Term
| arise in peripheral organs and travel to spinal cord and brain |
|
Definition
| sensory (afferent) fibers |
|
|
Term
| form the initial link in autonomic reflex arcs |
|
Definition
| sensory (afferent) fibers |
|
|
Term
|
Definition
|
|
Term
| autonomic nervous system control |
|
Definition
|
|
Term
| ANS component targeted pharmacologically |
|
Definition
|
|
Term
|
Definition
1. arise from thoracic and lumbar levels of the spinal cord (thoracolumbar)
2. cell bodies give rise to short preganglionic fibers, which synapse at paravertebral ganglia
3. organized for mass discharge |
|
|
Term
| synapses with many sympathetic ganglion cells through collateral fibers |
|
Definition
| single sympathetic preganglionic fiber |
|
|
Term
| innervate effector cells at the neuroeffector junction |
|
Definition
| sympathetic postganglionic fibers |
|
|
Term
| receive innervation from sympathetic preganglionic fibers carried over the greater splanchnic nerve |
|
Definition
| chromaffin cells of the adrenal medulla |
|
|
Term
| where do parasympathetic nerves arise? |
|
Definition
| from the midbrain and medulla (3,7,9,10 CN) or from the sacral part of the spinal cord craniosacral |
|
|
Term
| preganglionic parasympathetic fibers |
|
Definition
long
synapse with parasympathetic ganglion cells near or (more often) IN the organs innervated |
|
|
Term
| relationship between pre- and post-ganglionic PSNS fibers |
|
Definition
| 1:1 not organized for mass discharge like SNS |
|
|
Term
| *patterns of organ innervation |
|
Definition
1. dual innervation
2. single innervation
3. dual innervation with parallel function |
|
|
Term
| arms of ANS have opposite function on same target |
|
Definition
|
|
Term
| innervation by only one arm of the ANS |
|
Definition
|
|
Term
| 2 divisions produce similar effects |
|
Definition
| *dual innervation with parallel function |
|
|
Term
| homeostatic function of SNS |
|
Definition
1. normally regulates structures not under voluntary control (e.g. HR, contractility, BP, digestion, salivary secretion, pupil size)
2. control is moment-to-moment, but organization is for mass discharge |
|
|
Term
| excitatory function of SNS |
|
Definition
*"fight or flight"
1. increased cardiac activity
2. increased BP
3. dilation of skeletal muscle BV
4. dilation of pupils (mydriasis)
5. inhibition of gut, urinary bladder contraction
6. increase in blood glucose and free fatty acids
7. dilation of bronchial SM
8. secretions of viscous saliva |
|
|
Term
| responses of organs to SNS |
|
Definition
vaso-/veno- arterioles - contraction/stiffening
skin arterioles - contraction
skeletal muscle arterioles - dilation
bronchial muscle - dilation
eye - mydriasis
heart - increased force, rate
intestine - relaxation
pilomotor muscle - contraction
salivary glands - secretion (viscous)
urinary bladder - relaxation |
|
|
Term
| homeostatic functions of PSNS |
|
Definition
1. normally regulates structures not under voluntary control (e.g. relaxation, conservation, digestion, restoration of energy, rest and repair)
2. control is moment-to-moment, but organization is 1:1 |
|
|
Term
| non-excitatory function of PSNS |
|
Definition
*"rest, recovery"
1. slow HR
2. GI secretions - increased motility
3. contraction of urinary bladder
4. contraction of the pupil (miosis)
5. accomodation for near vision (lens gets fatter)
6. bronchial constriction |
|
|
Term
| responses of organs to PSNS |
|
Definition
heart - decrease rate/strength
bronchial muscle - contraction
salivary glands - secretions (mucous)
intestinal muscle - contraction
urinary bladder muscle - contraction |
|
|
Term
| communication between pre- and post-ganglionic neurons initiated by |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| PSNS pre- and post-ganglionic NT |
|
Definition
|
|
Term
| *5 steps of neurotransmission |
|
Definition
1. synthesis of transmitter chemical (in the pre-junctional neuron)
2. storage of transmitter chemical
3. release of transmitter in response to depolarization
4. diffusion of transmitter to the effector membrane
5. termination of action of NT |
|
|
Term
|
Definition
1. occurs in the cytoplasm of cholinergic nerves by esterification of choline with acetic acid donated by acetylchoenzyme A (acetyl CoA) in a reaction catalyzed by choline acetyltransferase
2. choline is derived from extracellular sources and taken up actively into the nerve terminal
3. after synthesis - Ach is stored in secretory vesicles |
