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Viva > VIVA august > Flashcards

VIVA august Flashcards

1
Q

Closed system neg

A

Long time to prime system

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2
Q

semiclosed define

A

Semi-closed systems have a full boundary with the surrounding atmosphere, and use a controlled source for fresh gas flow. Intake of ambient air is prevented, but excess fresh gas is vented into the surrounding atmosphere. Partial rebreathing of exhaled gas can occur. They are commonly subdivided using the Mapelson classification (see below).
Closed systems have a totally closed boundary across which no gas enters or is vented, meaning that complete rebreathing takes place. The commonest example is the circle system.

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3
Q

circle system

A

Circle system RB bag

CO2 ab is in line

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4
Q

monitoring NDMR

A

acceleromyography
-peizoelectric crystal

DBS
-if nil twitch then wait
-fade–>neo give neo 0.02mg-0.05mg/kg
no fade–>occurs when TOFCR =0.6 (so may be no DBS fade despite inadequate reversal!) so wait or Neo 0.02mg/kg as per up2date table 2

I presume if nil titch cant reverse with neo
ie only useful for assessing shallow block

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5
Q

TFOC

A 
Tofc (prop dreams) 
loss of...
4th at 75% occupancy
3rd 80%
2nd 90
1st almost 100%
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6
Q

normal volumes

A 
RV=15
ER=15
TV=10
IR=45
VC=70
TLC=85

so normal VC=5L
normal FEV1=3.5
normal FEV1/FVC=70%

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7
Q

NACHR types

A

aabde is adult NACHR
aabdg is fetal
stim of nerves–>mature

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8
Q

NMJ terms

A

sarcollemma is the membrane around the muscle fibre

sarcomere is a muscle unit

myosin is thick centre
actin is thin margin

Ca binds troponin –>move tropomyosin to expose my sin binding site on actin

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9
Q

sux MoA

A 
NDMR bind 1 of alpha of NACHR
sux binds 2
-accomation block
-bind-->conformational cange in NACHR-->depol-->end plate continually depolarisied-->M gate of near by NaCH opened but H gate can't reset
-also increased K perm-->hyperpol
-also decreased sens of NaCHR

yes phase I is sux

Sux doesnt cause fade as purely post synaptic

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10
Q

fade

A

fade

  • NDRM block presynaptic rec
  • the normal presynaptic NACHR–>positive feedback to release more Ach
  • blocked presynaptic–>fade as less Ach available for subsequent contractions
  • contraversion as snake venum which is purely postsynaptic causes fade.
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11
Q

Cx of anion gap

A

HCO3 Alb NH4

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12
Q

H3PO4

A

phosphoric acid

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13
Q

handling acids

A

buffer
compensate ie eliminate
Rx cx

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14
Q

ph

A

-log10H

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15
Q

pka

A

ka= A.H/AH
more stronger high ka–>low pKa

pka=-log10Ka

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16
Q

BIB which is ionized

A

B + H+–>BH+

BH+ is ionized (charge)

increase H–>ionized #BIB

A-.H+–>A- + H+

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17
Q

why propofol emulsified but thio not (yes)

A

pka propofol 11 hence cant make suffiently basic to ionized so emulsify

pka of thio 7.6 so by making solution pH 11 can ionize in water
ALSO enol form in alkaly form in vial
keto form at physiological pH

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18
Q

midazolam ph and why

A

3.5 as tautomerism to closed loop lipid sol at pH4

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19
Q

keto-enol tautomerism

A

THIOPENTON
enol form in alkaly form in vial
keto form at physiological pH

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20
Q

LACTATE DEHYDROGENASE

A

PYRUVATE TO LACTATE

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21
Q

lactate prod

A

nil mitochondria eg RBC

high demand low supply–renal medulla

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22
Q

lactate destination

A

–>pyruvate–>glucose with H+ consumed in process

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23
Q

procainamide

A

amide (2 I’s) antiarrhthmic

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24
Q

NH4 system

A

glutamine from protein metabolism then further metabolised in PCT cells
–>2NH4 and 2 HCO3
NH4 swapped for Na HCO# reab

NH3 als secreted in descedning LoH from medulla–>bind H+

BIGGER impact vs HPO4

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25
Q

min urinary ph

A

4.4 because active H transport enzymes ineffective beyond this pt

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26
Q

carbonic anhydrase

A

CO2–>carbonic acid

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27
Q

H+ in plasma

A

36nmol/L

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28
Q

renal acid Mx why required

A

shit tone of CO2 production=shit tone of resp loss so nil contribution normally

40-80mmol of fixed acids/day (small vs CO2 20K! yet still lots)–>renal requirement

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29
Q

CO2 0.03

A

SOLUBILITY CONSTANT

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30
Q

IC cells principal cells

A

principla a SALTED student

intercallated is interrelated h:K H

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31
Q

CO2 MV and MV vs CO2

A

MV as determinent –>hyperbola at both extremes

CO2 as derterminent–>linear until max and min platues

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32
Q

Smooth vs cardiac and sketal

A

cardiac and skeletal SR, ryanonide, T tubules, troponin.

cardiac has gap juctions skeletal doesnt

cardiac skeletal

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33
Q

inductor vs capacitor

A

evernote

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34
Q

voltage

A

potential difference

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35
Q

impedance

A

obstruction to flow

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36
Q

inductance

A

property of changing current in a conductor–>EMF–>change in current in another conuctor

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37
Q

capacitor

A

2 conductors and an insultor

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38
Q

micro macro shock

A

0.1ma vs 100ma

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39
Q

electrical safety touch active or neutral wire

A

patho of least resistance

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40
Q

accidental induction

A

capacitive coupling and stray capactitance

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41
Q

RCD

A

coil around active and nuetral if current difference–>leak–>trip 5-10mA

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42
Q

floating circuit

A

LIM alarm at 5mA

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43
Q

Hz from power socket and why

A

Why 50Hz?
The lower the frequency, the more efficient the delivery of electricity - less energy is lost from the system
Apparently 50Hz is the lowest frequency where flickering of lightbulbs is not noticeable, so this was chosen as the standard
Why do I care about this for the exam?
AC 50Hz is the most dangerous type of electrical current, in terms of causing ventricular fibrillation!

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44
Q

neutral to earth role

A

protect the electrical wires on streat from delivering huge current to houses with lightening strike complete curcuit from neutral to earth

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45
Q

case to earth

A

casing has wire–>earth socket–>closed system with low resistance if faults

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46
Q

soda lime

A

CO2+H20–>H2CO3
H2CO3 + NaOH–>H20 and heat and NaCO3
NaCO3+CaOH–>caCO3 and NaOH

water and heat speed up and NaOH is a fast reactor to mop CO2 quickly.

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47
Q

amsorb

A

CaCl instead of NaOH holds water so no base so less CO and compound A

FYI — Amsorb (we use)
Amsorb consists of calcium hydroxide lime (70%), water (14.5%), calcium chloride (0.7%), and two agents to improve hardness (calcium sulfate and polyvinylpyrrolidine). Amsorb has half the absorbing capacity of soda lime and costs more per unit. Calcium chloride serves as a moisture-retaining agent to allow for greater water availability. As a result, there is no need for alkali agents like NaOH or KOH. Without these strong monovalent bases, calcium hydroxide lime has fewer adverse reactions associated with the breakdown of inhalation agents (such as the formation of compound A or carbon monoxide [CO]).

