sept viva Flashcards

(259 cards)

1
Q

intralipid contents

A

Intralipid, which is an emulsion of soy bean oil, egg phospholipids and glycerin,

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2
Q

LA tox risk

A

LA drug factors Pr B and affinity to NaCH and pregame’s, acid, renal, hep

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3
Q

prev LA tox

A

USS
monitor
awake
test dose

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4
Q

AFOI blcok

A

Glossopharyngeal not oropharyngeal.

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5
Q

LA tox ecg

A

sinus bradycardia, intracardiac conduction defects (prolonged PR & QRS complex), ventricular arrhythmias, cardiac arrest.

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6
Q

Desc pain

A

PAG–>RVM–>DH

LC–>DH

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7
Q

Rexed Laminae

A

The Rexed laminae comprise a system of ten layers of grey matter (I–X),

P+H

Adelta–>laminae 2,5
C fibers–>2

The substantia gelatinosa is one point (the nucleus proprius being the other) where first order neurons of the spinothalamic tract synapse. (laminae II)
Many μ and κ-opioid receptors, presynaptic and postsynaptic, are found on these nerve cells;

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8
Q

gate theory

A

Ab touch and desc inhib in SUBSTANTIAL GENATINOSA (lamina II of DH)

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9
Q

glucose uptake

A

Glut1 the 1 most important thing so brain
Glut 2 food panc and hep
Glut 4 is lock in door (insulin dep)

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10
Q

BMR measurement

A

heat or indirect calaromitery

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11
Q

atp production cellular respiration

A

google
atp production cellular respiration

RB pyruvate oxidation CO2 prod

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12
Q

fatty acid

A

Fats into fatty acids and glycerol

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13
Q

ketogen

A

Fatty acid–>acetylcoa (b oxidation)
aceytl coa–>acetone, acetoacetate and betahydroxybutyrate via 3 steps including HMG coa synthase

When the body has no free carbohydrates available, fat must be broken down into acetyl-CoA in order to get energy. Under these conditions, acetyl-CoA cannot be metabolized through the citric acid cycle because the citric acid cycle intermediates (mainly oxaloacetate) have been depleted to feed the gluconeogenesis pathway. The resulting accumulation of acetyl-CoA activates ketogenesis.

Ketone bodies are produced mainly in the mitochondria of liver cells,

The production of ketone bodies is then initiated to make available energy that is stored as fatty acids. Fatty acids are enzymatically broken down in β-oxidation to form acetyl-CoA. Under normal conditions, acetyl-CoA is further oxidized by the citric acid cycle (TCA/Krebs cycle) and then by the mitochondrial electron transport chain to release energy. However, if the amounts of acetyl-CoA generated in fatty-acid β-oxidation challenge the processing capacity of the TCA cycle; i.e. if activity in TCA cycle is low due to low amounts of intermediates such as oxaloacetate, acetyl-CoA is then used instead in biosynthesis of ketone bodies via acetoacetyl-CoA and β-hydroxy-β-methylglutaryl-CoA (HMG-CoA). Furthermore, since there is only a limited amount of coenzyme A in the liver, the production of ketogenesis allows some of the coenzyme to be freed to continue fatty-acid β-oxidation.[8] Depletion of glucose and oxaloacetate can be triggered by fasting, vigorous exercise, high-fat diets or other medical conditions, all of which enhance ketone production

The three ketone bodies, each synthesized from acetyl-CoA molecules, are:

Acetoacetate, which can be converted by the liver into β-hydroxybutyrate, or spontaneously turn into acetone. Most acetoacetate is reduced to beta-hydroxybutyrate, which serves to additionally ferry reducing electrons to the tissues, especially the brain, where they are stripped back off and used for metabolism.
Acetone, which is generated through the decarboxylation of acetoacetate, either spontaneously or through the enzyme acetoacetate decarboxylase. It can then be further metabolized either by CYP2E1 into hydroxyacetone (acetol) and then via propylene glycol to pyruvate, lactate and acetate (usable for energy) and propionaldehyde, or via methylglyoxal to pyruvate and lactate.[10][11][12]
β-hydroxybutyrate

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14
Q

R quotient

A

CO2/R=0
CO2/O2=R

fat is .7 pr .8
feed COPD fat
stomach consumes CO2

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15
Q

lattent heat of…

A

melting

lattent TB= hidden

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16
Q

nicotine

A
Acute exposure to nicotine
–
HD effects last 1hr
Abstinence cigarettes 12hrs
–
10
-
20% increase in physical work capacity
T ½ COHb 4
-
6hrs so overnight abstinence helpful (10hrs
in men)
Peak benefit re: upper airway irritability at 10 days (effects start at 48hrs)
Autonomic ganglia
(N1 receptors)
–
blocked by hexamethonium
2.
NMJ
(N2 receptors)
–
blocked by tubocurarine
3.
CN

Initial stimulation then persistent depression of autonomic ganglia
CNS stimulant

tremor
Increased ventilation v
ia nicotine stimulating aortic/carotid body chemoreceptors
CVS: tachycardia, hypertension, increased SVR (via SNS increase)
Resp: initial stimulation of saliva/bronchial secretions then inhibition
GI: PNS activation causing vomiting, diarrhoea

ADrenal medulla ADr release

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17
Q

sweat glands ANS

A

In sweat glands the receptors are of the muscarinic type.