|
|
Term
| besides AchE - also catalyze hydrolysis of Ach |
|
Definition
| non-specific plasma cholinesterases |
|
|
Term
| inactivates Ach within the synapse |
|
Definition
|
|
Term
| where is acetylcholinesterase found in high concentrations? |
|
Definition
| *cholingergic ganglionic synapses and cholinergic neuroeffector junctions |
|
|
Term
|
Definition
| *rapidly cleaves ester function of Ach - in 100 microsecs it converts Ach to acetic acid and choline |
|
|
Term
|
Definition
| transported into the pre-ganglionic fiber |
|
|
Term
58 year old man
ER - chest pain that began 1 hr before; described as severe, dull, and pressure-like; substernal in location, radiates to both shoulders, a/w SOB; sweaty when pain began
patient has diabetes, HTN
takes hydrocholorothiazide and glyburide
BP 150/100; HR 95; RR 20/min; temp 37.3; O2 98%
patient is diaphoretic and appears anxious
auscultation - faint crackles at both lung bases
cardiac exam - S4 gallop; otherwise normal
abdomen - no masses or tenderness
EKG is performed
what is the most likely diagnosis? |
|
Definition
acute MI, probably anterolateral
58 year old man - presenting with acute severe chest pain, diaphoresis, and dyspnea; has a number of risk factors for underlying CAD |
|
|
Term
58 year old man
ER - chest pain that began 1 hr before; described as severe, dull, and pressure-like; substernal in location, radiates to both shoulders, a/w SOB; sweaty when pain began
patient has diabetes, HTN
takes hydrocholorothiazide and glyburide
BP 150/100; HR 95; RR 20/min; temp 37.3; O2 98%
patient is diaphoretic and appears anxious
auscultation - faint crackles at both lung bases
cardiac exam - S4 gallop; otherwise normal
abdomen - no masses or tenderness
EKG is performed
what therapies should be instituted immediately? |
|
Definition
aspirin is most important
O2, sublingual nitroglycerin, thrombolysis
decrease workload of heart (myocardial O2 consumption) is 1st goal - use beta blockers
nitroglycerin, herparin, clopidogrel (anti-platelet) |
|
|
Term
| long pre-, short post-ganglionic axon |
|
Definition
|
|
Term
| short pre-, ends in paravertebral ganglion, lots of collaterals, long post-ganglionic axon |
|
Definition
|
|
Term
| NT from the chromaffin cells of the adrenal gland |
|
Definition
|
|
Term
| when is epi released from adrenal medulla? |
|
Definition
|
|
Term
| why is epi not the prototypical NT in SNS? |
|
Definition
| nerves don't have enzyme necessary to make epi from NE |
|
|
Term
| what organ has dual innervation and what are the effects? |
|
Definition
heart
SNS increase HR and CO
PSNS decrease HR and CO |
|
|
Term
| what are 2 examples of single innervation and what are they innervated by? |
|
Definition
kidney - GFR is primarily controlled by SNS acting in afferent arteriole
peripheral resistance vessels/arterioles - primarily SNS |
|
|
Term
| what is an example of dual innervation with parallel function and what are the effects? |
|
Definition
| salivary glands - both arms increase production but composition is different |
|
|
Term
| SNS constriction response of arterioles mediated by |
|
Definition
|
|
Term
| constriction of arteriole |
|
Definition
1. provides pressure mechanism that will send blood downstream to organs
2. maintains pressure
3. divert blood from organ
constrict aorta - after-load increases to heart |
|
|
Term
| effect of 'stiffening' veins |
|
Definition
| don't constrict - would cause edema stiffen - become less compliant net effect - causes blood flow back to heart to increase; increases CO by stretching ventricle; increases preload |
|
|
Term
| ion that maintains resting membrane potential |
|
Definition
|
|
Term
| ion that causes depolarizing current |
|
Definition
|
|
Term
| communication between pre- and post-ganglionic neurons requires |
|
Definition
| requires release of Ach - for both SNS and PSNS |
|
|
Term
| communication between pre- and post-ganglionic neurons is propagated by |
|
Definition
| Ach-induced depolarization of the post-ganglionic neuron |
|
|
Term
| synthesis of Ach occurs in |
|
Definition
|
|
Term
| synthesis of Ach occurs by |
|
Definition
| esterification of choline with acetic acid |
|
|
Term
| what is acetic acid donated from in the synthesis of Ach? |
|
Definition
| acetylcoenzyme A (acetyle CoA) |
|
|
Term
| synthesis of Ach catalyzed by |
|
Definition
| choline acetyltransferase |
|
|
Term
