sept viva Flashcards
(259 cards)
intralipid contents
Intralipid, which is an emulsion of soy bean oil, egg phospholipids and glycerin,
LA tox risk
LA drug factors Pr B and affinity to NaCH and pregame’s, acid, renal, hep
prev LA tox
USS
monitor
awake
test dose
AFOI blcok
Glossopharyngeal not oropharyngeal.
LA tox ecg
sinus bradycardia, intracardiac conduction defects (prolonged PR & QRS complex), ventricular arrhythmias, cardiac arrest.
Desc pain
PAG–>RVM–>DH
LC–>DH
Rexed Laminae
The Rexed laminae comprise a system of ten layers of grey matter (I–X),
P+H
Adelta–>laminae 2,5
C fibers–>2
The substantia gelatinosa is one point (the nucleus proprius being the other) where first order neurons of the spinothalamic tract synapse. (laminae II)
Many μ and κ-opioid receptors, presynaptic and postsynaptic, are found on these nerve cells;
gate theory
Ab touch and desc inhib in SUBSTANTIAL GENATINOSA (lamina II of DH)
glucose uptake
Glut1 the 1 most important thing so brain
Glut 2 food panc and hep
Glut 4 is lock in door (insulin dep)
BMR measurement
heat or indirect calaromitery
atp production cellular respiration
google
atp production cellular respiration
RB pyruvate oxidation CO2 prod
fatty acid
Fats into fatty acids and glycerol
ketogen
Fatty acid–>acetylcoa (b oxidation)
aceytl coa–>acetone, acetoacetate and betahydroxybutyrate via 3 steps including HMG coa synthase
When the body has no free carbohydrates available, fat must be broken down into acetyl-CoA in order to get energy. Under these conditions, acetyl-CoA cannot be metabolized through the citric acid cycle because the citric acid cycle intermediates (mainly oxaloacetate) have been depleted to feed the gluconeogenesis pathway. The resulting accumulation of acetyl-CoA activates ketogenesis.
Ketone bodies are produced mainly in the mitochondria of liver cells,
The production of ketone bodies is then initiated to make available energy that is stored as fatty acids. Fatty acids are enzymatically broken down in β-oxidation to form acetyl-CoA. Under normal conditions, acetyl-CoA is further oxidized by the citric acid cycle (TCA/Krebs cycle) and then by the mitochondrial electron transport chain to release energy. However, if the amounts of acetyl-CoA generated in fatty-acid β-oxidation challenge the processing capacity of the TCA cycle; i.e. if activity in TCA cycle is low due to low amounts of intermediates such as oxaloacetate, acetyl-CoA is then used instead in biosynthesis of ketone bodies via acetoacetyl-CoA and β-hydroxy-β-methylglutaryl-CoA (HMG-CoA). Furthermore, since there is only a limited amount of coenzyme A in the liver, the production of ketogenesis allows some of the coenzyme to be freed to continue fatty-acid β-oxidation.[8] Depletion of glucose and oxaloacetate can be triggered by fasting, vigorous exercise, high-fat diets or other medical conditions, all of which enhance ketone production
The three ketone bodies, each synthesized from acetyl-CoA molecules, are:
Acetoacetate, which can be converted by the liver into β-hydroxybutyrate, or spontaneously turn into acetone. Most acetoacetate is reduced to beta-hydroxybutyrate, which serves to additionally ferry reducing electrons to the tissues, especially the brain, where they are stripped back off and used for metabolism.
Acetone, which is generated through the decarboxylation of acetoacetate, either spontaneously or through the enzyme acetoacetate decarboxylase. It can then be further metabolized either by CYP2E1 into hydroxyacetone (acetol) and then via propylene glycol to pyruvate, lactate and acetate (usable for energy) and propionaldehyde, or via methylglyoxal to pyruvate and lactate.[10][11][12]
β-hydroxybutyrate
R quotient
CO2/R=0
CO2/O2=R
fat is .7 pr .8
feed COPD fat
stomach consumes CO2
lattent heat of…
melting
lattent TB= hidden
nicotine
Acute exposure to nicotine – HD effects last 1hr Abstinence cigarettes 12hrs – 10 - 20% increase in physical work capacity T ½ COHb 4 - 6hrs so overnight abstinence helpful (10hrs in men) Peak benefit re: upper airway irritability at 10 days (effects start at 48hrs)
Autonomic ganglia (N1 receptors) – blocked by hexamethonium 2. NMJ (N2 receptors) – blocked by tubocurarine 3. CN
Initial stimulation then persistent depression of autonomic ganglia
CNS stimulant
–
tremor
Increased ventilation v
ia nicotine stimulating aortic/carotid body chemoreceptors
CVS: tachycardia, hypertension, increased SVR (via SNS increase)
Resp: initial stimulation of saliva/bronchial secretions then inhibition
GI: PNS activation causing vomiting, diarrhoea
ADrenal medulla ADr release
sweat glands ANS
In sweat glands the receptors are of the muscarinic type.
isometric isotonic
ismetric–>nil external work–>100% energyoutput as heat
isotonic–>some external work–>50% heat loss
brown fat
uncouples oxidative phosphorylation
not dep on consumption of ATP for ATP
heat produced through chemical reaction without ATP needing to be utilised
COX pathway
Sm muscle–>PG
cycloendoperoxidase
nerve twitch face
orbicularis occuli
nerve monitory placement
Typically smaller muscle groups are more sensitive
The positive (red) lead is placed proximal
Ulnar nerve
Electrodes are placed along the ulnar border of the wrist at the flexor crease, and thumb adduction is assessed.
Facial nerve
The positive electrode is placed at the outer canthus, and the negative electrode is placed anterior to the tragus. Eyebrow twitching is assessed. orbicularis occuli
Posterior tibial nerve
Electrodes are placed posterior to the medial malleolus, and plantar flexion is assessed. posterior tib
r vs s
rectus right clock
sirrius anticlock
levo vs dextro
A dextrorotatory compound is a compound that rotates the plane of polarized light clockwise as it approaches the observer (to the right)
Dr X