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18
Q

isometric isotonic

A

ismetric–>nil external work–>100% energyoutput as heat

isotonic–>some external work–>50% heat loss

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19
Q

brown fat

A

uncouples oxidative phosphorylation
not dep on consumption of ATP for ATP
heat produced through chemical reaction without ATP needing to be utilised

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20
Q

COX pathway

A

Sm muscle–>PG

cycloendoperoxidase

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21
Q

nerve twitch face

A

orbicularis occuli

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22
Q

nerve monitory placement

A

Typically smaller muscle groups are more sensitive
The positive (red) lead is placed proximal
Ulnar nerve
Electrodes are placed along the ulnar border of the wrist at the flexor crease, and thumb adduction is assessed.
Facial nerve
The positive electrode is placed at the outer canthus, and the negative electrode is placed anterior to the tragus. Eyebrow twitching is assessed. orbicularis occuli
Posterior tibial nerve
Electrodes are placed posterior to the medial malleolus, and plantar flexion is assessed. posterior tib

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23
Q

r vs s

A

rectus right clock

sirrius anticlock

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24
Q

levo vs dextro

A

A dextrorotatory compound is a compound that rotates the plane of polarized light clockwise as it approaches the observer (to the right)

Dr X

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25
stereoisomer
diff 3d orientation same bonds
26
diastereioismer
non enantiomers - ->geo (cis) - ->configurational (cant rotate around single bond)
27
thio tautomerism
So, as demonstrated by the diagram I nabbed from the net above, the ketone form C=O* is lipid soluble and is favoured in acidic environments. The enol form is favoured in alkaline environments and is water soluble. Enol forms for barbiturates are water-soluble at pH 10-11at 6% sodium carbonate
28
valsalva phase 3
BP drops as LV afterload worsened with release and prelead reduced
29
Valsalva quantification
highest HR in phase 4 over lowest in phase 4
30
ANS dx vasovagal
Figure 4.49 The Valsalva response in autonomic dysfunction: excessive fall in blood pressure in Phase II and absence of overshoot and bradycardia in Phase IV.
31
NSAID SE
CCF and fluid and salt rention NSAIDs promote sodium and water retention, and this has generally been explained by a reduction in prostaglandin-induced inhibition of both renal chloride reabsorption and the action of antidiuretic hormone
32
3 phases of heat loss
Rapid reduction Core temperature falls by 1-1.5°C in the first 30 minutes. Predominantly due to vasodilation, which is due to: Reduction in SVR, with generalised vasodilation and increased skin blood flow Heat redistribution is the major initial factor (rather than heat loss), as vasodilation leads to increased heat content of peripheries. Impairs thermoregulatory vasoconstrictive responses Inter-threshold range is widened to 4°C (up from 0.4°C) Gradual reduction Further drop in core temperature of 1°C over following 2-3 hours.
33
humidity
evernote
34
preg ABG
26-32mmHg CO2 | pO2 → essentially unchanged 100-105mmHg
35
resp drive preg
Hyperventilation centrally stimulated by | progesterone
36
preg CO
O2 Flux Measured as the product of blood O2 content and CO - ↑CO (30%)
37
normal HCT
40%
38
CVS changes preg %s
all about 25% except CO=50% and BV=50% https://primarysaqs.files.wordpress.com/2009/12/makeup-describe-the-cardiovascular-changes-that-occur-in-pregnancy.pdf
39
thyroid anatomy
inf to cricoid caritlage ext branch of sup laryngeal recurrent laryngeal
40
thyroid production
In follicular cells Iodine from basement memebrane Iodination of tyrosyl residue of thyroglobulin Lysosomal enzymes cleave T4 from iodinated thyroglobulin T4 cross into blood
41
thyroid effect
physiocal vs chemical catachol and insulin sens due to B rec upreg
42
hypothyroidism and GA
Hypothyroidism may result in depression of myocardial function, decreased spontaneous ventilation, abnormal baroreceptor function, reduced plasma volume, anaemia,82 hypoglycaemia, hyponatraemia and impaired hepatic drug metabolism Preventative measures should be adopted to protect against hypothermia. Because of an increased incidence of adrenocortical insufficiency and a reduced adrenocorticotropic hormone response to stress, hypothyroid patients should receive hydrocortisone cover during periods of increased surgical stress.
43
Hyperthyroidism
Of importance to the anaesthetist are the cardiovascular effects of hyperthyroidism including atrial fibrillation, congestive cardiac failure and ischaemic heart disease.4 In an attempt to prevent the dreaded complication of ‘thyroid storm’, patients should be euthyroid before surgery.4286 This is achieved by the use of antithyroid drugs, commonly carbimazole or propylthiouracil. These drugs block the synthesis of thyroxine but take 6–8 weeks to work. Beta‐blockers, particularly propranolol, are used to ameliorate the effects of thyrotoxicosis13 and are effective in the acute preoperative phase. Longer‐acting beta‐blockers such as atenolol or nadolol may achieve better control of symptoms.2736 Anaesthetic drugs may be affected by the hypermetabolic state of hyperthyroidism. For example, the clearance and distribution volume of propofol are increased in hyperthyroid patients. When total intravenous anaesthesia is used, propofol infusion rates should be increased to reach anaesthetic blood concentrations.9
44
Bohr effect
boring is stable #evernote and eqn
45
Bohr eqn
a-E/a as a is higher than e
46
humidity
renaults!!!!!
47
propofol infusion rate and CSHT
6mg/kg/hr bristol final stage onset 30s CSHT at infinity is 10min MILLERS CSHT 5hrs is 5min
48
THio presentaion
NaCO3 NaTP 2.5% stable 24 hrs
49
thio doa
10min
50
thio CVS CORE
neg ino with CO decrease 20% some VD compensatory tachy!!!!!!
51
thio resp
BC
52
thio hep
inducer of CYP450
53
thio other
arterial injection | porporia
54
porphyria
Porphyric crisis due to build up of porphyrins—>skin and nervous system effects * abdo and chest pain * vomiting fever * HTN tachy * Confusion * Blisteres Complication * seziure * Paralysis * Fatal Rx * IV haem or glocuse—>decreased haem synth—>less precursor accumulating
55
intraarterial injection thio
