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100 Cards in this Set
- Front
- Back
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ions high in extracellular fluid
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Na
Ca++ Cl- HCO- Mg++ pH 7.4 |
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ions high in Intracellular fluid
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K+
Bicarbonate Proteins pH 7.1 |
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use Na+ graident for secondary transport
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Glu
H+ Ca++ AA |
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amphipathic
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having both hydrophobic & phillic properties
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what isomer of glu is transported in facilitated diffusion
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D-Glu
D-galactose |
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what drug competes for the Glu transporter
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phlorizin
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what are 3 examples of active transport
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Na/K ATPase
Ca++ ATPase H+/K+ ATPase |
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Na/K ATPase
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3 Na out
2 K in alpha subunit has ATPase activity & binding sites Ouabain & digitalis inhibit Na/K ATPase activity by binding K binding site on Extracellular side & inhibits Pi release |
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Ca++ ATPase
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sarcoplasmic reticulum, mito
maintains low intracellular Ca++ 1 or 2 Ca++ transported/APT |
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H+/K+ ATPase
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gastric parietal cells
H+ from ICF into lumen of stomach Omeprezole inhibits H/K ATPase pump |
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Co transporters
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Na/Glu
Na/AA Na/K/2Cl- in ascending limb of Henle |
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b/c plasma has more protein, interstitial fluid has
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slightly higher Cl-
slightly lower K+, Na+ |
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Omeprezole
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inhibits H/K ATPase pump
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Ouabain
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inhibits Pi release from Na/K ATPase
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furosemide
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diuretic
blocks Na/K/2Cl cotransporter in ascending limb of Henle |
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Antiports
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Na/Ca++: 3 Na+ in/1Ca++ out
Na/H+ |
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what are 2 cardiac glycosides & how do they work
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Ouabain & Digitalis; Digoxin
inhibit Na/K ATPase --> inhibiting Na gradient -->cellular Ca++ spikes b/c Na/Ca can't work --> cardiac muscle contractility increases Used for treatment of heart failure; intropic action |
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vant Hoffs equation
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osmotic pressure (pi)
correlates with 1. Reflection coeefficient (sigma- solute permeability) 2. # of particles/mol of solution 3. Concentration (mM/L) |
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what causes fluid to move out of capillaries
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hydrostatic pressure
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what causes fluid to move into capillaries
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oncotic pressure
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symbol for hydrostatic pressure
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P
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symbol for oncotic pressure
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pi (osmotic pressure)
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example of paracrine signaling
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endochromaphin like cells in gastric mucosa release histamine to stimulate gastric HCl secretion
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cAMP can activate
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PKA
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cGMP can activate
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PKG
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Ca as a secondary messenger can activate
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calmodulin
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PKC can be activated by
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diacylglicerides
Ca++ membrane phospholipid (broken down) |
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2nd messenger targets of G proteins
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AD
cGMP phosphodiesterase Ca++ IP3 diacylglycerol |
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effectors of G proteins
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K & Ca++ channels
PLC, PLA2, PLD cAMP dependent kinases cGMP dependent kinases calmodulin dependent kinases PKC |
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what are some G protein receptors
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alpha & beta adrenergic receptor
Muscarinic acetylcholine receptor Adenosine receptor Olifactory receptor Rhodopsin receptor Peptide hormones |
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what are some peptide hormones that are linked to GPCR (4)
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nor/epinepherine
acetylcholine serotonin |
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how does PKC get activated?
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Ga activates PLC (PLC A2, PLD) --> IP3 & DAG
IP3 releases Ca++ from enoplasmic reticulum DAG + Ca++ activate PKC--> cell division |
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what releases arachnidonic acid?
