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ORTHO > 2nd test anestesio > Flashcards

2nd test anestesio Flashcards

1
Q

hx of ketamine

A

intoduced in 1970

syntheiitc drug (not derived from natural product - like propofol and benzos)

part of feniciclidina group

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2
Q

cx of ketamine

A

anesthetic agent - can be used unico for that

analgesia

not volatile

liposoluble derivative of fenciclidina

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3
Q

ketamine mechanism and action

A

not well understood

only EV that gives inhbition and excitation and simultaenously - selectively in one organ CNS (aka DISSOCIATIVE ANESTHESIA - keeps some reflexes intact and others depressed - other EV have to wait for px to close eyes not ketamine - produces fixed gaze tho scared - doesnt blockeyeball like oethers where eye rolls up - ketamine can cause nystagmus tho -)

excites limbic systrm, inc HR, VC, psychiatric deliriums (maybe resistant to others)

depresses cortex and thalamus

inetrrupts pain - anesthesia

blocks AcH at cortex

we think ketamine acts at same opiod rec due to reversal same

but also act in serotonin rec, NE rec, and muscarinic Ach rec

(@ muscarininc thats why salivation increases) -

maintain swallow reflex - px can cough, maintains suction reflex - defense mechanisms

@ NE rec liberates catecolamines, VC peripheral and increases BP

@acute processes dehydrated, hypotense state hypovolemic shock px give ketaine with anesthetic inductor helps cardiac precharge

produces hipnosis actina @ cortex BUT DIFFERENTLY and like barbs with excitation right before (not calm, agitated - unlike propofol)

analgesia > anesthesia –>
(need less inhaled gas) & (no pain at immediate postqx

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4
Q

antagonista puro de opiodes

A

naloxone

desireaed and undesired effects

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5
Q

FD ketamine

A

dissociative anesthesia ( suppresses some reflexes while others not)

maintains cough and corneal, suctionz

coordinated movements but not conciosu

eyes open, fixed gaze, nistagmus

potent hipnotic and analgesic

iincreases ICP
blood flow of brain
cerebral O2 cconsumption …metabolsm and intraocular pressure

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6
Q

can we measure depth of coma in ketamine

A

noooo

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7
Q

effect of ketamine on VC system

A

acts at NE rec and thats why it increases systolic arterial P 20-40mmHg - causes peripheralVC - more volume reaches heart (precharge) - CO increases as well

increases HR (increases LV work)) and O2 consumption of that muscle - so not good for px with coronary problems

elebates pulmonar vasc resistencees

relaxes bronquial SM - BD (@ asma px, BC px - ideaal_

secondary to increase in sympathetic activity

hepatic px (transplant px)are VD pysiologically, others VD from drugs (propofol, barbs, opiods) - ketamine ideal for VD px (NE causesVC)

anything that increases work of ventricle increases O2 consumption

not best in coronary px

BD (relaxes SM there)

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8
Q

ketamine @ resp

A

minimal effect - doesnt depress giving it biosecurity

problems alot of time when its used with another drug like opiods

transitory apnea < 5min

seen after intubation dose

relaxes broncial SM

betters pulm compliancy in anesthetic px

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9
Q

FK metabolism of ketamine

A

very liposoluble - used EV have effects in 1min

crosses BBB

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10
Q

duartion ketamine

A

10-15min (1min initiation)

IM effect by 5min (absorbs well)

produces qx anesthesia in 30-60sec

20 peak

oral dose produces max sedation in 20-45min

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11
Q

indications of ketamine

A

IV anesthetic inductor - can be alone

useful in hypovoelmic acute shock

good for kids - cardiac congenital (R to left), bronchial hyperactivity (BD)

used as inducgion agent in kids - IM
(before sevorane)

px with cardac tamponade
px with cardiac congenital diseases with right left shunt

px with reactive bronqual disease severe due to BD effect

useful in kids as an inducctor for less deliriums than in adults
IM inducer in px arent cooperating (with EV, studies)

can cause conscious sedation in kids that are doing minor procedures, como curas o cambios de apositos, desbridamiento of wounds, xray

IN these proceudres causes excellent analgesia wihtout respiratory depression

px that have to go everyday to get anesthesia for qxs

studies where we cant be in contact iwth px or px needs to be stilll/calm - CT, MRI, RT -good to canalize kid for short proceudres no resp or CV depresison

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12
Q

CI ketamine

A

px with ICP, mass in brain, cerebral infarct hx

NE rec @ chronic shock are depeleted so nooo, opposite effect , more VD (NE, epi wont work!)

px with open ocular lesions , glaucoma, (because ketamine increases intraocular pressure) ophtalmological qx

in px with coronary disease or pulm HTN, HTN,

in px with catecolamine depletion (in px with critical prolonged disease) - ketamine has
cardiodepressor effect which can manifest

bedridden px

px with psychiatric alteratiooncs - causes hallcuincations (auditive or visual), delirium

narcotrafficked, pleasure use-

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13
Q

ketamine interactions

A

potentiates relaxers NDNMRS

hipotension with halotane

prolongs inhaled anesthesia aka reduces CAM

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14
Q

dosis ketamine

A

IV
IM
recta;
oral

induction 0.5-2mg/kg IV (1mg/kg)

4-10mg/kg/IM (5 is enough)

maintenace 30-90mg/kg/min

10-20mg for concious sedation

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15
Q

benzodiazepines

A

dizepam, lorazepam, midazolan

preqx to sedate px - antianxiety

PROLONGED amnesia and good sedation - px wont remember

used in preanesthesia, preinduction, preqx to calm px down

EV anesthetics (right before qx)

also IM, VO (night before), parcho

NO ANALGESIA

NOT FOR INDUCTION OF SLEEP/ANESTHESIC

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16
Q

sturctures of benzos

A

diacepam and loracepam have similar structures

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17
Q

biodisposition diacepam

A

high liposoliblituy , hipofilic wait CNS initation

crosses BBB faster than midazolam (more hydrosoluble)

IM irritattes, hurts, acido bensoto, EV also irritates
somnolence, hipnosis slow irregular

very insoluble in water

slow initiaion - not ideal preinduccion

30min

slow recuperation

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18
Q

all EV decrease flow in hard organs

A

liver kidney bazo
all EV eliminate thru liver (benzos, opiods) - all prolonged if liver messed up…. except ketamine

keatmine doesnt decrease flow!!!!!! - can be used in px with pathologies of these organs

meatabolizes at liver (even at decreased flow or pathology, clears up well) eliminaeted life stays the same

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19
Q

metabolites of diacepam

A

3hidroxidicepan
oxacepan
dismetilodacepan

WITH sedative and pharmacological activity

like opiods , benzos use oxydation to metabolize

liver

duration of action of diacepam coorelates with these metabolites

in order for these metabolites to eleiminate undergo
2nd bioptransmformation to elimiante not oxidation this time , conjugation

forming acido glucoronico without farmacological activityg

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20
Q

fk DIACEPAM

A

1.5LT/k C - distribution volume

CLEARING 0.2-0.5CC/KG/MIN

ELIMINATION HALF LIFE 20-40hr

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21
Q

midazolan

A

most recent benzo
1995-97s

more soluble in water - less irritant via IM

fast initation action
effect on CNS fast
mx depresion > 1-3min

IM absorbs well - effect at less 30min

faster sedation

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22
Q

mech of action of all benzos (like opiods)

A

@ CNS potentiloze GABA in different areas,

rec of benzos of CNS @ cortex, black sustancia, hipocampo (these others are IIor presynaptic).. cerebelo (has postsynaptic aka type I rec) , medula espinal.

rec are post synaptic or presynaptic (so benzos can be type I or II))

increase clorine ion conductance in synapsis which hyperpolarizes cell - inhibitory

unlike barb, benz increases aperture o fCl- channels

frprnf on lovslxsyion

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23
Q

farmacological action of benzos

A

decrease necessity for inhaled agent

b/c they are sedatives

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24
Q

@ CV benzos..

