Vivas July Flashcards

(280 cards)

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
S vs R structure
chiral centre, lowest behind, then flat plane on pace ascending clokwise is Right Rectus vs Serious
26
high first pass
GTN, morphine, midaz,
27
prodrug
codeine, clopidogrel
28
midaz elim
pee out inactive met so CKD no biggy as per oxford
29
fat
increased alpha1 acid GP
30
roc offset factors
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
31
clondine PK
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
32
role BBB | core
1) chemical #kenicturus 2) immune # MS 3) ph 4) ion and glucose #manitol not effective in stroke 5) nt #ice abuse
33
BBB structure
tight junction of endo cells BM foot processesses podocytes enyzmes MAO AchE
34
Preg cvs
Oestrogen RAAS (all women are tense) Progesterone ->prostaglandin->vd->improve perfusion
35
SSx
most common is - hyperreflexia - clonus
36
OHBD shift right | CORE AS FUCK
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
37
deadspace preg
The lack of gradient is attributed to the reduction in alveolar dead space (increased blood perfusion from an increase in maternal CO).
38
preg resp
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 ```
39
fetal maternal CO2 levels
``` 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)
40
haldane effect wiki
deoxyHB binds H+ | shift H2CO3 eqn to right with more CO2 soaked up
41
bohr wiki
H+ stabilizes Hb in Tense state-->release O2 | essentially higher CO2-->more H+-->bump O2 off Hb
42
CVS changes in preg | core
1) humeral 2) mech 3) MRO2 HR.SV.SVR plus clotting and albumin and HCT plus regional plus transport OHDC
43
Hysteresis
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
44
deadspace effects
decreased AV -increased CO2, decreased O2 hypoxia easily reversible with Fio2 vs if shunt a cause.
45
resistance airway generation
moderate, high, +++low 17 division conductive including terminal bronchioles 17-23 respiratory including respiratory brioles
46
alv ventilation/min
5000ml/min =5L of BF=VQ=1
47
CO2 vs AV eqn CORE AF
PACO2=CO2 prod/AV.k
48
DS eqn | CORE AF
cardiac arrest PACO2-PECO2/PACo2 #expired Co2 in douglas bag diluted
49
Shunt eqn | CORE AF
Content o2 not Partial pressure ContentAlv o2-Content arterial/(Content Alv-mixed venous)
50
Diffusion capacity measurement
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
51
diffusion limitation axis
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.
52
O2 flux eqn
flux is delivery!!!!! Hb per L is 120 sol per L= 0.03 Hb per 100ml is 12 sol per 100ml is 0.003
53
diffusion limitation 2 components
diffusion to RBC O2 and CO2 reaction in RBC both contribute 50%
54
diffusion capacity error
VQ mm will fuck with things yet not a diffusion problem
55
Fick principle
Uptake=Qt(CaO2-CvO2)
56
measure PBF
fick prinicple uptake measure by measuring conc of expired O2 or indicator dillution method
57
why shunt cant be compensated
well oxygenated alveoli even with +++PAO2 can't carry much more O2 due to Hb maxed out #plateu of OHDC
58
asthma
airway obstruction-->shunt-->hyperventilate-->decreased PaCO2-->EXHAUSTED-->increased PaCO2 BC-->autopeep
59
copd
shunt+deadspace-->hypoxia and HYPERCAPNIA treat with PEEP to reduce shunt
60
hufners constant
each GRAM of Hb takes 1.34 ml of O2
61
OHDC figures
100: 100 90: 60 p50: 28 75: 40 venous Myoglobin 50point is 2.8mmHg
62
central venous vs mixed venous #teach
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
63
respiratory compliance curve
recoil P on x axis
64
wheatstone bridge
#galvinometer
65
aorta vs radius
Aortic incisura | Radius diastolic hump
66
glucose handling graph
glucose flux vs plasma glucose (x)
67
Warfarin met
Cyp450 CYP3A4 Met induced by STP And carbemazepine Met inhibited by amiodarone and cimetidine
68
Warfarin reversal
Remember prothonvinex
69
Hb BD
haem +globin haem-->fe and biliverdin-->bilirubin bili-->urobilinogen-->stercobilin
70
Conj vs uncong
uncong=prehepatic or hepatic eg cirrhosis conj=hepatocellular or post hepatic if any bili in urine=hyperconj
71
tryptase
