Western U Mcbm-Physiology

Front 1

4 Purposes of a Cell Membrane

Back 1

1. physical barrier
2. regulation of intake/outflow
3. communication with surroundings
4. structural support

Front 2

Components of a cell membrane (average)

Back 2

55% protein
25% phospholipids
13% cholesterol
4% lipid
3% carb

Front 3

permeability consequence of amphipathic membrane

Back 3

impermeable to most ions & polar molecules

Front 4

phosphatidylinositol role

Back 4

2nd messenger system

Front 5

Determining factor for variability among phosphoglycerides

Back 5

R group attached to the phosphate
i.e., if R=H then it's phosphatidic acid

Front 6

Variations between the inner & outer leaflets of cell membranes

Back 6

inner=modified for 2nd messenger system

outer=acidic

Front 7

True/False: Saturated fatty acid chains of phospholipids result in increased fluidity of the membrane?

Back 7

false

saturation results in decreased fluidity and and increase in melting temperature.

Front 8

Role of cholesterol in the cell membrane

Back 8

increases fluidity at temperatures lower than the melting temperature and reduces fluidity above the melting temperature (due to rigid steroid rings).

Front 9

Composition of lipid raft

Back 9

increased cholesterol and sphingolipids; marked by acylated and GPI linked proteins.

Front 10

Common position of cell signaling proteins

Back 10

in complexes formed on lipid rafts (attracted by acylated proteins)

Front 11

2 categories of proteins

Back 11

structural & functional

Front 12

miristoylation

Back 12

irreversible! co-translational protein modification

Front 13

Prenylation

Back 13

irreversible! lipidation of protein; adds hydrophobic molecules

Front 14

palmitoylation

Back 14

REVERSIBLE! attachment of F.A. chains to the cys residue of membrane proteins.

Front 15

6 functions of membrane proteins

Back 15

1. transport
2. enzymatic activities
3. signal transduction
4. cell to cell recognition
5. intercellular joining
6. cytoskeleton & ECM attachments

Front 16

4 Classes of Membrane Receptors

Back 16

1. ligand binding
2. receptor-enzyme
3. G-protein coupled receptor
4. integrin receptors (change cell shape)

Front 17

3 subunits of a G protein

Back 17

alpha, beta, gamma
beta/gamma bound to each other
alpha carries the ADP/ATP binding site

Front 18

monomeric G proteins

Back 18

family of GTPase
RAS, RAB, ARF, SAR, RAN, RHO

Front 19

GPCRs

Back 19

largest gene family; target of many best selling drugs (i.e., zyprexa, zantac, clarinex, zelnorm).

Front 20

Tyrosine Kinase Receptors

Back 20

ligand binding causes them to form a dimer & autophosphorylate to activate a relay protein for a specific cellular response; alpha & beta subunits.

Front 21

membrane carbohydrate function

Back 21

facilitate cell-cell recognition

Front 22

GAGs

Back 22

polymers of repeating disaccharides, one of which is always hexosamine.

Front 23

proteoglycans

Back 23

GAG + protein

Front 24

Heparin Sulfate Proteoglycans

Back 24

HSPGs; corecptors modulate ligand binding at the cell surface.

Front 25

Physiology

Back 25

science of normal functions and phenomena in the human body

Front 26

Cannon's Concepts of Homeostasis

Back 26

1. constancy requires control mechanisms
2. change automatically meets with resistance
3. regulatory system has cooperative and simultaneous mechanisms
4. homeostasis is an organized self-government

Front 27

Difference between steady state and equilibrium

Back 27

Steady state is an open system (like water behind a dam), while equilibrium is a closed system.

Front 28

3 components of steady state

Back 28

1. sensors
2. feedback
3. effectors

Front 29

Fluid compartments

Back 29

ICF (40% water)
ECF (5% plasma, 15% ISF)

Front 30

Mass Balance

Back 30

Body Load + Intake - Excretion

Front 31

Fluid Composition

Back 31

Plasma & ISF very similar
ICF very different b/c of plasma membrane barrier; mostly K+, PO4 3-

Front 32

Case example: after a motor vehicle accident, patient experiences severe blood loss and a threatening drop in BP. What do you do to raise the BP?

Back 32

ideally infuse new blood. If blood is unavailable, infuse a protein solution. Do not infuse saline b/c the ions will simply diffuse through the capillaries

Front 33

Blood Volume

Back 33

=amount (mg)/concentration (mg/L)

=plasma Vol (100/(100-hematocrit))

Front 34

How to calculate compartment volumes

Back 34

use substances like mannitol, inulin, iosotopes or sulfate

Front 35

Permeability of lipid bilayer

Back 35

readily permeable to hydrophobic molecules and gases

Front 36

Multicomponent Solution Diffusion

Back 36

Each component will diffuse according to its own concentration gradient.