alpha antag anticoag analgesia block
56
alpha anatag
phenoxybenzamine non selctive for pheochromocytoma | phentolamine
57
neo vs edro vs other
evernote
58
muscurinic antag
eyedrop to dilate
59
SE of neostig
CLINICAL FEATURES ``` confusion CNS depression weakness salivation urinary and faecal incontinence GI cramping vomiting sweating muscle fasciculations pulmonary oedema miosis brady or tachycardia seizures ```
60
QT prolonged
1,3 | sux, volatile, low K, low Mg
61
NO moa
Activates gyanalate cyclase
62
Oxytocin se
Phtn and coronary spasm ci in congenital hear tdx
63
Misoprostol
Pge1 analogue | Diarrhoea in the bum
64
Carbeprost
F2alpha BC and pulm HTN DIARHOEA VOMIT
65
central vs mixed venous
superior vena cava and proximal pulmonary artery,
66
reticulocytes
Like mature red blood cells, in mammals, reticulocytes do not have a cell nucleus. They are called reticulocytes because of a reticular (mesh-like) network of .
67
RBC production
google
68
rbc met
everntoe Bile secretion bilirubin
69
whole blood
Whole blood is typically stored under the same conditions as red blood cells and can be kept up to 35 days if collected with CPDA-1 storage solution or 21 days with other common storage solutions such as CPD. double if PRBC
70
PRBC additives
CONTINUED PROF DEV CPDA SAGM Sodium Chloride 0.92g • Adenine 0.02g • Dextrose Monohydrate 0.95g • Mannitol 0.55g
71
storage lesion
Blood can be stored for up to 35 days, which corresponds to 70% survival Hyponatraemia
72
oxy dose post infusion
> Prolonged use of oxytocin induces oxytocin receptor desensitisation and larger doses of oxytocin may be required to prevent or treat uterine atony and PPH 3
73
levosimendine
sensitizes Ca
74
milronone
Milrinone, commonly known and marketed under the brand name Primacor, is a medication used in patients who have heart failure. It is a phosphodiesterase 3 inhibitor that works to increase the heart's contractility and decrease pulmonary vascular resistance.
75
pulm HTN
Pulmonary Vasodilaters (generally referring to chronic Mx but some acute: http://www.rcjournal.com/contents/07.07/07.07.0885.pdf - O2—>reverse HPVC - CCB—>VD eg nifedipine and diltiazem - Nitric Oxide Gas - Low-dose intravenous sodium nitroprusside causes pulmonary vasodilation and reduces PAP, PVR, and right-ventricular afterload, but is not selective. - Nitroglycerin is another NO donor that has selective pulmonary vasodilation effects when delivered via aerosol - In vascular smooth-muscle cells, prostacyclins stimulate soluble adenylate cyclase and convert adenosine triphosphate to cyclic adenosine monophosphate (cAMP). In turn, protein kinases mediate a cAMP-induced decrease in intracellular calcium and produce relaxation and vasodilation (see Fig. 3).99,100 Prostaglandin I-2 and prostaglandin E-1 are both potent pulmonary vasodilators and inhibitors of platelet aggregation - -Epoprostenol, a short-acting prostaglandin I-2 - -Aerosolized epoprostenol is an effective alternative to INO in the acute care setting - Sildenafil, a phosphodiesterase type 5 inhibitor, approved for the treatment of erectile dysfunction, has been shown to be an effective treatment for PAH in several randomized controlled trials in adult patients154 –156 and was approved by the FDA in June 2005 as an oral PAH therapy. - -Phosphodiesterases are enzymes that inactivate cGMP and cAMP. Use of phosphodiesterase inhibitors to prevent the breakdown of cGMP and cAMP in vascular smoothmuscle cells can augment or prolong the vasodilator signaling pathways of both NO and prostacyclin
76
23dpg weeks
consumed-->increased sats in pRBC | 5% left at 4 weeks
77
storage lesion
K 28 at 28 days ph 6.7 PRBC 75% at 28 days
78
dex CVS
BRADY-->DEATH
79
Dex CNS
less deleirum
80
Dex PK
high Prb extensive hep with nil minimal renal dep vs clonidine 50% peed out unchanged
81
affect Pulm VR
Factors which influence pulmonary vascular resistance Pulmonary blood flow: Increased blood flow results in decreases pulmonary vascular resistance in order for pulmonary arterial pressure to remain stable This is due to: Distension of pulmonary capillaries (mainly), and Recruitment of previously collapsed or narrowed capillaries Lung volume: Relationship between lung volume and PVR is "U"-shaped Pulmonary vascular resistance is lowest at FRC At low lung volumes, it increases due to the compression of larger vessels At high lung volumes, it increases due to the compression of small vessels Hypoxic pulmonary vasoconstriction A biphasic process (rapid immediate vasoconstriction over minutes, then a gradual increase in resistance over hours) Mainly due to the constriction of small distal pulmonary arteries HPV is attenuated by: Sepsis and pneumonia hypothermia iron infusion Metabolic and endocrine factors: Catecholamines, arachidonic acid metabolites (eg. thromboxane A2) and histamine increase PVR Hypercapnia and (independently) acidaemia also increase pVR Alkalaemia decreases PVR and suppresses hypoxic pulmonary vasoconstriction Hypothermia increases PVR and suppresses hypoxic pulmonary vasoconstriction Autonomic nervous system: α1 receptors: vasoconstriction β2 receptors: vasodilation Muscarinic M3 receptors: vasodilation Blood viscosity PVR increases with increasing haematocrit Drug effects: Pulmonary vasoconstrictors: Adrenaline, noradrenaline and adenosine Pulmonary vasodilators: Nitric oxide, milrinone, levosimendan, sildenafil, vasopressin, bosantan / ambrisantan, prostacycline and its analogs, calcium channel blockers and ACE-inhibitors.
82
Stomache secretion
Stomache secretion evernote | g cells enterochroffin like cells
83
H2 blockers
H2 blockers are available by prescription or over-the-counter, and include ranitidine, famotidine, cimetidine
84
Hypothal thermo reg parts
anterior hypothalamus is sensitive to local warming of blood, which increases the ring rate, producing sweating and vasodilatation. e posterior hypothalamus responds to cold Cutaneous responses to heat 383 aerent impulses from the peripheral temperature receptors and causes increased shivering thermogenesis.
85
layers of adrenal medulla
zona glomerulosa: The outermost layer of the adrenal cortex, responsible for producing mineralocorticoids such as aldosterone. zona fasciculata: The middle layer of the adrenal cortex, responsible for producing glucocorticoids such as cortisol.
86
magnesium level vs side effects
magnesium level vs side effects google 5 SA AV 10 weak 15 AV block and resp paralysis 20 Arrest
