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117 Cards in this Set
- Front
- Back
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what is primary active transport
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SPENDING ENERGY
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USES ATP
DIRECTLY OR INDIRECTLY? |
DIRECTLY
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REQUIRES CARRIER PROTEIN
YES OR NO? |
YES
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PRIMARY ACTIVE TRANSPORT>>>
NA(SODUIM) WHERE? K+ PATASSUIM...WHERE? |
NA+ (SODUIM IS ON THE OUTSIDE OF CELL AND K+ IS ON THE INSIDE OF THE CELL.
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5 STEPS IN ACTIVE TRANSPORT. 1 N 2
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1) 3 NA+ MOVE INTO CELL
2) ATP BRKS DWN TO ADP AND ASPASE IS PHOSPHORYLATED |
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5 STEPS IN ACTIVE TRANSPORT...3,4
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3) 3NA+ RELEASED INTO ICF
4) PROTEIN CHANGES CONFIRMATION AND 2K+ FROM EDF BIND |
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5TH STEP IN ACTIVE TRANSPORT,
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PROTEIN CHANGES CONFIRMATION..
2 K+ RELEASED INTO ICF |
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PRIMARY PUMP IS IMPORTANT BECAUSE???
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IT BURNS ATP
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WHAT IS OUTSIDE THE PUMP IN THE EXTRACELLULAR FLUID?
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LOTS OF H+ (HYDROGEN)
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ACTIVE TRANSPORT MOVES
UP OR DOWN? |
UP! AND BECAUSE UPHILL IS WORK...ATP IS NECESS. ATP IS HYDROLYZED TO ADP
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what is primary active transport
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SPENDING ENERGY
|
|
|
USES ATP
DIRECTLY OR INDIRECTLY? |
DIRECTLY
|
|
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REQUIRES CARRIER PROTEIN
YES OR NO? |
YES
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PRIMARY ACTIVE TRANSPORT>>>
NA(SODUIM) WHERE? K+ PATASSUIM...WHERE? |
NA+ (SODUIM IS ON THE OUTSIDE OF CELL AND K+ IS ON THE INSIDE OF THE CELL.
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5 STEPS IN ACTIVE TRANSPORT. 1 N 2
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1) 3 NA+ MOVE INTO CELL
2) ATP BRKS DWN TO ADP AND ASPASE IS PHOSPHORYLATED |
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5 STEPS IN ACTIVE TRANSPORT...3,4
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3) 3NA+ RELEASED INTO ICF
4) PROTEIN CHANGES CONFIRMATION AND 2K+ FROM EDF BIND |
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5TH STEP IN ACTIVE TRANSPORT,
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PROTEIN CHANGES CONFIRMATION..
2 K+ RELEASED INTO ICF |
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PRIMARY PUMP IS IMPORTANT BECAUSE???
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IT BURNS ATP
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WHAT IS OUTSIDE THE PUMP IN THE EXTRACELLULAR FLUID?
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LOTS OF H+ (HYDROGEN)
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ACTIVE TRANSPORT MOVES
UP OR DOWN? |
UP! AND BECAUSE UPHILL IS WORK...ATP IS NECESS. ATP IS HYDROLYZED TO ADP
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2NDARY ACTIVE TRANSPORT DEPENDS OF WHAT?
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THE PRIMARY ACTIVE TRANSPORT
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MECHANISMS HARNESS ENERGY DERIVED FROM PRIM ACT TRANS OF 1 SUBSTANCE...WHY?
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FOR THE COTRANSPORT OFA 2ND SUBSTANCE.
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3TYPES OF ENDOCYTOSIS
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PHAGOCYTOSIS
PINOCYTOSIS RECEPTOR-MEDIATED ENDOCYTOSIS |
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WHEN SIGNAL IS INVOLVED ITS CALLED...
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RECEPTOR MEDIATED ENDOCYTOSIS
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WHY IONS MOVES ACROSS A CELL MEMBRANE?
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BECAUSE INSIDE AND OUTSIDE HAVE DIFFERENT CHARGE.
ELECTRICAL FORCE |
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INSIDE AND OUTSIDE OF A CELL HAVE DIFFERENT CONCENTRATIONS OF IONS
CALLED? |
CHEMICAL FORCE.
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THE COMBINATION OF FORCE ACTING ON IONS ARE CALLED?
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ELECTROCHEMICAL
GRADIENT |
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THE CYTOPLASM IS NEGATIVE IN CHARGE COMPARED TO EXTRACELLULAR FULID CUZ?
