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Viva > Vivas July > Flashcards

Vivas July Flashcards

1
Q

ideal breathing system

A
  1. Simple and safe to use.
  2. Delivers the intended inspired gas mixture.
  3. Permits spontaneous, manual and controlled ventilation in all age groups.
  4. Efficient, requiring low FGF rates.
  5. Protects the patient from barotrauma.
  6. Sturdy, compact, portable and lightweight in design.
  7. Permits the easy removal of waste exhaled gases.
  8. Ability to conserve heat and moisture.
  9. Easy to maintain with minimal running costs.
simple
safe-o2 in CO2 out, accurate
save-cheap system, low flow, efficeint
spont
strong
small
baro
heat
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2
Q

N20 bottle

A

For a cylinder that contains liquid and vapour, e.g. nitrous oxide, initially the pressure remains constant as more vapour is produced to replace that which was used. Once all the liquid has been used, the pressure in the cylinder starts to decreases. The temperature in such a cylinder can decrease because of the loss of the latent heat of vaporization leading to the formation of ice on the outside of the cylinder.

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3
Q

test bottle manufacturere

A

look
bend
pressurise
strip

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4
Q

mark bottle

A

chemical
test date
test p
tare weight (of empty bottle)

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5
Q

cylinder valve system

A

yoke (whole) with its pins
bodok washer
valve to turn on and off

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6
Q

PIping system

A

Cu-non rusting antibacterial

colour and hape matched
flexible hoses
pulltest
risk of fire frome warn hose and connection

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7
Q

cylinder manifold

A

series of cylinders

As nitrous oxide is only available in cylinders (in contrast to liquid oxygen), its manifold is larger than that of oxygen.

In either group, all the cylinders’ valves are opened. This allows them to empty simultaneously.

  1. The supply is automatically changed to the secondary group when the primary group is nearly empty. The changeover is achieved through a pressure-sensitive device that detects when the cylinders are nearly empty.
  2. The changeover activates an electrical signalling system to alert staff to the need to change the cylinders.
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8
Q

VIE

A 
#cu coil
#superheater
#-160C ie less than -118C crit temp
1000x vol at room temp
nil active cooling #LHV
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9
Q

entenox

A

pseudocritical temp -5C
therefore at -5.1C can be compressed to liquid–>poynting effect
N20 with 20% O2 on bottome with high O2 above

so >10C for 24hours before use, invert and shake, dip to take bottom before becomes hypoxic

only flows when sucked on (2 stage Pressure:demand regulator

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10
Q

renal feedback

A

macular densar are sensars of Na and release Adenosine
gRanular cells generate Renin
mesangial cells contract

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11
Q

N20 CBF

A

increased CMRO2

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12
Q

N20 production

A

NH4NO3–>H20 +N2O with impurities of NO and NO2

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13
Q

N20 SE resp

A

nil Change in MV despite small decrease in TV

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14
Q

N2O toxicitiy

A

oxidises the cobalt in B12 which means B12 can’t be a cofactor for methionine synthitase which makes methionine to produce activated folate and DNA

  • ->BM suppression–>agranulocytosis
  • ->subacute combined degreneration of spinal cord
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15
Q

N20 causing PTx

A

1) N2 is highly insoluble therefore TRAPPED IN THESE SPACES
2) N20 while insoluble vs other agents is more soluble in blood than N2
3) N20 out of blood into gas filled spaces (down conc gradient) much quicker than N2 exiting that space into blood

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16
Q

N20 lungs

A

PHTN-increased SNS

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17
Q

apheresis

A

Apheresis is a medical technology in which the blood of a person is passed through an apparatus that separates out one particular constituent and returns the remainder to the circulation

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18
Q

diasterioisomers

A

> 1 chiral centre

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19
Q

CO reduced Vd

A

V1 smaller i believe

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20
Q

t/2=

A

In2/k

k is rate constant for elimination

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21
Q

isomers definitions

A

structural=different bonds

stereoisomer=same bonds, different 3D arrangement

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22
Q

strucutural isomers

A

positional: butane vs isobutane

chain-iso vs enflurane

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23
Q

iso vs enflurane

all agent draw

A

chloride on diff carbon

similar O:G yet ENFLURANE has higher mac

Iso strong

Flouride stable, impotent increase VP less flammable decreased sol

  • halo 3 and old school Br (potent)
  • iso/en 5 and CHF2—>CO
  • sevo 6 and nil CHF2, has CF3, but compound A
  • des 7 and fuck it CHF2 but no compound A

Non polar and small—>high VP

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24
Q

geometric isomer

A

differ from each other in the arrangement of groups with respect to a double bond, ring, or other rigid structure.

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25
Q

S vs R structure

A

chiral centre, lowest behind, then flat plane on pace ascending clokwise is Right Rectus vs Serious

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26
Q

high first pass

A

GTN, morphine, midaz,

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27
Q

prodrug

A

codeine, clopidogrel

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28
Q

midaz elim

A

pee out inactive met so CKD no biggy as per oxford

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29
Q

fat

A

increased alpha1 acid GP

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30
Q

roc offset factors

A

Rb elderly and femal due to decreased m mass
rememeber Li

Amingoglyco and frusemide–>decreased AcH
aminolgycocyde also CCB

fenytoin speeds up recovery by increasing PrB to alpha 1 A GP and upreg of rec

Rb volatile inhibits NaCHR

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31
Q

clondine PK

A

99% OBA
50% hep 50% renal elimunchanged

MoA
presynaptic a2 stim–>decreased Nad
B stem–>decreased SNS out
DH–>opiate release and moduclate descening pain

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32
Q

role BBB

core

A

1) chemical #kenicturus
2) immune # MS
3) ph
4) ion and glucose #manitol not effective in stroke
5) nt #ice abuse

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33
Q

BBB structure

A

tight junction of endo cells
BM
foot processesses podocytes
enyzmes MAO AchE

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34
Q

Preg cvs

A

Oestrogen RAAS (all women are tense)

Progesterone ->prostaglandin->vd->improve perfusion

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35
Q

SSx

A

most common is

  • hyperreflexia
  • clonus
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36
Q

OHBD shift right

CORE AS FUCK

A

23dpg is PRODUCED IN hypoxia–>to release O2

23dpg is produced in pregancy

increase–>right shift (release O2)

23DPG is produced in alternative pathway for one of the steps of glycolysis (less efficient-consumes 1ATP inseatd of producing it)

decreased glycolysis in storage–>decreased 23DPG

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37
Q

deadspace preg

A

The lack of gradient is attributed to the reduction in alveolar dead space (increased blood perfusion from an increase in maternal CO).