| choline is derived from ___ and taken up actively into ___ |
|
Definition
| extracellular sources; nerve terminal |
|
|
Term
| after synthesis, Ach is stored in |
|
Definition
|
|
Term
| mechanisms of inactivation of Ach |
|
Definition
1. enzymatic degradation
2. spillover |
|
|
Term
|
Definition
| diffusion of NT from the junctional region to enter the bloodstream |
|
|
Term
| efficiency of non-specific plasma cholinesterases |
|
Definition
also catalyze hydrolysis of Ach
not sufficient to terminate synaptic transmission |
|
|
Term
| enzymatic hyrolysis of Ach occurs in how many steps |
|
Definition
|
|
Term
| first step of enzymatic hydrolysis of Ach |
|
Definition
| Ach interacts with the active sites of AchE by binding the positively charged ammonium head of Ach at the anionic site and by binding the carbonyl carbon at the esteric site |
|
|
Term
| second step of enzymatic hydrolysis of Ach |
|
Definition
hydrolysis of the ester function occurs quickly - freeing the choline portion of the molecule but leaving the acetate portion briefly attached to the esteratic site of the enzyme
the enzyme is momentarily acetylated |
|
|
Term
| third step of enzymatic hydrolysis of Ach |
|
Definition
| the acetate residue is then hydrolyzed - leaving the free enzyme active site and acetic acid |
|
|
Term
| product of hydrolysis of the ester of Ach |
|
Definition
|
|
Term
| norepinephrine is made from |
|
Definition
|
|
Term
| rate limiting enzyme in synthesis of NE |
|
Definition
|
|
Term
| SNS post-ganglionic axons don't have ___ which is why they can't make epi from NE |
|
Definition
| phenyl-n-methyl transferase (PNMT) |
|
|
Term
| cells that have PMNT; allows them to convert NE to epi |
|
Definition
| chromaffin cells in the adrenal medulla |
|
|
Term
| 3 mechanisms of inactivation of NE |
|
Definition
1. uptake 1 and enzymatic degradation by MAO
2. uptake 2 and enzymatic degradation by MAO or COMT
3. spillover |
|
|
Term
| inactivation of NE by uptake 1 |
|
Definition
neuronal transport system transports NE from extracellular fluid across the neuronal (axoplasmic) membrane into the cytoplasm of the nerve.
a vesicle or granule transport system transports the NE from the cytoplasm to storage vesicles. |
|
|
Term
| enzymatic inactivation of NE |
|
Definition
once taken up by uptake 1 pathway - some cytoplasmic NE in sympathetic nerve varicosity passively enters local mitochondria
in mitochondria - NE is oxidatively deaminated (inactivated) by monoamineoxidase (MAO) |
|
|
Term
| location of inactivation of NE by MAO |
|
Definition
|
|
Term
| inactivation of NE by uptake 2 |
|
Definition
effector cells take up NE - can also be inactivated by MAO
effector cells also contain catechol-O-methyl transferase (COMT) which donates a methyl group to form a ring methyoxyl analog of NE |
|
|
Term
| 2 enzymes that degrade NE after uptake 2 in effector cells |
|
Definition
|
|
Term
| diffusion of NT from the junctional region to enter the bloodstream |
|
Definition
|
|
Term
| too much NE or Ach causes |
|
Definition
|
|
Term
19 year old; 70 kg Lebanese female admitted for routine breast lump excision pre-operatively assessed as ASA grade 1 - no previous anesthetic experience no meds; no family history of anesthetic problems anesthesia was induced with propofol (short acting sedative), fentanyl (rapid acting opioid), and mivacurium (NM block); intubated uneventfully; anesthesia was followed with boluses of mivacurium at 7 and 16 mins after the initial dose supplements were given without waiting for recovery of muscle activity - O2, NO (anesthetic and analgesic), increments of propofol surgery was completed uneventfully in 25 min, 1 hour after onset of anesthesia patient did not recover muscle function despite discontinuation of anesthetics - declared to have prolonged muscle paralysis one hr after last dose of mivacurium - reversal was attempted with neostigmine (AchE inhibitor; prevent degradation of endogenous Ach) and atropine (muscarinic receptor blocker; prevents other effects of Ach); and again 1 hr later at higher doses ventilated with O2, NO and increments of midazolam (benzodiazepine derivative; keep patient unaware of what's going on) serum electrolytes - normal no recovery until 300 mins after last dose of mivacurium - some response noted as weak spontaneous resp efforts full recovery occurred with sustained and good resp activity; extubated suscessfully at 360 mins from start of procedure plasma cholinesterase level - 4795 IU (normal 7000-19000)
