block sodium voltage gated channels which doesn’t allow an action potential to conduct
TTX
Poison found in fish and is also an inhibitor of sodium voltage gated channels
Ligand-gated channels
Channels open when a ligand attaches
Occupied receptor= open channel
Free receptor= closed channel
Extracellular ligand
Neurotransmitters, hormones
Intracellular ligand
cAMP, ATP
Nictotinic receptor
Open in response to nicotine and acetylcholine. Found in skeletal muscles Will allow sodium to entertain the cell leading to contractions
Curare
Will inhibit the nicotinic receptor so that there are no muscular contractions
Muscarinic receptor
Muscarine and acetylcholine can open this channel. Found in heart muscles. Slows heart rate through an influx of potassium ions
Atropine+ insecticides
Block the muscadine channels leading to an increased heart rate
Mechanically-gated channels
Opens due to stretching, pressure, and touch
Ex: muscles, pressing on skin, hair cells of cochlea
Channelopathies
Problems in the channels. Can be due to inherited factors, trauma, or problems in translation/transcription (mutations)
Enhanced activation of sodium 17 channels
Is autosomal dominant and leads to painful hands and feet (erythromaligia)
Incomplete inaction of sodium 17 channels
Autosomal dominant and leads to paroxysmal pain disorder. Leads to ocular, mandibular, and rectal pain
Non-functional sodium 17 channels
Autosomal recessive. Feel no pain
Membrane potential
Voltage difference across the cell membrane. More sodium, chlorine, and calcium outside. More potassium inside
Depends on 2 things:
- Concentration of ion
- Permability of ion
Sodium potassium pump
Takes out three sodium and puts two potassium in. So net is losing one positive charge (making membrane more negative)
This is an electrogenic
Resting membrane potential
Membrane potential when the cell is at rest.
Positive charges on the outside will attract the negative charges in the inside forming a thin line of positive and negative charges respectively. Res5 of the positives and negatives will bind to each other neutralizing it
Equilibrium potential
When the concentration gradient and the electrical gradient is both at equilibrium
Potassium equilibrium potential
- Pottasium conc will want to come out of the cell
- Potassium electrical diff will want to come in the cell
Both will continue moving back and forth until equilibrium is established
Sodium equilibrium potential
- Sodium conc will want to go in the cell
- Sodium electrical will also want to go in the cell
Leads to a lot of positive charge accumulation so some sodium will leave the cell resulting in equilibrium
Permeability
Increase permeability if there are more leak channels of that ion.
Plasma membrane is more permeable to potassium than sodium
Non-excitable cells
RMP doesn’t change over time.
Ex: epithelial cells and adipose cells
Excitable cells
RMP can change due to a stimulus
Ex: muscle and nervous cells
Depolarization
Decrease in membrane potential. Cell is becoming more positive
Repolarization
Going back to RMP. Cell is becoming more negative
Hyperpolarization
Cell is below RMP so very negative
Graded potential
Changes in membrane potential that occur due to a stimulus
Vary depending on the strength and duration
Strength of stimulus grows weaker from the point of origin
Action potential
Fast changes in membrane potential
- Stimulus opens up sodium channels that allow it to enter the cell
- When it reaches threshold potential, sodium voltage gated channels open and allow rapid depolarization
- Sodium channels will close and potassium channels will open.
- Pottasium will enter the cell leading to repolarization
- Will close once hyperpolarization is reached
Properties of action potentials
- All or none
- Refractory period since sodium channel inactivation gate is closed. Have absolute refractory (can’t fire another action potential at all) and relative refractory (can fire another one if there’s a very strong stimulus)
Stimulus intensity coding
Higher strength of stimuli will cause a higher frequency of action potentials
Wave effect of conducting a nerve impulse
When one sodium-voltage gated channels opens, it opens the next one. By the time the next one opens, the original one is going back to repolarization and the cycle continues
Myelin-forming cells
Have myelin today insulate the cell and allow the response to go very fast. Myelin doesn’t allow sodium or pottasium to move. In between myelin, have nodes of Ranvier to allow potassium and sodium to move in and out of the cell
Two types:
- Oligodendrocytes
- Schwann cells
Oligodendrocytes
Small cells with few processes. Provide myelin to white matter of brain. Can wrap processes around axons
Schwann cells
Provide myelin for peripheral nervous system. Along the lengths of an a on
Saltatory conduction
AP along a myelin sheath
Multiple sclerosis
Condition in which the myelin sheath is damaged so have slow response
AP types
- Typical spike
- Plathea
- Rhythmic
Typical spike
Normal AP
Ex: motor neurons, skeletal muscle
AP with plateau
- Phase 0: depolarization through sodium voltage gated channels
- Phase 1: inactivation of sodium channels and activating pottasium channels
- Phase 2: calcium begins entering the cell but it does it really slowly. With calcium going in and potassium going out, leads to plateau phase
- Phase 3: calcium channels close and goes to normal repolarization
Ex: cardiac myocytes and smooth muscle
Rhthmic AP
In cells that are spontaneously active
Need 3 things for rhythmic AP:
- Permrability to sodium and in some cases calcium
- RMP is not maintained so less negative than normal
- Small hyperpolarization allows for re-excitation
Rhythmic AP in cardiac SA
At the end of an AP, have pacemaker potential which activates HCN channels (respond to hyperpolarization)
Allows cations to enter to enter but depolarization is through Ca. Repolarization is still through potassium
Thalami pacemaker potential
Depolarization through HCN with Ca coming in
Strong depolarization causes HCN channels to close leading calcium to not enter the cell leading to repolarization
Hyperpolarization will enter the next HCN channel
GI smooth muscle
Has rhythmic and repetitive
Repetitive due to electrical waves in intestinal walls
Don’t have HCN channels
Electrical synapse
Very fast. Involves the use of gap junctions which allow ions to move from one place to the other very fast.