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38
Q

preg resp

A

Cx 3

1) mech
2) humeral
3) MRO2 60%

Consumption
Drive-progesterone
Airway #BD due to progesterone
Compliance and work
Vol FRC decreased 20%
#IC mild increase in preg
VQ-shunt, DECREASED DS
OHDC
measurement
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39
Q

fetal maternal CO2 levels

A 
arterial gap of 15 
venous gap of 5
essentially mum takes 5 off baby
mum artery 37 (MEMORABLE alkalotic)-->42
fetal arter 52 (memorable acidodic)-->47

REMEMBER MOTHER IS ON BOTTOM (more O2)

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40
Q

haldane effect wiki

A

deoxyHB binds H+

shift H2CO3 eqn to right with more CO2 soaked up

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41
Q

bohr wiki

A

H+ stabilizes Hb in Tense state–>release O2

essentially higher CO2–>more H+–>bump O2 off Hb

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42
Q

CVS changes in preg

core

A

1) humeral
2) mech
3) MRO2

HR.SV.SVR
plus clotting and albumin and HCT
plus regional
plus transport OHDC

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43
Q

Hysteresis

A

1) surfactant -on expiration as volume decreases surfactant more concentrated to remaining volume—>reduced surface tension—>remains open for longer (less compliant)
2) visicoelastic properties
3) recruitement
4) dynamic compliance effected by airway resistance

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44
Q

deadspace effects

A

decreased AV
-increased CO2, decreased O2

hypoxia easily reversible with Fio2 vs if shunt a cause.

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45
Q

resistance airway generation

A

moderate, high, +++low
17 division conductive including terminal bronchioles
17-23 respiratory including respiratory brioles

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46
Q

alv ventilation/min

A

5000ml/min =5L of BF=VQ=1

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47
Q

CO2 vs AV eqn CORE AF

A

PACO2=CO2 prod/AV.k

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48
Q

DS eqn

CORE AF

A

expired Co2 in douglas bag diluted

cardiac arrest

PACO2-PECO2/PACo2

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49
Q

Shunt eqn

CORE AF

A

Content o2 not Partial pressure

ContentAlv o2-Content arterial/(Content Alv-mixed venous)

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50
Q

Diffusion capacity measurement

A

Flow=P.Diffusioncapictyoflung
Diffusion cap=P/flow

measure the uptake of something that is diffusion not perfusion limited ie CO

D of CO=sol/MW.A.P/T
CO uptake=diffusion capacity.Palv
PAlv=CO uptake/diffusion capacity of lung

SINGLE BREATH METHOD
measure insp with IR
hold for 10s then measure exp with IR

increases with exercise due to recruitment–>increased area

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51
Q

diffusion limitation axis

A

Partial pressure not diffusion %

things that are sol or sucked up by Hb–>dont build up an opposing partial P and keep sucking more and more in.

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52
Q

O2 flux eqn

A

flux is delivery!!!!!

Hb per L is 120
sol per L= 0.03

Hb per 100ml is 12
sol per 100ml is 0.003

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53
Q

diffusion limitation 2 components

A

diffusion to RBC
O2 and CO2 reaction in RBC
both contribute 50%

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54
Q

diffusion capacity error

A

VQ mm will fuck with things yet not a diffusion problem

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55
Q

Fick principle

A

Uptake=Qt(CaO2-CvO2)

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56
Q

measure PBF

A

fick prinicple uptake measure by measuring conc of expired O2

or indicator dillution method

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57
Q

why shunt cant be compensated

A

well oxygenated alveoli even with +++PAO2 can’t carry much more O2 due to Hb maxed out #plateu of OHDC

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58
Q

asthma

A

airway obstruction–>shunt–>hyperventilate–>decreased PaCO2–>EXHAUSTED–>increased PaCO2

BC–>autopeep

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59
Q

copd

A

shunt+deadspace–>hypoxia and HYPERCAPNIA

treat with PEEP to reduce shunt

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60
Q

hufners constant

A

each GRAM of Hb takes 1.34 ml of O2

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61
Q

OHDC figures

A

100: 100
90: 60
p50: 28
75: 40 venous

Myoglobin 50point is 2.8mmHg

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62
Q

teach

central venous vs mixed venous

A

yes confirmed

central is from atria normal is 70-80%
mixed venous is from Pulm artery

Central is RA
Mixed is pulmonary arter

Coronary sinus drains into RV so mixed is more hypoxic

myocardial oxygen consumption (given that the source of the discrepancy is probably blood washing out of the coronary sinus

can derive

  • OER to guide diag and Mx
  • CO from ficks prinicple
  • shunt eqn
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63
Q

respiratory compliance curve

A

recoil P on x axis

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64
Q

wheatstone bridge

A

galvinometer

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65
Q

aorta vs radius

A

Aortic incisura

Radius diastolic hump

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66
Q

glucose handling graph

A

glucose flux vs plasma glucose (x)

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67
Q

Warfarin met

A

Cyp450 CYP3A4

Met induced by STP And carbemazepine

Met inhibited by amiodarone and cimetidine

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68
Q

Warfarin reversal

A

Remember prothonvinex

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69
Q

Hb BD

A

haem +globin
haem–>fe and biliverdin–>bilirubin
bili–>urobilinogen–>stercobilin

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70
Q

Conj vs uncong

A

uncong=prehepatic or hepatic eg cirrhosis
conj=hepatocellular or post hepatic
if any bili in urine=hyperconj

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71
Q

tryptase

A

1,4,24 peaks, dropping, baseline. baseline will factor into interp

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72
Q

anaphylaxis

A 
Hist
leukotreine-chemotractic-->delayed effect
PG
bradykinin
TNFa
5HT
NO
Tryptase-->activate comp system, coag-->thombus and DIC
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73
Q

serum vs plasma

A

serum is what is left after blood has clotted ie plasma without coag factors

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74
Q

role of plasma proteints

A 
clings to...
water
pH
drugs
cations
clots
invaders
enzyme function
energy reserve
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75
Q

reticulocytes

A

new production of RBC

still have RNA fracgments

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76
Q

dibucaine number

A

is an amide LA that inhibits Butylcholinesterase

% of butylcholinesterase uneefected after challenge gives number

normal is 80%
genetic dx–>only 20% remain

%effective butylcholinesterase effective

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77
Q 
Esterases
#amanda diaz
A

hydrolyse esteres (BD by reaction with H2O)

non spec-remi and emsolol and atrac and cisatrac

butylesterease sux and miv and ester LA cocaine and heroine

achetylcholinesterase-Ach

RBC esterases esmolol and remi (small for remi)

