Vivas Flashcards
Henry law
Amount dissolved prop to pp
Soda lime moety
Chf2->co
Marsh
V1 bigger and growing
Schneider fixed V1 with variable Ke AND V2
Pap and res
Pap decreases res!!!!
Res and frc
EA compressed in collapse
Pulmonary v collapses in distended
Onset volatile
RB fi and n20
Laser
Propofol dreams
Prrg resp
decreased RV+ERV=FRC and TLC
increased TV
Pain pathway
ascending primary is Dorsal root ganglion
descending
- higher–>PAG–>RVM and Caudal raphe
- higher–>locus ceruleus
site of SNS and PSNS heart
The heart is innervated by vagal and sympathetic fibers. The right vagus nerve primarily innervates the SA node, whereas the left vagus innervates the AV node; however, there can be significant overlap in the anatomical distribution. Atrial muscle is also innervated by vagal efferents, whereas the ventricular myocardium is only sparsely innervated by vagal efferents. Sympathetic efferent nerves are present throughout the atria (especially in the SA node) and ventricles, including the conduction system of the heart.
transplanted heart
indirect wont work ephedrine and atropine
direct is EXAGGERATED due to increased rec density
Fat and washout
Summary:
complex, depends on O:G sol, duration, protected airway, balance of somethings that make it faster and some that make it slower, clinically insig with modern agents.
ANZCA primary lecture:
decreased FRC and increase MV—>fast wash in (foundational anaesthesia and phys and pharm book agree)
T/2=vol.sol/q=2110min for iso
Studies show nil clinical sig diff.
Foundational anaesthesia:
Right to left shunt slows wash-in (as would happen with reduced FRC) net:net decreased FRC in obese–>faster not slower as per text
Examiners report:
Increased CO—>slow
Duration relevant
O:G relevant
Katherine (Fellow):
Shunt–>slow
Millers:
Decrease TV due to poor compliance
CC>FRC—>shunt
Obese—>upper airway collapse
Ketamine nightmares: short case—>quicker as distributed, long case longer (perhaps for old very sol drugs)
PD and AD: nil answer
Summary:
complex, depends on O:G sol, duration, protected airway, balance of somethings that make it faster and some that make it slower, clinically insig with modern agents.
spont breathing feedback volatile
negative resp
positive cvs- decreased CO–>increased FA:Fi–>decreased CO
Closing capacity
INCREASES with age. ie it closes earlier at a larger vol
Hydralazine up2date
PO or IV with 30% OBA
for HTN, PET, CCF
onset 15min for 4hours
liver met with renal excretion of 50% of unchanged
SE CBF increased, flush headache, sweat, N+V
angina can occur
labetalol up2date
onset 5min peak 10min
duration 16 hours
pneumoperitoneum and BP
gentle squeeze–>balanced–>excess squeeze
Na:K
3Na out 2K in
RMP of diff cells
SA -65mvol
skeletal m and cardiac -90
neuron -70
ionconductance in cardaic AP
google CV phys
y axis is membran perm o at axis with nil crossing below
-90–>threshold and -70
K+ conductance blocked in phase 0 with opening of VDNaCH (as Na flows in less neg–>more Na in–>less neg)
Kt0 open in phase 1–>K+out transient and fast rapid drop in conductance of Na before Ca fully kicks in causes a drop too
L-type not T-type involved in 2 at -40mV
-unique to cardiac M
VDNaCH-open at threshold
-resting–>active–>inactive–>transient effect
-activation gate opened on stim
-inactivation gate closes shortly after
-reactivated once repol
once Ca Channels close after 200ms they can exert there unopposed effect to repolarise.
nerves don’t have the Ca ch for plateu!!!!!!
refractory period caused by
1) slow ca2+ maintaining Ca inflow against Koutflow
200ms ARP
50s RRP
T-ype Ca ch
only in pacemaker cells
Saltatory conduction
jump between insulating myelin (which would be slow) to nodes of ronvier
–>faster and more efficient
nerve fibre conduction
C-2m/s 0.5microm small unmyelinated
Ad-20m/s 5microm. large myelinated
Ab- touch myelinated
SA node as per POWER AND KAM
phase 4:
funny current–>Na influx
AND less K perm–>K not as effective leaking out
AND t-Ca ch leak in
phase 0
Ca t
Phase 3
Na and Ca deactived by positve membrane
K perm increased by positive memb
ANS SA
PSNS increased K perm–>hyperpol
SNS phase four quicker. This occurs by increasing If (“funny” pacemaker currents) and increasing slow inward Ca++ currents. Sympathetic activation also lowers the threshold for initiating phase 0 of the action potential.
