Basic Physiology Flashcards
How is ACh synthesized? Where is it stored?
- Acetyl CoA + Choline → choline acetyltransferase → ACh
2. Stored in the synaptic vesicles with ATP and proteoglycan
How is ACh degraded? What happens to the degradation products?
- ACh degraded to Acetyl CoA and choline by aceylcholinesterase
- Occurs at the muscle end plate
- 1/2 of the choline is taken back to the presynaptic cleft by Na-choline transport to make new ACh
Botulinum Toxin
Blocks ACh release from presynaptic terminals → total blockade
Curare
Competes with ACh for receptors on the motor end plate → decreased end plate potential
Neostigmine
Inhibits acetylcholinesterase → prolongs action of ACh at motor end plate
Hemicholinium
Blocks reuptake of choline into presynaptic terminal → depletes ACh stores
Excitatory neurotransmitters
- ACh
- Norepinephrine
- Epinephrine
- Dopamine
- Glutamate
- Serotonin
Inhibitory Neurotransmitters
- GABA
- Glycine
- Nitrous Oxide
Describe pathway for converting tyrosine into different neurotransmitters
Tyrosine → tyrosine hydroxylate → L-dopa → dopa decarboxylase → dopamine → dopamine β hydroxylase → norepinephrine → phenylethanolamine-N-methyltransferase → epinephrine
What does serotonin form from? Where is the highest concentration of serotonin?
- Tryptophan
2. Brainstem
What metabolizes norepinephrine and dopamine?
- Monoamine oxidase (MAO)
- Catechol-O-Methyltransferase (COMT)
* VMA metabolite of NE is increased in urinary excretion with pheochromocytomas
What is the most prevalent excitatory neurotransmitter in the brain?
Glutamate
GABA synthesis and receptors
- Glutamate → glutamate decarboxylase → GABA
- GABA(a) → Increase Cl conductance
- Benzodiazepines and barbiturates act here
GABA(b) → Increase K conductance
Nitric oxide synthesis
Arginine → NO synthase → NO
What is a major difference in myosin regulation between skeletal and smooth muscle?
Smooth has no troponin → Ca regulates myosin on the thick filaments
Type 1 muscle fibers
- Red, slow twitch
- Small diameter
- More mitochondria
- More blood supply
Type 2 muscle fibers
- White, fast twitch
- Large diameter
- Extensive sarcoplasmic reticulum
- Lots of glycolytic enzymes
- Less extensive blood supply
- Fewer mitochondria
What can occur with repeated thoracocentesis in chylothorax?
- Hyponatremia
- Hyperkalemia
* Third space loses of Na → subsequent decrease ECV and GFR causes increase K
What is the order of half-life duration of AST, ALP, and ALT?
- Dog
- Cat
- ALP>ALT»AST
2. ALP=ALT»AST
Sensitivity and Specificity (High/Low): ALP
- Dog
- Cat
- High sens (86%) but low spec (49%) for liver diseaes
2. Less Sens but more spec for liver disease
Reasons for increase:
- L-ALP
- B-ALP
- C-ALP
- Cholestasis, Hyperadrenocorticism, and drug induction (phenobarb and steroids - ~24-48 hours after exposure)
- Benign familial hyperphosphatemia in huskies and scotties results from increase B-ALP
- Steroids (10 days after exposure), Diabetes mellitus, primary liver disease, and HAC
Anion Gap Equation
(Na + K) - (Cl + HCO3)
Causes of increased calcium excretion
- Decrease PTH
- Increase ECV
- Increase BP
- Decrease P
- Metabolic alkalosis
* Opposites for decrease Ca excretion
Ions associated with vasodilation
- Increase Magnesium
- Increased H (acidemia)
- Acetate/Citrate
- CO2
- Vasodilate in brain
- Vasoconstrict periphery to increase flow to the brain