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78
Q

hoffman

A

spont degen in pH and temp

cleave of quarternary nitrogen link to central chain

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79
Q

local anaesthetic structure function

GOLD

A

COO is ester
NHCO is amide #amine

aromatic lipophilic group
hydrophilic group

Mepivacaine, bupivacaine, and ropivacaine are characterized as pipecoloxylidides (see Fig. 10-2). Mepivacaine has a methyl group on the piperidine nitrogen atom (amine end) of the molecule. Addition of a butyl group to the piperidine nitrogen of mepivacaine results in bupivacaine, which is 35 times more lipid soluble and has a potency and duration of action 3 to 4 times that of mepivacaine. Ropivacaine structurally resembles bupivacaine and mepivacaine, with a propyl group on the piperidine nitrogen atom of the molecule.

changing length and C attachments–>changed lipid sol DoA metabolism etc

piperadine nitrogen:
1) Methyl->4)butl–>bupivocaine ++lipid sol and doa
Butyl–>3)propyl–>ropivocaine

methyl ethyl propoyl butyl

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80
Q

LA pH

A

Local anesthetics are poorly soluble in water and therefore are marketed most often as water-soluble hydrochloride salts. These hydrochloride salt solutions are acidic (pH 6), contributing to the stability of the local anesthetic. An acidic pH is also important if epinephrine is present in the local anesthetic solution, because this catecholamine is unstable at an alkaline pH.

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81
Q

remifentanil vs fent potency

A

can simplistically be thought of as equipotent

classically remi called 2x more potent

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82
Q

pethidine

A

high sol low potency renal and fetal accum with active metabolite reacts with MAOi

action and SE antichol and SSRI and morphine
not reversed with naloxone

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83
Q

methadone

A

C-full opioid agonist, NMDA antag, SSRI
U-pain addition good for neuropathic pain
P-PO
A-opiate and NMDA
D-1/4 morphine (more potent)
O-relatively fast 2.5hrs (lipid sol) offset long due to large Vd
R-PO/IV

S

  • less sedation, euphoria, addiction
  • Qt prolongation in high dose
D
-PrB 90% highly lipid sol
A
-good OBA 75% due to low first pass met
M
-hep met (has large reserve) with inactive met
E inactive peed out
T/2 24 hours

Low cost
Individual unpredictable PK and PD so slow titration

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84
Q

naloxone naltrexone

A

naloxone crosses BBB, low OBA and fast and short effect–>IV reversal (yet also with targin as low OBA means it stops GI Sx without blocking neuro Sx)

Naltrexone
-good OBA nil BBB crossing

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85
Q

Opiate classification

A 
Endogenous
-encephalin, endorphine
Natural
-morphine
-codeine
-thebaine
Semi syth
-codiene changed to oxycodone
-morphine changed to heroine
Synthetic
-phenylpiperidine
-morphine deriv
-thebaine change-->naloxone and naltrexone
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86
Q

lafent offset

A

small Vd due to less lipid sol–>more rapid elimination despite less clearance

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87
Q

opiate change

A

incomplete cross tolerance

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88
Q

fent CSHT

A

better than alfent until2 hr infusion

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89
Q

quantal vs

A

graded

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90
Q

opiate rec

A

NOP is supraspinal

Cortex, Thal, BG, PAG, Resp centre, SC, periph

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91
Q

white vs grey matter

A

white is fat so middle of brain and outter tracts of SC

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92
Q

ANS

A

sympathetic spinal colum grey matter and peripheral ganglio

PSNS
CN nuclei
Sacral Rami

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93
Q

content O2 of blood Normal

A

200ml/L

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94
Q

bohr reason

A

H stab
Hb binding
ttttttoo boooooohring

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95
Q 
Hamburger effect
RV
RV
RV
GOLDEN
A

venous blood lower Cl vs arterial.

CO2 into RBC–>HCO3–>swapped from Chloride

Effect: mittigation of acidity in venous
increased CO2 carry cap in venous
increased offloading of O2 as Cl causes T state stabilization #allosteric change

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96
Q

henderson

A

ph=pka +log HCO/CO2x0.003

pka+log A-/HA

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97
Q

HCO3 in resp acidosis

A

INCREASES in acute and chronic 3x more in chronic

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98
Q

Predicted CO2

A

HCO3x1.5+8

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99
Q

Bicarb types

A

standard with real CO2
actual if CO2 normal

BE if real CO2
BExxx if normal Hb

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100
Q

NAG

A

10-16

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101
Q

CATMUDPILES

A

Cyanide, CO, aminoglycosides

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102
Q

measure osmolarity

A

2xNa +urea+glucose

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103
Q

Blood gas interp steps

A

met or resp or mixed
HAG or NAG
osmol gap
delta gap for HAG+other

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104
Q

HAG NAG renal

A

RTA is HCO3 loss hence NAG

ureamia is HAG

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105
Q

La Place

CORE

A

P=2T/r

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106
Q

surfactant and hysteresis

A

collapsing–>surfactant pressed together–>resist further collapse

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107
Q

Resp compliance

A

1/RC=1/L+1/Thoracic cage =1/100

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108
Q

surfactant

A

Prevention of fluid transudation. As the surface
tension forces are generally reduced by surfactant,
less interstitial fluid is sucked into the alveolus.