what was the diagnosis? |
|
Definition
pseudocholinesterase deficiency
can be given in presence of genetic abnormalities of plasma cholinesterase in patients who are hetero or homozygous for atypical plasma cholinesterase gene *plasma cholinesterase is important |
|
|
Term
| what determines half life of mivacurium, a nicotinic blocker? |
|
Definition
AchE or plasma cholinesterase
most drugs - kidney or CYPs |
|
|
Term
19 year old; 70 kg Lebanese female
admitted for routine breast lump excision
pre-operatively assessed as ASA grade 1 - no previous anesthetic experience
no meds; no family history of anesthetic problems
anesthesia was induced with propofol (short acting sedative), fentanyl (rapid acting opioid), and mivacurium (NM block); intubated uneventfully; anesthesia was followed with boluses of mivacurium at 7 and 16 mins after the initial dose
supplements were given without waiting for recovery of muscle activity - O2, NO (anesthetic and analgesic), increments of propofol
surgery was completed uneventfully in 25 min, 1 hour after onset of anesthesia
patient did not recover muscle function despite discontinuation of anesthetics - declared to have prolonged muscle paralysis
one hr after last dose of mivacurium - reversal was attempted with neostigmine (AchE inhibitor; prevent degradation of endogenous Ach) and atropine (muscarinic receptor blocker; prevents other effects of Ach); and again 1 hr later at higher doses
ventilated with O2, NO and increments of midazolam (benzodiazepine derivative; keep patient unaware of what's going on)
serum electrolytes - normal
no recovery until 300 mins after last dose of mivacurium - some response noted as weak spontaneous resp efforts
full recovery occurred with sustained and good resp activity; extubated suscessfully at 360 mins from start of procedure
plasma cholinesterase level - 4795 IU (normal 7000-19000)
what initiates muscle contraction? |
|
Definition
|
|
Term
19 year old; 70 kg Lebanese female
admitted for routine breast lump excision
pre-operatively assessed as ASA grade 1 - no previous anesthetic experience
no meds; no family history of anesthetic problems
anesthesia was induced with propofol (short acting sedative), fentanyl (rapid acting opioid), and mivacurium (NM block); intubated uneventfully; anesthesia was followed with boluses of mivacurium at 7 and 16 mins after the initial dose
supplements were given without waiting for recovery of muscle activity - O2, NO (anesthetic and analgesic), increments of propofol
surgery was completed uneventfully in 25 min, 1 hour after onset of anesthesia
patient did not recover muscle function despite discontinuation of anesthetics - declared to have prolonged muscle paralysis
one hr after last dose of mivacurium - reversal was attempted with neostigmine (AchE inhibitor; prevent degradation of endogenous Ach) and atropine (muscarinic receptor blocker; prevents other effects of Ach); and again 1 hr later at higher doses
ventilated with O2, NO and increments of midazolam (benzodiazepine derivative; keep patient unaware of what's going on)
serum electrolytes - normal
no recovery until 300 mins after last dose of mivacurium - some response noted as weak spontaneous resp efforts
full recovery occurred with sustained and good resp activity; extubated suscessfully at 360 mins from start of procedure
plasma cholinesterase level - 4795 IU (normal 7000-19000)
what causes paralysis? |
|
Definition
| sustained inhibition of nicotinic receptor |
|
|
Term
| 19 year old; 70 kg Lebanese female admitted for routine breast lump excision pre-operatively assessed as ASA grade 1 - no previous anesthetic experience no meds; no family history of anesthetic problems anesthesia was induced with propofol (short acting sedative), fentanyl (rapid acting opioid), and mivacurium (NM block); intubated uneventfully; anesthesia was followed with boluses of mivacurium at 7 and 16 mins after the initial dose supplements were given without waiting for recovery of muscle activity - O2, NO (anesthetic and analgesic), increments of propofol surgery was completed uneventfully in 25 min, 1 hour after onset of anesthesia patient did not recover muscle function despite discontinuation of anesthetics - declared to have prolonged muscle paralysis one hr after last dose of mivacurium - reversal was attempted with neostigmine (AchE inhibitor; prevent degradation of endogenous Ach) and atropine (muscarinic receptor blocker; prevents other effects of Ach); and again 1 hr later at higher doses ventilated with O2, NO and increments of midazolam (benzodiazepine derivative; keep patient unaware of what's going on) serum electrolytes - normal no recovery until 300 mins after last dose of mivacurium - some response noted as weak spontaneous resp efforts full recovery occurred with sustained and good resp activity; extubated suscessfully at 360 mins from start of procedure plasma cholinesterase level - 4795 IU (normal 7000-19000) how does mivacurium act? |