1,4,24 peaks, dropping, baseline. baseline will factor into interp
72
anaphylaxis
``` Hist leukotreine-chemotractic-->delayed effect PG bradykinin TNFa 5HT NO Tryptase-->activate comp system, coag-->thombus and DIC ```
73
serum vs plasma
serum is what is left after blood has clotted ie plasma without coag factors
74
role of plasma proteints
``` clings to... water pH drugs cations clots invaders enzyme function energy reserve ```
75
reticulocytes
new production of RBC | still have RNA fracgments
76
dibucaine number
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
77
``` Esterases #amanda diaz ```
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)
78
hoffman
spont degen in pH and temp | cleave of quarternary nitrogen link to central chain
79
local anaesthetic structure function | GOLD
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
80
LA pH
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.
81
remifentanil vs fent potency
can simplistically be thought of as equipotent | classically remi called 2x more potent
82
pethidine
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
83
methadone
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
84
naloxone naltrexone
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
85
Opiate classification
``` 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 ```
86
lafent offset
small Vd due to less lipid sol-->more rapid elimination despite less clearance
87
opiate change
incomplete cross tolerance
88
fent CSHT
better than alfent until2 hr infusion
89
quantal vs
graded
90
opiate rec
NOP is supraspinal Cortex, Thal, BG, PAG, Resp centre, SC, periph
91
white vs grey matter
white is fat so middle of brain and outter tracts of SC
92
ANS
sympathetic spinal colum grey matter and peripheral ganglio PSNS CN nuclei Sacral Rami
93
content O2 of blood Normal
200ml/L
94
bohr reason
H stab Hb binding ttttttoo boooooohring
95
``` Hamburger effect RV RV RV GOLDEN ```
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
96
henderson
ph=pka +log HCO/CO2x0.003 pka+log A-/HA
97
HCO3 in resp acidosis
INCREASES in acute and chronic 3x more in chronic
98
Predicted CO2
HCO3x1.5+8
99
Bicarb types
standard with real CO2 actual if CO2 normal BE if real CO2 BExxx if normal Hb
100
NAG
10-16
101
CATMUDPILES
Cyanide, CO, aminoglycosides
102
measure osmolarity
2xNa +urea+glucose
103
Blood gas interp steps
met or resp or mixed HAG or NAG osmol gap delta gap for HAG+other
104
HAG NAG renal
RTA is HCO3 loss hence NAG | ureamia is HAG
105
La Place | CORE
P=2T/r
106
surfactant and hysteresis
collapsing-->surfactant pressed together-->resist further collapse
107
Resp compliance
1/RC=1/L+1/Thoracic cage =1/100
108
surfactant
Prevention of fluid transudation. As the surface tension forces are generally reduced by surfactant, less interstitial fluid is sucked into the alveolus.
109
dynamic airway compression relevance
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
110
spiro dx
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
111
RR and TV and WoB in Dx
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
112
static compliance
oeophageal pressure measure
113
adding to alpha cardbon
BLOCKS MAO
114
classification of sympathomimetics
evernote gold
115
COMT mech
add a methyl group
116
MAO
oxidative deamination ie uses O2 to cleave amine
117
Sotalol
``` add salt to everything class I,II, III ```
118
low lipid bblocker
poor ab but minimal first pass met-->good OBA and long halflife as minimal met
119
adenosine
``` 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
why ohms law imperfect for lungs
elastic, non lamina, non-newtonian fluid F=P/R yet increase increase P-->decreased resistance
121
admix
"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
shunt
Shunt is the blood which enters the systemic arterial circulation without participating in gas exchange
123
anatomical shunt CORE
just 2! P+K and derranged phys thesbian which go to coronary sinus -->LA bronchial Veins-->LA
124
OLV CPAP
if blood going through may as well try add some O2 to it.