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109
Q

dynamic airway compression relevance

A

more apparent in lung Dx to restrict exp flow rate due to loss of lung elastic recoil and radial traction.
equal pressure point moves deeper into lungs on exp as airways get smaller in collapsing lung
determined by AlvP-Pleural pressure not mouth pressure

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110
Q

spiro dx

A

FEV1 decrease to GREATER EXTENT in COPD
FEV1 decreased to LESSER extent
west says in both FRC is decreased
i believe can be increased hence barrel chest copd

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111
Q

RR and TV and WoB in Dx

A

trap=elastic
curve=frictional (80% airway and 20% tissue)

in PF elastic work big and frictional work low so breath small TV with high RR

in COPD elastic work reduced and airway res increased–>take big breathes and low RR

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112
Q

static compliance

A

oeophageal pressure measure

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113
Q

adding to alpha cardbon

A

BLOCKS MAO

114
Q

classification of sympathomimetics

A

evernote gold

115
Q

COMT mech

A

add a methyl group

116
Q

MAO

A

oxidative deamination ie uses O2 to cleave amine

117
Q

Sotalol

A 
add salt to everything
class I,II, III
118
Q

low lipid bblocker

A

poor ab but minimal first pass met–>good OBA and long halflife as minimal met

119
Q

adenosine

A 
C-nat purine nucleoside
U-SVT reentry and diag
P 3mg/ml clear
A-
1)adenonsine sense K ch open -->hyperpol
2) inhibit cAMP excitation in ventricles
3)infusion-->drop SVR
D
O 10-20s doA
S
-CI in 2nd or 3rd degree heart block or SSSx
-can cx VF/VT as brady increases excitabiliy
-can Cx AF of Aflutter as decreased atrial refractory 
period
-can cx brady requiring pacing
Met-RBC and vasc endo to AMP
no dose change in renal or hep
120
Q

why ohms law imperfect for lungs

A

elastic, non lamina, non-newtonian fluid

F=P/R yet increase increase P–>decreased resistance

121
Q

admix

A

“venous admixture is the amount of mixed venous blood
required to mix with pulmonary capillary blood
to produce the observed alveolar–arterial Po2 difference.” (includes true shunt AND VQ scatter)

mixed venous blood is the venous blood drained from bronchi (via bronchial veins) and LV (via thesbian veins) to LA AND VQ SCATTER AND CARDIAC DEFECT R–>LSHUNT

Sources of venous admixture include:
“True” intrapulmonary shunt, blood which passes through lung regions where V/Q = 0
V/Q scatter, blood which passes through lung regions where V/Q < 1.0
Thebesian veins, which contribute myocardial venous blood with low oxygen content
Bronchial veins, which drain the bronchial walls
Intracardiac right-to-left shunts
Normal shunt fraction in healthy adults is 4-10%

!!!!SO TRUE SHUNT IS ZERO OXYGENATION
yet decreased VQ contributes to admix!!!!

122
Q

shunt

A

Shunt is the blood which enters the systemic arterial circulation without participating in gas exchange

123
Q

anatomical shunt CORE

A

just 2! P+K and derranged phys

thesbian which go to coronary sinus –>LA
bronchial Veins–>LA

124
Q

OLV CPAP

A

if blood going through may as well try add some O2 to it.

125
Q

Pulm HTN Mx

A

1) O2
2) NO donor (sodium nitropruside or GTN)
3) CCB
4) PDEi
- PDE3i cGMP inhibited BD Silden
- PDE35i CAMP inhibited BD milrinone
5) Prostaglandins–>VD

126
Q

silden

milrinone

A

S=5
M=3
visually looks that way
3->cAMP–>contractility

127
Q

peripheral chemo rec

A

CO2 and O2 CB and AoA

pH only in CB

128
Q

rotem

GOLD

A

clotting–>fibrin blocks–>platelet strength

CT–>CFT–>MCF–>plasmin

129
Q

vasopressin

A

VwF

130
Q

hypoplasmin

A

leukaemia, thrombolysis, bradykinin, ESLD due to impaired clearance of plasminogen activator

Trauma, DIC, thombolytic therapy, placenta acreta–>plasminogen activator from placeta–>lots of lysis

131
Q

resp centre

CORE

A

Medullar resp centre

Di
Ve
Be

pons

  • pneumotaxic-taxes slow
  • apneustic centre-aps speed up efficientcy
132
Q

HYperbaric Rx

A

CO poisoning
decompression
gas gangreen

133
Q

pendeluf and RR

A

worse with high RR as need prolonged exp oause to balance

134
Q

daltons law clinic sig

A

P=P1 +p2

so at everest less PP of O2

135
Q

avagadros law

A

at equal temp, vol and pressure different gases contain the same number of molecules

dilution of O2 in trachea–>decreased PP of O2

136
Q

henry’s law

A

conc proportional to pressure of gas in a liquid.

137
Q

gibbs donnan

A

KPr intracell KCL out

CL comes in K comes in water comes in

138
Q

osmotic p

A

the pressure that would have to be applied to a pure solvent to prevent it from passing into a given solution by osmosis,

139
Q

oncotic

A

osmotic p exerted by colloids ie protein

140
Q

albumin tonicity and effect

A

I agree albumin 20% (and 4%) are hypotonic and hyposmolar which as a fluid would mean they wouldn’t effectively expand much volume.
But
1) albumin remains much more intravascular without spreading interestitial fluid as fast as IVF
2) album 20% is 200g/l vs 45g/l in healthy patient, 4% is 40g/l so if giving it to someone will low albumin then it will increase the oncotic pressure despite the decreased osmotic pressure (colloid + electrolyte contribution). This will mean the starling forces (defined by oncotic pressures not osmotic) will pull fluid into blood and prevent peeing out at kidney
3) Gibbs donnan effect–>albumin pulls more water into IV space that would be expected

141
Q

albumin 20% tonicity

A

Alb 130mmol/L Na 130mmol –>260mmol–>hypotonic

142
Q

normal plasma osmolarity

A

280mols/L

143
Q

TWB splitts

A

60% TBW
1/3 EC
1/4 IV
5% of weight is plasma vol =3.5L then add cells

144
Q

Stewart theory

A

!!!!Strong, weak nonvolatile, weak volatile!!!!