|
Definition
| competitive inhibition of nicotinic receptor |
|
|
Term
19 year old; 70 kg Lebanese female
admitted for routine breast lump excision
pre-operatively assessed as ASA grade 1 - no previous anesthetic experience
no meds; no family history of anesthetic problems
anesthesia was induced with propofol (short acting sedative), fentanyl (rapid acting opioid), and mivacurium (NM block); intubated uneventfully; anesthesia was followed with boluses of mivacurium at 7 and 16 mins after the initial dose
supplements were given without waiting for recovery of muscle activity - O2, NO (anesthetic and analgesic), increments of propofol
surgery was completed uneventfully in 25 min, 1 hour after onset of anesthesia
patient did not recover muscle function despite discontinuation of anesthetics - declared to have prolonged muscle paralysis
one hr after last dose of mivacurium - reversal was attempted with neostigmine (AchE inhibitor; prevent degradation of endogenous Ach) and atropine (muscarinic receptor blocker; prevents other effects of Ach); and again 1 hr later at higher doses
ventilated with O2, NO and increments of midazolam (benzodiazepine derivative; keep patient unaware of what's going on)
serum electrolytes - normal
no recovery until 300 mins after last dose of mivacurium - some response noted as weak spontaneous resp efforts
full recovery occurred with sustained and good resp activity; extubated suscessfully at 360 mins from start of procedure
plasma cholinesterase level - 4795 IU (normal 7000-19000)
how is mivacurium cleared? |
|
Definition
| hyrolysis by plasma cholinesterases |
|
|
Term
19 year old; 70 kg Lebanese female admitted for routine breast lump excision pre-operatively assessed as ASA grade 1 - no previous anesthetic experience no meds; no family history of anesthetic problems anesthesia was induced with propofol (short acting sedative), fentanyl (rapid acting opioid), and mivacurium (NM block); intubated uneventfully; anesthesia was followed with boluses of mivacurium at 7 and 16 mins after the initial dose supplements were given without waiting for recovery of muscle activity - O2, NO (anesthetic and analgesic), increments of propofol surgery was completed uneventfully in 25 min, 1 hour after onset of anesthesia patient did not recover muscle function despite discontinuation of anesthetics - declared to have prolonged muscle paralysis one hr after last dose of mivacurium - reversal was attempted with neostigmine (AchE inhibitor; prevent degradation of endogenous Ach) and atropine (muscarinic receptor blocker; prevents other effects of Ach); and again 1 hr later at higher doses ventilated with O2, NO and increments of midazolam (benzodiazepine derivative; keep patient unaware of what's going on) serum electrolytes - normal no recovery until 300 mins after last dose of mivacurium - some response noted as weak spontaneous resp efforts full recovery occurred with sustained and good resp activity; extubated suscessfully at 360 mins from start of procedure plasma cholinesterase level - 4795 IU (normal 7000-19000)
how does neostigmine act? |
|
Definition
| reversible cholinesterase inhibitor binds to and inactivates AchE |
|
|
Term
19 yo; 70 kg Lebanese female.
admitted for routine breast lump excision.
pre-operatively assessed as ASA grade 1 - no previous anesthetic experience no meds; no family history of anesthetic problems.
anesthesia was induced with propofol (short acting sedative), fentanyl (rapid acting opioid), and mivacurium (NM block); intubated uneventfully.
anesthesia was followed with boluses of mivacurium at 7 and 16 mins. after the initial dose supplements were given without waiting for recovery of muscle activity - O2, NO (anesthetic and analgesic), increments of propofol.
surgery was completed uneventfully in 25 min.