A

depression of myocardium

increase HR

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25
Q

@ resp benzos

A

benzos cause transityry apnea
more pronounced if used opiod before (like propofol)

at dosis of 0.75 of midazolan or 0.015mg/kg of dizepan there will be no resp effects

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26
Q

uses of local anesthesics

A

residents
paramedics
anesthesiologits
everyone

@ colonization saw indigenus using oja de coca - adornacimiento on wounds and oropharynx,

used in clinic after development of jerninguilla

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27
Q

advangestes of LA

A

biosecurity

sold without perscription

cheap for alot of qx procedures - regional anesthesia

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28
Q

reuptake of NE causes by LAs

A

VC
stops bleeding of a wound

(also causes analgesia)

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29
Q

definition of local anesthetic

A

chemical substances that reversibly block, inhibiting gneration, and nerve umpulse conduction of nerve impulse without LOC (dont cross BBB)

peripihral regional nerve block

remove sensibility of a certain area of the body

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30
Q

presentation of LAs

A

can be tablet, parche, aerosol, etc all types (depending on objective)

(TODAY WE ONLY USE LIDOCAINE AND BUPIVACAINA)

with and without adrenaline added

without/with hypertonic dextrose –> hyperbaric anesthesia = known as anesthesicos pesados pesados
(deposit @ LCR and have higher baricidad than LCR)

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31
Q

cx necessary for local anesthetics

A 
be reversible
latency period
adquate duration that will guarantees qx (a bit longer than qx)
local toxicity minumum
potente de acuerdo a clincial use
stable ante light and heat
elimination and excretion in totality
can sterilize(50, 20ml containters with leftovers to not waste)
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32
Q

protein union of LAs @ nerve

A

procaine - 6%

lidocaine un 67%

ropivacaine - 94%

Bupivacaine un 97% (double duration time)

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33
Q

B fiber block

A

accion - increase of T and VD - one of the first MC of px (@ subaracnoid, epidural)

one of the smallest

smallest first to block, thickest last to block

@ dehydrated hypovolemic , VD px shock, it is CI to use LAs –> decreaases cardiac return –> hypotension

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34
Q

block of fiber A-delta and C

A

loss of sensation of T and pain sensibility

px cant differentiae hot from cold

use aguja to ask if px feels pain or not, vs gota de alcohol

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35
Q

blockage of fiber A-gamma

A

loss of propioception

dont know position of leg

dont move px until this is blocked??? - last px was in is what theyre in for whole qx in their memory

done when cant lift leg

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36
Q

block of fiber A-beta

A

loss of sensation al tact and prssure’

after can put bendaje elastico

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37
Q

block of fiber A -alfa

A

loss of motricity

px feel no deep pain

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38
Q

LAs

A

no shock, hydrated px necessary…. decrease venous return so first MC = hypotension

represent lack of sensbility in a certain area of the body

give analgesia in different parts of body when applied topically, injection in vecinity of nerve endings (principals ) or in epidural or subaracnoid

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39
Q

clinically useful LA agents

A

amino eteres or amino amines

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40
Q

primary action LAs

A

inhibition of peripheral nerves

very selective on which nerve fiber you want

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41
Q

when LAs are systematically administrated they can also affect

A

functions of cardiacl skeletal muscle and SM

asi como toda la transaccion de los impulsos en el CNS and in system speciliazed system in heart conduction

@ EV can affect purkinje1

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42
Q

most available antiarrythmic (or for tachycardia)

A

lidocaine

block purkinje to modulate cardiac rythm

2 presentations

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43
Q

constituents of nerve membrane, LA mechanism

A

…90% of constitutyents of a nerve membrane is lipid and 10% proteins

LA block sodium exit/flow, nerve transmission, depolarization

keep it repolarized

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44
Q

potency of LA depends on`

A

its liposolubility and duration of its effect (due to ala protiein affinity)

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45
Q

for LA to have an effect should

A

block no less than 3 nodules of ranvier or 3micras of diabmeter of a no mielinazed fiber

> 0.2 diameter mielinizado

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46
Q

only anesthetic local natural

A

cocain

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47
Q

cocaine cx

A

alcaloide with VC properties due to it blocking recatacion of NE in motor simpatico terminal nerve endings

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48
Q

2 groups of LAs…before

A

amino eteres derived = procaines , cloro proacina, tetracaine

amino- amine dervied -mepivacaine, prilocaine, lidocaine, bupivacaine, etidocaine

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49
Q

differentiating LAs

A

by metaboslims (where, some in plasma - those caused hpersensibility),

aminos, amina metabolize from hepatic microsomal (used today - at overdose can affect other tissues)

amino eteres from ataraza plasmatica

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50
Q

LAs depedning on duration are classfified into

A

low potency - procaine and cloro procaine (not really used) < 30min

intermediate - prilocaine, etidocaine - 60minn

high - bupicaina, tetracaina 120min

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51
Q

closer ph normal plasmatic to pka

A

will ahve more nonionized moleciels - pharmacological activity - faster intiation

further apart - less - prolonged intitation

if u give with bicarbonate (10cc-20cc lidocaine - 1cc of bicarbonate) = increase ionized molecules- more effeectivity - accelerates

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52
Q

what is pka

A

constant at which drug dissociates

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53
Q

choosing an LA depending on following factuors

A

duration of qx
duration of anesthetic should be > 50% on qx duration

type of regional anesthesia that will be done

size, constutution, general state of px and metabolic alteration

farmacocinetic

absorption, districution, excretion of LAs can say that oesnt mater where depsosited because distribution patter, metabolism and eliminatin is similar - althoug their velocities in these parameters is different

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54
Q

what does absorption of LAs depend on

A

whwere there was deposited and grade of preception of each zone

@ peripheral level, max plasmatic concentation reached within 15-30min , when applied EU reach these elvels immediatley

also depends on aditional VC drugs and fisciochemical properties of drug

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55
Q

in relation to plasma concentratio nfor every 100mg of lidocaine (intercostal very vascularized)

A

1mg of () PHM

(1.5 @ intercostal)

SC = 0.2

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56
Q

max plasmatic dose required to present toxic effect (of lidocaine)

