Physiology Lectures 1-2

Front 1

Various Units of Solute Concentration, their meaning

Back 1

1) mmol/L: Mole
2) mEq/L :Equivalents =Mole * Valence
e.g. 1 mmol of Ca2+ = 2mEq/L
3) mOsm/L: Osmole = Mole * # of particles dissolved into
e.g. 1 mmol NaCl = 2mOsm/L

Front 2

Principle of electroneutrality

Back 2

Each compartment in the body must have the same concentration, in mEq/L, of positive charges as of negative charges.

Front 3

Total Body Water

Back 3

Accounts for 50-70% of body weight

e.g. 75kg man with 65% body water has 45.5 kg = 45.5 L of water

Front 4

Proportion of body water in ICF, ECF

Back 4

ICF: two thirds of total body water

ECF: one third of total body water
ECF further divided into interstitial fluid (plasma ultrafiltrate that bathes the cells) and plasma.
ECF, ICF separated by cell membranes

Front 5

Composition of ICF, ECF

Back 5

ECF: cation is Na+, anions Cl- and HCO3-

ICF: cations are K+ and Mg2+, anions proteins and organic phosphates

Both ICF and ECF have same osmolarity

Front 6

Gibbs-Donnan equilibrium

Back 6

redistribution of small cations and anions across the capillary wall to equilibriate with the negatively charged plasma proteins in the blood. [Na+], [K+] increases in the blood, [Cl-] increases in the interstitium.

Front 7

What is the driving force for diffusion across a cell membrane?

Back 7

The concentration gradient.

Front 8

Partition coefficient, K

Back 8

K = [solute in oil]/ [solute in H2O]

describes the solubility of a solute in oil relative to its solubility in water. The great K is, the greater its ability to dissolve in oil/lipid bilayer

Front 9

Stokes-Einstein equation for Diffusion Coefficient

Back 9

D = KT/6πrη

D = diffusion coefficient
K = Boltzmann Constant
T = Absolute Temp
r = molecular radius
η = viscosity of medium

Front 10

Equation for permeability

Back 10

P = KD/Δx

P = permeability
K = Boltzmann's constant
D = diffusion constant
Δx = thickness of membrane

Front 11

Equation for Net Diffusion

Back 11

J = PA (Ca-Cb)

J = Net rate of Diffusion (mmol/sec)
P = Permeability
A = Surface area for diffusion (cm2)
Ca,Cb = concentration is solution a,b

Front 12

van't Hoff equation for Osmotic Pressure

Back 12

π = g*C*σ*RT

π = osmotic pressure/pressure required to stop the flow of water into a hypertonic solution
g = number of particles per mole in solution (Osm/mol)
C = concentration (mmol/L)
σ = Reflection coefficient (0-1), ease by which a solute crosses the membrane (1 = impermeable)
RT = gast constant * absolute temp

Front 13

Definition of Isotonic

Back 13

Two solutions that have the same osmotic pressure according to the van't Hoff equation: π = g*C*σ*RT

Water will flow from less pressure --> more pressure

Front 14

Nernst equation

Back 14

E = -2.3RT/zF*log10[Ci]/[Ce]

E = equilibrium potential (mV)
2.3RT/F = Constant (60mV at 37 deg)
z = charge of ion
Ci, Ce = concentrations intra,extra cellularly

Front 15

60-40-20 Rule

Back 15

60% of body weight is water
40% is ICF
20% is ECF

3/4 ECF in intersititium

Front 16

How to measure volume of a Body Fluid Compartment?

Back 16

1. Identify an appropriate marker
TBW: D2O
ECF: large molecular wt sugars
plasma: radioactive albumin
2. Inject a known amount of marker
3. Equilibriate and measure plasma concentration
4. Calculate Volume = Amt/Concentration

Front 17

Principles of Fluid Shifts between compartments

Back 17

1. The volume of the compartment depends on the amount of solute it contains
2. Osmolarity is the concentration of osmotically active particles, expressed as milliosmoles per liter (mOsm/L)
3. In a steady state, intracellular osmolarity is equal to extracellular osmolarity. To maintain this equilibrium, water shifts freely across cell membranes.
4. Solutes such as NaCl and NaHCO3 and large sugars such as mannitol are assumed to be confined to the ECF because they do not readily cross cell membranes.