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1...CELLULAR PROTEINS
2...PHOSPHATE GRPS OF ATP 3...BOTH ARE IMPERMEABLE SO THEY CANT LEAVE. |
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STIMULATION =
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EXCITABILITY
(IRRITABILITY) |
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THE AMOUNT OF CHARGE A CELL HAS IS CALLED?
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MEMBRANE POTENTIAL
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THE CYTOPLASMA IS NEG IN CHARGE COMPARED TO EXTRACELLULAR FLUID, WHY?
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1. CELLULAR PROTIENS
2. PHOSPHATE PROTEINS 3. BOTH ARE IMPERMEABLE SO THEY CANT LEAVE |
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GRADED POTENTIAL HAPPENS WHERE?
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IN THE CELL BODY AND DENDRITES
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THE STRENGTH OF THE DEPOLARIZATION IS DETERMINED BY?
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HOW MUCH CHARGE (NA+) ENTERS THE CELL.
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SYNAPSE
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A FUNCTIONAL CONNECTION
BETWEEN 2 NEURONS PRESYNAPTIC & POSTSYNAPTICE |
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CA ACTIVATES A PROTEIN
CALLED ? |
CALMODULIN
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CALMODULIN ACTIVATES AN
ENZYME CALLED ? |
KINASE
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PROTEIN KINASE PHOSPHORYLATES?
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SYNAPSINS IN THE MEMRANE OF THE SYNAPTIC VESICLES AND AID FUSION W/ PLASMA MEMBRANE
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DEPOLARIZING POTENTIAL IS CALLED?
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EXCITATORY POSTSYNAPTIC POTENTIAL
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HYPERPOLARIZING GRADED POTENTIAL IS?
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INHIBITORY POSTSYNAPTIC POTENTIAL...IPSP
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NOVEL MESSENGERS
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ATP AND DISOLVED GASES
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ACH..HAS 2 SUBTYPES OF RECEPTORS
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NICOTINIC
MUSCARINIC |
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AT SOMATIC MOTOR NERVE THE RECEPTOR IS ??
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NICOTINIC AND ACH IS EXCITATORY
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AT AUTONOMIC NERVE END
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IF RECEPTOR IS MUSCARINIC, ACH IS EITHER INHIBITORY OR EXCITORY
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WHERE DO U FIND NICOTINIC ACH RECEPTOR?
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AT THE NEURO MUSCULAR JUNCTION...NMJ
AND GANGLION |
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ANOTHER NAME FOR
AUTONOMIC NERV SYS SOMOMIC NERVE SYS ?? |
AUTO IS 2 NEURON SYSTEM
SONAMIC IS 1 NEURON SYS. |
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AUTONOMIC SYSTEM GOES TO THE
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GANGLION SYSTEM
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NICOTINE ALWAYS
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STIMULATES
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WHAT IS NICATINIC RECEPT
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IT IS A CHEMICALLY GATED CHANNEL
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WHAT IS A DIRCCT COUPLING
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IF RECPTOR AND CHANNEL ARE THE SAME STRUCTURE
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MUSCARINIC USES A LINK CALLED?
MIDDLE MAN! |
G-PROTEIN....
NOTE CALLED M2 WHICH IS USED IN HEART. |
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HOW DO WE REMOVE ACH
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ACETLCHOLINESTERA
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CATECHOLAMINES ARE?
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DOPA
DOPAMINE NOREPINEPHRINE EPINEPHRINE |
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INDOLAMINES ARE?
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SEROTININ
HISTAMINE DISTRIBUTED IN THE BRAIN |
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PHENYLALANINE IS
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AMINO ACID......
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WHAT IS THE SEQUENCE OF THE CATECHOLINES?
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PHENYLALANINE, TYROSINE, DOPA,DOPAMINE
NOREPINEPHRINE, EPINEPHRINE |
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HOW MANY RECEPTORS FOR
NOREPINEPHRINE (B1-HEART |
2...ALPHA AND BETA
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THE G-PROTEIN WILL BREAK DOWN N ATTACH TO WHAT TO CREATE ENZYME
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ADENYLATE CYCLASE....
BREAKS DOWN ATP TO cAMP CYCLIC-AMP(2ND MESSANGR |
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CYCLIC-AMP(cAMP)
WHAT DOES IT DO? |
IT ACTIVATES THE PROTEIN KINASE...OPENS NA+ OR K+ CHANNEL
MAKES HEART FAST/STRONG |
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HOW TO REMOVE NE
norepinephrine a break down of enzymes |
1. MOA.. PRESYNAPTIC REUPTAKE SYSTEM
2.POST SYNAPTIC IS COMT found in blood kidney,liver COMT...EVERYWHERE |
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puffy coat is
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wbc...platelets
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serum is
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plasma > fibrinogen
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force caused by protein?