87
ANS strucutre
ANS - SNS-efferent cell bodies in lateral grey column and in peripheral ganglion of T1-L2 - PSNS-efferent Brainstem CNs 3,7,9,10 and sacral primary rami—>pelvic splanchnic nerves
88
mass effect SNS
SNS-mass effect - exit lat grey column—>white rami communicans 3 options in the Sympathetic trunk 1. Synapse at that ganglion in white rami communicans 2. Travel upon down trunk to ganglions above # cervical ganglion 3. Pass through and synapse with a more distal ganglion - therefore blocking or stimulating one white rami communicans segment—>wide effect on many organs at many levels above and below
89
eqipment class
Class I Equipment that has an earth wire connected to its outer metal casing This protects against shock in case a fault causes the active wire to contact the outer case eg refrigerator, electric kettle Class II Double insulated equipment Has a plastic outer case in addition to the normal internal insulation An earth wire is not required as the outer casing is non-conductive eg hair dryer Class III Extralow voltage (< 40V) or battery powered equipment Doesn't require an earth wire, even if it has a metal case because the voltage is low so that the risk of macroshock is negligible eg mobile phone
90
avoid electricution
(i) general measures; (ii) equipment design; (iii) | equipotentiality; (iv) isolated circuits; and (v) circuit breakers.
91
warfarin MoA
inhibits reduction of vit K by inhibiting vit K epoxide reductase recuded form required as a coenzyme for carboxylation of glutamic acid residue
92
sux arrhythmias
Bradycardia  due to direct action on muscarinic ACh receptors in SA node o sinus brady, junctional/ventricular escape rhythm, asystole  worse if high vagal tone o children,  blocked, hypoxic, laryngoscopy  more commonly if repeat dose given  can be offset by co-administration of atropine Tachycardia / Hypertension  “large” / second dose of sux can directly stimulate nicotinic ACh receptors in sympathetic ganglia o  SNS nerve activity o  catecholamines released from adrenals  tachycardia, hypertension  ventricular arrhythmias
93
o2 storage in blood calc
150.1X1.34=200g | so 1L of O2 in blood
94
preoxygenation
PAo2=110/176 ie 13% 13% of 2.1L is 275ml 3.5ml.70 is 245ml
95
fuel cell vs other
clarke
96
HME
During expiration, the HME picks up some of the moisture from the expired humid air. These water droplets retain some of the heat from the gas which has carried them. During inspiration, the incoming torrent of air collects these warm water droplets, and carries them as vapour into the lungs of your patient.
97
Laplace
T=p.r/2 Tension is equal to TMP.RADIUS IN heart P=2T/R Pressure to collapse alv=ST/r to collaps
98
Surfactant
1.compkiance 2.oedema 3 stabilises
99
Surfactant oedema
Less ST so less oedema
100
Hb structure
4 heam | 4globin polypeptide chains 2a 2b
101
Methhb
Fe3+ Prilocaine nitrites Less able to bind O2 and less able to offload Treat with methelene blue and vit c
102
hep BF calc
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
103
renal BF calc
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
104
PaO2 at altitide
0.21(380-47)-50 | =19mmHg (5x worse)
105
neuropathic pain def
x
106
niceception def
x
107
neuropathic pain mech peripher
``` increased Na ch perm. microanatomical change-cross connection and sprouting central -migroglial activation -ca ch sens due to over expression -loss of large fibre inhibition -anamotical reorg (brain and SC) ```
108
cross and SC
decussate
109
paracetamol MOA
evernote
110
paracetamol met
evernote
111
NSAID flow chart | CORE
endoperoxidase
112
NMDA coagonist
Glycine is NMDA coagonist
113
NMDA rec
xenon NO2 ketamine methadone
114
post pit
ADH oxytocin
115
adrenaline secretion
enterochromafiin cells
116
COMT effect
The enzyme introduces a methyl group to the catecholamine, which is donated by S-adenosyl methionine (SAM).
117
phenylephrine dose
Initial dose: 50 to 250 mcg by intravenous bolus (most common doses: 50 to 100 mcg) 1ml is 100 microg
118
hep BF calc
INDOCYNIN GREEN
119
PLACENTA HORMONES
e placenta acts as an endocrine organ as it produces both peptide (human chorionic gonadotrophin [HCG] and human placental lactogen [HPL]) and steroid hormones (oestrogen and progesterone).
120
uterus blood supply
uterine and ovarian-->arcuate-->radial-->basal and spiral
121
uterine unit
chorionic villi fetal villi with chorioic external 2 layers -syncitiotrophoblast and cytotrophopblast (cyto near cytoplasm) intervillous space-maternal blood (YES)
122
MEAC
x fent is 3mcg/ml
123
uterine BF determ
alpha stim and uterine artery pressure
124
t.f in uterus
diff facilitated-glut1 active-Fe vit C endocytosis IgG
125
Selegiline
PDx Selegiline acts as a monoamine oxidase inhibitor,
126
nonobstetric anaesthetic
Neostigmine crosses the placenta and fetal bradycardia can occur, while glycopyrrolate does not. !!!! Non-steroidal anti-inflammatory drugs in early pregnancy may be associated with increasing fetal loss12 and in the third trimester may cause the premature closure of the ductus arteriosus. Single doses are unlikely to be harmful. T All volatile agents up to an MAC of 1.5 dilate uterine arteries and increase uterine blood flow, but at higher concentrations, this is offset by decreases in maternal arterial pressure and cardiac output. Volatile agents also reduce uterine tone. Nitrous oxide is avoided during the first trimester (see the Anaesthetic drugs and teratogenicity section). Light anaesthesia and pain are avoided to prevent maternal catecholamine release and consequent reduced uteroplacental perfusion.
127
Droperidol PK
extensive liver met 1% renal unchanged
128
acinus
The centre of the acinus is formed by the portal triads consisting of portal vein, hepatic artery and bile duct. The acinus is supplied by terminal branches of the hepatic artery and portal veins, which drain into sinusoids. The blood in the sinusoids drains into hepatic venules. The hepatic acinus may be divided into three functional zones: (1) periportal, (2) mediolobular and (3) centrilobular zones (Figure 6.1). Periportal hepatocytes (zone 1) receive blood with the highest oxygen content and have the highest metabolic rate and are especially involved in protein synthesis. Centrilobular hepatocytes (zone 3) receive the least oxygen but contain high concentrations of cytochrome P-450 and therefore are important sites for drug biotransformation.