125
Pulm HTN Mx
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
silden | milrinone
S=5 M=3 visually looks that way 3->cAMP-->contractility
127
peripheral chemo rec
CO2 and O2 CB and AoA | pH only in CB
128
rotem | GOLD
clotting-->fibrin blocks-->platelet strength | CT-->CFT-->MCF-->plasmin
129
vasopressin
VwF
130
hypoplasmin
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
resp centre | CORE
Medullar resp centre Di Ve Be pons - pneumotaxic-taxes slow - apneustic centre-aps speed up efficientcy
132
HYperbaric Rx
CO poisoning decompression gas gangreen
133
pendeluf and RR
worse with high RR as need prolonged exp oause to balance
134
daltons law clinic sig
P=P1 +p2 so at everest less PP of O2
135
avagadros law
at equal temp, vol and pressure different gases contain the same number of molecules dilution of O2 in trachea-->decreased PP of O2
136
henry's law
conc proportional to pressure of gas in a liquid.
137
gibbs donnan
KPr intracell KCL out | CL comes in K comes in water comes in
138
osmotic p
the pressure that would have to be applied to a pure solvent to prevent it from passing into a given solution by osmosis,
139
oncotic
osmotic p exerted by colloids ie protein
140
albumin tonicity and effect
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
albumin 20% tonicity
Alb 130mmol/L Na 130mmol -->260mmol-->hypotonic
142
normal plasma osmolarity
280mols/L
143
TWB splitts
60% TBW 1/3 EC 1/4 IV 5% of weight is plasma vol =3.5L then add cells
144
Stewart theory
!!!!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
G+S+Xmatch
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
immunoglob
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
immune system pneumonic
Innate PGN Cs | Addaptive immune BAT
148
complement cascade
Complement - proinflamatory proteins activated by classic: Ig:Antigen or alternative or proteolytic enzymes—>inflammation, lysis - reaction in ABO incompatability - inhibited by C1 esterase
149
collegiate
increase BP, osmotic P | decreased freezing point and SVP
150
actual and standard HCO3
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
BE and standard base excess
Hb 50 (anaemic-->standardized)
152
Mannitol
RV adme and PD
153
Des PD
Decreased TV Increased RR | Nil neg into more VD more hypotensive more tachy
154
Frusemide
Pulm and systemic VD | Cl channel block can't conc medulla
155
SNP met
OHb-->met-->cyanomet Rhodanase adds sulfur group B12-->cyanocobalamine Bicobolt chelates
156
Heparin
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
HITTS RX
direct thrombin inhibitor
158
4Ts
timing 5-10days oTher Cx thombosis thrombocytopenia
159
CYP450 types
3A4 midaz warfarin, clopid | 2D6 tramadol
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Naturalf freq stiffness eleasticity
on top
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damping effect
yes does decreased freq a little and increase freq response window (ie the range of frequency of before resonance occurs)
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damping anzca text
2. 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.
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resonant freq
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.
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damping coeff
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
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HM
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
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Morphine met
CYP450 demethylation and glucornidation M3G-->neuroexcitatory M6G-->13x more potent
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octenol:water coeff
morph=1 | fent=600
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oxcodone met
noroxycodone inactive and oxymorpphone-->WEAKLY active 3A4 → inactive noroxycodone 2D6 → active oxymorphone Naloxone is an “Nalkyl derivative of oxymorphone”
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buprenorphine
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
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Mannitol
decreased CSF produ cross glom and not reab-->wash out medulla-->no reab nil met small Vd HTN transiently target osmol 300-320 hypokalaemia
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Hypertonic saline
``` 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 ```
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porphyrin
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
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parietal cell stim and inhibition
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 ```
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filling ratio N2O
0.75 or 0.66 in tropics
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yoke pins etc
yoke is the outside c grip with pins as 1 componenet and fresh gas flow outlet washer valve is part of cylinder
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Heat vs temp
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.