Stewart theory from Melbourne course
H+/HCO3 are dependant on 3 variables
1. SID #electrical neutrality
    1. Na + K-Cl =42
    2. Other Strong ions Ca Mg, lactate, ketones, 
    3. Weak ion HCO3, Albumin
2. Weak inorganic acids
    1. Alb
        1. IVF—>dilute albumin (an acid)—>increased HCO3
        2. (Note in SID decreased Alb—>increased HCO3 
    2. Phosphate
3. CO2 
benefit
Acknowledges
- hydration status effects
-Albumin conc effects
-identifies SID as MOST IMPORTANT FACTOR
145
Q

G+S+Xmatch

A
  1. ABO (what Antigens are present on RBC)
    1. Forward test
      1. Recipient RBC vs control
    2. Backward test (confirm forward)
      1. Recipient plasma vs control RBC
  2. Screen for non ABO antigens (these are not on RBC! So patients serum is tested for antigens!!!!!)
    1. Recipient plasma vs control RBC
  3. Xmatch (Will the recipient reject this offering)
    1. Is screen and Hx negative for ABs then 2 options
      1. Algorithm based on data—>choice
      2. Immediate saline spin (check screen really right with real donor sample)
        1. Recipient plasma vs donor RBC
    2. Screen positive or sig hx
      1. Indirecirect Antiglobulin test (IDAT) to see if ABO and other antigens present
        1. Incubation of recipient plasma and donor RBC
        2. Wash this combo to remove any plasma Ig not bound to RBC (this would react with the anti-human immunoglobulin about to be added
        3. Glutination-add anti-human-IG to bind the Ig that is bound to antigens—>little clumps—>positive result (bad thing: means recipient has antibodies against donor RBC that then clump when bound by antihuman Ig)
146
Q

immunoglob

A

Role of immunoglobulins

  1. Labelled for NK to destroy
  2. Labelled for phagocytosis #opsinization of viruses
  3. Compliment activation
  4. Bound to Bcell wall—>make a befell an Antigen presenting cell

Immunoglobulins tip is variable so specific to antigens

147
Q

immune system pneumonic

A

Innate PGN Cs

Addaptive immune BAT

148
Q

complement cascade

A

Complement

  • proinflamatory proteins activated by classic: Ig:Antigen or alternative or proteolytic enzymes—>inflammation, lysis
  • reaction in ABO incompatability
  • inhibited by C1 esterase
149
Q

collegiate

A

increase BP, osmotic P

decreased freezing point and SVP

150
Q

actual and standard HCO3

A

pCO2 – Measured directly
 Actual HCO3 – Measures pH and pCO2 from blood sample and then
calculates HCO3 from the H‐H Equation
 Standard HCO3 – Calculated parameter when the blood sample is
equilibrated with a gas mixture with PCO2 level of 40mmHg – attempt
to represent the True metabolic component in patients with dual Acid –
Base AbN.

151
Q

BE and standard base excess

A

Hb 50 (anaemic–>standardized)

152
Q

Mannitol

A

RV adme and PD

153
Q

Des PD

A

Decreased TV Increased RR

Nil neg into more VD more hypotensive more tachy

154
Q

Frusemide

A

Pulm and systemic VD

Cl channel block can’t conc medulla

155
Q

SNP met

A

OHb–>met–>cyanomet

Rhodanase adds sulfur group

B12–>cyanocobalamine

Bicobolt chelates

156
Q

Heparin

A

mucopoly

ACS

REVERSIBLE BINDING TO
ATIII
9,10,11,12,13
PL

8000 SC TDS/BD

T/2 1.5hrs

bleeds, HITS, osteoporosis, ald inhib

Vd 100ml/L
Ab same SC
M hep and liver and ER system-->de polymerated
-slowed in hypothermia
E-renal fine

target APTT 2x normal

157
Q

HITTS RX

A

direct thrombin inhibitor

158
Q

4Ts

A

timing 5-10days
oTher Cx
thombosis
thrombocytopenia

159
Q

CYP450 types

A

3A4 midaz warfarin, clopid

2D6 tramadol

160
Q

Naturalf freq stiffness eleasticity

A

on top

161
Q

damping effect

A

yes does decreased freq a little and increase freq response window (ie the range of frequency of before resonance occurs)

162
Q

damping anzca text

A
  1. To determine the optimum damping of the system, a square wave test (fast flush test) is used ( Fig. 11.9 ). The system is flushed by applying a pressure of 300 mmHg (compress and release the flush button or pull the lever located near the transducer). This results in a square waveform, followed by oscillations:
    a. in an optimally damped system, there will be two or three oscillations before settling to zero
    b. an overdamped system settles to zero without any oscillations
    c. an underdamped system oscillates for more than three to four cycles before settling to zero.
163
Q

resonant freq

A

The lowest resonant frequency of a vibrating object is called its fundamental frequency. Most vibrating objects have more than one resonant frequency and those used in musical instruments typically vibrate at harmonics of the fundamental.

Resonant Frequency is the Oscillation of a system at its natural or unforced resonance.

164
Q

damping coeff

A

reflection of freq response of system

actual damping/critical damping

zero damping=o

optimal damping=0.64

critical damping =the point at which there is just no overshhoot =1

overdampe=no overshoot and takes more time than critical damping to get there >1

165
Q

HM

A

HM6G is INACTIVE but neuroexcitatory and accum in renal

more lipid sol vs moprhine–>faster onset vs morph
smaller Vd vs fent–>longer DoA vs fent

166
Q

Morphine met

A

CYP450 demethylation and glucornidation
M3G–>neuroexcitatory
M6G–>13x more potent

167
Q

octenol:water coeff

A

morph=1

fent=600

168
Q

oxcodone met

A

noroxycodone inactive
and oxymorpphone–>WEAKLY active

3A4 → inactive
noroxycodone

2D6 → active
oxymorphone
Naloxone is an “Nalkyl derivative of
oxymorphone”

169
Q

buprenorphine

A

partial ag
slow dissocaition from rec–>long action and unpredictable reversal and low dependancy
-resp dep not completely reversed by naloxone
biliary excretion
25x potency of morphine

SL BA=50%
PO is well ab but high FPM
Vd 4l?kg
CYP450–>bile

severe resp dep with high midaz

elim T/2 5hrs

170
Q

Mannitol

A

decreased CSF produ

cross glom and not reab–>wash out medulla–>no reab

nil met

small Vd

HTN transiently

target osmol 300-320

hypokalaemia

171
Q

Hypertonic saline

A 
ICP
rhabdo
preserve renal function
start diuresis in renal transplant
bowel prep
glaucoma
titrate to target Na 155
benefit nil osmolar testing
cheap available
antioxidant
less likely to cause hypovolaemia
10min on for 1 hr
Disad
hypernatraemia
hyperchlo acid
hypokalaemia
central pontine demiolosis
renal failure
phlebitis, necrosis
hypervolaemia
seizure encephalopathy
rebound raised ICP
172
Q

porphyrin

A

porphyrin ring of Hb

precurser of Hb
req p450 to change forms
genetic or acquired dysrufption–>accum–>toxic

skin and nervous system

  • tachy, HTN
  • fever
  • confusion
  • seizure, paralysis
  • death
  • abdo, chest pain,
  • blisters
173
Q

parietal cell stim and inhibition

A

Highly specialised
Mitochondria ++
Proton pump (apical H+/K+-ATPase) moves H out of cell againstsignificant gradient