Direct communication between the cytoplasms
Each gap junctions is made of 6 connexin proteins that make up one connexon
Chemical synapse
Involves the use of chemicals in vesicles and the influx of calcium. Slower than electrical synapse. The cytoplasms are farther away than in the electrical one.
Depolarization from the action potential allows calcium to enter the cell and it binds to its protein that allows the neurotransmitter to be exocytosed out of the cell
Neurotransmitter
Chemical that is released at the presynaptic terminal.
To be a neurotransmitter:
- Synthesized within the presynaptic membrane or be present in the cell
- Lead to a response in the postsynaptic membrane and the response is the same every time
- Have some sort of termination of the neurotransmitter
Postsynaptic receptors
Two types:
- Ionotrooic (ligand-gated ions channels)
- Metabatropic
Ionotropic receptors
Very fast. Binding of neurotransmitter allows ions to pass through
3 types of receptors
- Pentametic
- Glutamate
- ATP
Pentametic receptors
Composed of 5 subunits around a central channel.
Contains ACh, GABA, and glycine
Nicotinic acetylcholine receptors
Ionotropic receptors that allow sodium to enter the cell leading to excitatory postsynaptic potential. 2 acetylcholine molecules open up the channel
Type A gamma aminobutryic acid receptors (GABA A, Rs)
Ionotropic receptor. GABA binds to receptors and allows chlorine to enter leading to an inhibitory postsynaptic potential
Glycine receptors
Ionotropic receptors. Allows chlorine to entered leading to an IPSP
Metabotric receptors
Slow transmission. Linked to a G-protein. When the ligand binds, the alpha subunit of the G protein dissociates from the beta-gamma. Either the alpha portion will open up a channel or the beta-gamma
Muscarinic ACh receptors
Metabotropic receptors. When acetylcholine binds, beta-gamma complex binds to potassium channels and opens it.
Potassium leaves the cell leading to a slowed heart rate
GABA b receptor
Metabotropic receptor. Opens pottasium channels that leave and cause IPSP
EPSP
When the membrane become closer to depolarization. So when sodium and calcium ions come into the cell
If it hits threshold potential, it can lead to an action potential
IPSP
When the membrane potential gets farther away from the threshold potential. So when chlorine enters the cell or potassium leaves the cell
Spatial summation
Adding all the IPSPs and EPSPs at all synapses
Temporal summation
Adding all the IPSPs and EPSPs at only one synapse
Termination of neurotransmitter
- Enzymatic degradation
- Reuptake
- Diffusion
Termination of acetylcholine
Enzymes degrade it and choline is taken back to the presynaptic membrane to form acetylcholine again
Termination of glutamate
Taken up by specialized membrane transport proteins
Gap junctions
Most simple form of communication. Ions pass between them. Allows for the cells to work as one uniform unit. Made up of connexons
Ex:heart muscle, smooth muscle, lung, liver, neurons
Contact-dependent signaling (CAMs)
Known as juxtacrine signaling. Have cell adhesion molecules on the surface for a ligand to bind to it
Different types:
- Nerve cell adhesion molecules
- Integrins
- Selectins
- Cadherins
Nerve-cell adhesion molecules
Help in nerve cell growth when the nervous system is developing
Integrins
Cell signaling found in cell-matrix junctions
Cadherins
Used in adhesion molecules (desmosomes)
Selectins
Temporary cell-cell adhesion during inflammation
Intracrine
Molecule synthesizes within the cell and acts within the cell
Ex: angiogenesis II in neurons
Paracrine
Cell secretes a molecule and goes to another cell through diffusion or through local circulation
Ex: histamine, NO
Autocrine
Cell makes a molecule that acts on itself
Ex:growth factors
Neurocrine
Neurotransmitters are secreted by a neuron and goes to another cell by diffusion or by the local circulation
Ex: hormones of the hypothalamus and pituitary
Endocrine
Hormones secreted by glands or cells and go to cells through the general circulation
Neuroendocrine
Secrete neurohormoes that go to cells by the general circulation