1 hour after onset of anesthesia patient did not recover muscle function despite discontinuation of anesthetics - declared to have prolonged muscle paralysis.
one hr after last dose of mivacurium - reversal was attempted with neostigmine (AchE inhibitor; prevent degradation of endogenous Ach) and atropine (muscarinic receptor blocker; prevents other effects of Ach); and again 1 hr later at higher doses.
ventilated with O2, NO and increments of midazolam (benzodiazepine derivative; keep patient unaware of what's going on).
serum electrolytes - normal.
no recovery until 300 mins after last dose of mivacurium - some response noted as weak spontaneous resp efforts.
full recovery occurred with sustained and good resp activity.
extubated sucessfully at 360 mins from start of procedure.
plasma cholinesterase level - 4795 IU (normal 7000-19000)
why was neostigmine administered? |
|
Definition
| given to increase Ach at the NMJ to compete with mivacurium |
|
|
Term
| 19 year old; 70 kg Lebanese female admitted for routine breast lump excision pre-operatively assessed as ASA grade 1 - no previous anesthetic experience no meds; no family history of anesthetic problems anesthesia was induced with propofol (short acting sedative), fentanyl (rapid acting opioid), and mivacurium (NM block); intubated uneventfully; anesthesia was followed with boluses of mivacurium at 7 and 16 mins after the initial dose supplements were given without waiting for recovery of muscle activity - O2, NO (anesthetic and analgesic), increments of propofol surgery was completed uneventfully in 25 min, 1 hour after onset of anesthesia patient did not recover muscle function despite discontinuation of anesthetics - declared to have prolonged muscle paralysis one hr after last dose of mivacurium - reversal was attempted with neostigmine (AchE inhibitor; prevent degradation of endogenous Ach) and atropine (muscarinic receptor blocker; prevents other effects of Ach); and again 1 hr later at higher doses ventilated with O2, NO and increments of midazolam (benzodiazepine derivative; keep patient unaware of what's going on) serum electrolytes - normal no recovery until 300 mins after last dose of mivacurium - some response noted as weak spontaneous resp efforts full recovery occurred with sustained and good resp activity; extubated suscessfully at 360 mins from start of procedure plasma cholinesterase level - 4795 IU (normal 7000-19000) how does atropine act? |
|
Definition
| muscarinic receptor antagonist |
|
|
Term
| 19 year old; 70 kg Lebanese female admitted for routine breast lump excision pre-operatively assessed as ASA grade 1 - no previous anesthetic experience no meds; no family history of anesthetic problems anesthesia was induced with propofol (short acting sedative), fentanyl (rapid acting opioid), and mivacurium (NM block); intubated uneventfully; anesthesia was followed with boluses of mivacurium at 7 and 16 mins after the initial dose supplements were given without waiting for recovery of muscle activity - O2, NO (anesthetic and analgesic), increments of propofol surgery was completed uneventfully in 25 min, 1 hour after onset of anesthesia patient did not recover muscle function despite discontinuation of anesthetics - declared to have prolonged muscle paralysis one hr after last dose of mivacurium - reversal was attempted with neostigmine (AchE inhibitor; prevent degradation of endogenous Ach) and atropine (muscarinic receptor blocker; prevents other effects of Ach); and again 1 hr later at higher doses ventilated with O2, NO and increments of midazolam (benzodiazepine derivative; keep patient unaware of what's going on) serum electrolytes - normal no recovery until 300 mins after last dose of mivacurium - some response noted as weak spontaneous resp efforts full recovery occurred with sustained and good resp activity; extubated suscessfully at 360 mins from start of procedure plasma cholinesterase level - 4795 IU (normal 7000-19000) why was atropine administered? |
|
Definition
| was given to increase Ach available to the NMJ to compete with mivacurium |
|
|
Term
| how does chemical neurotransmission occur? |
