week 7 ANS Flashcards
Foxglove plant
makes digoxin
Marijuana schedule
1
Teratogenic med=
could cause harm to fetus (cross placenta blood barrier) most effects during 1st trimester
ASD Atrial Septum Defect
blood shunt from hole in septum in between atrium
4 components of pharmacokinetics
absorption, Distribution, metabolism, Excretion
Pharmacodynmaics=
What med does in body
Pharmacokinetics=
What body does to med
Medication affinity=
force of attraction between medication & a receptor
Adrenergic receptors
Sympathetic receptors “adrenaline”
Chlorogenic receptors
Parasympathetic “C for Chill”
chronotropy=
Heart rate
dromotropy=
Heart’s Electrical impulse activity
Inotropy=
Ventricle squeeze strength
Neuron anatomy=
Soma, dendrites, axon, nucleus
Neuron Threshold:
Neuron Resting Potential:
Neuron Reversal of Charges:
Neuron Refractory period:
= -55mV
= -70mV
= +30mV
= goes more - than baseline before recovering
Neuron Depolarization:
Neuron Polarization:
=action up & -mV down
=going down & -mV up
Sodium effect on neuron:
Potassium effect on neuron:
:Depolarization
:Repolarization
BENZOs effect on neurons:
make cells more negative to slow down cells by binding to GABA sites
RAAS→ Renin-angiotensin-aldosterone system steps:
- reg/s cardiovascular system → make sure fluids there
- JG cells Juxtaglomerular granular cells= kidney cells
- kidneys send renin to liver angiotensin to form angiotensin 1
- angiotensin 1 flows around to heart to lungs for ACE to produce angiotensin 2 & aldosterone
RAAS→ Renin-angiotensin-aldosterone system in short
Kidneys monitor blood pressure (Low pressure = more renin & vice versa) & Angiotensin 2 to vasoconstrict produced from lungs
ACE inhibitors
“-Pril”s
Hypertension meds
EX lisinopril
Sympathetic NS adrenergic receptors:
ACh binds to Nn receptor preganglionic fiber & NORepi for postganglionic (only exception for sweating has ACh post ganglionic)
Albuterol:
B agonist w/ preference for B2 receptors, // indications: bronchospasm, allergies, hyperkalemia// Contraindication: hypersensitive, anxiety, dizzy/HA,
Terbutaline (Brethine):
B selective agonist relaxation w/ high affinity, can give to asthma dependent and/or heart prob PT // asthma, emphysema, preterm labor, reversible airway, //contraindication: same as albuterol & no pedis
EPI 1:1000:
potent A & B agonist // indications: bronchospams, anaphylaxis
Atropine:
Parasympatholytic & selectively blocks Muscarinic receptors inhibiting the parasympathic NS // contra: allergy, EXTREME CAUTION USE W/ MIs & hypoxia→ increase O2 med, avoid hypothermic (82degrees)
Ipratropium (Atrovent):
anticholinergic, selectively blocks Muscarinic receptors // ind: bronchospasm w/ obstructive lung diseases
Alpha 2 inhibits
Release of NORepi
parasympathetic cranial nerves:
3,7,9,10 cranium (10 prominent vagus nerve)
Parasympathetic neurotransmitter
acetylcholine post & pre ganglion
Lavine’s sign
clenching chest
Muscarinic 3-(5) receptors found in
M1: CNS, GI, salv glands
M2: SA & AV nodes
M3: Smooth Muscles
OD on parasympatholytic=
Anticholinergic Toxidrome→ “blind as a bat, Red as a beet, mad as a hatter”
Physostigmine medication .5mg/ml slow
Over stimulation of parasympathetic NS=
SLUDGEM Atropine to revese
Prototype=
medication that best demonstrates the class’s common properties & illustrates its particular characteristics.