129
NAPQI
phase I glutathion mop-->cysteine
130
Nociception
Nociception (also nocioception, from Latin nocere 'to harm or hurt') is the sensory nervous system's process of encoding noxious stimuli.
131
sevo SVP
20kpa 158mmHg 2% with 90% bipass
132
artline MAP
AUC per cardiac cycle
133
SE RE
SE max 91=awake
134
Evoked potentials (EP)
``` Evoked potentials (EP) Evoked potential monitors measure electrical activity in certain areas of the brain in response to stimulation of specific sensory nerve pathways. ```
135
entropy CI
patient-brain dead neonat Surgical-MRI Drug-ket, N20
136
entropy
entropy, freq, time
137
bis
freq, phase, duration
138
doppler shift
shift=v/c x freq0. cos theta
139
measure BF
tracer uniquely handled by organ and doesnt change BF itself
140
innate vs adaptive
nonspec vs targetted protein triger
141
Anaphylaxis def
``` Anaphylaxis is an acute severe type I hypersensitivity reaction affecting multiple organ systems (there is currently no consensus definition) ```
142
adaptive immune
Over next 10 – 14 days produces IgE specific to the antigen
143
late anaphylaxis
TNF-α with a cumulative mean difference of 22.81 ng/ml is also an inflammatory soluble mediator and is released as both pre-formed and late-phase mediator and has the ability to activate neutrophils, recruits other effector cells and enhances the synthesis of chemokine
144
normal ICP
ICP is defined as 5 to 15 mm Hg
145
MAP to CBF linear
TBI
146
altered Ach at NMJ
sux, NDMR producution blocked with Hemi release blocked with Bot LA blocks post synaptic Volatile blocks positive feedback and Ca and Nach res and Na Ch aminoglyco blocks presynaptic ca frusemide blocks camp for less release.
147
gibbs donan
uneven distribution of permiable charged ions on either side of SPM due to distribution of impermiable charged ions "The Gibbs-Donnan effect describes the unequal distribution of permeant charged ions on either side of a semipermeable membrane which occurs in the presence of impermeant charged ions. " derranged phys
148
AFOI
internal of sup laryngeal is sens (inside)
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m. of larynx
intrinsic m- | CT is sole adductor ext sup lary n.
150
laryngeal cartilage
evernote
151
AP tissues
In physiology, an action potential occurs when the membrane potential of a specific cell location rapidly rises and falls:[1] this depolarization then causes adjacent locations to similarly depolarize. Action potentials occur in several types of animal cells, called excitable cells, which include neurons, muscle cells, endocrine cells, glomus cells, and in some plant cells.
152
pain in elderly
evernote
153
Conc effect
In the study of inhaled anesthetics, the concentration effect is the increase in the rate that the Fa (alveolar concentration)/Fi (inspired concentration) ratio rises as the alveolar concentration of that gas is increased. In simple terms, the higher the concentration of gas administered, the faster the alveolar concentration of that gas approaches the inspired concentration. In modern practice is only relevant for nitrous oxide since other inhaled anesthetics are delivered at much lower concentrations due to their higher potency.
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remi pka onset t/2
7.1 so 68% unionized at 7.4 onset 90s t/2 5min so doa 10min or so. clearance ++ fast 5l/min clearance remi>morp>fent>alfent !!
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why does morph have a longer t/2 vs fent
fent bolus offset is due to redistribution!!
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why does alfent have a smaller t/2 vs fent
t/2=vd/cl | as Vd is smaller t/2 is shorter
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why does remi have fast onset
pka 7.1 | lipid sol
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why does remi have short doa
non spec plasma and tissue esterase hydrolysis t/2=Vd/Cl vd small and clearance large
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FGF req for T piece
2.5xMV | MV of 30kg=300mlx20=6L-->15L/min FGF
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he dilution
V1.C1=C2.(V1+V2) V2=TLC!!!!! then with TLC known spirometry can determine FRC
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mole
The mole (symbol: mol) is the unit of measurement for amount of substance in the International System of Units (SI). A mole of a substance[1] or a mole of particles[2] is defined as exactly 6.02214076×1023 particles, which may be atoms, molecules, ions, or electrons.[1] In short, for particles 1 mol = 6.02214076×1023
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Avogadro's law
Avogadro's law states that "equal volumes of all gases, at the same temperature and pressure, have the same number of molecules."[1] 1mole=22L at STP
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gas cylinder size
E=emergency | J=juganaut
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vol in anaesthetic clinder
V1.P1=V2.p2 O2 4.7x137/1=629L from size E bottle NOTE N20 is a vapour so not applicable -it is stored at 44bar and produces 1800L (as liquid can produce a shit tone of gas) 137 bar for air, o2, entenox
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VIE figures
VIE figures BP=-180 Crit temp -118 VIE -150C
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psuedocrit temp
at 147 bar is -5.5 | at 4 bar (ine pipeloine is-30C)
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partician coeff
x
168
USS limitations errors
x
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APL pos
distal to Bag to avoid PTx!
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scavenging
* Active or passive systems are incorporated to collect gas waste. * This method consists of a collecting and transfer system, a receiving system and a disposal system. * Both excessive positive and negative pressure variations in the system are limited. * Other methods are used to reduce theatre pollution: theatre ventilation, circle system, total intravenous and regional anaesthesia.
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sample line vol
120ml/min O2 consumption 3.5ml/kg/min= 250 | hence 350ml min.
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la place
To appreciate the afterload on individual muscle fibers, afterload is often expressed as ventricular wall stress (σ), where AL=2.r.p/thickness In alv P to collapse= T/r