A

5mcgxdl

we can dedcuce that max lidocaine we can put is 500mg of lidocaine with epn and 400mg without epnef

max at intercostal 350mcgxdl

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57
Q

plasma concentration depends on

A

lugar of block

Ej: in intercostal level for every 100mlg of lidocaine will have 1.5mcg of { } plasmatico

in a B . epidural = 0.1mg {}plasmatic

in a B. plexo b. will have 0.6mg {} plasmatic

in a B. Plexo cutaneo will have 0.2mg { } plasmatic (can put mroe in places with less irrigation -

these places take into account using adrenaline can cause damage, infection, necrosis - nasal, pabellon oreja, dermis of skin - dont use too superficially - put it SC )

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58
Q

LA metabolism and excretion

A

destoxicaiton and excretion of local anesthesics are metabolized in liver or in plasma ,

metaboliztes are excreted in urine

VC decreases velocity of venous clearing of LA, from site of injection

this duration is more attenduated in block of peripheral nerve where injectio sites are avascular

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59
Q

local block inititation accelerates with

A

use of carbonated solutiones combined with LA producing more free particlses

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60
Q

cardiav toxicity of LAs

A

CV system is more resitent to toxic effects of LAs, (CNS more sensitive)

dose to cause CV depresion is > than dose to provoke depresion in CNS

this doesnt happen with bupivacain, the mostcardiotoxic toxic…

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61
Q

Signs and Symptoms of LA cardiac toxicty

A

EKG: increases PR interval

prolonges QRS complex

sinusal bradicardia

severe ventricular arrythmia (give lidocaine)

ventricular fibrillation (doesnt happen with lidocinae) - so attached to proteins hard to revese - make sure when giving it youre not in luz of vazo - can kill px

higher threshold when pre give benzo but not level of CNS

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62
Q

tx to toxic response

A

maintenance, resp route PERM, circulatory assistence

tx convulsion w/ small doses of EU short acting barbituric like triopental in 1-2m/kg and sucinil coline in 0.5mg/kg dose

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63
Q

if maintenace of respiratory airways is compromised with convulsions.

A

endotraqueal intubation is urgent

also that will avoid bronco respiration of gastric secreionts

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64
Q

first step to prevent toxicity of LAs

A

use in small quantity for any regional anesthetic

if toxic reaction of bupivacaine and cloro procain shoudl consider using slow injection or fractioned dosis in particular for epidural block to reduce leaste toxiiity potential in am maccidental IV injection

premedication with benzodiacepine like diazepam 1-2mg/kg increases toxic threshold in CNS, nevertheless, influences in CV toxicity

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65
Q

subaracnoidal anesthesia

A

used with LA base

seen daily, gynacologists for cesarean, hacer mama

regional block of hemicuerpo

raquianesthesia - thru vertebral column

have to do LP (need to know where medula finishes)

localizing spots isnt too hard

blocks different nerve fibers depending on size (thinnest first - A beta ) –> VD –> hemodynamic changes, hypotension –> changes T (cant differntiate)

doesnt feel sensitivity nor motor

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66
Q

where does medula finish

A

L1-L2 - lesioned causes pernmanaent damage, less sensibiliy

L2-L3 - inadult inferior border

all should be below L2

neonate - until S2

covered by PAD w/ LCR

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67
Q

absolute CI of subaracnoid anesthesia/ LP

A

vessels in the way,factors to bleeding –> grand hematoma - compresses medula with irreversilbe medula damage - altered coag factors to form trauma

infectious process @ SKIN and puncture area - can cause bacterial translocation

px denies

labor attitutes

deformities of spine (palapate spinooous apofisis)

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68
Q

elements to go thru

A

skin (insulin, LAs with bigger agujas)
between apofisis espinosasa - interspinous ligament
yellow ligament
epidural space (another site for block)
dura madre
exit of LCR - must happen to know youre in subaracnoid space *cx of liquid

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69
Q

important subaracnoid, osmolarity

A

isovaric (LCR = osmolarity) vs.. hipovaric (nerve block under where yo u adminstetered -) vsl. hyperovaric (block will be above where administered - to block T10 - the higher the block more VD - more hemodynamic changes more hypotension)

isovaric bloacks in same place of deposition

election depends on which block level you desire

subaracnoide casues regional anesthesia - hemicuerpo (not specific limb)

lidocaine 1min (heavy , hypervarica - have dextrosa hypertonic, adrenaline_

surgeon has to mark exact of qx excision - ombligo T10 - block fibers above it too T8

first 5min

incline head of px - physical effect to diffuse faster - anesthetic osmolarity is decreasing (hypervaric evenutally becomes isovaric = se fijo - doesnt increase more thant that no matter what more you do to head - wont ascend more)

duration depends on which used
lidocaoine 1 min
bupiv - 2hr

lidocaine pesado , hypervaric with hypertonic dextores

can use adrenaline to increaseduration 30%-40%

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70
Q

max # of LA (volume) can deposit to avoid hypertension of toxicity of any drug

A

4ml

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71
Q

max lidocaine to avoid toxicity

A

100-(200mg)

100 i smax @ subaracnoide

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72
Q

postanesthetic cefalea

A 
not always
feminine
multiple tries of finding space
aguja was too big
not appropriate hydration of px

NOT because px walked or due to pillow or sat up

differnt types

sat or awake NOT when laying down

anesthesia causes weight occiptofrontal sensation

do a differentaial )hx of anesthesia from 24hr -14d

vs pulsatile in temporo parietal (if vascular headache)

hard in kdis and oldies (more in normal fertile age - anesthesia cefalea)

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73
Q

tx cefalea

A

hytdration
steroids
meningeal irritation or no?
parche hematico - not really used , risky

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74
Q

advantatges of epidural anesthesia

A

analgesic (less dose) and anesthesic (more dose)

relaxes less than subaracnoide

al depends on dose

today we are using opiod subdural for analgesic

LAs, lidocaine are not used as analgesics in subaracnoide but they are used in epidural dpeending on dose

any level - doesnt cross dura madrea - wont injur medula

thicker neeedle and catheter can go thru (this determines headage) - can be there 1 wk - long duraion

px can feel pressure but not Pain

much slower or resistent to hemodynamic changes (firssst MC in subarachnoide) USE FOR CESAREA - hypotension affects fetus

much more selective on where to block

complications fo subaracnoide not present here (doesnt perforate dura madre)

of anesthesia depends on how high block (the higher the block, # of anesthetic will be less)

px that dont need too much muscle relaxation - epidural is ideal

plastic surgery

more sensitive block - feels hand of dr but no pain

the higher the block, the less # of anesthetic needed why because the spacers are diffferent (higher medula occupoes mroe aguerjo below more space)

desambular faster - recovers faster

can block 2 places at once

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75
Q

blocking of braquial plexus

A

we want to decrease risk for px
fast recuperation

specific anatomical block = to inhibit pain transmission @ calcium channels that liberate @ nerve fibers

in px with severe pulm or cardiac px - can just block hand - putting them full to sleep is a bit risky for that kind of px

can go straight home

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76
Q

what forms form first primary trunk

A

(roots/raizes) C4, C5, C6

DRAW

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77
Q

segundo tronco primario is formed by

A

C7

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78
Q

tercer tronco primario is formed by

A

C8, T1

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79
Q

innervation of hand

A

C4-T1

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80
Q

each primary trunk has

A

anterior and posterior branches

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81
Q

anterior branch of first trunk unites with

A

anterior branch of second primary trunk to form tronco secundario anterinterno

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82
Q

anterior branch of thrid trunk forms..