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osmotic
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albumins?
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most connon carrier protein...
keeps fluids in |
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globulins
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group of protiens that are round
antibody enzymes |
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fribinogen
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plasma proteins
in liver |
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albumns
globulins fibrinogen transferrin |
carrier
clot'g factor, enzyme antibody forms fibrin treads for clot'g iron transport |
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3 blood cell w/ granulocytes
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neutrophil.....50-70%
eosinophils...1-4% basophil .....<1% |
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2 blood cells--- agranulocytes
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lymphcytes..20-40%
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hematopoisis is
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formation of blood cells from stem cells in red
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cytodines?
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chemical factor responsible for blood cell production
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erythropoisis is?
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formation of rbc
released in kidney |
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thrombospoiesis is?
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formation of platlets
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red blood cells burn what? ...and have no??
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2 atp ....anarobicly
no nucleus no ribosome no mitochondria |
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RBC IS HB
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carrier of oxygen.
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hemotopoisis is
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a formation of blood cells from stem cells in red bone marrow.
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cytikines?
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chemicle factor that is responsible for blood cell production.
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rbc hb carries?
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carries oxygen
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spectrin?
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plasma membrane protien
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Hemoglobin protein is a ?
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peptide chain-4
alpha 1 alpha 2 beta 1 beta 2 |
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fetus carries what hb
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alpha 1 alpha 2
g1 g2 |
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porphyrin is?
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Iron...Fe2
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4 globular protein chains consist of?
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porphyrin ring w/ Fe2 in the middle
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old red blood cells die and go?
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to red bone marrow or liver and mostly spleen.
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met-hemoglobin has?
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Fe# in blood and no o2
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excess Iron is stored?
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in the macrophages of the bone marrow ...called ferritin
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liver changes fat soluble to?
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water soluble
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albien is a ?
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protein carrier
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neutrophils production increases where?
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in the bone marrow.
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nutrophils cells production will go up when?
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only in acute bacterial infections due to nucrosis
death of cell. |
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neutophil has how many lobes?
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can have 2 or more lobes
w/granules |
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eosinophil are where?
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primarily in the spleen and blood marrow but also in blood circulation
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eosinophil can limit the rx's
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by histaminase and
arylsulfatase following most cell release. |
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eosinophil increases when?
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invasion of parasitic worms
and allergies. |
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basophil has large granuales in the cytoplasm and helps?
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allergies
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heparin is?
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anti clot'g
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lymphocyte is the smallest wbc and increases when?
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increases during viral infection and r- arthritis
mostly in lymphoid tissues |
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monocyte is?
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large in size w/ lrg cytoplasm and large nuclei
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monocytes leave blood and become?
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macrophages
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dendrictic cells are made from?
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monocyte and will trap the pathogens/antigens
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monocytes increase when?
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with disease..crones, ibd, collegen vasscular disease
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platelets do?
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maintain the integrety of the blood vessele walls
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magakaryocytes are ?
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giant cells w/multiple copies of dna
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magakaryocytes release?
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vonwilbran factor and also platlets
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glycoprotein recepter for the VWF is?
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gph1b
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glycoprotein receptor binds what?
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platlets bind to each other and to fibrinogen using gp2b and gp3
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glycoprotein and adp?
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the adp causes insertion to platlet membrane using gp2 and gp3
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platelets stick to collegen and release?
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release adp to stick(aggregation)
causing serotonin in platlets to constrict |
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cell structure 1...release of NO 2. VWF then ???
3. CD39 |
clot'g to stop
acts as a bridge so collegen can attach to blood enzyme brks down adp in blood |
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pectechin?
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pin point hemmorage due to lack of plts
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ecchymosis?
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bruise due to clot'g factor
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clot'g factors w/ vitamins?
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2,7,9,10
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factor 4
factor 2 factor 6 |
coaggulation
converts fibrinogin to fibrin leads to b deficientcy and hemophilia |
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extrinsic pathwy.
intrinsic |
3,7,10,2,1
12,11,9, |
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CA controls contraction....
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thin pulls over thick filiment
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what causes calk'g
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ATP
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rigor stage?
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is the pull not the contraction
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what is power stroke?
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is the attachment taking place pulling back to gain for force
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