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contractility factors
The Frank-Starling law holds that increased stretch on the myocytes (to a point) increases the force of their contraction. (indep of preload-simple stretch in a lab)
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afterload
Afterload can be defined as the resistance to ventricular ejection - the "load" that the heart must eject blood against. It consists of two main sets of determinant factors: Myocardial wall stress, which represents intracardiac factors Input impedance, which represents extracardiac factors Wall stress is described by the Law of Laplace ( P × r / T) and therefore depends on: P, the ventricular transmural pressure, which is the difference between the intrathoracic pressure and the ventricular cavity pressure. Increased transmural pressure (negative intrathoracic pressure) increases afterload Decreased transmural pressure (eg. positive pressure ventilation) decreases afterload r, the radius of the ventricle Increased LV diameter increases wall stress at any LV pressure T, the thickness of the ventricular wall A thicker wall decreases wall stress by distributing it among a larger number of working sarcomeres Input impedance describes ventricular cavity pressure during systole and receives contributions from: Arterial compliance Aortic compliance influences the resistance to early ventricular systole (a stiff aorta increases afterload) Peripheral compliance influences the speed of reflected pulse pressure waves (stiff peripheral vessels increase afterload) Inertia of the blood column Ventricular outflow tract resistance (increases afterload in HOCM and AS) Arterial resistance Length of the arterial tree (the longer the vessels, the greater the resistance) Blood viscosity (the higher the viscosity, the greater the resistance) Vessel radius (the smaller the radius, the greater the resistance)
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what changes contractility
homeometric-frank starling heterometric-HR bowditch and Anrep (AL) HR, preload, afterload drugs, electoolytes, disease.
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anrep
AL Sustained myocardial stretch activates tension dependent Na+/H+ exchangers, bringing Na+ ions into the sarcolemma. This increase in Na+ in the sarcolemma reduces the Na+ gradient exploited by sodium-calcium exchanger (NCX) and stops them from working effectively. Ca2+ ions accumulate inside the sarcolemma as a result and are uptaken by sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pumps. Calcium induced calcium release (CICR) from the sarcoplasmic reticulum is increased upon stimulation of the cardiac myocyte by an action potential.
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bainbridge
The Bainbridge reflex, also called the atrial reflex, is an increase in heart rate due to an increase in central venous pressure. Increased blood volume is detected by stretch receptors (Cardiac Receptors) located in both sides of atria at the venoatrial junctions.
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bezold jarish
The Bezold–Jarisch reflex (also called the Bezold reflex, the Jarisch-Bezold reflex or Von Bezold–Jarisch reflex[1]) involves a variety of cardiovascular and neurological processes which cause hypopnea (excessively shallow breathing or an abnormally low respiratory rate), hypotension (abnormally low blood pressure) and bradycardia (abnormally low resting heart rate) in response to noxious stimuli detected in the cardiac ventricles
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CO autoregulation Golden
heterometric-HR,AL-->contract. Pressure-->HR homeometric-FS-->cont 40-180 CO indep of HR in vitro
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what makes prop good for TCI
t/2=vd/cl | relatively predictable vd, cleara,ce redistribution, and half time
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CVP information
ΔCVP = ΔV / Cv end-expiration, PEEP — PEEP of 10 cmH20 usually results in increase of CVP by ~3 cmH20
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swan ganz
evernote
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GABA rec CORE AF
aa,bb,g ab x2=GABA binding site ag=modulatory allosteric BNZ binding site (increased activation) b= propofol, volatile site, barbituates (increased duration) Although benzodiazepines and barbiturates produce the same electrophysiological action (increase in chloride conductance) at the macroscopic level, studies of channel kinetics indicate that benzodiazepines act primarily by increasing channel activation/ reactivation whereas barbiturates act by increasing the duration
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allosteric
relating to or denoting the alteration of the activity of an enzyme by means of a conformational change induced by a different molecule.
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how do drugs works | CORE
1) PC 2) rec a) LGIC b) second messenger - GPCR, TKR, GCyclase c) steroid 3) enzymes 4) VGIC
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DV
UV-->IVC and liver the shunt is the DV
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umbi vein artery Po2
verin 28 artery 18
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max MV
30xnormal | cardiac output not even close
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Resp exchange ratio
CO2 EXPIRED/O2 CONSUMED. varies dep on metabolic and non metabolic facotrs. RQ is fixed and simply reflects substrate. In the body, the volume of CO2 expired and the volume of O2 consumed vary with metabolic, as well as non-metabolic, factors. During exercise, the RER approaches a value of 2 because a greater volume of CO2 is expired due to hyperventilation. In metabolic acidosis, the RER increases because the respiratory compensation for acidosis causes the amount of CO2 expired to increase, whereas, in contrast, the RER decreases in metabolic alkalosis as the hypoventilatory compensatory response reduces the amount of CO2 expired.
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anaesrobic threshold
e workload above which the blood concentration of lactic acid rises is called the ‘anaerobic threshold’.
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pasteurs point
The Pasteur point is the partial pressure of oxygen at which oxidative phosphorylation ceases, and is ~1mmHg
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measure CO2