A

tronco secoundario anteroexterno

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83
Q

3 anterior branches from 3 troncos form

A

tronco secundario posterio

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84
Q

from tsai

A

medial
cubital
musculocutaneo
ECM

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85
Q

tsae

A

raiz external of medial
coracobraquial nerve
another he forgets

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86
Q

tronco secunario posterior

A

radial nerve

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87
Q

raizes come out of osea where i sthe braqueal plexus

A

agujeros de puncion? in neck between anterior and medial scalenes

then passes under clavicle (already in paquete with veins and artery) - hueca supracavliculara a nivel de la sida

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88
Q

3 levels of blocking brauql plexus

A

interexcalenico - at raiz exit

hueco supraclavicular

axilar

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89
Q

advantages of interecalenico

A

can block entire plexus - all roots

of anesthesia needed is less

px doesnt have to move hurt arm

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90
Q

disadvantages of interecalenica

A

need paresthesia - with aguja #22 superficially, px feels sensation when it touches nerve - thats when you deposit anesthesia - around cricoid thyroid

(now we have electric stiulators)

can block vago and frenico

cant do parrallel, bilateral

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91
Q

supraclavicular tecnhique

A

has been discontinued

@ inspiration vertix of lung comes up and can cause a neumotorax even if done correctly

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92
Q

axillar techinqieu avantages

A

can be done bilaterally

no need for paresthesia

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93
Q

disadvantages of axillar technique

A

need large volumes for blocking all plexus

blocks can be partial (T1 not fully blocked)

can easily punture artery or vein of axillar, if put anesthesics in luz of vessel causing intoxication when looking for nerve - orient with pulse

px would have to move injured arm

smelly

if you puncture vessel just go all the way throught, nothing out, dont move needle
dont take it out and try again

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94
Q

IV blocks

A

thru vein
antebrazo is the only place to do it
effective, useful

exsanguinate all forearm, presure bandage to avoid reflux perfusion (180mmhg/ 2 tourniquetse)

take 1% lidocaine , 20cc, thru acatherer that was put earlier
(without adrenaline) or bupivacaine

arm is asleep

used most for hand, trauma. lavado qx, phalangeal fractures

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95
Q

risk of IV block

A

if tourniquets get lose,

lidocaine through circulation can cause cerebral toxicitu

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96
Q

how long for tourniquet max

A

1.5hr
no perfusion to arm
qx should be over by then (1hr lidocaine should be absorbed up by now)

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97
Q

lidocaine presentation

A

2%

every ml/cc there is 20mg

dilute with saline solution
1% - every cc - 10mg

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98
Q

max dose of IV block without epi

A

400mg max of lidocaine

more 5mg/dl

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99
Q

today we can do selective blovks of specific nerve fibers of plexus - most popular

A

cubital and radial

especially when working on hand

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100
Q

organ according to books that most gets injured

A

the hand

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101
Q

where to block cubital

A

funny bone area

fossa epitrofia/craneal?

here only covered with skin

with 3-5cc withoutepi

need paresthesia

need asepsia

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102
Q

causes of ER infections

A

poor asepsia (block cubital first)q

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103
Q

medial nerve blockage

A

between palmar major and palmaro minor - on sides

laterally punctinging medial nerve

dont need paresthesia

5cc of lidocain without epi

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104
Q

radial nerve block

A

easily blocked by
agujera thru tabacera anatomica under skin and pentrate needle max and then administer

fine needle

know which fingers are innervated by it

ALWAYS ASPIRATE before infiltrating to makre sure youre not in an artery

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105
Q

interdigital blocks

A

2 cc o f lidocaine blocks all distal phalanges

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106
Q

pudendal nerve blocks

A

also done

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107
Q

crystalloides (aka suero)

A

anesthesiologists regulate hydration
were used for hemodilutions
similar to plasma

substances with water, electrolyetes and or sugars in different pro-portions and osmolarities (dextorse) - may or may not contain dextrose

(some substances have only dextrose and water - hypertonic solutions)

water with disorbente universal and electrolytes

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108
Q

basis for hadningl px hydration

A

water or electrolytes

know normal rnage of elecrolytes

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109
Q

normal Na+

A

135-145meq/dl

most abundant electrolyte

command osmolarity of solutions - decides

> 145 = hypernatrmic/hyperosmolar solution

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110
Q

K+ normal

A

3.5-4.5

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111
Q

Cl- normal

A

107ish

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112
Q

calcium normal

A

8-10

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113
Q

magnesium normal`

A

1.7-2

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114
Q

if you give 1000ml distributes in coporal liquids as

A

2/3 to IC space (666ml) and 1/3 to EC space (333ml)

since EC space is divided into intersticial and intravascular (250ml to intersticial - 75% and 83ml to IV space 25%)

takes 2-4min to diffuse to diffeent spaces

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115
Q

capacity for crystaoilds o expand volume is related to

A

consentration of sodium in solution and this sodium is what provokes osmotic gradient between Extravasuclar and intravasuclar space

different for each solution - depends on how much sodium

hypernatremic drags more water from EV space to IV space (osmosis - ability to mbilize liquid from one space to antoerh)

IV is where we want liquid in hypotense VD px, to imrpove precharge

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116
Q

crystaloids are considered …

A

non toxic, no eadverse effects,
dont cause allergies,, are not vitamins, dont need refridgeration or light
dont interact with regular blood components

only should maintain equilibrium

can present certian alterations related to indiscriminated use and without control of medical team -

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117
Q

hyperhydration can cause

A

edema in all tissues and membranes

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118
Q

normal osmolarity of plasma

A

280-300

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119
Q

nutrient in orgnaism

A

dextrose

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120
Q

types of dextrose in water

A

for every g of dextrose 4kcal

5% - 5g

10%, 50% for food formulas

energy only in hypoprotein px

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121
Q

hypernatremic px needs…

A

WATER
give 0.45% saline

Ringer lactate (130 Na+)

dextrose in water

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122
Q

px losing cl- and na+ , bleeidng, acute hypovolemic

A

give normal saline

drags water , osmosis, less liquid needed

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123
Q

careful for saline solutions

A

in px with cardiopathies

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124
Q

adverse effects of ringer lactate

A

has bicarbonate (to elimate has to be CO2 and H2O)

in px with hepatopathies will cause metabolic alkalosis form too much lactate in blood

has calcium - can cause hypercalemia in renal px with high infusions

dont use in px with liver and kidney probems

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125
Q

adverse effects of normal saline solution

A

too much cl - hypercloremia

hypercloremic acidosis in px with poor renal function

hypernatremia in renal px

edema (all solutions cause this)

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126
Q

hypertonic saline solution

A

hypernatremia
metabolic acidosis
hypocalemia
cerebral dehydration with ingracraneal blleed
mielinolisis pontica from abrupt changes in sodium concentration
pulm edema in cardio px