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48
Q

cardiac reflexes

A

COntract
-Increased SVR—>increased contraction

BOWDITCH force frequency relationship

  • increased HR—>increased contractility
  • Bowed Box in a ditch—>little kid gets heart rate up and then it contracts to nothing

Bainbridge
Atrial stretch—>baro—>decreased HR
-Bain barorec

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49
Q

Group
screen
Xmathc

A

screen is patient plasma vs lab RBC (loooking for patient plasma antigen/antibodies)

Xmatch
-will body reject donor RBC

INCUBATION
WASH
glutination

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50
Q

IOP

A

As the globe has typically poor compliance, a small increase in volume can cause a large increase in intraocular pressure. Factors affecting volume include:

Volume of aqueous humor
Aqueous humor is a clear fluid that fills the anterior and posterior chambers of the eye, and provides avascular tissues with nutrients and oxygen whilst still allowing light to pass freely between the lens and retina. Volume of aqueous humor is a function of:
Production
Aqueous humor is produced by secretion and filtration from capillaries in the ciliary body in the posterior chamber, and circulates through into the anterior chamber.
Production is accelerated by β22 agonism
Production is inhibited by α2 agonism
Carbonic anhydrase inhibitors decrease aqueous humor production probably by decreasing sodium secretion into the eye
Reabsorption
Aqueous humor is reabsorbed into venous blood in the canal of Schlemm.
The trabeculae meshwork is the main source of resistance to reabsorption
If this is blocked, a significant reduction in reabsorption can occur and IOP will increase.
Reabsorption is affected by:
Haemorrhage
Blocks trabecular meshwork.
Muscarinic antagonism
Dilates pupil, which brings the iris closer to canal and decreases absorption.
α1 agonism
Dilates the pupil, decreasing absorption.
PGF2α
Relaxes ciliary muscle, increasing absorption.
Volume of blood within the globe
Affected by:
MAP
Venous obstruction
External factors
Other factors affecting volume or compliance of the globe:
Extraocular muscle tension
Extraocular compression

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51
Q

CSF in stroke

A

SAH–>block arachnoid villir reab (arachnoid projections through dura
SDH not an issue
#

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52
Q

monroe kelly

A

liquids are incompressible

CSF production in constnat
Reabsorption is pressure dependant and increases linearly above 7mmHg

Prod in lateral vent chorocoid plexus and in ependymal cells of 3rd and 4th ventricle
150ml constant
500ml prod/day (3x cycle per day)

Ultra filtrate and secretions from fenestrated endothelial cells
Na active glucose fascilitated
Co2 higher pH lower glucose lower

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53
Q

TEG PL change

A

MA change indep of K and alpha

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54
Q

TEG fibrinolysis

A

imediate drop in MA once formed

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55
Q

PL function analyser

A
  • Citrated whole blood is drawn through a hole in a collagen-coated membrane which is bound to adrenaline or ADP
  • Under the shear stress influences, platelets aggregate and seal the hole
  • This is sensed by a pressure transducer
  • The time taken for platelets to occlude the hole is referred to as the closure time
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56
Q

MAC requirement at everest

A

double the MAC as half the barometric pressure

2% of half instead of 2% of the whole.

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57
Q

increased MAC

A

P+K p 107

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58
Q

propofol to LoC

A

2.5

to loss of motor respon 14

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59
Q

MAC ANS

A

MAC BAR

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60
Q

sens and spec

A

A burglar alarm is highly sensitive if it goes off every time someone breaks in.
It is highly specific it is rarely triggered by possums on the front porch (my thoughts)

The result is that sensitivity is a measure of the probability of getting a positive result out of all the positive cases, and that specificity is a measure of the probability of getting a negative result out of all the negative cases.

  • Sensitivity (also called the true positive rate, the epidemiological/clinical sensitivity, the recall, or probability of detection[1] in some fields) measures the proportion of actual positives that are correctly identified as such (e.g., the percentage of sick people who are correctly identified as having the condition). It is often mistakenly confused with the detection limit,[2][3] while the detection limit is calculated from the analytical sensitivity, not from the epidemiological sensitivity.
  • Specificity (also called the true negative rate) measures the proportion of actual negatives that are correctly identified as such (e.g., the percentage of healthy people who are correctly identified as not having the condition).

The positive and negative predictive values (PPV and NPV respectively) are the proportions of positive and negative results in statistics and diagnostic tests that are true positive and true negative results, respectively

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61
Q

Can O2 measurement be done with IR

A

no need two different atoms to absorb IR

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62
Q

IR set up

A

filter to select freq through

reference chamber

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63
Q

TEG

A

R/V

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64
Q

main stream vs side stream

A

Side stream:

fixed volume of gas continuously sampled from the circuit

aspirated through tubing, released to atmosphere or returned to circuit

rate adjusted between 50-500ml/min

errors:

sampling as close to patient as possible to minimize circuit dead space

sampling rate exceeds expiratory flow rate & inspired gas sampled

hypoventilation is sampling exceeds fresh gas flow

water vapour condensed in sample tubing/accumulates in measurement chamber – erroneous readings (filters and water traps in systems)

may have gas leakage, CO2 diffusing out

Main stream:

incorporate the infrared sensor into the circuit very close to the endotracheal tube.

Directly measure in circuit, no gas subtracted

Effects of breathing circuit and sample tubing dead space minimized, response time faster

Problems/errors:

Need to be warmed to prevent condensation

Avoid skin contact (warm, burns)

Heavy, risk circuit kinking of ETT

Requires frequent calibration

Prone to soiling with saliva, mucus

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65
Q

mass spectrometry

A

postively charged not neg!

Clinical use of mass spectrometry for expired gas analysis began in respiratory care units in the mid-1970s. They were introduced into operating rooms and anesthesia practice shortly thereafter. Because of their size and complexity, hospitals often connected many operating rooms to a single spectrometer and had the results relayed back to the anesthesiologist. The convenience plus low cost of infrared analyzers has largely phased mass spectrometry out of clinical use.

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66
Q

power alpha beta

A

Alpha value: value chosen (convention alpha = 0.05) for ‘acceptable’ level of Type 1 error. Thus accept 5% chance of incorrectly rejecting the null hypothesis (i.e. stating that there is a difference between the groups when there is not). This is important in medicine as stating that there is a difference between two drugs may cause harm to patients by incorrectly changing practice.

Beta value is a chosen value (convention 0.2) that relates to the chance of making a Type 2 error.
This means that we accept a 20% chance of incorrectly accepting the H0 and stating that there is no difference between the two groups, when actually there is a difference. This is less important as although may result in delay of discovery of important advances in medicine, it is less likely to harm the patient population as would be with Type 1 error.

Power = 1 – beta, usually 80%.

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67
Q
  1. What are the determinants of sample size?
A
  1. What are the determinants of sample size?
    a) Chosen alpha value: smaller value requires larger sample size
    b) Chosen beta value: smaller B (higher power) means larger sample size
    c) Effect size ie Delta value: if looking for small difference between two groups, sample size increases
    d) Theta: underlying variance in population tested (cannot control) – large variance will increase sample size.
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68
Q

thermo dilution

A

AUC Cl dose

not ficks prinicple

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69
Q

ficks principle

A

CO = 250ml / (200ml – 150ml)

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70
Q

HER

A

High HER
-metabolises free drug so quickly that PrB releases bound drug to maintain equilibrium hence PrB % irrelevant for high HER but ++ RELEVANT for low HER #P+H

(a-v)/a

The hepatic extraction ratio is determined largely by the free (unbound) fraction of the drug and by the intrinsic clearance rate

With increasing hepatic blood flow, hepatic extration ratio will decrease for all drugs

drugs with low intrinsic clearance:
Hepatic extraction ratio will drop more rapidly with increasing hepatic blood flow
Hepatic clearance will not increase significantly with increasing blood flow

The last point is important. Consider a drug which is completely absorbed and undergoes 95% clearance by first pass metabolism, making its systemic bioavailability 5%. With enzyme inhibition, a minor 5% drop in hepatic enzyme activity will result in a doubling of systemic bioavailability (to 10%), which could represent a toxic concentration for drugs with a narrow therapeutic index.

verapamil as a stereotypic drug with high individual variability due to high first pass
ALSO MORPHINE

The liver also forms a reservoir of blood with a volume of 450 mL (30 mL/100 g liver tissue), half of
which may be mobilized if hypovolaemia occurs.
The portal blood can bypass the sinusoids as blood
is shunted from portal venules to hepatic venules
by the relaxation of hepatic venule sphincters.
Catecholamines can mobilize blood from the sinusoids. The liver can also buffer against an increase
in blood volume. Hepatic compliance (i.e., distensibility) is higher at high venous pressures than at
low venous pressures.

