Pop

Front 1

*What is the substrate for Acetylcholine (Ach) synthesis?

*How is it removed?

*What receptors does it act upon?

Back 1

*It is synthesized from Acetyl-CoA that is made from glucose and Choline. it is transported via secondary active transport.

*It is metabolized by acetylcholinesterase, and Choline reuptake for reuse via secondary active transport

*It acts on Nicotinic and Muscarinic receptors

Front 2

* What are the key types of nicotinic receptors and what types of receptors are they?

*What are the key types of muscarinic receptors and what type of receptors are they?

Back 2

*N1 (neuromuscular junctions) and N2 (autonomic ganglia) ionotropic receptors

*M 1,3,and 5 via Gq which increases phospholipase C which increases intracellular calcium and M 2,4 via Gi which inhibits PKA which increases potassium coduction to hyperpolorize the cell and reduce vesicular traffic

Front 3

* What is the substrate for catecholaminergic synthesis?

* What is the rate-limiting enzyme in sythesis and how is it regulated?

*How is it removed?

Back 3

*It is synthesized from tyrosine that is transported via secondary active transport

*Tyrosine hydroxylase, because it increases synthesis via cAMP kinase or increases TH production. It is regulated by secondary actiive transport and reuptake of neurotransmitter presynaptically

*it is metabolized viia monoamine oxidase (CNS) and catechol-O-methyltransferase (other sites)What en

Front 4

What enzymes converts tyrosine to dopamine?

Back 4

L-tyrosine -> {tyrosine hydroxylase} -> L-DOPA -> {Aromatic L-amin acid decarboxylase} -> dopamine

Front 5

Which neurotransmitters are catecholamines and what receptors do they act upon?

Back 5

Dopamine (DA), Norepinephrine (NE), Epinephrine (Adrenal medulla only-acts as hormone); NE (and Epi) alpha1 via Gq, Alpha Gi, Beta 1, 2, 3 via Gs; dopamine 1, 5 via Gs - dopamine 2, 3, 4 via Gi

Front 6

What factors deetermine if the signal at the synapse is passed on to the next cell (another neuroon or effector)?

Back 6

The amount of neurotransmitter released, the number of receptors, and cell polariization (partially depolarized or hyperpolarized)

Front 7

What is the basic anatomic structure of ANS

Back 7

Originate: CNS (brain stem and spinal cord); preganglionic neuron -> autonomic ganhlia ->postganglionic neuron -> effector

Front 8

What neurotransmitter is released in the ganglionic synapses of the autonomic nervous system? On what receptor does it act?

Back 8

Acetylcholine: N2 or Nn (Nicotinic acetylcholine receptor)

Front 9

What is the primary neeurotransmitter released for voluntary skeletal movement? Or whatreceptor does it act?

Back 9

Acetylcholine, N1 or Nm (Nicotinic acetylcholine receptor)

Front 10

*Which component of the autonomic nervous system is characterized by a long pre - and shortpost-ganglionic fiber?

*Which is characterized by a short pre- and long post-ganglionic fiber?

Back 10

*Parasympathetic

*Sympathetic

Front 11

What neurotransmitters are released by post-ganglionic nerve fibers?

Back 11

Acetylcholine and Norepinephrine are released by post ganglionic nerve fibers; Epinephrine is released from the adrenal medulla

Front 12

To what receptor does acetylcholine bind in the ganglia of the ANS

Back 12

N2 or Nn receptor

Front 13

What diffrences exist between the SNS and PNS regarding origin and the connecions between pre- and post-ganglionic neurons?

Back 13

ANS: dual innervation with generally opposite effects

SNS: thoracic and lumbar origin, highly interconnected via chainganglia near spinal cord that extend from the cervical to sacral regions, highly branched at the ganglia allowing for widespread actions

PNS: Cranial and sacral origin; ganglia close to effector with limited branching allowing for more specific effects on organ or tissue

Front 14

14.What receptors are located on the effector cells of the PNS? What receptors are located on the effector cells of the SNS? What target tissues in the SNS act via muscarinic receptors?

Back 14

14. Muscarinic; Adrenergic (alpha and beta); Sweat glands, piloerector muscles, some blood vessels.

Front 15

15.Where is the primary location of Beta1 receptors? What is the effect?