ABG: Carbon dioxide tension is measured with a Severinghaus electrode, which is based on the pH electrode, as PaCO2 is related to [H+]. The Severinghaus electrode consists of: expired IR mass spec ramand spec
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anaesthetic gas measurement
evernote
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phase capno
1,2,3,4
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beerlambert
absorpptoin=molarabcoeff.c.l
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NSAID SE
rash, allergic, | AKI-->heartfailure, hyperkalaemia, HTN
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double bohr
so easy to get wrong mum gives freely fetus clings
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metabolic role placenta
COMT, MAO, butylcholinesterase
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long term potentiation
In neuroscience, long-term potentiation is a persistent strengthening of synapses based on recent patterns of activity.
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central sens
glutamate, NO, glia sensitization of wide dynamic range neurons wind up is short term and progresses if sustained to long term potentiaion #sdney Expansion of receptive field size Increase in magnitude and duration of response to stimuli Reduction in threshold of firing
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picco vs swancanz
Picco: if swan canz CI PICO insert a central line place PiCCO into a large artery, usually the femoral (axillary is an alternative) CO and pulse contour analysis
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RMP def
The resting membrane potential of a cell is defined as the electrical potential difference across the plasma membrane when the cell is in a non-excited state. Traditionally, the electrical potential difference across a cell membrane is expressed by its value inside the cell relative to the extracellular environment.
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Vapour pressure =fi.barometroc pressure
Vapour pressure
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CSHT definition
Context-sensitive half time is the time required for a 50% decrease in the central compartment drug concentration after drug administration has ceased; where the "context" is the duration of a “BET” (bolus, elimination, transfer) infusion that maintained a steady concentration in the central compartment.
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Ka
``` 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 DR/D.R=K1/K2=Dk Kd=dissociation constant inverse of Ka Ka= K2/K1=A.R/AR KA=association constant and is reciprical (strenght of sticking on once bound) ```
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starling forces numbers and principle
MAP=60 PBC=15 oncCap=21 loosely 60-20-20=20 filtration coef=SA.p reflection coef=1/proptein perm=glycocalyx function
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steroids dose potency
dex 4=pred 25=hydrocort 100 | dex spec glucocort!!
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Moa Dex
increased enceph-->eat decreased sub P decreased 5HT decreased PG
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getn
positive effect-conc dep, post Abx and small degree time above MIC SE determined by time above crit level. block ribosome s30-->mistranslate tNRA--.weak protein-->wall breaks -->cidal -->synergistic with b lactams SE nephrotox ATN reversible, Dx ototoxicity not met-->excreted unchanged kidneys +water sol. muscle weakness
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prolonged block
Patient: PK, PD drug: choice Anaesthetic: intereactions 2006a(6): Explain the possible mechanisms for prolonged neuromuscular blockade after a 4hr procedure using a non-depolarising muscle relaxantGeneral: Non-depolarising muscle relaxants work by competitively antagonizing ACh at the nAChR on the motor endplate of the NMJ. Prolonged blockade after 4 hours can be due to:Pharmacokinetics- AbsorptionoRepeated administration of NMBD during the case oAccidental administration of long-acting NMBD during the case Drug error- DistributionoInfusion (eg of vec which is lipid soluble) would lead to accumulation in lipid rich tissue without monitoring level of blockadeoInappropriately large doses→ high conc in synaptic cleft- MetabolismoImpaired metabolism: Hepatic failure preventing the metabolism of active drug into less active/inactive metabolites (eg pancuronium)o↓T°C if Pt not adequately warmed during the case: slows down drug metabolism- EliminationoRenal failure:↑ amount of active drug remaining in the body PancuroniumoRenal failure: active metabolite (vec) not eliminated fast enoughoHepatic failure: ↑ active drug remaining Vecuronium, Rocuronium, pancuroniumPharmacodynamics - Electrolyte disturbances:o↓K+, ↑Mg2+(competes w Ca2+), ↓Ca2+- ↓pH: ↑affinity of non-depolarising NMBDs (except gallamine) for nAChRo↑risk during a long case- Drugs:oVolatiles (prolonged exposure during a long case)- ↓ACh release at NMJoLithium -↓Na+ transmission at NMJoAminoglycosides - ↓ACh releasedby ?competition w Ca2+oLA – may block Na+ channel at NMJ (variable)oDiuretics – may effect cAMP production (variable)oCa2+ blockers - ↓ACh releaseoMg- Neuromuscular abnormalityomyasthenia gravis→ defective nAChRoEaton-Lambert → impaired Ca reuptake
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Define the term "hepatic extraction ratio"
# Define the term "hepatic extraction ratio" "Hepatic extraction ratio ... is the fraction of the drug entering the liver in the blood which is irreversibly removed (extracted) during one pass of the blood through the liver".
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determinants of HER
BF, uptake, enzyme capacity
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HER drug types
high HER-->BF is relevant. Prb and HF not low HER ->low Prb-->protein binding irrel -->high Protein binding-->protein binding change-->toxicity
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nerve test palcement
Typically smaller muscle groups are more sensitive The positive (red) lead is placed proximal Ulnar nerve Electrodes are placed along the ulnar border of the wrist at the flexor crease, and thumb adduction is assessed. Facial nerve orbicularis occult The positive electrode is placed at the outer canthus, and the negative electrode is placed anterior to the tragus. Eyebrow twitching is assessed. Posterior tibial nerve Electrodes are placed posterior to the medial malleolus, and plantar flexion is assessed. post-tibial nerve-flexor hallucis brevis
