MD2002 Week 2 Flashcards
(82 cards)
what connect the actin filaments in smooth muscle?
dense bodies
outline smooth muscle contraction
- Ca binds to calmodulin
- Ca-calmodulin-MLCK complex leads to phosphorylation of MLC (part of myosin head)
- myosin binds to actin and power stroke occurs
outline smooth muscle relaxation
- Ca is released from calmodulin
- MLCP removes P from MLC
- myosin head detaches from actin filament
what must the free energy change be for a reaction to occur spontaneously?
free energy change must be negative for this to occur
chemical formula of phosphate
PO4^3-
what factors affect metabolism? (3)
- amount of substrates/products
- amount of key enzymes
- activity of key enzymes
steps in the cross-bridge cycle (4)
- energized myosin binds to actin when [Ca2+] > 10^-5
- energy is discharged and cross bridge rotates. ADP and P are released
- ATP binds to myosin and breaks link
- ATP is split, producing energized myosin
stiffening of skeletal muscles after death
rigor mortis
source of ATP in muscle that provides 100 twitches
creatine phosphate
source of ATP in muscle that provides 20000 twitches
aerobic glycolysis provides this many twitches in muscle
source of ATP in muscle that provides 600 twitches
anaerobic glycolysis provides this many twitches in muscle
molecular structure of sugar
OH at every C + aldehyde group
keto acids
compound where amine group of amino acid is replaced by carbonyl and can be used for energy
NADH
nicotinamide adenin dinucleotide
niacin (B3) deficiency
pellagra: sensitive to sunlight, dermatitis, alopecia (hair loss), glossitis, weakness, ataxia
enzyme catalyzing glucose –> glucose-6-P
hexokinase
phosphofructokinase
catalyses fructose-6-P –> fructose-1,6-bisphosphate
factors affecting phosphofructokinase activity in glycolysis (5)
- high [ATP] allosterically inhibits
- low pH inhibits (lactate accumulation)
- high [citric acid] inhibits
- high [pyruvate] inhibits
- high [fructose-6-P] stimulates
energy products of glycolysis
2 ATP and 2 NADH produced
3 ways to block NMJ transmission
- inhibiting Ach synthesis
- inhibiting Ach release
- postsynaptically
how depolarising/agonistic NMJ blockers work
- persistent depo of motor end plate
- prolonged end plate potential and depo of muscle membrane
- MP above threshold for resetting of V-gated Na channels
- no more muscle action potential generated
Phase 2 of depolarizing NMJ blocker
prolonged exposure to drug causes “desensitization blockade” (depo cannot occur, even in absence of drug)
onset and duration of rocuronium
this NMJ blocker has fast onset and medium duration
side-effects of pancuronium and rocuronium
side effect of these NMJ blockers is tachycardia