|
Definition
| through site specific expression of receptors |
|
|
Term
| nicotinic receptors are what type? |
|
Definition
| ligand gated ion channels |
|
|
Term
| adrenergic receptors are what type? |
|
Definition
| G-protein coupled receptors |
|
|
Term
| muscarinic receptors are what type? |
|
Definition
| G-protein coupled receptors |
|
|
Term
| which limb of the ANS do you target therapeutically? |
|
Definition
|
|
Term
| what is the structure of the ligand gated nicotinic receptor? |
|
Definition
| 5 subunits that form the receptor channel |
|
|
Term
| how does the nicotinic receptor work? |
|
Definition
Ach binds the ligand gated channel
it becomes a 'poor man's' Na channel - Na trickles through
depolarizes the membrane
activates fast Na channels
have fast Na entry and rapid depolarization
eventually activates Ca channels - Ca rushes in
vesicles are released at the synapse |
|
|
Term
| what are they 2 types of nicotinic receptors? |
|
Definition
nicotinic ganglionic - Ng
nicotinic muscular - Nm |
|
|
Term
|
Definition
| autonomic ganglia and adrenal medulla |
|
|
Term
| location of NM receptors? |
|
Definition
| NMJ - responsible for skeletal muscle contraction |
|
|
Term
| how do the Ng and Nm receptor differ? |
|
Definition
anatomically the same except for one subunit: 2 alpha, beta, delta +
Nm - epsilon
Ng - gamma |
|
|
Term
| when Ach binds nicotinic receptor, what ions move through the ion pore? |
|
Definition
|
|
Term
| drugs that inhibit Ng receptor block what? |
|
Definition
|
|
Term
| how does hexamethonium work and what is it used for? |
|
Definition
non-specific nicotinic blocker
used in HTN treatment |
|
|
Term
| phase 1 clinical trials, primary goal |
|
Definition
safety
non-specific drugs are potential disasters |
|
|
Term
| adrenergic G-protein coupled receptors |
|
Definition
|
|
Term
| cholinergic G-protein coupled receptors |
|
Definition
M1-M5 (1,2,3 most important)
bind Ach |
|
|
Term
| structure of G-protein coupled receptors |
|
Definition
7 transmembrane spanning domain
extracellular N- and intracellular C-terminus (cytosolic carboxy tail) |
|
|
Term
|
Definition
1. ligand binding activates heterotrimeric G proteins (G refers to GTP binding proteins)
2. heterotrimeric G proteins - comprised of a, B, and gamma subunits
3. GDP binds a - not B or g at rest
4. after ligand binding - GTP for GDP exchange occurs --> leads to dissociation of G protein from receptor
5. a subunit has bound GTP - dissociates from Bg complex
6. a-GTP and Bg - both signal inside the cell |
|
|
Term
| in all GPCRs, what initiates activation of heterotrimeric G proteins? |
|
Definition
|
|
Term
| what is the duration of the signal in GPCR signaling dependent on? |
|
Definition
how long GTP lasts
once GDP again --> its inactive and a binds back Bg |
|
|
Term
| how are G proteins named? |
|
Definition
| based on their biological function |
|
|
Term
| what are the 3 types of G proteins? |
|
Definition
|
|
Term
| what is the function of Gi? |
|
Definition
|
|
Term
| what is the function of Gs? |
|
Definition
stimulatory
increases cAMP |
|
|
Term
| what is the function of Gq? |
|
Definition
|
|
Term
| what receptors increase cAMP? |
|
Definition
|
|
Term
| which receptors are linked to Gs? |
|
Definition
|
|
Term
| what receptors decrease cAMP? |
|
Definition
|
|
Term
| which receptors are linked to Gi? |
|
Definition
|
|
Term
| what receptors increase Ca? |
|
Definition
|
|
Term
| which receptors are linked to Gq? |
|
Definition
|
|
Term
| vascoconstriction and bronchoconstriction are linked to which G protein? |
|
Definition
|
|
Term
| vasodilation and bronchodilation are linked to which G protein? |
|
Definition
|
|
Term
| B2 agonist effect in bronchioles |
|
Definition
|
|
Term
| a1 agonist in the BV causes |
|
Definition
|
|
Term
| what are 2 times you give a a1 agonist? |
|
Definition
hypotensive crisis in ICU
nasal stuffiness |
|
|
Term
| how is HR/strength of contraction of a cardiac myocyte determined? |
|
Definition
balance of SNS vs PSNS action
both B1 and M2 receptors
SNS - activate B1, increase cAMP via Gs, increase contractility, increase HR, increase CO
