Vivas Flashcards

(86 cards)

1
Q

Henry law

A

Amount dissolved prop to pp

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2
Q

Soda lime moety

A

Chf2->co

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3
Q

Marsh

A

V1 bigger and growing

Schneider fixed V1 with variable Ke AND V2

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4
Q

Pap and res

A

Pap decreases res!!!!

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5
Q

Res and frc

A

EA compressed in collapse

Pulmonary v collapses in distended

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6
Q

Onset volatile

A

RB fi and n20

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7
Q

Laser

A

Propofol dreams

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8
Q

Prrg resp

A

decreased RV+ERV=FRC and TLC

increased TV

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9
Q

Pain pathway

A

ascending primary is Dorsal root ganglion

descending

  • higher–>PAG–>RVM and Caudal raphe
  • higher–>locus ceruleus
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10
Q

site of SNS and PSNS heart

A

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.

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11
Q

transplanted heart

A

indirect wont work ephedrine and atropine

direct is EXAGGERATED due to increased rec density

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12
Q

Fat and washout

A

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.

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13
Q

spont breathing feedback volatile

A

negative resp

positive cvs- decreased CO–>increased FA:Fi–>decreased CO

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14
Q

Closing capacity

A

INCREASES with age. ie it closes earlier at a larger vol

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15
Q

Hydralazine up2date

A

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

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16
Q

labetalol up2date

A

onset 5min peak 10min

duration 16 hours

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17
Q

pneumoperitoneum and BP

A

gentle squeeze–>balanced–>excess squeeze

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18
Q

Na:K

A

3Na out 2K in

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19
Q

RMP of diff cells

A

SA -65mvol

skeletal m and cardiac -90

neuron -70

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20
Q

ionconductance in cardaic AP

A

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

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21
Q

T-ype Ca ch

A

only in pacemaker cells

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22
Q

Saltatory conduction

A

jump between insulating myelin (which would be slow) to nodes of ronvier
–>faster and more efficient

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23
Q

nerve fibre conduction

A

C-2m/s 0.5microm small unmyelinated
Ad-20m/s 5microm. large myelinated
Ab- touch myelinated

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24
Q

SA node as per POWER AND KAM

A

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

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25
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.
26
Goldman hodgekin katz
O-outside | I-inferior
27
lipid raft
broken-->enzyme can act on substrate-->open K channel
28
GPCR enzyme
GDP-->GTP alphaGTP-->target either AC or PLC PLC PIP->IP3+DAG-->PKC
29
ATP prod
atp synthase
30
How anaesthetics work
1)classic lipid theory increased MW-->increased sol to ceiling 2a) modern lipid theory: crowded 2b) hydrophobic pr b
31
why prod lactate
glycolysis NAD-->NADH | pyruvate-->lactate NADH-->NAD
32
mitochonidrae
1) 2 layers of membrane | 2) cristea -->increased SA
33
23 DPG
produced in RBC in response to hypoxia and anaemia | release O2
34
Ach
acetic acid+choline
35
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)
36
PDEi
nonselective caffeine and theophylin -inodilator and BD Selective PDE3i- Milronone ino PDE5i- sildenofin-VD including pulm PDEi-dipyridamole
37
GPCR q i u
HAVE1 MM MAD2 rest
38
glyconeo
both renal excr
39
hyosine
HB cross BBB | Hyoscine butyl bromide doesnt cross
40
moxonidine, methyldopa
a2 ag
41
block alpha
phentolamine | prazosin
42
lipid sol and met and ellim GOLD
high lipid sol-->liver mer | low lipid sol GI absorption good-->renal excretion
43
BBlockers
``` aim for black sally with the salt and pepper AME B BLACK SAlly SP PPL AP ```
44
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
45
COMT
catechol o methyl transferase | change OH to CH3
46
MAO
Hydroxylates
47
ephedrine and pseudoephedrine
lipid sol so treat headache cold and flu
48
glom membrane charge
neg to repel Pr-
49
Hend hascel
ph=pka+log A-/HA
50
Pr binding acid base drugs
Alb bind acid and spill over base | alpha1 acid glycoprotein base
51
allosteric
bind at different site to cause change | eg benzo
52
NMDA rec
AMPA-glut | NK1-sub P
53
efficacy
Emax Intrinsic activity is a relative term for a drug's efficacy relative to a drug with the highest observed efficacy
54
Extraction ration
1-Conc out/Conc in ???? surely its (Ci-Co/Ci) (70-63)/70=10% ER
55
Elim
clearance.conc
56
Vd 3 measures
1) extrap 2) AUC -AUC=x/cl -t/2elim=vd.0.693/cl 3)Vss Vd=Cl.MRT (from AUC model)
57
ketamine binding site
phenyl cyclidine protien binding site PCP site | allosteric binding site (separate from glut and glycine)
58
flecanide
1c) nil change to ARP slowed conduction decreased excitability rate rependant blockade on NaCh-->breaky tachyarrhthmia
59
correlation between AP and ECG
#evernote
60
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
61
ketamine met
CYP450 demethylated and hydroxylated to norket 1/3 active-->gluronation-->inactive met peed out
62
OBA
ab.(1-ER)
63
ER
1-out/in
64
Vd measure 3
1,2,3
65
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
66
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
67
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−
68
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
69
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
70
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)
71
ABG PH measure and issues | GOLD core
http://www.partone.lifeinthefastlane.com/blood_gases.html
72
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.
73
PL store
22C 5 days aggitate
74
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
75
Phenothiazine
prochlorperazine ie stemetil DA 1st hist and chol highest EPSE-->dystonia drowsy
76
ondans SE
consitpation HA Qtc
77
Droperidol
butyrophenones 0.25mg dose SE -hyperprolactin hep emt 1% renal excretion unchanged
78
metoclopramide
DA and 5HT NNT=30! OBA 30-90% arrhythmia and hypotension with bolus
79
Dex MoA
endorphin-->mood antiinflam-->reduced 5hT release in gut ENTEROCHROFFIN CELLS prostaglanin antag steroids stimulate lipocortin-->suppress PLA2 (first step in prostaglandin synth)!
80
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
81
aprepitant
NK! antag (bind sub P)
82
nabilone
CB1 rec ag (periph and central
83
maoI
SERLEGELINE FOR pdX IS MAOB SO IS OK ANTIDEPRESSANT mao-->risk cease on DOS -beware indirect agent-->prolonged intense effect
84
H1 rec
``` first gen -phenergen second gen -loratadine -less antichol sedatin effects ```
85
class 1 drugs
a prolong procaaaaaainomide b shortens phenytoin and lig c nil flecainide
86
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,