3 agonists:
Gastrin
ACh
Histamine

Inhibited by:
Somatostatin
B-adrenergic activity
High acidity 
PGE2
174
Q

filling ratio N2O

A

0.75 or 0.66 in tropics

175
Q

yoke pins etc

A

yoke is the outside c grip with pins as 1 componenet and fresh gas flow outlet

washer

valve is part of cylinder

176
Q

Heat vs temp

A

Heat is potential and kinetic energy that is transferred from a substance of higher temp to lower temp.
J or Cal

Temperature is not energy but a measure of the hotness or coldness of a substance (measure of average kinetic energy of a single particle in a system per degree of freedom)
K or C

heat can be added to increased the temp OR change the state.

177
Q

SHC

A

The amount of heat energy required to increase one Kg of a substance by one Degree Centigrade/Kelvin

178
Q

Renal BF reg

A

Autoreg

SNS
Renin
ATII
ANP
PGs
179
Q

Tubulorglomerular balance

A

glucose

increased oncotic P in pertubular cap–>increased reab

180
Q

oliguria mech

A 
osmorec
HP baro
LP baro
renal Baro
renal autoreg
181
Q

cardiovascular centre

A

HTN–>…

NTS stims Nambig stims PSNS
NTS inhibits RVLM hence decreased SNS

182
Q

how is medulla gradient created

A

LoH

ACSENDING pulls NaCL into interstium (reab) H20 impermeable.
DESCENDING pulls allows H20 to be pulled out by NaCl

300 osmole–>400 in desc and 200 in ascending
play over until 1400 in loop pin

183
Q

Vasa recta

A

water out as descending replaced as ascending

184
Q

potassium Ch blocker antiarrhythmic

A

rb sotalol

185
Q

digoxin tox

A

phenytoin

186
Q

SVT and VT options

A

amiod, flacainide, sotalol

187
Q

sotalol

A

class 1,2,3
Rx VT
prevent SVT

188
Q

adensoisne rec

A

Where are the adenosine receptors?
A1: Gi, in SA/AV node, cause decrease in HR. 
A2A: Gs, coronary arteries (vasodilatation)
A2B: Gs, bronchiole smooth muscle (bronchospasm)
A3: Gi, cardioprotective in ischaemia, inhibits neutrophils degranulation

189
Q

Cardiac SE adenonsine

A

decreased atrial refractory–>AF or flutter

190
Q

adenosine met

A

plasma and RBC esterase

191
Q

digoxin

A 
25% PrB-->large Vd
minimal hep met
largely excreted unchanged in urine
narrow TI
level 1-2mcg/L
OBA 70%

increase Ach releaseat M rec

ECG

  • PR prologn
  • ST dep reverse tick
  • t wave flatterening
  • Short Q T

anorexia,N/V/D

192
Q

Rx digoxin tox

A 
ABC
electrolytes
brady Rx
Phenytoin
Dig ABs if >20mcg/L
2 weeks to steady state post PO
half line alph 1 day beta 3 weeks
193
Q

Ester vs amide structure

A

COOR
vs
NHCO

194
Q

nerve block onset types

A

B>Ad>Ab>C

ANS>sens>motor

195
Q

neuro tox common LA

A

CIRCUMORAL TINGLING

196
Q

thiopentone vial

A

500mg in 20ml
25mg/ml

NaCO3 NOT HCO3

197
Q

thio vs prop CVS

A

Sodium thiopental generally produces less hypotension than an equivalent dose of propofol when used for induction of anaesthesia. This is partly because both drugs decrease systemic vascular resistance, but thiopentone (as opposed to propofol) tends to preserve the reflex tachycardia seen in states of acute hypotension, which can restore cardiac output.

198
Q

Adx

A

Htn brady–>pulmonary oedema seizure

Nil betablcoeker

199
Q

Muscle relaxants class SE

A

Aminosteroids anaphylaxis

Benzylisoquinoliniums histamine release

200
Q

Hoffman

A

Cleave nh4 from central structure
Laudenosine
Temp and oh dep

201
Q

Butylecholinesterase prod

A

Liver

202
Q

Leg block monitor

A

Post tibial nerve

Plantaflexion of big toe

203
Q

Onset muscle

A

See Evernote

204
Q

FRC as o2 buffer

A

constant o2 supply. stops swing of insp O2 with none on exp

205
Q

full body plethysomgraphy

A

V1.P1=(V1-changeV).P2 of box

V2.P3=(V2+changeV).P4 of lung

gauge pressure =alv pressure when zero flow

206
Q

estimate pao2 by age

A

100-a/3

207
Q

po2 tissue

A

5

mitochondria 1

208
Q

Hep BF and volatiles

A

It is generally accepted that all the inhalational anesthetics alter hepatic blood flow and oxygenation that may lead to changes in hepatocellular functions [22-24]. The decrease in total hepatic blood flow (THBF) is primarily because of decreased cardiac output and imposes various compromising effects on hepatic oxygen supply [22]. Sevoflurane, like isoflurane, preserved THBF at up to 1 MAC, but THBF was reduced in tandem with increased MAC [23]. However, desflurane is shown to better preserve THBF than halothane or isoflurane in animal studies

209
Q

hepatic unit

A

acina

central hepatic venules

peripheral bile duct, heaptic arterioles and portal venules

  • portal triad
  • ->sinusoids

3 zones

1) periportal-high O2 protein synth
2) mediolobular
3) Centrilobular-CYP450 low O2.