In the presence of portosystemic shunts, some portal blood bypasses first pass clearance and therefore bioavailability of drugs with a high first pass clearance will be increased

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71
Q

low HER

A

phenytoin

methadone

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72
Q

HIGH HER

A 
Glyceryl trinitrate
Verapamil
Propanolol
Lignocaine
Morphine
Ketamine
Metoprolol
Propofol
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73
Q

HER

A

High lipid sol—>good GI ab and high HER #bblockers P+H

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74
Q

osmolality measured in lab

A

Measured by: Movement of a stick on thawing solution, 1 mole will depress freezing point by 1.86 Kelvin.

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75
Q

mosmol

meq

A

measure of osmols

measure of osmols*valency of that osmol

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76
Q

osmoloarity

A

avagadros number of molecules/L

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77
Q

solvent solute

A

vent is the water
ute is the salt

How to remember ‘solute & solvent’ in a solution: A thief broke into a building and filled a bag with loot. Then the police came. The thief hid the loot in a vent, so he wouldn’t get caught. The solute goes into the solvent

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78
Q

how does hyperglycaemia cx low Na

A

hypersomolar–>draw fluid in (and i assume trigger ADH)

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79
Q

psuedo hyponatraemia

A
  • normally plasma contains 93% water, 7% solids (5.5% proteins, 1% salts, 0.5% lipids)
  • hyperlipidaemia & other disorders increase solid phase up to 10%
  • [Na+] in aqueous phase
  • most methods for plasma [Na+] measure Na+ content of fixed volume of plasma, yield misleadingly low [Na+] as lipid accounts for larger than normal % of plasma
  • concentration of sodium in plasma water is unchanged, but there is less water and therefore less sodium in a given volume of plasma
  • osmolality will be normal
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80
Q

ineffective osmoles

A

glucose and urea

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81
Q

hep BF

A

evernote

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82
Q

HER Prb

A

p10 P+H
low metabolic capacity–>Prb relevant as free drug overwhlems system and then ER reduced after brief Mx–>narrow window so test.

Intrinsic Cl, unbound drug

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83
Q

HER big 2 determinants

A

Intrinsic Cl, unbound drug

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84
Q

SHC water

A

4.2Kg/kg/C

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85
Q

ITR margins

A

sweat=effective
VC=effective
Autonomic response

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86
Q

ITR lower margin term

A

threshold temp

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87
Q

TNZ lower margin term

A

Critiical temp

VC and VD can occur here as don’t really fuck with metabolic rate (regulated by controlling heat loss not producing heat)

The thermoneutral zone is defined as the range of ambient temperatures where the body can maintain its core temperature solely through regulating dry heat loss, i.e., skin blood flow.

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88
Q

temp rec path

A

Ad delta cold <25
c warm raffini 30-46
STT
post HT Poles cold efferent

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89
Q

LHV number

A

2.4kj?kg at 37C

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90
Q

thiazide

A

block Na reab–>hyponatraemia

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91
Q

prod of aqueous humer

A

B2 increase

a2 inhibit

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92
Q

Drainage of aqueous humur

A

haemorrhage blocks

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93
Q

formular name thermodilution

A

stewart hamilton

?law of conservation of energy?

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94
Q

Loop diuretic

A

Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus causing sodium, chloride, and potassium loss in urine.

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95
Q

thiazide

A

Thiazide diuretics control hypertension in part by inhibiting reabsorption of sodium (Na+) and chloride (Cl−) ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl− symporter

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96
Q

spironolactone

A

causes less K secretion ie potassium sparing diuretic

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97
Q

aldosterone

A

Na:KATPase PRINICPLE ASSAULTED DCT AND CD
HATPas INTERCALATED CELLS CD
HK ATPase INTERCALATED CD

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98
Q

GFR EQUATION

A

GFR=kf.NFP NOTE: afferent Cap pressure hydrostatic is 60mmHg ie MAP oncotic is 24

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99
Q

low pressure baro

A

IVC SVC atrial Pulm art and vein

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100
Q

calculate Hep BF

A

Like CO AUC (ficks prinicple is more complex with a fixed infusion)

ICG has a known HER 0.74

AUC (measured)=x (known)/cl
AUC=x/(Q.0.74)

HER is 0.74 for ICG
Cl is vol cleared per min=Q.HER ie Q.0.74

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101
Q

renal clearance calc

A

Renal clearance can be calculated by dividing the
amount of a substance in urine (collected over a
given time) by the plasma concentration, P:
P
Renal clearance =
Amount of substance in
urine per unit time
Plasma concentration of
substance,
The amount of a substance in urine over a given
time is the volume of urine produced in that time,
V, multiplied by the urinary concentration of the
substance, U. Thus, for any substance,
U V
P = × Renal clearance
(plasma volume/unit time; mL/min,L/day

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102
Q

CrCl vs GFR

A

Creatinine is filtered by the renal tubule and is not
reabsorbed. Creatinine clearance is used routinely
as a method of estimating GFR. However, a small
amount of creatinine is secreted by the tubules
into the lumen so that the creatinine clearance is
slightly greater than the true GFR.

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103
Q

GFR calc

A

RENAL CL and GRF
Clearance= amount removed so what do you need vol, conc urine and conc plasma
Renal clearance can be calculated by dividing the amount of a substance in urine (collected over a given time) by the plasma concentration, P: P Renal clearance = Amount of substance in urine per unit time Plasma concentration of substance, The amount of a substance in urine over a given time is the volume of urine produced in that time, V, multiplied by the urinary concentration of the substance, U. Thus, for any substance, U V P = × Renal clearance (plasma volume/unit time; mL/min,L/day

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104
Q

Renal BF calc

A

RENAL BF
Clearance of a drug that is peed out every time
PAH is filtered at the glomerulus, and any remaining in the peritubular capillaries is secreted into the lumen by proximal tubules. When the PAH concentration is low, all the plasmaperfusing, -filtering and -secreting parts of the kidney (the effective renal plasma flow is 85%–90% of the total renal plasma flow) are completely cleared of PAH. The renal clearance of PAH is therefore equal to the effective renal plasma flow, from which the effective renal blood flow can be calculated: = − Effective renal blood flow Effective renal plasma flow 1 Blood haematocrit

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105
Q

GFR vs eGFR

A

eGFR is simple plasma Cr with nitl urine monitoring

plasma cr is inversely proprotional to CrCl (requires urine monitoring) which is similar to GFR (requires inuline)

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106
Q

HCT normal

A

45%

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107
Q

%BF organs

A

Having Sex usually brings man kids later

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108
Q

oncotic pressure normal

A

24mmHg #half to hydrostatic as a rule of thumb

60-15-24=21 at afferent

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109
Q

fluid shift in haemorrhagic shock

A

decreased hydrostatic out increased oncotic in–>autotransfuse

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110
Q

high dose ADH renal

A

decreased RBF and gfr as constrict afferent

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111
Q

intralipid

A

fat emulsion soya and egg phosphatatide and glycerol

1.5ml/kg of 20%

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112
Q

risk of LA tox drug factors

A

VD or VC!

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113
Q

pathomneumonic of bupivocaine tox

A

refractory VT or VF

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114
Q

motor neuron

A

AALPHA

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115
Q

ONSET LA AND LIPID SOL

A

Slower

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116
Q

LA tox ration neuro and cardiac

A

Cardiac collapse:CNS

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117
Q

nerve block onset by nerve type

A

1st C fibres are large unmyelinated (ache and SNS fibres) blocked at same time as A delta pain and cold (small myelinated)
-stoelting “Both types of pain-conducting fibers (myelinated A-δ and unmyelinated C fibers) are blocked by similar concentrations of local anesthetics, despite the differences in the diameters of these fibers.”