Front 18

Diarrhea

Back 18

Isosmotic volume contraction:
volume lost from GI tract is isosmotic to that of ECF. Thus, disturbance in diarrhea is loss of isosmotic fluid from ECF.
ECF volume decreases, but because it's isosmotic, there's no change in ICF volume.
Results in concentration of hematocrit/blood proteins.

Front 19

Water deprivation (Lost in Desert)

Back 19

Hyperosmotic Volume Contraction
Sweat is hyperosmotic relative to ECF: loss of sweat reduces ECF volume, increases ECF osmolarity. Water shifts from ICF to ECF, increasing ICF osmolarity. End result: decreased ICF, ECF volumes, increased ICF, ECF osmolarities. [Plasma protein] increases, but not hematocrit (RBC's lose water volume too!)

Front 20

Adrenal Insufficiency

Back 20

Hormonal problem leading to Na+ malresorption in distal tubule; excess NaCl excreted in urine. NaCl is an ECF solute, so ECF osmolarity decreases. Water shifts from hypotonic (ECF) to hypertonic (ICF) until equilibrated.
Both [plasma protein] and hematocrit increased because of decrease in ECF volume (water INTO RBC's!)

Front 21

Infusion of NaCl

Back 21

Isotonic Volume Expansion:
NaCl stays in ECF, isotonic means no water will travel from ICF; ECF volume increases, [plasma protein] + hematocrit decrease.

Front 22

Syndrome of inappropriate antidiuretic hormone (SIADH)

Back 22

Hypoosmotic Volume Expansion
Too much ADH --> too much water resorbed, added proportionately to ICF, ECF. [plasma protein] decreases, hematocrit remains the same

Front 23

Colloidosmotic pressure

Back 23

AKA oncotic pressure: the osmotic pressure in capillaries generated solely by proteins

Front 24

Starling Equation

Back 24

Jv = Kf [(Pc-Pi) -(πc-πi)]
Jv = Fluid movement (ml/min)
Kf = Hydraulic conductance (ml/min*mmHg)
Pc = capillary hydrostatic pressure (mmHg)
Pi = Interstitial hydrostatic pressure (mm Hg)
πc = Capillary oncotic pressure (mm Hg)
πi = Interstitial oncotic pressure (mm Hg)

Fluid flow direction

Front 25

Hydraulic Conductance, Kf

Back 25

Water permeability of the capillary wall that varies amongst tissues. Highest in fenestrated capillaries (glomerulus) and lowers in cerebral capillaries. Kf independent of hypoxia, metabolite buildup, or changes in arteriolar resistance.

Front 26

Capillary hydrostatic pressure

Back 26

Pc: force favoring filtration out of the capillary, determined by arterial and venous pressures (closer to arterial pressure).
Pc affected MORE by changes in VENOUS pressure than arterial pressure.
Except in glomerular capillaries, Pc decreases along length of capillaries because of filtration of fluid; thus Pc highest at arteriolar end, lowest at venous end.

Front 27

Interstitial hydrostatic pressure

Back 27

Pi: force opposing filtration, normally 0 or slightly negative.

Front 28

capillary oncotic pressure

Back 28

πc: a force opposing filtration, is the effective osmotic pressure of capillary blood due to presence of proteins, and is determined by [proteins] of capillary blood.

Front 29

interstitial oncotic pressure

Back 29

πi: force favoring filtration. πi is determined by the interstitial fluid protein concentration. Normally, this is low.

Front 30

What could cause an increase in filtration?

Back 30

Increase in any Starling parameter that favors filtration (Pc, πi, Kf), or decrease in a parameter that favors absorption (Pi, πc).

Front 31

Describe lymphatic capillaries

Back 31

Lymphatic capillaries lie in the intertitial fluid, close to vascular capillaries, and possess one-way valves which permit interstitial fluid and protein to enter, but not to leave, the capillaries. These merge with other lymphatic vessels and eventually end in the thoracic duct.

Front 32

Edema

Back 32

An increase in interstitial fluid volume: occurs when the volume of interstitial fluid (due to filtration out of the capillaries) exceeds the ability of the lymphatics to return it to the circulation.