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127
Q

dextrose in water adverse effects

A

water intoxication due to overdose of glucosalated solution
hyperglicemia -dont use in diabetics
addison px can cause crisis due to cell edema and water intoxication
cell dehydration in cerebraltrauma

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128
Q

hypotonic solutions

A

have less solute concentrations than other solutions

solutions with osmolarity less than plasma ( < 280mOsmol/l)

used for hypernatremia

saline 0.45, 0.33?
dextrose 2.5, 5

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129
Q

isotonic solutions

A

solutoins that have the same concentration of solutes as other solution

an isotonic solutoin has an osmolarity similar to plasma between 272-300mosmol/l

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130
Q

most cardiotoxic LA

A

bupicavaine

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131
Q

low potency LA

A

procaine

cloro procaine

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132
Q

initiation of procaine vs cloro procaine

A

1 (procaine)

cloro procaine (0.8)

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133
Q

pka of procain vs cloroprocain

A

procaine (8.9)

cloro procaine (8.7)

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134
Q

low potency LA with protein uniont

A

procaine - 5.8

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135
Q

intermediate potency LAs

A

mepivacaine

etidocaine
prolocaine

lidocaine

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136
Q

initations of intermeidate potent LAs

A

mepivacaine - 1.5

etidocaine - 8
prolocaine - 1.5

lidocaine - 0.8

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137
Q

pka of intermediate potency LAs

A

mepivacaine - 7.6

all the rest are 7.7
etidocaine
prolocaine

lidocaine

7.7 lidocaine - 7.4 normal plasma pka - 64% particles

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138
Q

protein union of intermediate potency LAs

A

mepivacaine - 77

etidocaine - 94
prolocaine - 55

lidocaine - 64

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139
Q

high potency LAs

A

tetracaine

bupivicaine

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140
Q

intitation of high potency LAs

A

8 both tetracaine

bupivicaine

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141
Q

oka of high potency LAs

A

tetracaine - 8.5
bupivicaine - 8.1 (initation action will be slower 20% noninonized particles)

decide by duration of qx

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142
Q

protein union of high potency LAs

A

tetracaine - 76

bupivicaine - 95

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143
Q

max dose of lidocaine wihtout toxicity

A

we can dedcuce that max lidocaine we can put is 500mg of lidocaine with epn and 400mg without epnef

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144
Q

LAs pH

A

local anesthetics are drugs of weak bases, when their PKA > pH will have a > # of ionizaed molecules

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145
Q

year that cocain was clinically introduced and use

A

1884

topical use

polvo prep

146
Q

max dose of cocaine

A

200

147
Q

year benzocaine was introduced in clinic and use

A

1900

topical use

pomada and aerosol prep

148
Q

year procaine was clinically introduced and use

A

1905

spinal use

prep sol 10/20g/ml

149
Q

max dose of procaine

A

1000

150
Q

year tetracaine was clinically introduced and use

A

1930

spinal use

sol 10/20g/ml

151
Q

max dose of tetracaine

A

200

152
Q

year lidocaine was clinically introduced and use

A

1944

2 presentation types

????? periphral neve block, epidural

10/20g/ml

max dose 500
spinal
topica = pomada 2.5

153
Q

history and use of mepivacaine

A

1957

epidorual and peripharl nerve block

sol 10/20g/ml

154
Q

max dose of mepivacaine

A

500

155
Q

prilocaine histoy and use

A

1960

epidorual and peripharl nerve block

sol 10/20g/ml

156
Q

max dose of prilocaine

A

900

157
Q

bupivicaine history and use

A

1963

epidorual and peripharl nerve block

sol. 2.5 and 5mg

158
Q

max dose of bupiviaine

A

200

159
Q

cx of class C fibers

A

myelinic? - no

D-M (0.3-1.3)

conduction velocity 0.7 - 1.3

sympathetic, func. auto post gan diverso

160
Q

cx of class D fibers

A

myelinic? - no

D-M 0.02

Veloc-conduction 0.1-2.0

pain temperature and tact

161
Q

cx of class A alpha fibers

A

myelinic (> 0.02 are myelinic….he said)

D-M (6-22) - thickest

cond vel 30-120

motor

162
Q

cx of beta A fibers

A

myelinic

D-M (6-22) - biggest

cond vel 30-120 metro por milecima seg

motor

163
Q

cx of gamma A fivers

A

myelinic

D-M (3-6)

cond vel 15-35

muscular tone

164
Q

cx of delta A fivers

A

myelinic

D-M 1-4

conduction velocity 5-25

pain and temperature and tact

165
Q

cx of B fibers

A

myelinic

D-M -3

conduction velocity
3-15 pregnagionar sympathetic

diverse autonmaous functions

166
Q

where do LAs act

A

act in n. membrane

(what they do is the inhibit the flow of sodium acting on specific receptros responsible for changes in conductance of sodium channels)

specifically in internal channesl is blocked by local anesthetics used in clinics

167
Q

duration of anesthetic effect can lengthen how

A

increasing the dosis or by abolition of VC like adrenaline or fenilatrine

168
Q

3 main benzos with special interest for anesthesia

A

dizepam, lorazepam, (he doesnt use) midazolan

diazepam and loracpam have similar structures

midazolan is completely different

169
Q

what differentiates midazolam from diazepam since each molecule has hydrogen atoms also has a ring strucuture called….and its importance in midazolan

A

imidazol

( i think this is only in midazolan….the imidazol in midazolan converts this drug to hydrosoluble with a pH < 4)

midazolan different (dormicun) (doesnt irritate, less liposoluble than diazepam immidasol ring) - BBB fast, fast initiaion
imidazol ring

but we cant explain why midazolam is faster initation

170
Q

why does diacepam irritate

A

prepared in benzoic acid which irritates alot

171
Q

loracepan prepared in what solution

A

propilenglicol acid

172
Q

solubility of loracepan

A

just as insoluble in water as diacepam

173
Q

flumacenil

A

inidication

revert depressive effects of benzos @ central level

174
Q

dose of flumacenil for an overdose of benzos

A

bollus of 0.2mg

@ 30min

0.3

then 0.5 until reacing 3.0mg

175
Q

Pedro Cieza de leonn - described that incas chewed coca (kunka) sukunka means faringe adormecida

A

1532

176
Q

charles gabiriel prevaz, crystal jeringa

A

1853

177
Q

alexander wood, aguja hypodermic

A

1885

178
Q

who and when was cocaine isolated

A

1860 - Nieman

179
Q

who and when describes pharmacology of cocaine

A

1878 - anrep describes farmacology of cocaine

180
Q

who and when show first clinical demonstration of cocaine in ocular conjuntiva

A

1884 - k. koler and sigmund freud

181
Q

who and when realized first block with cocaine

A

1885 - Halsted

182
Q

who and when used frist time adrenaline to prolong a regional block

A

1903 - Braun , uses adrenaline to prolong regional block

183
Q

when and by whom was logfren synthesized

A

1943 - logfren synthethizes lidocain

184
Q

when was bupivacaine synthesized

A

1963 - synthesizes bupivacaine

185
Q

in respect to plasma crystalloids can be

A

can be hypo, hyper or isotonic

186
Q

components of cloruro de sodio of 0.9% (normal saline) vs 0.45% (SS al medio)