2nd touch and pressure Abeta

3rd motor A alpha

—>D,C,B,A

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118
Q

lipid sol of LA number

A

octenol: water coeff

lig 350
rop 700
bup 3000

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119
Q

pka LA

A

7.9 and 8.1

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120
Q

ester LA met

CORE

A

rapid organ indep hydrolysis by butlycholinesterase
metabolite is PABA–>hypersens reaction

cocaine has hepatic hyrolysis –>inactive–renal ecretion

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121
Q

amide LA

A

amidase–>hydroyxlation and N-de-alkylation
dep on liver
minimal renal excretion of unchanged drug

prilocaine
–>o toludeine—>metHb (oxidized Fe2+–>Fe3+ –>metHb–>cant carry O2)–>Rx with methylene blue

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122
Q

ester example

A

procaine
tetracaine
cocaine

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123
Q

dibucaine number

A

INHIBITS BUTYLCHOLINESTERASE
Inhibits normal allel but hardly touches mutant allel
So more inhibition with Normal enzymes
hence
Normal number >80
Homogenous atypical is 20. (Less inhibition. Less change. Lower number)

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124
Q

BIB equation

A

B + H+—>BH+ BH+ is IONIZED B Is unionized

125
Q

AIA EQquaion

A
  • AH—>A- + H+. NOTE THAT BASE AND ACID HAVE NO CHARGE AH AND B
126
Q

Hb structure #evernote

A

If Fe3+—>methaemoglobinaemia—>can’t carry O2

O-tolulene from prilocaine in EMLA causes this

127
Q

Fuel cell

A

Cathode electrons consumed (RIG) in presence of O2—>more current
Cath has a great rig and consumes lots of O2 and energy

At the anode: Pb + 2(OH) → PbO + H 2 O + 2e –
(OIL) oxidation of lead at anode (spits of electron)

128
Q

Pulse ox absorption

A

660 deoxy absorbs RED 660nm (990nm is IR on right)

beer lambert not strictly applied due to scatter hence calibrate with pop study so…
A copy of this correction calibration graph is available inside the pulse oximeters in clinical use. When doing its calculations, the computer refers to the calibration graph and corrects the final reading displayed.

LED pattern different to 50Hz to minimize interference

129
Q

pulse ox memorable errors

A

dye, MetHb, COhb
nail pollish
arrhythmias

anaemia irrelavnt

PATHOLOGY, PATIENT, PROGRAMME, PROBE

130
Q

draw pulse ox curve for 75% sats

A

half way between oxy and deoxy ;)

131
Q

pulse ox AC DC

A

So the final signal picture reaching the pulse oximeter is a combination of the “changing absorbance” due to arterial blood and the “non changing absorbance” due to other tissues.

132
Q

LED benedit

A

Are cheap ( so can be used even in disposable probes)
Are very compact (can fit into very small probes)
Emit light in accurate wavelengths
Do not heat up much during use (low temperature makes it less likely to cause patient burns)

133
Q

LED pattern

A

LED pattern different to 50Hz to minimize interference

lights off–>detect baseline interference
red on–>change
IR on–>change

134
Q

R ratio

A

R absorbance AC/DC red / AC/DC IR

modulation ratio. gives the ratio of change to both EM ranges in relation to one another. this number is then clinically correlated with study pop

R is derrived from population study. different population–>different R value in different brands–>difference

R = (ac absorbance/dc absorbance) red / (ac absorbance/dc absorbance )IR

R corresponds to SaO2
— SaO2 100% = R 0.4
— SaO2 85% = R 1
— SaO2 0% = R 3.4

135
Q

Cvs changes in obesity mak95

A

evernote

136
Q

laplaces law and PPV

A

P=4T/r

if T stable then decreasing r–>increasing pressure inwards to collapse

(P, ventricular pressure; r, ventricular radius; h, wall thickness).

Decreased afterload due to a reduction in LV end-systolic transmural pressure and an increased pressure gradient between the intrathoracic aorta and the extrathoracic systemic circuit

Mechanisms affecting the right ventricle and the pulmonary circulation are:

Increased intrathoracic pressure is transmitted to cenral veins and the right atrium, decreasing right ventricular preload
Increased intrathoracic pressure is transmitted to pulmonary arteries
Transmitted alveolar pressure increases pulmonary vascular resistance
Increased pulmonary vascular resistance increases right ventriular afterload
Thus, increased afterload and decreased preload has the net effect of decreasing the right ventricular stroke volume.
Mechanisms affecting the left ventricle and the systemic circulation are:

Decreased preload by virtue of lower pulmonary venous pressure
Decreased afterload due to a reduction in LV end-systolic transmural pressure and an increased pressure gradient between the intrathoracic aorta and the extrathoracic systemic circuit
Thus, decreased LV stroke volume
The consequences of this are:

Decreased cardiac output
Decreased myocardial oxygen consumption

137
Q

Closing collapse-why base

A

base of lung smallest due to gravity

138
Q

FRC in ovese GA

A

Under anesthesia, the FRC of the obese patient decreases about 50% as compared to 20% reduction for the nonobese patient.

CLOSING CAPACITY UNCHANGED

139
Q

closing capity changed with

A

effort, flow
age
COPD

not obesity

140
Q

WOB graph

A

Elastic work
About 65% of total work, and is stored as elastic potential energy. Energy required to overcome elastic forces:
Lung elastic recoil
Surface tension of alveoli
Resistive work
About 35% of total work, and is lost as heat. This is due to the energy required to overcome frictional forces:
Between tissues
Increased with increased interstitial lung tissue
Between gas molecules

141
Q

ARP

A

Phases 0, 1, 2 and most of 3 are refractory to stimulation. In fact, until the membrane reaches -50 mV the myocyte cannot contract again. This is the ABSOLUTE REFRACTORY PERIOD.

Ca keeps them above the reset point Na Ch are time dep

Nerve refractory period 2ms
Myocyte 200ms+50ms RRP (due to ca ch)

142
Q

antiplatelets

A

dipyridamole potentiaties ie augments adeonisine not inhibit–>increased cAMP it alsoe is PDEi to increase cAMP–>send messangers–>PLi

clopidogrel p2y12 subunit of ADP rec
also -prasugrel
-ticagrelor

143
Q

tramadol met

A

desmethyl tramadol active
renally cleared
CYP2D6–>genetic variability

144
Q

tapentadol

A

nil active met

minimal but some renal clearance

145
Q

PL granules

A

alpha
fibronectin, fibrinogen, vWF, PDGF, and Thrombospondin, platelet factor 4.

δ-granules
Contain 5-HT, ATP, ADP, and Ca2+.

146
Q

platelet storage duration

A

5 days

147
Q

Pl stroage treatment

A

wiki

Platelet aphoresis vs pooled whole blood platelets

  • aphoresis–>sufficient dose from a single donor–>better
  • pooled–>from whole blood in insuffient dose from any single donor so pool together–>more risk of bacteria and virus

Both apheresis and pooled platelets are leucodepleted during or soon after collection and are also irradiated before release from Lifeblood, unless other specific arrangements have been made with the receiving laboratory/institution.

Platelets can be stored for 5 days after collection at 20 - 24º C with gentle agitation. Platelets can be irradiated at any stage during their 5 day storage and thereafter can be stored up to their normal shelf life of 5 days after collection.

The first advantage is that the whole-blood platelets, sometimes called “random” platelets, from a single donation are not numerous enough for a dose to give to an adult patient. They must be pooled from several donors to create a single transfusion, and this complicates processing and increases the risk of diseases that can be spread in transfused blood, such as human immunodeficiency virus.[citation needed]

Collecting the platelets from a single donor also simplifies human leukocyte antigen (HLA) matching, which improves the chance of a successful transfusion. Since it is time-consuming to find even a single compatible donor for HLA-matched transfusions, being able to collect a full dose from a single donor is much more practical than finding multiple compatible donors.