Front 33

Somatic Nervous System: number of neurons, cell body location, effector organ, neurotransmitter, receptors

Back 33

consists of single motoneuron --> skeletal muscle fibers
cell body location: CNS
effector organ: skeletal muscle
neurotransmitter: ACh
receptors: nicotinic receptors on motor end-plates

Front 34

Autonomic Nervous System: number of neurons, effector organ, neurotransmitter, receptors

Back 34

two neuron system: pre and postsynaptic
effector organ: smooth muscle, heart, glands
neurotransmitter: ACh for presynaptic; postsynaptic can be ACh (PSNS, somatic, SNS sweat-glands), NE (SNS), or neuropeptides
receptors:

Front 35

origin of preganglionic neurons in SNS, PSNS

Back 35

SNS: T1-L3 spinal level (thoracolumbar)
PSNS: Nucleic of CN II, VII, IX, and X;
spinal cord segments S2-S4 (craniosacral)

Front 36

Receptor types in organs with sympathetic innervation

Back 36

α1, α2, β1, β2

Front 37

Receptor types in organs with parasympathetic innervation

Back 37

Muscarinic ACh

Front 38

Adrenal medulla

Back 38

A specialized ganglion in the sympathetic division of the ANS, with cell bodies in the thoraco spinal cord. Preganglionic neurons travel via greater splanchnic nerve to synapse on chromaffin cells, and release ACh onto Nicotinic receptors. This causes the chromaffin cells to release catecholamines (20% NE, 80% Epi)

Front 39

Chromaffin cells

Back 39

Cells in the adrenal medulla which are innervated by presynaptic sympathetic neurons. Upon stimulation, they release catecholamines (20% NE, 80% Epi) into the bloodstream.

Front 40

SA Node ANS activity: action and receptors

Back 40

SNS: Increases HR via β1 receptor

PSNS: Decreases HR via M receptor

Front 41

AV Node ANS activity: action and receptors

Back 41

SNS: Increases HR via β1 receptor

PSNS: Decreases HR via M receptor

Front 42

Heart Contractility ANS activity: action and receptors

Back 42

SNS: Increases contractility via β1 receptor

PSNS: Decreases atria contractility only via M receptor

Front 43

ANS activity of Skin-- Splanchnic/Vascular Smooth Muscle

Back 43

SNS: Constricts vascular smooth muscle via α1 receptors

Front 44

ANS activity of Vascular Smooth Muscle/Skeletal Muscle: Receptors and Actions

Back 44

SNS: Dilates via β2 receptor, and Constricts via α1 receptor

Front 45

Endothelium ANS activity: Actions and receptors

Back 45

PSNS: Release of EDRF (relax!) via M receptors

Front 46

Bronchioles ANS activity: Actions and receptors

Back 46

SNS: Dilates bronchioles via β2 receptor

PSNS: Constricts bronchioles via M receptors

Front 47

ANS activity in the smooth muscle walls of the GI tract

Back 47

SNS: relaxes smooth muscle in walls of GI tract via α2, β2 receptors

PSNS: Contracts smooth muscles in walls of GI tract via M receptors

Front 48

ANS activity in the sphincters of the GI tract

Back 48

SNS: Contracts smooth muscle sphincters in GI tract via α1 receptors

PSNS: Relaxes smooth muscle sphincters in GI tract via M receptors

Front 49

ANS activity of Saliva secretion

Back 49

SNS: Increase Saliva secretion via β1 receptors

PSNS: Increases Saliva secretion via M receptors

Front 50

α1 receptors: location, action, mechanism

Back 50

α1 receptors
Found in vascular smooth muscle of skin, skeletal muscle, and in splanchnic regiong, in sphincters of GI tract + bladder, and in radial muscle of iris.

Activation leads to CONTRACTION of these tissues via G-protein activation of phospholipase C.

Front 51

α2 receptors: location, action, mechanism

Back 51

less common than α1 receptors, α2 receptors are found in the wall of the GI tract and in presynaptic adrenergic nerve terminals.

Act by inhibiting adenylyl cyclase (reducing cAMP levels).

Front 52

β1 receptors: location, action, mechanism

Back 52

β1 receptors: Prominent in Heart (increase HR), also located in salivary glands, adipose, kidney (renin secretion).

Act via Gs protein activation of adenylyl cyclase.

Front 53

β2 receptors: location, action, mechanism

Back 53

β2 receptors are found in the vascular smooth muscle of skeletal muscle, in the walls of the GI tract and bladder, and in the bronchioles.

Act via Gs protein activation of adenylyl cyclase.