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PLC A2
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arachidonic acid is a precursor to
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prostaglandins
prostacyclins thromboxanes leukotrienes |
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corticosteroids work by
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inhibiting cycloxygenase --> stopping PLC A2 derivatives of arachidonic acid
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kind of receptor insulin binds to
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RTK
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order of synthesis of biogenic amines
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dopamine --> Norepi--> epi
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what enzymes are needed for dopamine
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tyrosine hydroxylase
dopa decarboxylase |
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enzymes for norepiephrine
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tyrosine hydroxylase
dopa decarboxylase dopamine beta hydroxylase |
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enzymes for epinephrine
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tyrosine hydroxylase
dopa decarboxylase dopamine beta hydroxylase phenylehtanolamine-N-methyltransferase |
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serotonin
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produced from tryptophan
seroteginic neurons in brain & GI precursor to melatonin in pineal gland |
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glycine
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inhibitory neurotransmitter
spinal cord & brain stem increases Cl- |
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nicotinic receptor
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ion channel : Na, K, Ca++
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equilibrium potential
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diffusion potential that opposes the tendency for diffusion
inversly related to charge Na +65mV Ca +120mV K -85mV Cl -90mV |
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Dendrite spines
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cerebrum
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multiple sclerosis
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autoimmune, destruction of myelin in CNS
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inward current
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flow of cations into cell, depolarizes
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outward current
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flow of cations out of cell, hyperpolarizes
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AP threshold
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-60mV
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blocks voltage sensitive channels
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lidocne
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overshoot
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AP where interior is positive
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undershoot
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hyperpolarization
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absolute refractory period
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closure of inactivation gates in response to depolarization
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nodes of ranier
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lotes of Na channels
salutatory conduction |
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used to maintain sympathetic & sensory neurons
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NGF
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NGF
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sympathetic & sensory neruron
high in submandibular salivary glands of men Cholinergic neurons in forebrain reduced cell death |
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prevents damage of embryonic spinal cord neurons
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CNTF
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CNS neuroglia
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Microglia
Oligodendrocytes Astrocytes |
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Microglia
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CNS
~ macrophages |
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Astrocytes
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maintain BBB, take up K, GABA
Fibrous astrocytes- intermediate filaments (white matter) Protoplasmic astrocytes: granular cytoplasm (gry matter) |
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Burgman glia
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take up Glutamine & convert it back to glutamate in cerebellum
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Neuromuscular junction structure
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Ach receptor mmouths of junctional folds
active zones (pre) release vesicles |
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puffer fish toxin
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Tetrodoxotin
blocks Na voltage gated channel on pre neuromuscular junction |
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Neuromuscular transmission
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AP at pre --> open of Ca++
--> release of neurotransmitter ACh vesicles --> ACh binds opening Na & K channels |
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this causes spastic paralysis
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tetanus toxin
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causes flaccid paralysis
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botulism
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curare
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drug that competes w/ACh
relazation of skeletal muscle during aneshthesia |
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binds irreversibly to ACh receptor
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bungarotoxin
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ACh receptors
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Muscarine: smooth muscles & glands
nicotinic - sympathetic, post ganglion neurons |
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Muscarin chol receptor
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GCPR
--> AC K channels PLC |
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connexin
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allow passage of water soluble molecules at gap junctions
heart, liver, intestinal smooth muscle, lens |
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1:many synapse
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renshaw cells in spinal cord
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Many: 1 spnapse
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spinal motor neuron
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EPSP
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opening Na & K
ACh, nor/epi, dopamine, glutamate, serotonin |
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IPSP
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opening Cl
GABA, Lysine, glycine |
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75% of excitatory neurotransmitter in CNS
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Glutamate
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curare
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drug that competes w/ACh
relazation of skeletal muscle during aneshthesia |
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binds irreversibly to ACh receptor
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bungarotoxin
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ACh receptors
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Muscarine: smooth muscles & glands
nicotinic - sympathetic, post ganglion neurons |
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Glutamate receptors in CNS
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Metabotropic - GPCR
Ionotropic |
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Metabotropic
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glutamate receptor
GPCR --> cAMP --> DAG & IP3 |
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Ionotropic
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glutamate receptor
ion channel 3 types: Kainite, AMPA, NMDA |
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Kainite
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ionotropic glutamate receptor
Na channel presynaptic on GABA nerve |
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AMPA
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ionotropic glutamate receptor
Na channel Na & Ca++ channel |
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NDMA
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ionotropic glutamate receptor
cation channel receptor: K, Na, Ca++ only in neurons hippos needs glycine |
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produces amnesia, dissociation from environment
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Keatmine - blocks AMPA & NMDA glutamate receptors
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LTP
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mossefeild
Shaffer- excess glutamate keeps NMDA channels open longer |
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LTD
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dephosphorylation of AMPA
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glutamate decarboxylase (GAD)
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needed to make GABA from glutamate
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GABA receptors
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GABA-A Cl ion channel
GABA-B metabotropic & GPCR, K channel, inhibits AC & Ca++ influx GABA C- retina |
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progesteron & deoxychortcosteroid bind what receptor
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GABA-a & increase Cl (inhibatory)
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Benzodines
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bind GABA-a --> muscle relaxer, anticonvulents, sedatives
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alchohol & barbituites
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opens GABA-c Cl channel
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thin filaments in muscle
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actin
tropomyosin troponin |
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thick filaments in muscle
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myosin (heavy & light)
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z line
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connects thin filaments
actinin binds actin |
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H zone
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no myosin heads, thin filaments
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M line
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binds thick filaments
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muscle action
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ACh --> AP down T tubule
--> conformation change in voltage sensitive dihudropyrdine --> conformation change in ryanodine opening Ca++ channel Ca binds troponin C causing tropomyosin to more --> letting actin/myosin bind tenstion Ca pumped back into SR & actin/myosin no longer cross bridge |
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What stops neuromuscular junction
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Tetrodoxotin
Lambert-Eaton syndrom- Ab Ca++ channel Mathis Gravis - Ab blocks Ach receptors Curare competes w/Ach 5 |