Plateletpheresis products are also easier to test for bacterial contamination

148
Q

leukodeplete and irradiation role

A

Irradiated blood components are used to prevent Transfusion-associated graft-versus host disease (TA-GVHD) the primary cause of which is proliferation and engraftment of transfused donor T-lymphocytes

The leucocytes present in donated blood play no therapeutic role in transfusion and may be a cause of adverse transfusion reactions. Removal of leucocytes may therefore have a number of potential benefits for transfusion recipients, including:

Reduced risk of platelet refractoriness
Reduced risk of febrile non-haemolytic transfusion reactions (FNHTR)
Reduced risk of CMV transmission
Reduction in storage lesion effect
Reduction in the incidence of bacterial contamination of blood components
Possible reduced risk of transfusion-associated graft vs host disease (TA-GVHD)
Possible reduction in transfusion related immunomodulatory (TRIM) effects, including cancer recurrence, mortality, non-transfusion transmitted infection
Possible reduced risk of transmitting variant Creutzfeldt-Jakob Disease (vCJD)

149
Q

betablocker BSL

A

decreased BSL cellular uptake as less glucose and less insulin to facilitate uptake and less response.

BSL can go high or low (low is more classical)

CV phys: B1-glycogenolysis and pancreatic release of glucagon, which increases plasma glucose concentrations. β1-adrenoceptor
pub med: Specific beta(2)-agonist effects on the pancreatic beta cell result in increased insulin secretion, yet other mechanisms, (b1)such as increased glucagon secretion and hepatic effects, cause an overall increase in serum glucose and an apparent decrease in insulin sensitivity.

150
Q

nerve type onset

A

—>D,C,B,A

151
Q

lignocaine met

A

hep–>MEG–>lower sezirue threshold
>600mg–>methhb–>impaired O2 transport
10% renally eliminated

152
Q

adenosine hepatic arterial

A

It is suggested that this buffer response is due to intrahepatic levels of adenosine. With reduced portal blood flow, a build-up of adenosine occurs that vasodilates the hepatic artery.

TUBULOGLOMERULAR FEEDBACK In the juxtaglomerular apparatus, the macula densa lies in the wall of the ascending limb of the loop of Henle, close to the renal arterioles. The contraction of the smooth muscle of the afferent arteriole to the glomerulus is controlled by a vasoconstrictor, adenosine, from the macula densa (although the vasoconstrictor was previously thought to be renin). The macula densa releases more adenosine if the renal perfusion pressure rises and reduces production if the pressure falls. Adenosine production by the macula densa is determined by the composition of the fluid in the ascending loop of Henle. If the perfusion pressure increases, the glomerular capillary pressure and glomerular filtration also increase. The macula densa senses the increased flow of sodium and chloride in the ascending limb of the loop of Henle and releases more adenosine, which constricts the afferent arterioles, reducing the glomerular capillary pressure and the GFR. The vasodilator nitric oxide may be produced by the macula densa when the renal perfusion pressure falls.

153
Q

laser

A

light amplification by stimulated emission of radiation; an optical device that produces an intense monochromatic beam

154
Q

ant STT

A

The anterior spinothalamic tract, also known as the ventral spinothalamic fasciculus, is an ascending pathway located anteriorly within the spinal cord, primarily responsible for transmitting coarse touch and pressure. The lateral spinothalamic tract (discussed separately), in contrast, primarily transmits pain and temperature.

155
Q

chronic opioid use

A

In addition, chronic opioid exposure can lead to hypogonadism, opioid-induced hyperalgesia, sleep-disordered breathing, and potentially increased risk of cardiovascular disease and neurocognitive impairment.

156
Q

classify inhalational anaesthetics

A

gas and volatiles

157
Q

Xenon bad

A 
PONV
Low O2
Cost
raised ICP
dense-->increased Wob
158
Q

volatile define

A

Volatile anaesthetic agents share the property of being liquid at room temperature, but evaporating easily for administration by inhalation.

159
Q

anatomical DS measure and changes

A

fowlers

-size, large insp–>traction, position/posture

160
Q

CVS change with PEEP in CCF

A

depends if dehydrated or overfilled

161
Q

resp q

A

derived from ration of CO2 prod per O2 consumed
Carbs is 1
lipid is 0.7

162
Q

ANS BP control question

A

HR.SV.SVR alpah1 B1 B2 rec

163
Q

Pulse pressure determ

A

HR.SV.SVR

WIDENED: Increased stroke volume, and stiff arterioles or Run off due to Aortic dissection of CVM—>wide

  • SV: exercise, preg, AR
  • increased SVR: atherosclerosis, hyperthyroidism

Narrow

  • SV:hypovol, CCF, AS
  • compliant arteries
164
Q

winkessell

A

elasticity of aorta allows damping of the pressure wave–>

Decreased AL in systole as aorta compliant

AND flow in diastole.

peripheral arteries less compliant–>resistance–>stored volumed to be more evenly released to allow flow in diastole

165
Q

regional BF left and right heart wiggers

A

frown in systole for both

166
Q

tramadol classification

A

centrally acting synthetic PARTIAL opioid AGONIST
also NMDA rec antag and SNRI
met desmethyl-tramadol

167
Q

descedning pain pathway

A

from brain stem nuclei–>DH

tract unclear in my mind

168
Q

Serotonin Sx

A

hyperreflexia, tremor, rigidity, hyperthermia, tachy, sweat–>seizure

Rx with cyproheptadine +/-benzo and activated charcoal

169
Q

potentiate attenuate

A

x

170
Q

USS CO

limitation

A

Hr.SV=CO
SV=VTI.LVOTarea

limitation

  • nonuniform flow
  • arrhyhtmias
  • theta
  • heart moves
  • only measures flow in DESCEDNING aorta=70% of CO
171
Q

doppler shift eqn

A

changed freq proprtional to changed velocity.Costheta

172
Q

USS wavelength

A

20mHz

definition is 20kHz

173
Q

receptor theory of drug effect

A

The main points to describe receptor theory are:

Drugs interact with receptors in a reversible manner to produce a change in the state of the receptor
This interaction can be modeled mathematically and follows the Law of Mass Action
The binding of drug and receptor determines the quantitative relationship between dose and effect.
Mutual affinity of drugs and receptors determines the selectivity of drug effects
Competition of mutually exclusive molecules for the same receptors explains agonist, partial agonist and antagonist drug activity

174
Q

law of mass action

Gold

A

Law of mass action:
Rate of reaction is proportional to conc of reactants
A+R—>AR
V1=V2 at equillibrium
V1=D.R.k1
V2=DR.k2
So D.R/DR=K2/K1=Dk
Kd=dissociation constant also called Ka= K2/K1=A.R/AR
KA=association constant and is reciprical (strenght of sticking on once bound)

175
Q

pharm

A

The main points to describe receptor theory are:

  1. Drugs interact with receptors in a reversible manner to produce a change in the state of the receptor
  2. This interaction can be modeled mathematically and follows the Law of Mass Action
  3. The binding of drug and receptor determines the quantitative relationship between dose and effect.
  4. Mutual affinity of drugs and receptors determines the selectivity of drug effects
  5. Competition of mutually exclusive molecules for the same receptors explains agonist, partial agonist and antagonist drug activity

Law of mass action:
Rate of reaction is proportional to conc of reactants
A+R—>AR
V1=V2 at equillibrium
V1=D.R.k1
V2=DR.k2
So D.R/DR=K2/K1=Dk
Kd=dissociation constant also called Ka= K2/K1=A.R/AR = conc of drug in plasma to get 50% rec occupancy in mmol/L
KA=association constant and is reciprical (strenght of sticking on once bound)
L/mmol (which is annoying)

If affinity is high then DR»»>D.R at equilibrium so DR/D.R is high so KA is high so KD (inverse) is low

176
Q

affinity

A

50% rec occupied Kd

177
Q

potency

A

ED50% 50% max response

178
Q

efficacy

A

once bound Emax

179
Q

IA

A

ration of Emax:full ag

180
Q

COHb ab

A

As the graph show the light profiles in the chosen areas (red = 660 nm and infrared = 940 nm) overlap considerably for carboxyhemoglobin and oxyhemoglobin (as it does for methgb and deoxyhgb). This means that the pulse oximeter will see the reflected light for carboxyhgb and oxyhgb as the same when measuring in the red light spectrum and thereby measure a combined reflection. Carboxyhgb is not reflected/absorbed in the infrared spectrum and therefore does not add to this part in the ratio. Remember, the ratio between these measurements is checked against the pulse oximeters database. This ratio will correspond with the displayed SpO2.