210
Q

hepatic failure first effected

A

synthetic function

enzyme function ++late

211
Q

coags made by liver

A

fibringoen, ATIII, prothrombin,2,7,9,10

212
Q

osmolarit of blood and NACL

tonicity of NACL

A

290 vs 308 (close enough)

blood is not a perfect fluid so NaCL doesn’t completely dissociate so 308 x osmotic coef of 0.93=286

213
Q

tonicity define

A

effective osmotic pressure

214
Q

normal osmolar gap

A

10 due to normal unmeasured osmoles

215
Q

osmolar gap cx

A

mannitol, ethanol, methanol

216
Q

colligiate properties

A

osmotic pressure, depressed freezing point

217
Q

solute vs solvent

A

U—>V

218
Q

how to measure (not calc) osmolarity

A

osmometer: HP vs osmotic
vapour pressure depression
FP depression with platue pressure using thermister

219
Q

pendulum chest

A

Seen in flail chest when several ribs are fractured at multiple sites so that a portion of the
Chest wall moves independently
• The negative intrathoracic pressure during inspiration causes the fractured ribs to be
sucked in, thereby preventing expansion of the lung and during expiration, this segment
moves outwards.
• When the injury is unilateral, air from the affected lung passes into the opposite healthy
lung during inspiration and air moves back from the normal lung into the affected lung
during expiration = “Pendulum breathing”.

220
Q

why PTx resolves

A

O2 absorbed down conc gradient

N2 absorbed down conc gradient

  • 593 in atm
  • 573 in blood as alv air is humidifed and then equillibrates with blood

second gas effect as O2 absorption–>conc further

221
Q

slow vs fast twitch

A

slow is Type I

222
Q

RAP normal

A

0-5

223
Q

fluid bolus starling curve

A

increased RAP and MSFP

224
Q

cefazolin allergy or MRSA Abx

A

clina/ticoplanin

vanc for MRSA

225
Q

GI absorption

A

mor lipid sol–>more absorption
Most drugs are weak organic acids or bases, existing in un-ionized and ionized forms in an aqueous environment. The un-ionized form is usually lipid soluble (lipophilic) and diffuses readily across cell membranes. The ionized form has low lipid solubility (but high water solubility—ie, hydrophilic) and high electrical resistance and thus cannot penetrate cell membranes easily.

226
Q

bacterial wall

A

g+ve thick PG wall (peptidoglycan)

g ive thin PG wall with lipopolyysacharide layer

227
Q

ABx moa anaesthetics

A

evernote

all renal clearance except metronidazole which has an active met–>renal Cl

228
Q

contamination class and ABx

A

clean elective (nil ABx)
clean contam emergency anything or elective hernia
contam NONPURULENT penetrating <4
dirty PURULENT penetrating >4. or bowel p

give <24 hours

229
Q

nerve block

A

Supraclav: commet with subclavian artery

interscalene: between scalenes
infraclavicular: surrounds axillary artery cephalad
axillary: surrounds axillar

230
Q

metabolic alkalosis

A

https://litfl.com/metabolic-alkalosis/

H loss

1) GI
2) renal
- diuretics

HCO3 gain
-Antacid HCO3 iatrogenic

So easy to piss away HCO3 so something has to maintain the HCO3 reab issue
1) low Cl
-diuretics
-HCL vomit
2) dehyd
aldosterone–>reab Na. nut not as much chloride saved.
3) low K due to high minercorticoids
–>minerocorticoids–>aldosterone–>reab Na and spit out K and H+

Sx
resp
-cling to O2
-resp comp-->hypovent
impaired contractility
decreased CBF
confusion, obtunded
231
Q

LA tox

A 
circum oral tingling and numbness
tinitus
vertigo
NOT TASTE or VISION
EXCITABLE TWITCHING
seziure
coma

HTN tachy
VD prolonged QRS and PR and brady

232
Q

semiopen

A

mapelson

T
extended
freq
disabled
A for efficeincy
Bain for BRAIN MRI
233
Q

closed benefit and loss

A

slow onset

warm

234
Q

how does afterload affect contractility

A

The increased afterload causes an increased end-systolic volume. This increases the sarcomere stretch. That leads to an increase in the force of contraction.

235
Q

withdraw reflex

A

afferent–>several interneuron–>alpha motor neuron
–>flexor stim extensor relax.

  • interneurons from pathway that cross the spinal cord can stimulate the extensor motor neurons on the opposite side of the body to produce the cross-extensor reflex
236
Q

SNS cell bodies and structure

A

lateral grey col (since cell body has no myelin)
and in peripheral ganglion

preganglionic is myelinated yes–>NaCHR

paravertebral ganglia

exit from grey collum (unmyelin)–>white rami COMMUNICANS
–>synapse with paravertebral ganglion OR
–>up or down to other paravertebral ganglia # cervical sympathetic ganglia OR
–>skip and create more distal ganglia
So… blocking on white rami communicante–>effects at multiple levels

237
Q

ANS structure

A

SNS and PSNS

  • efferent: visceral and somatic
  • afferent (just visceral): organ sens, reflex loop, refered pain
238
Q

A delta vs C fibre lamin

A

A delta lamina 1,5 #15As rugby team pain
C is lamina 1 2 3
as per ANZCA talk and a model answer

239
Q

pain fibre rec modulation

A

evernote pain pathway goldne

240
Q

once NMDA stim

A

cations in
changed gene transcription
activate kinases
central sensitization

241
Q

peripheral sensitation

A

at nociceptor

central is at DH and brain

242
Q

central sens

A

1) wind up
- increased no of action potentials per noxious stim
2) Long term potentiation
- C fibres activated to transmit pain
3) altered gene transcription
- persistant neural inflam
4) abnormal connection between cells in DH

243
Q

spinoreticular tract

A

spine to reticular formation then thalamus and hypothal–>emotion

244
Q

neuropathic pain mech

A

dysfunction of nervous system

1) changed NaCH–>spont depol
2) changed K –>less breaks
3) changed Ca –>more NT

due to changed gene transciption and phsphorylation of ion ch

245
Q

paracetamol meta

A

phase I (cyp450)–>NAPQI–>neutralized by glutathione (replenished by NAC)

phase II (simultneous) non toxic

246
Q

NSAID in IHD risk

A

both selective and nonselective CI

247
Q

paracoxib benefit

A

less asthma
less PLi (PL is cox1)
less GI

248
Q

pain Mx options

A
  • Simple
  • Opiate
  • Neuropathic #ducktape
    • Duloxetine
    • Clonidine
    • Ketamine
    • Tramadol/talent
    • Amitriptyline
    • Pregabalin
  • Adduvent ie psych immobilize enviro
  • Regional
decrease ascedending
-nsaid, paracetamol
-opiate
-LA NaCH
-gabapentinoids CCB
-ketamine
-clonidine
-regional
increased descending
-SNRIs
-tramadol
249
Q

gabapentinoids soa and SE

A

VGCCB at DH

Gabapentinoids prevent VGCC getting to presynaptic membrane in dorsal horn. inhibit alpha2delta subunit (the tugboat that pulls VGCC to membrane)

drowsy and fat

Other SoA
-NMDA rec antag #neuropathic

250
Q

Gabapentin vs pregabalin

A

Gabapentin
A -active uptake, changes with dose–>unreliable
-non linear dose response curve
M-neither is metabolised!!!!!!
E -elimination zero order for gabapentin at high doses