Goldman hodgekin katz
O-outside
I-inferior
lipid raft
broken–>enzyme can act on substrate–>open K channel
GPCR enzyme
GDP–>GTP
alphaGTP–>target either AC or PLC
PLC
PIP->IP3+DAG–>PKC
ATP prod
atp synthase
How anaesthetics work
1)classic lipid theory
increased MW–>increased sol to ceiling
2a) modern lipid theory: crowded
2b) hydrophobic pr b
why prod lactate
glycolysis NAD–>NADH
pyruvate–>lactate NADH–>NAD
mitochonidrae
1) 2 layers of membrane
2) cristea –>increased SA
23 DPG
produced in RBC in response to hypoxia and anaemia
release O2
Ach
acetic acid+choline
excitation contraction skeletal
2 ach. Ligand gate cationic ch–>depol–>AP–>T tubule–>VDCaCh–>ryanodine rec on SR–>Ca
ca binds to troponin C –>move tropomysin on actin–>expose myosin binding site
ca pumped back into SR actively by ryanodine 1 rec (#MH)
PDEi
nonselective caffeine and theophylin
-inodilator and BD
Selective
PDE3i- Milronone ino
PDE5i- sildenofin-VD including pulm
PDEi-dipyridamole
GPCR q i u
HAVE1 MM
MAD2
rest
glyconeo
both renal excr
hyosine
HB cross BBB
Hyoscine butyl bromide doesnt cross
moxonidine, methyldopa
a2 ag
block alpha
phentolamine
prazosin
lipid sol and met and ellim
GOLD
high lipid sol–>liver mer
low lipid sol GI absorption good–>renal excretion
BBlockers
aim for black sally with the salt and pepper AME B BLACK SAlly SP PPL AP
burns Nach
GBS vs MG
Normal is 2abde
extrajunctional is 2abdg
denervation, GBs stroke, M dystrophy, burns >24hrs
Myasthenia=muscle weakness Gravis= grave
AI antibodies block or destroy NAChR at NMJ
-Think Myastenia—>muscle
GBS
-AI attach of peripheral nerves
—>raised potassium with SUX
-think Succy Syndrome
COMT
catechol o methyl transferase
change OH to CH3
MAO
Hydroxylates
ephedrine and pseudoephedrine
lipid sol so treat headache cold and flu
glom membrane charge
neg to repel Pr-
Hend hascel
ph=pka+log A-/HA
Pr binding acid base drugs
Alb bind acid and spill over base
alpha1 acid glycoprotein base
allosteric
bind at different site to cause change
eg benzo
NMDA rec
AMPA-glut
NK1-sub P
efficacy
Emax
Intrinsic activity is a relative term for a drug’s efficacy relative to a drug with the highest observed efficacy
Extraction ration
1-Conc out/Conc in
????
surely its (Ci-Co/Ci)
(70-63)/70=10% ER
Elim
clearance.conc
Vd 3 measures
1) extrap
2) AUC
-AUC=x/cl
-t/2elim=vd.0.693/cl
3)Vss
Vd=Cl.MRT (from AUC model)
ketamine binding site
phenyl cyclidine protien binding site PCP site
allosteric binding site (separate from glut and glycine)
flecanide
1c) nil change to ARP
slowed conduction
decreased excitability
rate rependant blockade on NaCh–>breaky tachyarrhthmia
correlation between AP and ECG
evernote
amiodarone
met and elim
class 1,2,3,4 -partial a and beta agonist active metabolite frome liver excreted in bile elim-bile! hence fine in CKD WPW
SE
neuropathy, thyroid, photosens, GI
CI in porphoria
ketamine met
CYP450 demethylated and hydroxylated to norket 1/3 active–>gluronation–>inactive met peed out
OBA
ab.(1-ER)
ER
1-out/in
Vd measure 3
1,2,3
paramegnetic O2
mainstay ;)
2 unpaired electrons in outer orbit (attracted to EMF (volatiles etc repelled)
insp and exp limb
lasts for ages
fast
water fucks with it and all O2 measuring techniques require claibration
glavanic Fuel cell
GOLD
OXIDATION OF LEAD
#godlen rig RIG at anode (+) #derrangedphys O2+ e- —>OH-
Lead gets oxidised at cathode (-)
OIL
OH- +Pb—>PbO H2O + e-
The redox reaction requires a reagent, which gradually becomes depleted, and this means the oxygen cell needs to be replaced regularly
Clark electrode LITFL
Mr’s clarke has silver hair.