181
Q

collegiate

A

Boiling point increases in proportion to the molar concentration of the solutes
Freezing point decreases in proportion to the molar concentration of the solutes
Vapour pressure is dependent on the vapour pressure of each chemical component and the mole fraction of that component in the solution (Raoult’s law)

182
Q

how drugs work

A

evernote

183
Q

pulse ox two types

A

Pulse oximetry is a noninvasive method for accurately estimating oxygen saturation (SaO2) by reading the peripheral oxygen saturation (SpO2). As SaO2 and SpO2 are sufficiently correlated and pulse oximetry has the advantages of being safe, convenient, inexpensive, and noninvasive, this approach is clinically accepted for monitoring oxygen saturation [1], [2].

Pulse oximetry is simple to carry out; it only uses two different light sources and a photodiode [3], [4], [5]. Depending on the measurement site, either the transmissive or the reflective mode can be used. In the transmissive mode, the light sources and photodiode are opposite to each other with the measurement site between them. Light then passes through the site. In the reflective mode, the light sources and photodiode are on the same side, and light is reflected to the photodiode across the measurement site.

Currently, the transmissive mode is the most commonly used method because of its high accuracy and stability. Nevertheless, the demand for reflective-mode oximetry is continuously increasing because it does not require a thin measurement site. It can be used at diverse measurement sites such as the feet, forehead, chest, and wrists. In particular, if the wrist is the available measurement site, pulse oximeters can be conveniently used in the form of a band or watch. To the best of our knowledge, reflectance pulse oximetry, specifically for monitoring oxygen saturation at the wrist, is currently not practiced clinically. In recent years, many reflectance pulse oximeters have become commercially available, but they are only for personal monitoring of oxygen saturation and for entertainment purposes. Obviously, the focus is on developing oximeters for medical purposes, and research is being carried out in this regard. Furthermore, most research papers discuss only the basic principle of pulse oximetry and its utilization in smart devices; only a few papers discuss the challenges associated with reflective pulse oximetry.

In this study, we developed a reflectance pulse oximeter and addressed the practical issues and limitations associated with its use. Using this oximeter, we investigated the results of AC amplitudes and DC offsets of the red and infrared signals, including modulation ratio, which are critical factors to estimate SpO2. We first tested our device by measuring oxygen saturation at a fingertip and wrist and analyzed its performance. Finally, we summarized all issues and discussed the feasibility of using the device for clinical purposes.

184
Q

hep met phases

A

evernote

185
Q

ester met

A

The product of phase I has an oxygen species that reacts better with enzymes involved with phase II reactions. Phase II reactions conjugate the metabolites created in phase I to make them more hydrophilic for secretion into blood or bile.

186
Q

cocaine moa

A

DA and NARUI
3mg/kg for 30 min
excitatory Sx of any LA

187
Q

Poynting effect

A 
Bubbling O2 through N20 produces a mix with a lower critical temp than that of O2 
#pseudocrit temp temp below which can be compressed-->lamination
188
Q

sympathomimetic def and cat

A

compounds that mimics the effect of endogenous agonists of SNS
DIRECT vs mixed vs indirect
Selective vs nonselective
(Catechol is a shitty classification as it doesn’t narrow MoA or use)
-catechol ring benzen and OH at 3,4

189
Q

Levosimenden

A

tropC sens and K:atpase open–>VD

acute decomp CCF

190
Q

milronone

A

PDE3i
-heart and VD
CCF in cardiac surg

191
Q

QTc

prolong Cx

A

QT/square RR risk in tachy
<440

all LOW
Hypokalaemia
Hypomagnesaemia
Hypocalcaemia
Hypothermia
Myocardial ischemia

TYPE1 AND 3 ANTIARRHYTHMICS
antipysh and TCA

192
Q

crystalloid vs colloid

A

Crystalloids are aqueous solutions of mineral salts or other water-soluble molecules. Colloids contain larger insoluble molecules, such as gelatin; blood itself is a colloid.

193
Q

colloids

A

https://derangedphysiology.com/main/required-reading/electrolytes-and-fluids/Chapter%20225/colloids-vs-crystalloids-resuscitation-fluids

gelafusin is from pig fat–>coagulopathy and anaphylaxis

starch and dextran–>AKI and anaphylaxis

starch lasts for 5 days

albumin as an antioxidant

194
Q

NDMA def and rec

A

N-methyl-D-aspartate receptor

glutamate
glycine
PCP

195
Q

Ketamine MoA

A

NMDA rec antag-blocking Ca in
inhibit presynaptic glutamate release
interact with opiate rec

196
Q

ket met

A

CYP450–>inactive–>pee hence CKD fine

197
Q

cori

A

Lactate–>pyruvate–>glucose (GNG)

198
Q

key parts of cellular resp

A

https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/overview-of-cellular-respiration-steps/a/steps-of-cellular-respiration

glycoslysis
pyruvate oxidation
kreb cycle
ETC

Eectrontransport is call oxidative phosphorylation

CO2 prod in kreb cycle and pyruvate oxidation

199
Q

eGFR vs GFR

A

eGFR is based on an isolated Cr level which is inversely related to CrCl which slightly overestimates GFR

200
Q

CrCL

A

cockcroft gault eqn

(140-age).wt/(72.Cr)

less clearance with old, small, females

201
Q

RBF

A

Effective renal
blood flow
=Effective renal plasma flow/1- Blood haematocrit

202
Q

washin factors

A

drug patient anaesthetic #n20 AND DURATION

203
Q

o2 tank size

A

E=emergency J=juganaut

204
Q

how much O2 in a cylinder

A

50Bar 4.5L–>50.4.5=225

205
Q

pipeline pressure O2

A

4bar

O2 tank 50bar

206
Q

cylinder pattern

A

bottles shoulders evernote

207
Q

Motion sickness

A

Hyoscine anticholinergic

208
Q

Cyclizine

A

Anti hist and ach

209
Q

Stenetil

A

Prochloperaxine

DA H ACh

210
Q

Ondans

A

Can cx Qt change

211
Q

Rx epse

A

Benztropine

212
Q

Tnr kids

A

Thethermoneutral zoneis the range across which the basal rate heat production (and oxygen consumption) is balanced by the rate of heat loss

For an adult it istypically 27-31°C

In neonates it is higher,typically 32-34°C.

213
Q

Phase two heat loss

A

2.5hr

214
Q

Critical temp heat

A

critical temp is for ITR

TNZ lower limit

215
Q

Laser

A

PHOTON–>decay to base level

Argo for cataract highest freq
Chlorhex n20

216
Q

Sugamadex

A

Hydrophobic ring to bind steroid aminosteroids as per Kate. OxCHB says anionic inner ring binds Amine cationic ends
Hydrophilic–>peed out stable
High association low disassociate

The intermolecular (van der Waals) forces, thermodynamic (hydrogen) bonds, and hydrophobic interactions of the sugammadex-rocuronium complex make it very tight. (stoelting)

  • ->fluclox
  • ->altered haemostasis (stoelting)
  • ->OCP
  • ->postoperative nausea/vomiting
217
Q

BSL

A

mmol/L

218
Q

OAG

A

x

219
Q

metformin

A

biguanide

220
Q

gliclazide

A

sulfonylurea

Binds and inhibits ATP-sensitive K+
channels on pancreatic β cells
! depolarisation ! open voltage-gated Ca2+ channels !
↑intracellular [Ca2+] ! ↑release of insulin vesicles
S/fx – hypoglycaemia, GIT upset

221
Q

sitaglipton

A

DPP-4i prevent GLP breakdown

These agents work by activating the GLP-1R, rather than inhibiting the breakdown of GLP-1 as do DPP-4 inhibitors,

222
Q

Glucagon-like peptide-1 agonist

A 
Glucagon-like peptide-1 agonist
inhibit glucagon (it's like it's own negative feedback)

a lower risk of causing hypoglycemia.

