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Vivas Flashcards

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
Q

ANS SA

A

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.

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26
Q

Goldman hodgekin katz

A

O-outside

I-inferior

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27
Q

lipid raft

A

broken–>enzyme can act on substrate–>open K channel

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28
Q

GPCR enzyme

A

GDP–>GTP

alphaGTP–>target either AC or PLC

PLC
PIP->IP3+DAG–>PKC

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29
Q

ATP prod

A

atp synthase

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30
Q

How anaesthetics work

A

1)classic lipid theory

increased MW–>increased sol to ceiling

2a) modern lipid theory: crowded
2b) hydrophobic pr b

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31
Q

why prod lactate

A

glycolysis NAD–>NADH

pyruvate–>lactate NADH–>NAD

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32
Q

mitochonidrae

A

1) 2 layers of membrane

2) cristea –>increased SA

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33
Q

23 DPG

A

produced in RBC in response to hypoxia and anaemia

release O2

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34
Q

Ach

A

acetic acid+choline

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35
Q

excitation contraction skeletal

A

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
Q

PDEi

A

nonselective caffeine and theophylin
-inodilator and BD

Selective
PDE3i- Milronone ino
PDE5i- sildenofin-VD including pulm
PDEi-dipyridamole

37
Q

GPCR q i u

A

HAVE1 MM
MAD2
rest

38
Q

glyconeo

A

both renal excr

39
Q

hyosine

A

HB cross BBB

Hyoscine butyl bromide doesnt cross

40
Q

moxonidine, methyldopa

A

a2 ag

41
Q

block alpha

A

phentolamine

prazosin

42
Q

lipid sol and met and ellim

GOLD

A

high lipid sol–>liver mer

low lipid sol GI absorption good–>renal excretion

43
Q

BBlockers

A 
aim for black sally with the salt and pepper 
AME B
BLACK
SAlly
SP
PPL
AP
44
Q

burns Nach

GBS vs MG

A

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
Q

COMT

A

catechol o methyl transferase

change OH to CH3

46
Q

MAO

A

Hydroxylates

47
Q

ephedrine and pseudoephedrine

A

lipid sol so treat headache cold and flu

48
Q

glom membrane charge

A

neg to repel Pr-

49
Q

Hend hascel

A

ph=pka+log A-/HA

50
Q

Pr binding acid base drugs

A

Alb bind acid and spill over base

alpha1 acid glycoprotein base

51
Q

allosteric

A

bind at different site to cause change

eg benzo

52
Q

NMDA rec

A

AMPA-glut

NK1-sub P

53
Q

efficacy

A

Emax

Intrinsic activity is a relative term for a drug’s efficacy relative to a drug with the highest observed efficacy

54
Q

Extraction ration

A

1-Conc out/Conc in

????

surely its (Ci-Co/Ci)

(70-63)/70=10% ER

55
Q

Elim

A

clearance.conc

56
Q

Vd 3 measures

A

1) extrap
2) AUC
-AUC=x/cl
-t/2elim=vd.0.693/cl
3)Vss
Vd=Cl.MRT (from AUC model)

57
Q

ketamine binding site

A

phenyl cyclidine protien binding site PCP site

allosteric binding site (separate from glut and glycine)

58
Q

flecanide

A

1c) nil change to ARP
slowed conduction
decreased excitability
rate rependant blockade on NaCh–>breaky tachyarrhthmia

59
Q

correlation between AP and ECG

A

evernote

60
Q

amiodarone

met and elim

A 
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
Q

ketamine met

A

CYP450 demethylated and hydroxylated to norket 1/3 active–>gluronation–>inactive met peed out

62
Q

OBA

A

ab.(1-ER)

63
Q

ER

A

1-out/in

64
Q

Vd measure 3

A

1,2,3

65
Q

paramegnetic O2

A

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
Q

glavanic Fuel cell

GOLD

A

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
Q

Clark electrode LITFL

A

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
Q

anaesthetic gas analysis

A

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
Q

ABG MEASUREMENT OF CO2

A

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
Q

ABG measurement of SaO2

A

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
Q

ABG PH measure and issues

GOLD core

A

http://www.partone.lifeinthefastlane.com/blood_gases.html

72
Q

N20 ptx

A

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
Q

PL store

A

22C 5 days aggitate

74
Q

Clonidine

A 
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
Q

Phenothiazine

A

prochlorperazine ie stemetil
DA 1st hist and chol
highest EPSE–>dystonia
drowsy

76
Q

ondans SE

A

consitpation HA Qtc

77
Q

Droperidol

A

butyrophenones
0.25mg dose

SE
-hyperprolactin

hep emt

1% renal excretion unchanged

78
Q

metoclopramide

A

DA and 5HT
NNT=30!
OBA 30-90%
arrhythmia and hypotension with bolus

79
Q

Dex MoA

A

endorphin–>mood
antiinflam–>reduced 5hT release in gut ENTEROCHROFFIN CELLS
prostaglanin antag

steroids stimulate lipocortin–>suppress PLA2 (first step in prostaglandin synth)!

80
Q

cyclizine

A

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
Q

aprepitant

A

NK! antag (bind sub P)

82
Q

nabilone

A

CB1 rec ag (periph and central

83
Q

maoI

A

SERLEGELINE FOR pdX IS MAOB SO IS OK
ANTIDEPRESSANT mao–>risk cease on DOS
-beware indirect agent–>prolonged intense effect

84
Q

H1 rec

A 
first gen
-phenergen
second gen
-loratadine
-less antichol sedatin effects
85
Q

class 1 drugs

A

a prolong procaaaaaainomide
b shortens phenytoin and lig
c nil flecainide

86
Q

antipsych

A

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,

Viva (7 decks)

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