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SHC
The amount of heat energy required to increase one Kg of a substance by one Degree Centigrade/Kelvin
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Renal BF reg
Autoreg ``` SNS Renin ATII ANP PGs ```
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Tubulorglomerular balance
glucose | increased oncotic P in pertubular cap-->increased reab
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oliguria mech
``` osmorec HP baro LP baro renal Baro renal autoreg ```
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cardiovascular centre
HTN-->... NTS stims Nambig stims PSNS NTS inhibits RVLM hence decreased SNS
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how is medulla gradient created
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
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Vasa recta
water out as descending replaced as ascending
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potassium Ch blocker antiarrhythmic
rb sotalol
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digoxin tox
phenytoin
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SVT and VT options
amiod, flacainide, sotalol
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sotalol
class 1,2,3 Rx VT prevent SVT
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adensoisne rec
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
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Cardiac SE adenonsine
decreased atrial refractory-->AF or flutter
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adenosine met
plasma and RBC esterase
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digoxin
``` 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
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Rx digoxin tox
``` 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 ```
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Ester vs amide structure
COOR vs NHCO
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nerve block onset types
B>Ad>Ab>C | ANS>sens>motor
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neuro tox common LA
CIRCUMORAL TINGLING
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thiopentone vial
500mg in 20ml 25mg/ml NaCO3 NOT HCO3
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thio vs prop CVS
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.
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Adx
Htn brady-->pulmonary oedema seizure Nil betablcoeker
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Muscle relaxants class SE
Aminosteroids anaphylaxis Benzylisoquinoliniums histamine release
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Hoffman
Cleave nh4 from central structure Laudenosine Temp and oh dep
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Butylecholinesterase prod
Liver
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Leg block monitor
Post tibial nerve | Plantaflexion of big toe
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Onset muscle
See Evernote
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FRC as o2 buffer
constant o2 supply. stops swing of insp O2 with none on exp
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full body plethysomgraphy
V1.P1=(V1-changeV).P2 of box V2.P3=(V2+changeV).P4 of lung gauge pressure =alv pressure when zero flow
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estimate pao2 by age
100-a/3
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po2 tissue
5 | mitochondria 1
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Hep BF and volatiles
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
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hepatic unit
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.
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hepatic failure first effected
synthetic function | enzyme function ++late
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coags made by liver
fibringoen, ATIII, prothrombin,2,7,9,10
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osmolarit of blood and NACL tonicity of NACL
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
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tonicity define
effective osmotic pressure
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normal osmolar gap
10 due to normal unmeasured osmoles
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osmolar gap cx
mannitol, ethanol, methanol
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colligiate properties
osmotic pressure, depressed freezing point
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solute vs solvent
U--->V
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how to measure (not calc) osmolarity
osmometer: HP vs osmotic vapour pressure depression FP depression with platue pressure using thermister
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pendulum chest
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".
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why PTx resolves
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
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slow vs fast twitch
slow is Type I
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RAP normal
0-5
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fluid bolus starling curve
increased RAP and MSFP
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cefazolin allergy or MRSA Abx
clina/ticoplanin vanc for MRSA
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GI absorption
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.
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bacterial wall
g+ve thick PG wall (peptidoglycan) | g ive thin PG wall with lipopolyysacharide layer
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ABx moa anaesthetics
evernote | all renal clearance except metronidazole which has an active met-->renal Cl
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contamination class and ABx
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
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nerve block
Supraclav: commet with subclavian artery interscalene: between scalenes infraclavicular: surrounds axillary artery cephalad axillary: surrounds axillar
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metabolic alkalosis
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 ```
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LA tox
``` circum oral tingling and numbness tinitus vertigo NOT TASTE or VISION EXCITABLE TWITCHING seziure coma ``` HTN tachy VD prolonged QRS and PR and brady
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semiopen
mapelson ``` T extended freq disabled A for efficeincy Bain for BRAIN MRI ```
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closed benefit and loss
slow onset | warm
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how does afterload affect contractility
The increased afterload causes an increased end-systolic volume. This increases the sarcomere stretch. That leads to an increase in the force of contraction.