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onset of different muscle group block
onset is determined by BF since larynx and diaphragm equal and larynx more sens order is L, D adductor has poor BF and as a peripheral muscle group is most sensistive offset is determined by resistance D>L>Adductor Orbicularis occuli corresponds well with larynx but depth of block can be underestimated by direct stim of muscle anddecause facial nerve is quite reistant clinical imp: AD is safe indicateor of when to tube and extubate diaphragm recovery is not equal to larynx recovery which is not equal to upper airway muscle tone. (wait for adductor)
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venous drainage brain
dural venous sinus-->IJV
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CSF foramen
foraemen of munroe aqueduct of silvia goes to arachnoid villi outpouches from dura in sagital sinus
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arachnoid villi
Arachnoid granulations (also arachnoid villi, and pacchionian granulations or bodies) are small protrusions of the arachnoid mater (the thin second layer covering the brain) into the outer membrane of the dura mater (the thick outer layer).
219
coricoid plexus
in ventricles | ultrafiltration glucos facilitated Na actively transported Cl fo;llows
220
hi HER
prop, GTN, ketamine #only IV or +++ dose
221
low HER
methadone, roc, phenytoin, thio
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nerve fibre types
``` A alpha somatic motor beta touch delta cold sharp B preganglion ANS C post gang ANS and pain and temp ```
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resistance unit
dyne.s/cm^5 or mmHg.Min/Lx80 normal is 100
224
muscle of artery
media=muscle
225
PVR factors
luminal-r4 intraluminal-PAP extraluminal-lung vol, PEEP
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PTC
It consists of applying a 50-Hz tetanic stimulus to the ulnar nerve for 5 s, followed by single twitch stimulation at 1 Hz. The number of twitches observed in the period of post-tetanic facilitation, the post-tetanic count, correlates inversely with the degree of neuro- muscular blockade.
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PTC to TOFC
TOFC 1=PTC of 9 | PTC of 2-->10min until TOFC of 1
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rec occupancy for depression
75% NDMR, depol is only 20%
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placenta
IgG
230
ketamine bidning site
Phencyclidine (PCP
231
preg and prB
α1‐acid glycoprotein decreased during pregnancy with the lowest value around week 30
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changes in preg
peaks: map 20 CO30 https://primarysaqs.files.wordpress.com/2009/12/makeup-describe-the-cardiovascular-changes-that-occur-in-pregnancy.pdf
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roc met | CORE
NIL!!!
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VEC
CVS SE: nil P+H (NIL BRADY) active met with short half life peed out also bile out
235
panc
active met with half potency unchanged peed mets in bile
236
Atrac met
hoffman hydrolysis-->lordenosine | nonspec esterases-->ludenosine
237
Cisat met
hoff-->nonspec esterases
238
miv
isomers | histamine release
239
ED 95 | CORE AF
In anaesthesia, the term ED95 is also used when referring to the pharmacology of neuromuscular blocking drugs. In this context, it is the dose which will cause 95% depression of the height of a single muscle twitch, in half of the population.
240
secondary immune response
2nd time seen it ++ quick 1 vs 5 days
241
opiate terms
phenanthrene thebaine phenylpiperadine
242
opiate receptors
all act suprasinally, SC and peripherally yet predominate at mu-supraspinal #Morphine delta-spinal kappa-spinal NOP-supra and spinal
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GqpCR
evernote
244
CYP450
3A4 is midaz and alfent and warf | 2D6 is codeine tramadol
245
dabagat vs riva #evernote
Dabagatran Double DURATION +Double action + DIALYSIS proDRUG. Min prB Thrombin inhibitor #coag cascade and PL agg
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ropivocaine strucutre
propyl group on its piperadine nitrogen S enantiomer less lipid sol-->more discriminatory block elim half life 150min 2.5hrs
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AchEi
physiostigmine crossed BBB to treat central antichol Sx neostig-reacts with amide site to cause conformational change alowing esteratice site to forma covalent bond #carbamylated
248
micromacro
0.01ma ie 10microamp vs 100ma
249
earthing
completes circuit when fault-->trip and path less resistant than through you. in powerlines -->escape
250
aladin caseete
electrical injection of liquid (doesnt change volume with temp much.)
251
flow meteres viscosity density
5. At low flow rates, the clearance is longer and narrower, thus acting as a tube. Under these circumstances, the flow is laminar and a function of gas viscosity (Poiseuille’s law). 6. At high flow rates, the clearance is shorter and wider, thus acting as an orifice. Here, the flow is turbulent and a function of gas density.
252
mannitol end point
should be discontinued if Na+ > 160 or osmolarity > 320mosmol/kg
253
hypertonic salien end point
end point of therapy Na+ 145-155
254
STP
NaCO3
255
propofol contains
benzyl alcohol | NaOH ph 7.4
256
TEG
What is r? r = reaction time (normally <6 minutes) Measured from sample placement until the amplitude reaches 2 mm Represents activation of the coagulation cascade (intrinsic) Prolonged with heparin, coagulation factor deficiency If abnormal, consider FFP Initiation What is k? k = clot formation time (normally <6 minutes) Measured from r until the amplitude reaches 20 mm Represents fibrin formation Requires normal intrinsic clotting factors, fibrinogen and platelets Amplification What is the α angle? Measured from the top of r to the k value Normally 60 degrees Represents the rate of clot propagation If abnormal, consider fibrinogen = cryoprecipitate What does the maximum amplitude represent? Represents clot strength Normally 60 mm Significantly disturbed by platelet abnormalities
257
midaz
0.5mg/kg PO 0.1mg/kg IV
258
flumazenil
0.5mg ie 1ml
259
naloxone
50-100mcg Q5min