223
Q

SGLT2i mech

A

eg sergliflozin

By reducing glucose blood circulation, gliflozins cause less stimulation of endogenous insulin secretion or lower dose of exogenous insulin that results in diabetic ketoacidosis
block 180g/day=180 jelly beans

224
Q

insulin met

A

liver and kidney

225
Q

insulin

A

polypeptide hormone

226
Q

diathermy

A 
Resistancethrough body-->heat high current density
monopolar 
10cm away
short bursts
ICD-->back up external
227
Q

Volatile stability

A

Cl stabilizers

ether has O2 bonds–>explode

228
Q

CSL ton and osmo

A

hypoosmolar

isotonic as per government website

229
Q

Cx of Anion gap

A

So4 po4

230
Q

Freeze dep

A

0.003 permmol

231
Q

Remi hyperalgesia

A

TLR stim by remifentanil acid longer t/2 vs Remi renslly cleared

232
Q

Morph met

A

M3G

TLR neurexcite hyperalgesia

233
Q

Carvedilol

A

Indications. Carvedilol is a non-selective adrenergic blocker indicated for the chronic therapy ofheart failurewith reduced ejection fraction (HFrEF),hypertension, and left ventricular dysfunction followingmyocardial infarction(MI) in clinically stable patients.

234
Q

Propranalol

A

Old school shitty
B1 AND 2

MEMBRANE STABLE

SALT AND PRPOER
PPL

NOT BLACK OR SALLY
NIL ALPHA NOT LOW LIPID

235
Q

mole

A

6*10^23 molecules

236
Q

tonicity

A

Tonicity is the measure of the osmotic pressure gradient between two solutions.

237
Q

NACL AND CSL TONICITY

CORE

A

Osmolarity=Nax2=308 RRRRREALLY EASY
Osmolality=Osmolarity*0.93 as Nacl 97% dissociates
So NaCL0.9% has osmolarity 308 and osmolality of 287—>isoosmolar and isotonic
Vs CSL osmolarity of 276. So osmolality is 256 (hypoosmolar) THEN the lactate disappear—>hypotonic!!! BAD FOR CEREBRAL OEDEMA OR HYPONATRAEMIA

238
Q

CSL and CL

A

increase 1.5mmol/L every L
plasmalye only increase 0.4
(normal level of cloride is 98-105 and plasmalyte has 98)

239
Q

non electric thermometer

A

Non-electrical techniques
(1) mercury or alcohol thermometer
- thin column of mercury or alcohol ! expands when heated
- height of column reflects degree of expansion ! proportional to temperature
- mercury solidifies at -39ºC ! not suitable for low temperatures
- alcohol boilds at 79ºC ! not suitable for high temperatures
- disadvantages = takes 3 ~ 5 min to reach thermal equilibrium, glass can break
causing injury
(2) bimetallic strip thermometer
- 2 strips of metal with different thermal expansion coefficients fixed together in
coil ! expands different extent when heated ! moves dial
(3) Bourdon gauge thermometer
- sensing element contains volatile fluid ! content expands when heated !
moves dial

240
Q

electric thermo

A

resistance wire linear increase

thermister curved decrease

241
Q

heat loss

A

R-50
E-30
C and C-15 tot
resp 5%

242
Q

AND loop

A

NTS inhibts RVLM–>less SNS output

243
Q

midaz dose

A

.5mg/kg PO

0.1mg/kg IV

244
Q

ketamine

A

5mg/lg PO

245
Q

clonidine

A

4mcg/kg PO kids

OBA 98%

246
Q

glucose filtered dayly

A

180g

247
Q

defibe I and V

A

high current (#capacitor) high voltage (2000)

248
Q

monopolar diath limitation

A

penis, ears, fingers–>nil collateral

short burst
back up external defiub if ICD

249
Q

NSAIDS in preg

A

third trimester terrible!!! DA closure

t/2 2H

250
Q

Obuprofen met

A

CYP–>renal elim

251
Q

ED space contents

A

fat, nerve roots, blood vessels and

lymphatics.

252
Q

COXi

A

PL, endo (cyclin), sm m PGs

253
Q

LA add to EDB

A

increase duration without motor block, improve quality of block

254
Q

pethidine

A

active met norpeth–>seizure
addiction
ach LA onset 6min for 4hrs

255
Q

sufent

A

old school opioid induction and post op analgesia
lipid sol –>rapid onset
hep and renal dep
hypotension, histamine release, tachy brady
minimal change in CSHT

256
Q

Pneumoperitoneum

A

resp neuro GI

257
Q

antifreeze

A

ethylene glycol

258
Q

TRUP Sx

A

glycine tox

259
Q

CVP in AF, tricuspi path etc

A

https://derangedphysiology.com/main/cicm-primary-exam/required-reading/cardiovascular-system/Chapter%20783/interpretation-central-venous-pressure-waveform

260
Q

des vs sevo

A

des
methy-ethyl

sevo
methyl-isopropyl

both highly F

261
Q

VOlatile met

A

Halothan The major metabolite is trifluoroacetic acid (TFA), which is protein-bound and this TFA–protein complex can induce a T-cell-mediated immune response resulting in hepatitis ranging from mild transaminitis to fulminant hepatic necrosis and possibly death.

The production of inorganic fluoride by the metabolism of halogenated agents may cause direct nephrotoxicity. Studies investigating methoxyflurane demonstrated an association between high fluoride levels (serum fluoride >50 μmol litre−1) and polyuric renal failure. Serum fluoride levels peak earlier and decrease more rapidly with enflurane than with methoxyflurane, making enflurane less nephrotoxic. Isoflurane is more resistant to defluorination and can be used for prolonged periods without significant increases in serum fluoride levels. Sevoflurane undergoes significant defluorination

sevo–>3-5% CYP2E1 metabolism to hexafluoroisopropanol and inorganic F- (which may be nephrotoxic)

Hepatic CYP450 (CYP2E1) metabolises C-halogen bonds to release halogen ions (F-, Cl-, Br-), which can be nephrotoxic and hepatotoxic. The C-F bond is minimally metabolised compared to the C-Cl, C-Br, and C-I bonds. All agents undergo hepatic oxidation, except for halothane which is reduced.

CHF2–>CO with soda lime (not present on sevo!

262
Q

Halothane

A

Cl,Br–>potentent unstable, metabolismed
CF3–>inflammable
met trifluroacetic acid–>Pr:TFA–>t cell immune hepattis

neg ino, VD, impaired baro, vagal–>brady–>++decreased BP, decreased work and consumption
arrhytmogenic

catechol sens

263
Q

ester amide linkage

A

evernote

264
Q

LA hydophilic side

A

NH4

lipophilic is aromatic ring

265
Q

LA S:F

A

Increasing carbons in hydrocarbon linkage aromatic ring or on the tertiary amine—>increased lipid sol and potency
Methy, propyl butyl group to amine end of molecule

266
Q

methadone agonist

A

FULL not partial

267
Q

Mg

A 
PR prolong and AV SA ERP
inhibit excitation of Adrenaline
inhibit Ach release at NMJ and NAd in SNS
uterine
BD
PETs
MI
bleed due to Cablock

minor
-flush, HA, Nausea

–>arrest

268
Q

Mg level to Sx

A

googe: magnesium toxicity and plasma conc

269
Q

Des BP

A

23C

270
Q

N20 crit temp

A

36

271
Q

prop HR

A

INITIAL EXCITATORY PHASE then peak effect coincides with drop in HR as tachy reflex inhibited.
Hence instrument Paeds airway as heart rate just starts to back off

272
Q

anaphylactoid

A

Search Results
Featured snippet from the web
Anaphylactoid reactions are defined as those reactions that produce the same clinical picture with anaphylaxis but are not IgE mediated, occur through a direct nonimmune-mediated release of mediators from mast cells and/or basophils or result from direct complement activation.

