Path Phys Test 1

Front 1

steady state

Back 1

a condition that doesn't change with time.
- energy - may be required e.g. ion gradients

Front 2

equilibrium

Back 2

- opposing forces are balanced and their is no net movement between compartments
- type of steady state equilibriium
- energy - not required for equilibrium.

Front 3

components of a control system

Back 3

- sensor - measures variables you're trying to control.
- integrating center - compares the input to the set point
- effectors- change the system

Front 4

negative feedback systems

Back 4

- brings it back into normal range

Front 5

reason temp. regulation is needed

Back 5

- maintain rxn. rates at optimal level.

Front 6

pathologic consequences of temp. deviations.

Back 6

excessive heat - 43 deg. C or up is fatal
- excessive cold - less than 77 deg. farhenheit is fatal.

Front 7

core vs. peripheral temp.

Back 7

- core = brain, thoracic/abdominal cavities
- imp. to control these areas temp.

Front 8

control system

Back 8

- sensors (thermoceptors)
peripheral - monitor shell temp.
- central - hypothalamus of brain and abdominal cavities
- integrating center
- hypothalamus - compares set point to input (thermoceptors)

Front 9

responses to the cold

Back 9

- decreased blood flow to the skin
- inc. symp. ns. activity --> skin vasoconstriction --> dec. blood flow--> decreased heat loss

Front 10

shivering response to the cold

Back 10

- hypthalamus --> motor neuron actiivty --> skeletal muscle contraction

Front 11

responses to cold increased metabolic rate

Back 11

- increased epinepherine and thyroid hormone release
- increased fat breakdown
brown fat - lot of mitochondria in it and this produces more metabolic activity and more heat.

Front 12

responses to heat -

Back 12

behavioral adjustments
- increased blood flow to skin
- decreased s.n.s. activity --> skin vasodilation --> increased blood flow --> increased heat loss

- sweating - evaporatin cools off the skin.

Front 13

pathological conditions of temp. range

Back 13

- fever - increase in setpoint, the bodies thermostat goes up
- mechanism - infection, traums --> macrophages --> increased pyrogens --> increased prostaglandins in hypothalamus --> increased setpoint.

Front 14

hyperpyrexia

Back 14

- greater than 41 deg. cel. is life threatening.

Front 15

hypothermia

Back 15

- less than 35 deg. cel. is mild
- less than 28 degres cels. is severe
- less than 25 deg. cels. is fatal.
- CNS effects - confusion
- cardiac effects - arrhythmias due to faulty ion channels in heart.

Front 16

heat exhaustion

Back 16

- profuse sweating --> fluid loss --> dec. blood volume --> dec. blood pressure --> fainting.

Front 17

heat stroke

Back 17

- immediately life threatening
- GI vasoconstriction --> ischemia --> endotoxins from intestines released into the blood
- signs - increased body temp., often no sweating;
- CNS: delirium, coma, siezures

Front 18

phospholipids

Back 18

3 carbon backbone, 2 fatty acids, phsophate adn alcohol
- amphipathic - polar and non polar regions
- headgroup alcohol group is polar
- fatty acids - non polar regions.

Front 19

cholesterol

Back 19

- decreases membrane fluidity and may alter membrane protein function.

Front 20

membrane protein

Back 20

integral - in the membrane and they cross or embedded)
- peripheral - loosely associated

Front 21

carbohydrates

Back 21

- can be attached to protein or lipid
- glycolipids and glycoproteins - almost always face outside of cell.

Front 22

membrane transport

Back 22

- simple diffusion - occurs by random thermal motion.
- rate increased with concentration
- direct relationship between concentration and solute concentration.

Front 23

factors determining diffusion through cell membrane

Back 23

- size - smaller passes easier
- polarity - non polar pass more readily
- osmosis - (diffusion of water)
- H2O moves from area of high H2) conc. to low H2O concentration, and stops moving when hydrostatic pressure exactly opposes osmotic pressure.

Front 24

osmolarity

Back 24

- cell osmolarity is approx. 300 mosm.

- hypoosmotic - solution has lower number of solutes.

- hyperosmotic - solution has a higher number of solutes.

Front 25

tonicity

Back 25

- the molar concentration x the number of osmotically active impermeant molecules
THIS IS WHAT DETERMINES IF CELL SHRINKS OR GROWS. NOT osmolarity

Front 26

tonicity in review

Back 26

- hypotonic solution - solution has less solute than cell
- H2O moves into the cell and it grows

isotonis solution - no movement and cell volume remains the same.

- hypertonic solution - cell has less solute than solution so water moves out and the cell shrinks.

Front 27

clinical relevance of tonicity

Back 27

- hypnatremia/ water intoxication - low tonicity and H2O moves in.

- kidney and liver disease - late stage alcoholism - tonicityof peritoneal fluid is much higher than blood so fluid flows out and pot belly follows.

Front 28

facilitated diffusion

Back 28

- carrier proteins (transporters or exchangers) -
passive - moves from area of high to low conc. of molecules
- substrate size - can move large molecules that wouldn't pass otherwise
- transport max. velocity (Vmax) - max. velocity you can have at any given conc. because their are only so many receptors.

competition - if 2 substrates compete the rate for each goes down.

Front 29

ion channels

Back 29

- rapid movement after gate opens
- passive -
- substrate size - small molecules
- specificity - selective ( varies)
- flux rates - very high rate of ion streaming.
- 3 main types - activated by NT's, voltage or stretch.

Front 30

active transport

Back 30

- primary - directly breaking down ATP to move molecules
NaATPase
goes against conc. gradient.

- secondary - indirectly using energy stored in conc. gradient created from primary active transport
two types - symport - move molecules in the same direction
- antiport - move molecules in opposite direction

Front 31

vesicular transport

Back 31

- endocytosis
- pinocytosis - small particles/ fluid taken in
- phagocytosis - large particles
- receptor mediated endocytosis - ligand that binds surface protein and that molecules are then taken up into vesicle (ex. ion receptor)

- exocytosis - intracellular vesicle diffuses thru plasma membrane.

- exocytosis - intracellular vesicle diffuses thru plasma membrane

Front 32

second messenger systems

Back 32

- intracellular - takes EC signal and transmits it inside via receptors
- amplificaiton - make signal stranger because theyre catalytic.

- speed - fast responses (seconds to minutes)

Front 33

adenylyl cyclase/ cyclic AMP

Back 33

- G protein signal to adenylyl cyclase creates cAMP (2nd messenger)

- PDE - breaks down cAMP -

Front 34

phospholipase C/inositol triphosphate (IP3)

Back 34

Protein lipase C --> activates DAG or it creates IP3 which causes the cascade (DAG activates protein kinase c makes atp into ADP)
- di acyyl glycerol is the 2nd messenger (lipid soluble) -->activates protein kinase C

-- IP3 is the other 2nd messenger

-- synthetic enzyme --> hormone