Analgesic:
Anesthetic:
=medications that relieve the sensation of pain
=med that relieves ALL SENSATIONS
Endorphins:
= hormones that bind to opioid receptors aka natural painkillers
Opiate receptors physiology
different receptor→ different effect
Opiate receptor M1:
Opiate receptor M2:
Opiate receptor Kappa:
Opiate receptor Sigma:
Opiate receptor Epsilon:
Opiate receptor Delta:
=angelsia & euphoria
=respiratory & physical depression, miosis, less GI m-vt
= Analgesia, sedation, miosis, respiratory depression, dysphoria
=Psychotomimetic (i.e., hallucinations), dysphoria, possibly mydriasis
= Effects uncertain
=Analgesia, dysphoria, psychotomimetic effects (hallucinations), respiratory & vasomotor stimulation
Common non-opioid angelistics= 3 types of non-opioid med/s w/ analgesic & antipyretic (fever-fighting) properties:
=salicylates= EX aspirin
=Nonsteroidal anti-inflammatory drugs (NSAIDs)=EX ibuprofen,
=Para-aminophenol derivatives= acetaminophen.
Opioid agonist-antagonist=
have both agonistic & antagonistic properties. like opioids, decreases pain response, & antagonist b/c it has fewer respiratory depressant & addictive side effects
Neuroleptanesthesia
type of anesthetic that combines with effect of w/ amnesia (useful in procedures that require PT calm & responsive )
BENZOdiazepines:
frequently prescribed for oral use & are relatively safe & effective for treating general anxiety/insomnia
Barbiturate
have broader general depressant activities & a higher potential for abuse, are used much less frequently than benzodiazepines.
Both benzodiazepines & barbiturates effect on neuron:
hyperpolarize the membrane of CNS neurons, thus decreases response to stimuli.
Gamma-aminobutyric acid (GABA)=
Chief inhibitory neurotransmitter in the CNS.
GABA receptors location
dispersed through CNS on chloride ion channels in the cell membrane.
GABA receptors job:
- When combines w/ the receptors the channel “opens”
- chloride diffuses & B/c is a anion (neg/ ion),makes inside of cell more negative than the outside.
- Thus hyperpolarizes membrane making more difficult to depolarize
- Depolarization therefore requires larger stim/ to cause cell to fire
Benzodiazepines & Barbiturates
increase GABA receptor–chloride ion channel affinity
Romazicon:
med that is competitive antagonist of Benzo’s
Phenytoin (Dilantin) & Carbamazepine (Tegretol)
=inhibit sodium influx decreasing cell’s ability to depolarize & propagate seizures.
Benzodiazepines & Barbiturates:
interact w/ GABA receptor–chloride ion channel complex
Valproic acid & Ethosuximide=Valproic acid & Ethosuximide=
inhibit influxation & interact w/ calcium channels in hypothalamus absence seizures typically begin.
Partial seizure meds:
Phenytoin
Carbamazepine
Oxacarbazepine
Felbamate
Lacosamide
Lamotrigene
Levetiracetam
Absent seizure meds:
Valproic acid
Ethosuximide
General seizure meds:
Carbamazepine
Phenytoin
Phenobarbital
Lamotrigene
Levetiracetam
Gabapentin
Amphetamines High-dose pharmacodynamics=
Can increase concentration of dopamine in synaptic cleft & similar effect on NORepi neurons; it can induce release of NORepi into the synaptic cleft & inhibit the norepinephrine reuptake transport
Methylxanthine pharmacodynamics=
unclear, but it seems to block adenosine receptors.
Mental dysfunction A&P:
= inbalance of monoamine neurotransmitters in CNS being: norepinephrine, dopamine, serotonin
Nicotinic Acetylcholine Receptors Muscle type location=
AMS type preganglion=
Anatomy L=
Agonist=
Antagonist=
=neuromuscular junction of skeletal (only) muscles
=parasympathetic ganglion
=Found on many neurons in the brain
=Nicotine is an agonist
=Curare is an antagonist
Muscarinic Acetylcholine Receptors Muscle type location=
AMS type preganglion=
Anatomy L=
Agonist=
Antagonist=
=neuromuscular junction of smooth & cardiac muscle
=sympathetic ganglion
=Found on glands
=Muscarine is an agonist
=Atropine is an antagonist
2 basic types of indirect-acting cholinergic med/s:
Reversible inhibitors pharmacodynamics:
Irreversible inhibitors pharmacodynamics:
= reversible inhibitors and irreversible inhibitors. Both bind w/ cholinesterase (ChE), acting as a substitute for ACh thus prevent ChE from destroying ACh.
=bound w/ ChE longer than ACh but eventually release it.
=Release cholinesterase but bound so long considered irreversible.
Atropa belladonna “nightshade” plant=
Creates atropine
hormones released by adrenal medulla=
80% Epi & 20% NORepi
Foxglove plant=
Digoxin