A

saline 0.9% only has Na+ and Cl- (154 each) - hypercloremica, hypernatremica_ - mild hypertonic - 308 osmolarity (mosm/L)
put if losing sodio (hiponatremia_), bleedning (improve hemodynamic state of px), acute hypovolemic px

saline 0.45% 77,77, hyposomlar, hypochloric, hyponatremic - 154
reponer with nutrition not to hydrate
@ hypernatremc px

know what px needs at rehydration

187
Q

other saline solution components 0.21 vs 3% vs 5%

A

0.21%
Na and Cl - 34 each
68 mosm/L

3% - 513 each
1026mosm/L

5% 856 each
1712 mOsm/L

188
Q

components of dextrose in water (5 vs 10 vs 50%)

A

dextrose in water - only to give energy and nutrients @ hypoglicemia, for heart and brain, no other electrolyte

5% has 50g of glucose /L with 252 osmolarity

10% - 100g/L, 505mosm/L

50% - 500 g/L - 2525mOsm/L

@ hypernatremic px
energy only in hypoprotein px

189
Q

components of Ringer solution

A

Ringer solution has 148 Na+, and 156 Cl-,
K+4,
Ca 3
(310mosm/L)

190
Q

ringers lactate or Haartmann (baxter) solution components

A 
lactate ringer 
Na+ 130, - hyponatremic
Cl 109, 
28 bicarbonate, 
K+ 4, 
Ca - 3, 
(272 mildy hypotonic)
@ hypernatremic px
191
Q

Components of dextrose in 5% saline solutoin

A

= SOLUCION MIXTA = 154, 154, Na+ and Cl-
50g of dextrose (560mosm?L)

slaine 9 + dextrose 5 together

192
Q

dextrose/glucosated solutions are CI in

A

CI - diabetic px

193
Q

use for hypotonic solutions

A

used to correct electolytic anomalies like

in px with hypernatremia from loss of free water

in diabetic px

or px with chronic dehydration donde prima IC volume loss

194
Q

examples of isotonic solutions

A

SSN (normal saline solutoin) al 0.9% and Ringer lactate

195
Q

hypertonic soltions

A

those that have higher concentraiton of solutes than other solutoins and higher osmolarity than plasma ( >300mosm/L) and higher sodium concentration

196
Q

dextrose in distilled water al 5% (DAD 5%)

A

is a hypotonic solution between 252-261mOsmol/L of glucose

energy only in hypoprotein px

197
Q

main 2 indications for DAD 5%

A

rehydration in hypertonic dehydrations and as an agent to give energy

gives significant calories to reduce proteic catabolism and acts as a producer combustible of tissues that most need it likw CNS and myocardium

198
Q

every L of DAD5% gives what

A

50g of glucose = 200kCal

199
Q

dextore in distilled water al 10%,20%, and 50%

A

these are hypertonic glucsolated soltions that same as 5% glucose once they metabolize they give energy and transform in water

only for food boli

also glucose is considred as an indirect provider of K+ to the cell because it mobilizes sodium from the cell to the EC space and K+ in the opposite direction

200
Q

most importnat indications of dextorse in distilled water al 10, 20, 50%

A

tx circulatory collapse

cerebral edemas

pulm edema

because glucose produces cell dehydration and attracts water to vascular space decreasing the pressure of CSF liquid and lung

201
Q

colloid solutoins

A

contain particles in suspension of high molecular weight that dont cross capillary membrane

so they are capable of increasing osmotic pressure in plasma and retaining water in IV space

basicllay they increase oncotic pressure and effectivity of movement of fluids from intersitical space to deficient plasmatic compartment aka they are PLASMA EXPANSOR AGENTS

202
Q

hemodynamic effects of crystaloids vs colloids

A

colloids produce hemodynamic effects faster and more sustained than crystaloids in less amount

precisandose less volume than crystaloids

cost is much higher

ARS makes you justify use of these synthetic solutions

203
Q

cx that coloidal solution should have

A

should have the capacity to maintain osmotic coloidal pressure for some hours

lack of other farmacological actions

lack of antigenic effects, alergenic or pirogenic effects

lack of interference with tipification or compatbilization with blood

stability during prolonged periods of storing y bajo amplias variaciones of temperature

easy sterilization

cx of viscocity that are adequate for infusions

204
Q

classification of coloids… 2 types

A

natural coloidal solutoins - only one

artificial coloidal solutoins

205
Q

natural coloid sollutions

A

albumin

206
Q

albumin is produced where

A

in the liver

207
Q

albumin

A

responsible for 70-80% of oncotic pressure of plasma making it an effective colloid

208
Q

molecular weight of albumin

A

its molecular weight osscilates between 66.3 and 66.9

209
Q

distributioin of albumin

A

between IV compartnemtn (40%) and intersticial 60%

210
Q

albumin synthesis stimulated by

A

stimulated by coritol and tyroid hormones

while albumin decreased when there is a decrease ? in oncotic pressure of plasma - edema to peripheral tissue

211
Q

normal concentration of albumin in serica in suero

A

3.5-5g/dL

it correlates with nutritional state of subject
<3.5 - hipodenutrido

212
Q

1gr of albumin increases plasmatic volume by

A

18ml,

more mobliity of liquid form one space to another

213
Q

100ml of albumin al 25% increases plasma volume by

A

una media de mas o menos 465 +/- 47 mL

20gr albumin - 455-500cc in plasma

214
Q

1L of ringerlactate increases plasma volume by

A

194cc +/- 18mL

215
Q

90% of administrated albumin stays where

A

plasma for 2hr

after this it equilibrates between intra and extravascular spaces for a period of 7-10d (1gr)

75% dissapears from plasma by 2d

216
Q

catabolism of albumin

A

in digestive tract, kidney, mononuclear phagocytic system

217
Q

clinical condutions thtat can be associated with decrased albumin prodcution in blood include

A 
malnutrition
cirrosis - hepatopata
qx
trauma
hypothyroidism
inflammatory systemic states like sepsis

less albumin produced in all these states because albumin is simualted by cortisol in liver, malnutrat…

218
Q

possible benefits of albumin

A

capacity to decrease edemas

improving oncotic vascular pressure avoiding edema in lung and other organs

not justified for NUTRITION - even tho measured for that $2500 por frasco

219
Q

artifical coloidal solutions

A

dextranos

HEA (hidroxietil-almidon)

Pentalmidon

220
Q

dextranos orgin

A

polysaccarides with bacterial orgin (Leuconostoc mesenteroids)

solucion hemased - helafundi?? commercial names

221
Q

capacity of dextranos

A

oncotic protperties are adequate but cant transport oxygen

fast glumerular fast

222
Q

elimination of dextranos

A

renal

223
Q

dextranos on kidney

A

concentrated infusions of low molecular weight rapidly cross glomerular filter and can increase urine viscocity causing renal insufficiency from tube obstruction

this is reversible if you rehydrate px (IR)

224
Q

HEA

A

hetaalmidon is a synthetic almidon prepared from amilopectine using hydroxietil eter groups in glucose residus