Back 15

15. Heart; Increased heart rate and contractility

Front 16

16.Where is the primary location of Beta2 receptors? What is the effect?

Back 16

16. Lungs; Smooth muscle relaxation – bronchodilation; Dilates vessels in skeletal muscle; promotes glucose production in liver

Front 17

17.Where is the primary location of Beta3 receptors? What is the effect?

Back 17

17. Adipose and bladder; Calorigenesis and bladder wall relaxation.

Front 18

18.Where is the primary location of Alpha1 receptors? What is the effect?

Back 18

18. Blood vessels; vasoconstriction; Dilates pupils; slows GI motility; Contracts bladder

Front 19

19.Where is the primary location of Alpha2 receptors? What is the effect?

Back 19

19. Presynaptic to decrease NE release; Vasodilates selected blood vessels; Decreases insulin release; Promotes platelet aggregation

Front 20

20.What is the mechanism when nicotinic receptors are activated?

Back 20

20. Ligand gated Ion Channels (Sodium)

Front 21

21.What is the mechanism when muscarinic receptors are activated?

Back 21

21. M1,3,5 via Gq  PLC  IP3 and DAG  increase intracellular calcium and M2,4 via Gi  decrease cAMP  inhibition of PKA  increased potassium conductance

Front 22

22.What is the mechanism when beta receptors are activated?

Back 22

22. Gs  adenylyl cyclase  increased cAMP

Front 23

23.What are some of the key sites of autonomic tone for the SNS and PNS?

Back 23

23. SNS: blood vessel (arteriole) walls – resting BP; PNS: Heart – resting heart rate (decrease) and GI tract between meals

Front 24

25.Which part of the ANS is responsible for sweating? What receptors are involved?

Back 24

25. Sympathetic nervous system; Apocrine glands – alpha receptors; Eccrine glands – muscarinic.

Front 25

26.In the adrenal medulla what neurotransmitter is released in response to activation of the N2 or NN receptor? What are the physiologic effects when this neurotransmitter is released?

Back 25

26. Epinephrine giving a more prolonged effect. Many answers (slide 21): increased heart rate / respiratory rate, “fight or flight” response.

Front 26

27.What higher centers regulate the autonomic nervous system? What are some examples of local autonomic reflexes?

Back 26

27. Hypothalamus, cortex, limbic system; Pain, Mechanoreceptors, Chemoreceptors, and Nociceptors

Front 27

1.What is homeostasis? What are the key physiologic mechanisms involved in maintaining physiologic homeostasis?

Back 27

1. Maintenance of a stable internal environment (around an ideal set point or within a normal range) by physiologic mechanisms (i.e. blood pressure, HR, serum sodium). Negative feedback most common mechanism. Also, positive feedback and feedforward loops play a role in selected situations (especially when adjusting the set point in response to a stimulus).

Front 28

2.How do equilibrium and steady state differ?

Back 28

2. Equilibrium implies balance with no NET change and no energy is required to maintain it. Steady state usually requires energy or some action to maintain the set point and is the correct term for most physiologic systems

Front 29

3.What are the key components of feedback systems? What are some examples of negative feedback systems?

Back 29

3. Receptor (monitors the variable for possible change due to a stimulus); Control center (set point established); Effector (Adjusts variable through a response). Examples: Blood pressure, body temperature, blood glucose levels, most hormones

Front 30

4.What is the primary purpose of feedforward control? What is an example?

Back 30

4. Response to an anticipated physiologic change for a particular variable resulting in a temporary change in the set point value above or below its normal range. Increased HR and RR when proprioreceptors are activated during exercise.

Front 31

5.How does positive feedback differ from feedforward control? What are some examples of positive feedback?

Back 31

5. Instead of adjusting to a temporary new set point, positive feedback results in the variable continuing to change in response to the stimulus. Requires negative feedback systems to bring it back to homeostasis. Childbirth is a normal example. Excessive coagulation or inflammatory response are examples of pathologic positive feedback where the normal control mechanisms don’t work.

Front 32

6.What are some of the key components of the cell membrane that impact its physiologic function?