A voltage of 0.6V is applied across the electrodes, causing the silver to reactive with chloride in the solution to produce electrons:
Ag+Cl−⇒AgCl+e−
This potential difference is required to start the reaction
0.6V is chosen because it is enough to start the reaction but will have minimal effect on measured current flow
At the cathode, oxygen combines with electrons and water to produce hydroxyl ions: O2+4e−+2H2O⇒4OH−
anaesthetic gas analysis
IR (CO2, anaesthetic vapours and N2O, NIL O2)
The amplitude of the spectral shape represents the amount of vapour present in the mixture. The amplitude is inversely proportional to the amount of agent present.
peizoelectric quarts crystal oscillation (volatile only)
- lipid sol anaesthetic agents alter resonant freq of crystals
- non specific to differenet agents
raman scattering (o2 co2, anaesthetic gas and vapour) -argon laser-->90 degree scattering of different energy of light. each agent has a different characteristic property
mass spectrometry (02, CO2, anaesthetic gases and vapour)
- charge all particles with an e- beam in a vacuum
- magnet permanent
- now weight is the only determinant
- unique spectrum for each agent
ABG MEASUREMENT OF CO2
The Severinghaus electrode is a modified glass electrode;
The electrode contains some sodium bicarbonate, which reacts with the CO2;
The reaction changes the pH in the electrode, which corresponds to a change in potential difference, and this is measured.
The CO2 is then inferred from the change in pH.
reference electrode with nil CO2 exposure
ABG measurement of SaO2
spectrophotometric measurements (IR light absorption)
oxyHb/(oxyhb+deoxyhaemoglobin)
DANGER IS CO:Hb looks similar to O:Hb
OR calculated
-for given Po2 and pH
Partial pressure of O2 (pO2) is measured by amperometry by CLARKE ELECTRODE (LIFTL)
ABG PH measure and issues
GOLD core
http://www.partone.lifeinthefastlane.com/blood_gases.html
N20 ptx
The difference in the rate of increase in nitrous oxide concentration in the bowel compared with the pleural space was thought to be because of a greater blood flow to the pleura. The difference in the blood gas partition coefficient of nitrous oxide (0.46) and nitrogen (0.014) resulted in the preferential transfer of nitrous oxide into a compliant air filled cavity faster than nitrogen could exit.2 This is considered responsible for the rapid increase in size of a pneumothorax when a patient inspires a mixture of oxygen and nitrous oxide.
PL store
22C 5 days aggitate
Clonidine
Uses -shiver and prolong LA 0.5-1mcg/kg Onset 5 peak 25min Partial agonist NIL RESP DEP Rebound htn and transient rise Block adh block insulin Dry mouth common
Lipid sol–>well ab
50% hep met vs renal excretion unchanged
Prolonged in CKD
Phenothiazine
prochlorperazine ie stemetil
DA 1st hist and chol
highest EPSE–>dystonia
drowsy
ondans SE
consitpation HA Qtc
Droperidol
butyrophenones
0.25mg dose
SE
-hyperprolactin
hep emt
1% renal excretion unchanged
metoclopramide
DA and 5HT
NNT=30!
OBA 30-90%
arrhythmia and hypotension with bolus
Dex MoA
endorphin–>mood
antiinflam–>reduced 5hT release in gut ENTEROCHROFFIN CELLS
prostaglanin antag
steroids stimulate lipocortin–>suppress PLA2 (first step in prostaglandin synth)!
cyclizine
piperazine derive
antichol SE #confusion tachy
sedating mild
Met liver minimal 1% renal excretion
care in severe cardaic failure as HR–>decreased preload
CI in porphyria
aprepitant
NK! antag (bind sub P)
nabilone
CB1 rec ag (periph and central
maoI
SERLEGELINE FOR pdX IS MAOB SO IS OK
ANTIDEPRESSANT mao–>risk cease on DOS
-beware indirect agent–>prolonged intense effect
H1 rec
first gen -phenergen second gen -loratadine -less antichol sedatin effects
class 1 drugs
a prolong procaaaaaainomide
b shortens phenytoin and lig
c nil flecainide
antipsych
typical
-relatively DA specific eg halo and drop
Atypical
- more 5HT –>increased some DA activity–>less prolactinaemia and EPSE
- eg quetiapine and olansapine
- ->SE of antichol, alpha block,