225
Q

Pentaalmidon clearance - advantage

A

90% is cleared in 24hr and is practically indetectable in 3d

226
Q

pentaalmidon

A

volume expander takes longer than albumin - 12hr effect

due to incrased oncotic pressure (40mmhg) - expands more than albumin 5% or hetaalmidon 6%

227
Q

duration of pentaalmidon

A

12hr

228
Q

lactate ringer or Hartmann solution (vs SSN)

A

isotonic solution with 51mEq/L of Cl less than SSN generating only transitory hypercloremia so less possibility to cause acidosis

its a balanced electrolytic solution - part of sodium of isotonic saline solution is replaced with calium and potassium

229
Q

use when hartmann or ringer lactate

A

when we need to administer massive amounts of crystaloid solutions

230
Q

hypertonic saline solution actions

A

expands IV volume by extracting liquid from extravascular compartment

inotropic and pulm VD affect as well

231
Q

use for hypertonic saline solution

A

in burned px

decreases edema and supplies well hydric demands

232
Q

hypertonic saline solution mechanism

A

increase in sodium concentration and osmolarity when infusing hypertonic serum in extracelular space

233
Q

gel derived solutions history

A

first used in WWI due to increasing viscosity and low freezing point

234
Q

how to buffer psyychiatric affects of ketamine

A

buffer with benzo

235
Q

methods of metabolism

A

oxydation,
conjugation reduction, hydrolysis

elimination can be transcutaneous, pulmonary, urine

236
Q

who shouldnt use diazepam

A

accumualtes in fetal blood risk for RN - cross BBBand placenta

px with IR, IH, VD px dont use , but if u have to pseudosis to relax

these px have increased GABA rec # so more sensible to EV anesthesics

prolongs action duration

237
Q

fk midazoloam

A

decrease volemu similar to others 1-5lt/kg and clearance 4-8ml/kg/min - higher

half life of elinianted 2-4hr therefore much shorter

dissapears faster

238
Q

metabolism midazolam`

A

metabolizes in liver - oxidation

metabolites hidroximetil midazolan - excreted thru urine - not farcaologically active

239
Q

best sedatin

A

midazolam

dont wake up fucked like with diazepam

smooth relaxation properties

240
Q

amnesia of diazepam vs midazolam

A

diacepam more amnesia thqan mid midazolam

241
Q

use what to revert resp affects of benzos

A

revert with flumazenil

dosis dependent

242
Q

causes of high doses of diacepam

A

\

high dosis can cause severe cerebral depression

suicide method

243
Q

only ev anesthetics with analgesic affects

A

opiods and ketamine

not barbs, not benzos, not propofol

244
Q

best EV anesthesia for biosecurity margin

A

ketamine

wont cause ventialatory arrest (like propofol and benzos and opiods - wrost, barbs)

245
Q

1 cause of death from EV anesthesia

A

resp arrest

246
Q

only EV and IM of same effectivity

A

ketamine (maybe initaion action a little longer)

nuvaine opiod SC

247
Q

only drug that can inhibit or excite at same time

A

ketamine

248
Q

reversing ketamine side effects

A

same opiod reverser = naloxone

we think it involves opiate rec due to reversion of efects of ketamine from naloxone

we think ketamine acts in same opiod rec

249
Q

(antagonsita puro de opiode to revert_

A

naloxone

250
Q

how to decrease salivation effects of ketamine

A

decreaseed with anticholinergic drugs- atropine, –> broncoaspiration

if px needs itcant use in px with isquemia, myocardial infarct
coronary infartc unstable angina problem you fuck up giving them ketamine - they have excess salivation - dont double fuck up and give atropine - increase HR even MORE

give glicopirulato (exclusive salival rec) - atropine has rec in heart and salivary or give psuedosis of atromine (0.1mg) b/c salivary galnds are very sensitive to atropine so pseudosis is enough

251
Q

anticholinergics

A

….

252
Q

only anesthetic that helps CO, pregcharge and causes peripheral VC

A

adrenaline

stimulated by ketamine

increases BP and HR (not like others that u can use bradicardia to see depth of anesthesia)

253
Q

how to measure depth of anesthesia with ketamine

A

incoordinated movments

no way to know if its pain or part of the effect …. cant really know

254
Q

drug ideal for VD px

A

ketamine

255
Q

when do LAs cause cerebral and cardiac alterations

A

cerebral changes only if overdosage as well as cardiac alterations — so all is well if you stay in therapuetic dosis

256
Q

nerve fiber composed of what

A

2 layers of lipid and one protein layer

257
Q

determines potency of LA

A

affinity anesthesia has to lipid - liposolubility

258
Q

duration action of LA depends on

A

depends on affinity to plasma protein of nerve

259
Q

are LAs composed of what

A

organic compounds

carbons, H ions

260
Q

myelinic vs amyelinic nerve fibers

A

(amyelinica < 0.03 micra diamter - with)
transmission of pain impulse is all along nerve fiber
various symptoms - tachy cardia, altered glicemia, endocrine MC< CV MC psycoholgical MC, apendicular process like, discomfort
non localized pain

myelinic > 0.03 miras diamter
form of tranmission of pain alatrorio a traves de ranvier nodules
localized pain

261
Q

transmission velocity is usally in LAs

A

(usually 20-25 x diabeterm of fiber it blocks

262
Q

pH affect on LAs

A

LAs weak to pH changes
dont act at acid envirtonment - cant transform and dissociate into pharmacological parts, ionized/nonionzed part
(odontological proceudres) - also affects initiation action time

at cardiac arrest we look for resp acidosis from bad ventilation it doesnt matter what adrenaline or atropine you give they wont react….thats why ventilation is so important

263
Q

FK of LAs

A

all same

absorpption \depends on irrigation of deposit area

lecho venoso - immediatley
peripheral 15min

raiz nervioso - depends on if has adrenaline or not with it (where there isa vein, arenaline caues VC –> passage to bloodstream is slower, 30-40% superior - longer block) - with adrenaline can put more dose - less possibility of toxicity

without adrenaline - immediate passage - less dose allowed
SC less irrigation

264
Q

CNS adverse affects of LAs

A

tinnitus
meningeal irritation
no response al cuander vale?
convulsions tonic clonic (give regular meds)

265
Q

@ lidocaine toxicity causing bradicardia

A

can give anticholinergic like atropine

266
Q

important cx of liquid at subaracnoid space

A

pressure which it comes out
serosanguinolent - abort mission
lechosa - abort - take sample

267
Q

max bupicaina to avoid toxicity

A

20mg

268
Q

complications of raqui

A

meningitis encefalitis
hypotension manage with hydration

infecting

cefalea post puncture

269
Q

complications of epidural

A

catheter folded on itself

cant take it out

more catherer intoduced can fall out of site desired

270
Q

max LA at lumbar

A

20cc

271
Q

max LA at cervical or thorax

A

10-15cc

272
Q

apofisis espinosa anatomy for aguja

A

thoaax and cervix perpendicular

lumbar - they are reactas

273
Q

use what to block braquial plexus

A

lidocaine without adrenaine (5…..400 max dose for toxicity)

or bupicaina1

15cc = 350mg

interecalaneico 10cc = 200mg (still below dose)