251
Q

tramadol met path

A

o desmethyltramadol–>opioid rec

CYP2d6 (genetic variability)

252
Q

ketamine routes

A

Rb oral 40min

nasal 15min

253
Q

clonidine vs dex

A

DH and locus ceruleus and SNS peripheral nerves and reticular n. GiPCR–>changed Na and K ch conductance

dex is full agonist (higher ceiling vs clonidine)
peak at 10min similar
t/2 2 vs 15hrs hence doa 1 vs 6 hrs

severe brady

hi Pr Bound

no renal clearance ok in CKD!
decrease in hep failure

254
Q

pain pathway

A

Tissue damage/Nociception/Pain Experience

255
Q

Buprenorphine

A

C: partial Mu agonis. Kappa antag. 25xpotency vs morphine hence 200-400microg SL dose (OBA 70%)

U: acute with poor oral, chronic, opiate replacement/wean
P: SL, patch, iv
A:
D
Onset: peak after IV is 80min: due to slow distribution to effect site and other sites
Give doses Q8H for pain IV or SL
Offset: terminal elim 24 hrs, elimination half life 5 hours due to high affinity to rec. binds and doesn’t let go
R
S
-less resp dec as kappa blocked
-less euphoria ?as slow?
-less tolerance And depressiondependance as slow on and off
-antagonise full
-unpredictbale reversal with naloxone
E
T
D-large 3.2L/kg due to high PrB
A-good ab but large first pass met hence SL not PO
M-liver phase I and II—>bile
E-70% in bile with some renal
Elim T/2 is 5 hours
No dosage adjustment is required in patients with renal impairment or mild to moderate hepatic impairment. Patients with severe hepatic impairment may accumulate buprenorphine and Bupredermal patch should be used with caution, if at all, in such patients. (MIMS)

256
Q

fentanly clearance and effect site term

A

10% renal excretion unchanged 90% is inactive met

clearance rate and Vd is similar to morphine

t/2Keo 4.5 min vs 4.5 hrs morphine

257
Q

codeine met

A

15%–>morphine hence give 6xdose

Poor
-2 shitty allells
Intermediate
-1 shitty allel
Extensive (normal
-2 normal
Ultrameta
-multiple repeats of funcitoning allel

aftricans–>ultrafast
poor white man–>poor

258
Q

nociception

A

def

259
Q

substantia geletanosa

A

The apex of the posterior grey column, one of the three grey columns of the spinal cord, is capped by a V-shaped or crescentic mass of translucent, gelatinous neuroglia, termed the substantia gelatinosa of Rolando (or SGR) (or gelatinous substance of posterior horn of spinal cord). C fibres from primary afferents terminate here with some fibres projected to deeper layers of spinal grey matter, from which arises the spinoreticular tract to the ascending reticular activating system. However, some A delta fibers (carrying fast, localized pain sensation) also terminate in the substantia gelatinosa, mostly via axons passing through this area to the nucleus proprius. Thus, there is cross talk between the two pain pathways.

260
Q

wind up

A

Wind-up = repeated stimulus with no change in strength causes an increase in response from dorsal horn neurons mediated by the release of excitatory neuromediators. Wind-up is dependent on activation of NMDA receptor

261
Q

Ca to NT release

A

Ca binds calmodulin– calmodulin dep kinases–>doc and release

262
Q

Ca in second order afferent neuron pain

A

Ca in due to NMDA, AMPA, NK1

Ca:calmodulin–>changed gene transcription
altered K perm
second messangers–>NO–>neurotoxic

263
Q

silent nociceptor

A

unmyelinated primary afferents, normally do not respond, but in presence of inflammation or chemical sensitization may become responsive and discharge vigorously

264
Q

blood supply to kidney in shock

A

reduced!

ATII and SNS–>VC afferent and efferent
PG–>VD afferent and effent
normally ANP–>VC efferent and VD afferent–>increase filtration

265
Q

ADH trigger

A

high osmol (VOLT etc in Hypothal) >280
low pressure baro rec >5-10% blood vol
-but bumps threshold left and steepens

above 20% BV ADH has caused maximal renal reab and continues to rise and now is its VC effect becomes apparent.

266
Q

ADH

A

see evernote

267
Q

WOB diagram

A

trapezium=ELASTIC (TISSue and alv ST)

curve=RESTRICTIVE: 80% airway 20% tissue (increased in interesitial Dx)

268
Q

static vs dynamic

A

Dynamic compliance=vol/(Pmax-PEEP)
-hence no eosoph
Static Compliance=vol/PlateuP-PEEP)
-hence eosoph

269
Q

potassium channels cardia AP

A

K1 RMP
Kto special transient at peak of 1
Kr rectifying

270
Q

excitatory and inhib NTs

A

glut, NAd ach, 5HT

inhib
GABA glycine

271
Q

time constnat

A

time to complete if rate cont

t=C.R
t=0.63of completion (loner than half life)
t/2= 0.5 completion
t/2=t.0.63

272
Q

oxycodone met

A

CYP450
noroxycodone active

15% of parent renally elliminated so imperfect but a fair option for PO renal Dx

273
Q

pethidine

A

Mu, SSRI, VGSC, SE Ach

met to norpethadine 50% as potent but renally accumulates

accumulates in renal
delerium
anticholinergic
addictive
seziures due to
274
Q

Na Ch types

A

resting (closed) –>active–>inactive

ARP due to NaCh in inactive stage (need time and repol to reset both gates)

275
Q

Botulin etc

A

botuline stops release of Ach

hemicolinium inhibits Choline recycling

276
Q

T tubule

A

invagination of sarcolemna

277
Q

MEPP

A

small small small big

278
Q

cardiac vs smooth vs cardiac

A

evernote

279
Q

midaz met

A

a little bit of active met yet renal excretion no problem

280
Q

MG vs GBS

A

GBS succhy syndrome –>K so use NDMR

MG->muscles weak ACHR Dx–> more sens to 10% of NDMR dose or use sux (less sensitive to sux as less agonist rec).

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