PSNS - activate M2, activates Gi, lowers cAMP, lower contraction strength, lower HR, decrease CO |
|
|
Term
| vaso-/veno- arterioles response to NE/epi |
|
Definition
|
|
Term
| skin arterioles response to NE/epi |
|
Definition
|
|
Term
| skeletal muscle arterioles response to NE/epi |
|
Definition
|
|
Term
| bronchial muscle response to NE/epi |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| increased force, rate - B1 |
|
|
Term
| intestine response to NE/epi |
|
Definition
|
|
Term
| pilomotor muscle response to NE/epi |
|
Definition
|
|
Term
| salivary glands response to NE/epi |
|
Definition
|
|
Term
| urinary bladder response to NE/epi |
|
Definition
|
|
Term
| site specific responses are mediated by? |
|
Definition
| receptor expression pattern |
|
|
Term
|
Definition
| decrease rate/strength - M2 |
|
|
Term
| bronchial muscle response to Ach |
|
Definition
|
|
Term
| salivary glands response to Ach |
|
Definition
|
|
Term
| intestinal muscle response to Ach |
|
Definition
|
|
Term
| urinary bladder muscle response to Ach |
|
Definition
|
|
Term
| smooth muscle contraction due to |
|
Definition
|
|
Term
| relaxation of smooth muscle due to |
|
Definition
|
|
Term
| response of Ca to increase cAMP in a smooth muscle? |
|
Definition
decrease Ca - leads to relaxation
heart is different |
|
|
Term
| response of Ca to increased cAMP in the heart? |
|
Definition
increase Ca
B1 --> Gs --> increase cAMP --> phosphorylates L channel --> Ca influx --> increase Ca in the heart --> contraction |
|
|
Term
| response of heart to binding of the M2 receptor? |
|
Definition
| lowers cAMP and therefore decreases Ca and contraction |
|
|
Term
|
Definition
| NE - B1 - Gs - cAMP - increase Ca - increase contraction strength |
|
|
Term
| response of bronchial smooth muscle to epi? |
|
Definition
| epi - B2 - Gs - increase cAMP - Ca decreases - relaxation |
|
|
Term
12 yo girl
presents - sore throat, fever
dx - pharyngitis caused by group A hemolytic strep
given IM injection of PCN
5 mins later - found in resp distress with audible wheezing, skin is mottled and cool, she is tachy and BP is 70/20
what is diagnosis? |
|
Definition
| anaphylactic allergic reaction |
|
|
Term
12 yo girl
presents - sore throat, fever
dx - pharyngitis caused by group A hemolytic strep
given IM injection of PCN
5 mins later - found in resp distress with audible wheezing, skin is mottled and cool, she is tachy and BP is 70/20
immediately give an injection of? |
|
Definition
|
|
Term
12 yo girl
presents - sore throat, fever
dx - pharyngitis caused by group A hemolytic strep
given IM injection of PCN
5 mins later - found in resp distress with audible wheezing, skin is mottled and cool, she is tachy and BP is 70/20
what effect does epi have on this patients vascular system? |
|
Definition
vasoconstriction
any BV dominated by a1 receptors constricts; b2 receptors dilate
net - increased BP and peripheral vascular resistance; HR increases, SV increases |
|
|
Term
12 yo girl
presents - sore throat, fever
dx - pharyngitis caused by group A hemolytic strep
given IM injection of PCN
5 mins later - found in resp distress with audible wheezing, skin is mottled and cool, she is tachy and BP is 70/20
which adrenoreceptor primarily mediates the vascular and resp response to epi? |
|
Definition
a1
BUT epi also get B2 going to skeletal muscle
airways dilate - B2 receptors; increase cAMP and decrease Ca |
|
|
Term
| effect of epi on patient with septic shock, persistent hypotension |
|
Definition
| constricts ateriolar smooth muscle via acting on a1 receptors |
|
|
Term
acute asthmatic attack
give epi subcutaneously
how does it dilate bronchiole SM? |
|
Definition
acts on B2 receptors to relax the bronchi
due to adverse CV effects of epi (B1), more selective B2 agonists are now used (albuterol) |
|
|
Term
| what is the cellular action of epi in heart and bronchial SM? |
|
Definition
| activation of adenylyl cyclase |
|
|
Term
| a2 receptor is physiologically activated by? |
|
Definition
|
|
Term
| epi's physiologically relevant receptors? |
|
Definition
|
|
Term
| epi mediated B1 activation results in? |
|
Definition
|
|