Back 32

6. Lipids (phospholipids, glycolipids, sphingolipids), Proteins (channels, receptors, carriers), Cholesterol (structural support), Lipid rafts (aggregate of sphingolipids/cholesterol/proteins allowing for key protein interactions), Caveolae (location for receptors, tranducers, channels, pumps, exchangers)

Front 33

7.What is the role of cell membrane permeability in normal physiology? What are some examples of molecules that will freely diffuse? How do other molecules cross the membrane?

Back 33

7. Allows for gradients (steady state!) to be established across the membrane (intracellular/extracellular, intravascular/extravascular). Oxygen, carbon dioxide, other gases and alcohols freely diffuse. Water diffuses to a lesser extent (requires a channel to move in large quantities). Other molecules require channels, carrier proteins or other physiologic process (pinocytosis, exocytosis) to move across the membrane.

Front 34

8.What are some of the key functions that transmembrane proteins play in normal physiology?

Back 34

8. Transporters, Anchors, Receptors, Enzymes

Front 35

9.What are three common mechanisms for movement of substances across a cell membrane?

Back 35

9. Passive diffusion (for permeable substances; impermeable substances via channels), Active transport (primary and secondary), Vesicle fusion (Movement of macromolecules or larger quantities - phagocytosis, endocytosis, exocytosis)

Front 36

10.How does diffusion differ from active transport?

Back 36

10. Diffusion moves down a concentration gradient, may or may not require a carrier or channel and does NOT require energy; Active transport is against a concentration gradient, requires a carrier, and requires energy (ATP or an ion gradient, usually sodium)

Front 37

11.What is the most important physiologic variable important to simple diffusion? Why?

Back 37

11. The relative concentration of the substance across the membrane (concentration gradient). Other components (membrane thickness (distance), diffusion/permeability coefficient, cross sectional area, temperature) don’t acutely change in normal physiology.

Front 38

12.How is facilitated diffusion similar / different from simple diffusion? What is an example of facilitated diffusion?

Back 38

12. Similarities: Move down concentration gradient and do not require ATP; Differences: Utilizes a carrier protein, has a maximum rate (Vmax) of transport, rate can adjust over time by changing density (#) of carrier proteins. Examples: Glucose transporters, Amino Acid transporters

Front 39

13.What are some key features of membrane ion channels? What is the process which drives net movement of a substance through a channel?

Back 39

13. Usually specific to a specific substance (ion); May be ungated (leak channel) or gated; Gate channels can open due to voltage changes, chemically (ligand, hormone, neurotransmitter) or other stimulus (pressure, temperature, etc.); Simple diffusion down gradient.

Front 40

14.What are the key differences between primary and secondary active transport?

Back 40

14. Primary uses ATP to move molecules against their concentration gradient. Secondary uses energy created by another concentration gradient.

Front 41

15.What is the Na+/K+ ATPase pump and what role does it play? What are some other key substances regulated by primary active transport?

Back 41

15. A primary active transport carrier protein present on all cells. Establishes and maintains the intracellular/extracellular Na+/K+ gradients and regulates cellular osmotic balance. Minimal role in determining the actual resting potential across the cell membrane. Others: Calcium, Hydrogen, Cholesterol/lipid metabolism, organic anion and cation transporters

Front 42

16.How are facilitated diffusion and active transport similar?

Back 42

16. Both have a Vmax since they involve carrier proteins.

Front 43

17.Describe the energetics of secondary active transport. What are the two basic types of transporters?

Back 43

17. Involves a transport carrier protein where the energy of one molecule (usually sodium) moving DOWN its transport gradient moves another molecule AGAINST its concentration gradient. Can move in the same (Co-transporter or Symporter) or opposite (Counter-transporter or Antiporter) direction as the molecule creating the energy.

Front 44

18.How are pumps used to move substances from the luminal to basolateral side of an epithelial cell?

Back 44

18. Typically involves a combination of primary (Na+/K+ ATPase pump) and secondary active transport pumps. Different pumps on the apical and basolateral sides moves the substance of importance (example: glucose or amino acids) in one direction across the cell.

Front 45

19.What is osmosis and osmotic pressure? What are some key roles physiologically?

Back 45

19. Osmosis is the net diffusion (passive) of water molecules across a membrane from a higher concentration of water / less osmotically active particles to a lower concentration of water / more osmotically active particles. Osmotic pressure is the “pulling” for being exerted by the osmotically active particles. Maintenance of cell volume (changes in extracellular osmotic pressure will cause cells to swell or shrink, especially if changes occur rapidly. Maintenance of intravascular volume (osmotically active proteins in the blood keep fluid from “leaking” out of the blood vessels).