273
Q

anaphylaxis crossreaction

A

NDMR ammoniumgroup coumpound in cosmetic cough and cleaning

274
Q

NDMR review

A

evernote

275
Q

DoA morphine vs fenty why

A

nil redisp

active met

276
Q

morphine and fentanyl clearance

A

similar (infact morphine slightly more!)

yet nil redistrib and active met

277
Q

bup Moa and PK

A

NIL NMDA WRONG (methadone only)

peak 80min post IV!
kappa blokced-->less resp dep
less tol and euphoria
high PrB
yes renal impairment relevant
278
Q

anaphylactoid

A

Anaphylotoxins c3,4,5–>bind to mast or basophil–>anaphylactoid

classic anaphylactoid: trigger–>Ag:Ig->comp–>mast
alternative: no clear trigger–>com–>mast

279
Q

complement system

A

protolytic inflam cascade
reg by C1 esterasei 0defecient in angiooedema
comp–>ABO incompat reaction

280
Q

CI

A

2STD from mean

281
Q

adenosine and rec

A

Adenosine AGONIST
aslo iCamp–>neg inotropy

A1: Gi, in SA/AV node, cause decrease in HR. (k CH OPEN–>HYPERPOL–>neg chrono
A2A: Gs, coronary arteries (vasodilatation)
A2B: Gs, bronchiole smooth muscle (bronchospasm)
A3: Gi, cardioprotective in ischaemia, inhibits neutrophils degranulation

282
Q

digoxin

A 
digitalis lantana
nat occuring cardiac glycoside
min hep met
non dialysable
Rx hyperkalaemia and brady and use phenytoin
283
Q

half life in textbooks

A

Each phase has its own halflife; usually the “overall” halflife quoted by textbooks is the halflife for slowest of the phases, which tend to massively ovepredict the “real” halflife of a highly fat-soluble drug

284
Q

compartment

A

“A pharmacokinetic compartment is a mathematical concept which describes a space in the body which a drug appears to occupy. It does not need to correspond to any specific anatomical space or physiological volume”.

285
Q

bi exponential washout phases

A

The distribution phase is the initial rapid decline in serum drug concentration
The elimination phase is the slow decline in drug concentration, sustained by redistribution of drug from tissue stores.

286
Q

triexponential

A

https://derangedphysiology.com/main/cicm-primary-exam/required-reading/pharmacokinetics/Chapter%202.0.1/single-and-multiple-compartment-models-drug-distribution

The distribution phase finishes with the concentrations reaching their peaks in the peripheral compartments.

To call the next phase the “elimination phase” is probably incorrect, but it is a period during which the main effect on drug concentration is in fact elimination. This phase ends when the slow compartment concentration becomes higher than the tissue concentration and the total clearance is slowed down by the gradual redistribution of the drug into the blood compartment.

The last phase is called the “terminal” phase, also sometimes confusingly referred to as the elimination phase. In actual fact during this phase elimination is rather slow because the concentration of the drug in the central compartment is minimal. The major defining factor affecting drug concentration during this phase is the redistribution of stored drug out of the slow compartment.

287
Q

triexponetial equation

A

Ae^-alpha.t + Be^beta.t +Ce&gamma.t

288
Q

triexponential phases

A
  1. distribution V1->other compartments
  2. elimination is main process from V1–>Vo as high conc and NO REDISTRIBUTION FROM V2 OR V3 TO V1 some ongoing distribution V1–V3
  3. terminal elimination V1–> Vo occurs but is slow as El=Cl.c and c is low. it is further slowed due to redistribution from V3–>V1
289
Q

limitation of compartment model

A

1) That the central compartment is the only compartment from which the drug is eliminated. Of course that is not the case, as for example in the case of cisatracurium where the drug degrades spontaneously no matteer where it is in the body, i.e. elimination takes place in numerous compartments simultaneously.

290
Q

propofol half life

A

alpha is 2 min

beta ie terminal elimination is 6 hours

291
Q

salbutamol met

A

liver inactive
OH 4,5–>nil COMT
nil MAO

292
Q

anticholinergic in asthma

A

yes ipratropium

293
Q

aminophylinne

A

methylxantine nonselective PDEi

294
Q

heliox in asthma

A

79:21 or 60:40

295
Q

reynolds number

A

radius!!!!!!!! air in a large tunnel–> turbulent
honey in a straw –>lamina

2r.v.d/viscoistiy

> 2000

296
Q

why density irrelevant form lamina flow

A

R=8nl/pir^4

viscosity relevant density irrelvant

297
Q

lamina vs turbulent flow consequence

A

lamina V=P.k with nice central fast spike

turbulent V= square root of p.k

298
Q

naturally occuring levo or dextro

A

Most naturally occurring molecules are all one isomer (e.g. all levo)
so more potent

299
Q

microcirc

A

smallest arterioloes, precap sphincter cap and venules

  • ->SVR
  • ->cutaneous shunt for temp
  • ->exchange

Flow through capillaries is also intermittent, controlled by contraction or vasodilation of precapillary, terminal arterioles. Periodic contraction and vasodilation in microvascular beds (vasomotion) causes the flow through capillaries to increase and subside approximately every 15 sec.

300
Q

figures for starling forces in microvasc

A

https://en.wikipedia.org/wiki/Starling_equation#Reflection_coefficient

301
Q

placenta metabolic

A

the placenta contains enzymes that synthesize hormones such as oestrogen, progesterone,
chorionic gonadotrophin and placental lactogen.

It also contains pseudocholinesterase, alkaline
phosphatase, monoamine

302
Q

butylcholinesterase

A

In humans, cocaine is detoxified to pharmacologically inactive products primarily by butyrylcholinesterase. Butyrylcholinesterase also hydrolyzes aspirin, succinylcholine, mivacurium, and heroin

303
Q

roles of placenta

A

TIME

304
Q

BF to placenta

A

At term, maternal blood flow to the placenta is approximately 600–700 ml/minute.

305
Q

time of closure of fetal parts

A

FO 4-6weeks OR NEVER
DA 14 hrous then 14 days
DV hours #V8

306
Q

neonatal cardio changes

A

The cardiovascular changes above can be modified
Elevation of RAP ! persistence of foramen ovale
Decrease PVR ! persistence of ductus arteriosus
Prostaglandins and hypoxia ! inhibit closure of ductus arteriosus

(1) Umbilical vessels are obliterated when the cord is clamped externally ! ↓blood
flow through IVC and ductus venosus
(2) Ductus venosus closes over 3 ~ 10 days
(4) First breath ! negative intrathoracic pressure ! oxygen enters lungs ! opening
of pulmonary vessels + ↓hypoxic pulmonary vasoconstriction ! dramatic fall in
pulmonary vascular resistance
(5) ↓↓pulmonary vascular resistance ! ↑pulmonary blood flow ! ↑venous return to
left atrium ! ↑left atrial pressure ! LAP exceeds RAP ! functional closure of
foramen ovale within minutes to hours of birth ! all RA blood passes into RV
(6) Anatomical closure of foramen ovale occurs over several days
(7) Ductus arteriosus constricts (high PaO2) and complete closure within 48 hours
(8) Other changes take several weeks after birth – ↓RV wall thickness, ↑LV wall
thickness, etc

307
Q

first breathe

A

MAKEUP: Describe the first breath
Before birth: 20ml/kg fluid present in the lungs
- Most expelled during passage through birth canal (absorbed / expelled)
- Much is replaced by air with the 1st breath
o ↑compliance lung tissue
First breath: Requires large negative pressures (-50 – -60cmH2O)
Subsequent breaths easier
- establishment of air-liquid interface
- Surfactant action in ↓surface tension
FRC is established quickly
- 10min → 17ml/kg
- 30 – 60 min → 30ml/kg (adult value)

308
Q

N20 to anaemia

A
  • N2O oxidises Cobalt ion on B12—> co factor for methionine synthesise for folate

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