Front 37

Fick's Law

Back 37

J = -PA (C1-C2)

C=concentration of solutes
A=diffusable surface area
P=permeability coefficient of molecule

Front 38

Graphical relationship btw J & C in diffusion

Back 38

J is on the Y axis, C is on the X axis; linear relationship.

Front 39

Relationship btw molecule size and its permeability

Back 39

larger molecules have smaller permeability

Front 40

Factors affecting P (permeability coefficient of a molecule)

Back 40

lipid solubility
substance size
membrane thickness

Front 41

osmolarity

Back 41

concentration of solution and the number of particles a compound dissociates into.

O=GC

G=# particles

Front 42

Colligative properties

Back 42

dependent on only the # of particles, not the nature of those particles in a given solution

Front 43

Osmotic pressure's impact on freezing point, boiling point and vapor pressure

Back 43

incr BP
decr FP
decr Pvapor

Front 44

gated channels controlled by

Back 44

allosteric regulation (voltage, ligand, phosphorylation and membrane stretch)

Front 45

Structures of protein channels

Back 45

multiple subunits converge to create a channel with a pore; Cl- and H2O channels have 2-4 subunits each with their own pores.

Front 46

Patch Clamping

Back 46

removal of a piece of cell membrane and using electrodes to study action of ion channels.

Front 47

TTX effects

Back 47

closes Na+ channels, thereby preventing action potentials.

Front 48

BuTX effects

Back 48

blocks nicotini receptors in muscles (muscle spasms)

Front 49

Glc delivery method

Back 49

via carrier proteins that work solely on conformational change; much slower than voltage or ligand gated channels.

Front 50

Km (Michaelis-Menten kinetics)

Back 50

Concentration of substrate required to reach 1/2 the maximum flux

Front 51

Glc isomers

Back 51

D & L; carriers specific to D.

Front 52

Anion exchange (RBC)

Back 52

in respiring tissues, CO2 enters cell & converts to HCO3- which exits the RBC via exchange protein while Cl- is entering. This process reverses at the lungs for gas exchange.

Front 53

Na/K pump

Back 53

moves 2K IN and 3Na OUT
creates/maintains membrane potential

Front 54

Secondary transport

Back 54

couples energy of a molecule moving down a gradient with moving another against its gradient.

Front 55

Na/K pump subunits

Back 55

alpha-binds Na/K, ATP, Ouabain
beta

Front 56

Ca pump method

Back 56

1. 2 Ca bind on cytosol side
2. phosphorylate active site to cause conformational change
3. Ca moved to and dissociates into ER lumen
4. Dissociation sends protein back to its rest state.

Front 57

Properties of Primary active transporters

Back 57

high specific
use ATP
slower than ion channels
uses conformational change to transport
operates at 50% Vmax under normal [S]

Front 58

Types of Active Transporters

Back 58

P type-Phosphorylates
V type-Vacuole/H+ pump
F type-energy coupling Factor
ABC-ATP binding casette

Front 59

Coupling of primary & secondary active transporters

Back 59

moves both substrates against their concentration gradients.
Symport
Antiport

Front 60

Symport

Back 60

both molecules move in same direction against gradient
i.e., Na/D-glc & Na/L-AA

Front 61

Antiport

Back 61

Substrates move in opposite directions against their gradients.
i.e., Na/H, 3Na/Ca exchangers

Front 62

Na/Glc transport method

Back 62

1. Na binds & incr affinity for glc bind
2. Glc binds & changes conformation of protein
3. Pump opens to inside of cell, drops Na which decr affinity for glc
4. glc disassociates & conformation returns to rest

Front 63

Glc uptake in small intestine method

Back 63

1. Na/Glc symport into cell at apical end
2. Na/K pump moves Na to bloodstream at basal end
3. GLUT2 facilitates glc uniport to bloodstream at basal end

Front 64

Ouabain mechanism

Back 64

1. blocks na/k pump action
2. therefore, incr [Na] in cell
3. causes Na/Ca antiporter to malfunction
4. therefore, incr [Ca] in cell
5. therefore incr muscle strength of contractions

Front 65

Parietal Cell anion antiport mechanism (produces HCl)

Back 65

1. H2O & CO2-->HCO3- & H+
2. HCO3- exchanges with incoming Cl- on basal side
3. Cl- exits on apical side via Cl- channel into stomach
4. H+ exits apical side via H+ pump (driven by ATP) into stomach

Front 66

Omeprazole (Prilosec) mechanism

Back 66

inhibit H+ pump in parietal cells

Front 67

Cimetidine (Tagamet) mechanism

Back 67

blocks HK ATPase via histamine receptors.