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withdraw reflex
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
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SNS cell bodies and structure
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
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ANS structure
SNS and PSNS - efferent: visceral and somatic - afferent (just visceral): organ sens, reflex loop, refered pain
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A delta vs C fibre lamin
A delta lamina 1,5 #15As rugby team pain C is lamina 1 2 3 as per ANZCA talk and a model answer
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pain fibre rec modulation
evernote pain pathway goldne
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once NMDA stim
cations in changed gene transcription activate kinases central sensitization
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peripheral sensitation
at nociceptor | central is at DH and brain
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central sens
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
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spinoreticular tract
spine to reticular formation then thalamus and hypothal-->emotion
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neuropathic pain mech
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
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paracetamol meta
phase I (cyp450)-->NAPQI-->neutralized by glutathione (replenished by NAC) phase II (simultneous) non toxic
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NSAID in IHD risk
both selective and nonselective CI
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paracoxib benefit
less asthma less PLi (PL is cox1) less GI
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pain Mx options
* 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 ```
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gabapentinoids soa and SE
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
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Gabapentin vs pregabalin
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
tramadol met path
o desmethyltramadol-->opioid rec | CYP2d6 (genetic variability)
252
ketamine routes
Rb oral 40min | nasal 15min
253
clonidine vs dex
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
pain pathway
Tissue damage/Nociception/Pain Experience
255
Buprenorphine
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
fentanly clearance and effect site term
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
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codeine met
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
nociception
def
259
substantia geletanosa
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
wind up
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
Ca to NT release
Ca binds calmodulin-- calmodulin dep kinases-->doc and release
262
Ca in second order afferent neuron pain
Ca in due to NMDA, AMPA, NK1 Ca:calmodulin-->changed gene transcription altered K perm second messangers-->NO-->neurotoxic
263
silent nociceptor
unmyelinated primary afferents, normally do not respond, but in presence of inflammation or chemical sensitization may become responsive and discharge vigorously
264
blood supply to kidney in shock
reduced! ATII and SNS-->VC afferent and efferent PG-->VD afferent and effent normally ANP-->VC efferent and VD afferent-->increase filtration
265
ADH trigger
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
ADH
see evernote
267
WOB diagram
trapezium=ELASTIC (TISSue and alv ST) | curve=RESTRICTIVE: 80% airway 20% tissue (increased in interesitial Dx)
268
static vs dynamic
Dynamic compliance=vol/(Pmax-PEEP) -hence no eosoph Static Compliance=vol/PlateuP-PEEP) -hence eosoph
269
potassium channels cardia AP
K1 RMP Kto special transient at peak of 1 Kr rectifying
270
excitatory and inhib NTs
glut, NAd ach, 5HT inhib GABA glycine
271
time constnat
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
oxycodone met
CYP450 noroxycodone active 15% of parent renally elliminated so imperfect but a fair option for PO renal Dx
273
pethidine
Mu, SSRI, VGSC, SE Ach met to norpethadine 50% as potent but renally accumulates ``` accumulates in renal delerium anticholinergic addictive seziures due to ```
274
Na Ch types
resting (closed) -->active-->inactive ARP due to NaCh in inactive stage (need time and repol to reset both gates)
275
Botulin etc
botuline stops release of Ach | hemicolinium inhibits Choline recycling
276
T tubule
invagination of sarcolemna
277
MEPP
small small small big
278
cardiac vs smooth vs cardiac
evernote
279
midaz met
a little bit of active met yet renal excretion no problem
280
MG vs GBS
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).