Front 46

20.How does tonicity differ from osmotic pressure?

Back 46

20. Tonicity is based upon solutes impermeable to the cell membrane. The reference is the tonicity of extracellular fluid (determined by primarily by sodium, chloride, glucose, urea). Isotonic – similar to extracellular fluid; Hypertonic – higher than extracellular; Hypotonic – lower than extracellular.

Front 47

21.In most cells, what components are involved in maintaining the steady state resting membrane potential of sodium and potassium?

Back 47

21. Ungated Sodium and Potassium “leak” channels; Na+/K+ ATPase pump establishes and maintains the gradient (limited effect on actual RMP)

Front 48

22.Since most cell membranes are fairly impermeable to water, how is most water exchanged across a cell membrane?

Back 48

22. Via aquaporin channels. Different types present on different cells. Some are hormonally regulated.

Front 49

23.Which ions are in higher concentration in the EXTRAcellular space? Which ions are in higher concentration in the INTRAcellular space? Why is this important?

Back 49

23. Intracellular: Potassium, Anions (Phosphate, Proteins, Bicarbonate), Hydrogen (slightly higher). Extracellular: Sodium, Magnesium, Calcium, Chloride. These gradients allow for membrane potentials to be established and to allow for actions to occur within the cell when the relative concentrations of the ions changes in response to a stimulus

Front 50

24.What is membrane potential? Based upon the Nernst equation, what relationship is important in determining the potential of a particular ion?

Back 50

24. Membrane potential is the charge difference across a cell membrane. The ratio of the concentration of the ion across the membrane determines the Vm for a particular ion.

Front 51

25.What is the membrane potential for most cells? What key ions are involved in determining the potential? Which ion is the most important in determining the membrane potential?

Back 51

25. The membrane potential for most cells is -80 to -90 mV (more negative on the inside of the cell); Sodium, Potassium, Chloride (also calcium in some cells); Potassium is the most important – resting potential is the closest to potassium for most membranes. Potassium has the highest permeability (through ungated channels).

Front 52

26.What are the three types of “local” communication of cells?

Back 52

26. Gap junctions (ions moving through channels from one cell to another); Autocrine (receptors on self); Paracrine (substance released from one cell signals adjacent cell)

Front 53

27.What are some examples of “local” communication of cells?

Back 53

27. Gap junctions – smooth muscle and cardiac muscle; Autocrine – none given yet – cytokines like interleukins are one example; Paracrine – nitric oxide from endothelial cells resulting in smooth muscle relaxation

Front 54

28.What are the three types of “remote” communication of cells? What are some examples of each?

Back 54

28. Nervous (release of neurotransmitter at a synapse), Endocrine (release of a hormone into the blood stream having effects on numerous tissues – insulin and glucagon), Neuroendocrine (release of a hormone as a result of nervous system – hypothalamus/pituitary - thyroid hormone, cortisol, epinephrine)

Front 55

29. What is cellular signaling? What are the key components of cellular signaling?

Back 55

29. Tightly regulated pathways that allow transduction of a signal within a target cell. First messenger (ligand), receptors, transducers/effectors, second messengers.

Front 56

30. What are some of the key transducers?

Back 56

G protein-coupled receptors; ion channels; Tyrosine kinase receptors

Front 57

31. for G-protein receptors: What are the key effector targets? What are the two effector molecules?

Back 57

Targets are ion channels and membrane proteins; Effector molecules are adenylyl cyclase and phospholipase C

Front 58

32. For G Protein-coupled receptors: What activates the G protein? What subunit binds to adenylyl cyclase? What results from this binding?

Back 58

GTP binding to the alpha subunit; Alpha subunit; converts ATP tp cyclic AMP (cAMP)

Front 59

33. For G Protein-coupled receptors: What happens when cAMP is fromed? What effects can result? How is cAMP removed?

Back 59

cAMP activates Protein Kinase A - kinases phosphylate proteins causing biologic effects which include enzyme activation, open (or close) ion channels and activation of gene transcription factors; Phosphodiesterase - degrades cAMP to 5' AMP