EV (20cc 1%)

dilute with saline solution (10cc with water and convert 2%usual presentation to 1%)

274
Q

types of solutions

A

colloid, blood, crystaloid or , blood derived (total blood, plasma, complete blood)

suero = …

were used for hemodilution

all crystalloids different

depends what px needs

base for handling hydration - reposicion in a px

275
Q

what is osmosis

A

ability to mbilize liquid from one space to antoerh

276
Q

why edema in px

A

pump problem

depletion of albumin, hypoproteinemic px

px iwth osmotic factor low
cardiopathic px
pulm px
px with too much water

px with IR

discover and tx cause

277
Q

balanced solution expensive in markets

A

vaster solution, crystalloid de baster

and

normosol? nono sol - solution prototype very equibilirated - too expensive

tapon system
no bicarbornate for tapon

278
Q

types of blood derived solutions

A

blood derived (total blood, plasma, complete blood)

279
Q

colloid solutions only used for

A

severe hypotension
improve perfusion in these px

NOT FOR HYDRATION

280
Q

preanesthesic evaluation objective

A

drugs with more security, hemodynamic changes, less heapto/neuro/nephrotoxic = best advanceses

qx used to be awful, death

px never met anesthesiologist before

best px conditions before taking to qx sala not IN it

general - bigger integration between professional, family and px

specific - know history and physiological anatomical aspects of px

all this used to be while px was hospitalized the day before surgery…too late really

px taking aspirin , antiplatelets - SUSPEND px better a week before

avoid getting sued by informed px

last filter to make sure they got all their other evavlautions done (endocrinological, cardiological etc)

alst chance to suspend or cancel qx

281
Q

preanesthetic evaluation divided into 3 aspects (2 parts)

A

Inform - give infor to px aboust his case and what the deal with anesthesia (type, why that one); familiarity between px and

dr should know all about px (any questions?)

know the risks, conversate with family (he saild pilas not just 2 or 3 aspects)

Mental preparation - px prepared for qx, px will be anxioius, scarier than actual qx - taboos (decrease tensions) - spread good vibes

previously visisint pzx in room to decerease stress

benzos are important for that (10mg of diazemapm)

282
Q

after infomring medical part begins…

A

medical history from childhood

family hx - (women gynelogical history)

toxic habits (marijuana or cocaine can inhibit recapatioan of catecolamines) - can modulate tx type, drugs? (som suspended some not)

pathological hx, transfusions, allergics

history of actual disease and subyacentes

283
Q

physical exam in preanesthetic evaluation

A 
general
inspection
palpation
auscultatoin 
percusion

all we care about is pulmonary function - how px is ventilating!! (ronco, sibilantes, crepitantes??)
check oropharynx in case of intubation (save yo ass)

284
Q

Gabinete studies

A 
hemogram
platelets, bleeding times
urea creatinina
transminases
depurinando?
CVr risk? HTN, > 60-70yr - do echo, 
history of angina - stress strength test (qx is one)
psycological evalutation/support

know and explain risks

all this to establish anesethetic conduct to someone who has ASA or risk factors
(pre and post anesthetics and trans qx - which drugs to have, what to expect)

285
Q

ASAs

A

ASAI - healthy px without other important pathology

ASA II - px that besides prodcedure has other diseases that dont limit physical function (HTN, diabetic - controlled)

ASA III - px depite this problem have another diesase that limits their physical activity (not controlled , unstable BP, not taking meds regularly, angina a year ago - maybe some HF - fatigues after some effort)

ASA IV - px that even at rest presents potentially mortal risk (instable angina) - need ICU

ASA V - moribundo px ( we will do everything possible but idkkkk - no prognosis)

286
Q

ASA III an dup

A

alert family

287
Q

concentimiento

A

concentimiento legal medical document - px should have signed

specific to anesthsia

if you have to change must explain first - shouldnt have to change

it tells you if you have high risk

288
Q

premeds

A

anticolinergic, atropine, ecopalomine, glicopiralate
heparin if risk for pulm emb, nebulziation at asma px

benzo night before or an hour before

gastric juice blocker decrease acidity at fasting (omeptrazol) - H2 blocker antiacid - particulated (leche qu se yo que) or nonparticualted (fervecente)

monitorization of anesthized px to help identfy phenomenon or accumulated events transanesthesic

monitorization should begin since the moment px arrives to OR

289
Q

consults started

A

2006-2008

290
Q

general concepts of resp insufficiency

A

px in resp insuff when thru arterial gasometry presents PO2, < 80 mmhg (hypoxemia) and PCO2 < 40mmhg (hipocapnea)

291
Q

mortality of anesthesia

A

overdose of drugs (when we didnt have BIS, depth of coma, not knowing px)

NOW ITS RESP problems/depresson/px not ventilating. black blood (all drugs we use alters resp. , EV cause apnea, opiods #1 enemy of resp)

worse if px has chronic bronquitis, emphysiema, asma

292
Q

even after should be handled

A

relajante, post qx drugs ??? recording

293
Q

normal oxygen parameters

A

PO2 - indicates oxygenation of px (partial pressure at blood)

85-95mmHg

@ FIO2 21%

294
Q

indicator #1 of how px is ventilating

A

PCO2

35-45 mmHg

if abnormal - affection of gasometry - changes blood pH

295
Q

normal pH of plasma

A

7.4

indicates H+ ions in a substance (tells if acid or alkaline) - arterial blood in this case

296
Q

bicarbonate

A

…

relation between HCO3 and pH, CO2

any supplement of HCO3 - excesso o deficit de base EB1

297
Q

hipoxemia can be

A

leve 75-/80
mod - 60-75
severa < 60

298
Q

methods to tx resp insuff

A

canula nasal first to assimilate 3-4L (PCO2 will go up 4mmhg for every L O2 appliled)

so if px came in with 75 O2, and we put 4L we are giving 16 mre = total will be 91 - in normal range no longer hypoxemic

if it kept descending, canula isnt enough so give simple mask - elevates 4mmhg of mercury for every L of O2 applied - can assimilate up to 6 (ppt says 4L) - should give 94 - breathes from mouth and nose

if keeps going down PO2 use mask with resevoir - last element - px can assimilate up to 10 L of O2 (ppt says 8) and PO2 up 4mmhg for every L O2 applied

px that was hyperventilating is now hypoventilation (hypercapnea) hemoglobin curve to the right bemglobin not letting go of O2 to tissues and CO2 isnt being eleiminated its being retain by cells now we have fracaso resp

299
Q

fracaso resp

A

px isnt ventilating properllay

geting resp acidosis and hypoxemia severa

RBC nots diong function (retaining CO2 , not giving O2 to tissues)

no longer clinical, px cant change cuadro himself

have to connect px to artifical respiratory until cuadro is fixed

time we dont know how long

PO2 < 60mmhg severe hypoxemia and PCOr > 45mmhg

after 7 days do tracheotomy for profilaxis (undo intubaiton)

evelvate ventilation to take out Co2

100% oxygen

modify based on gasometries

300
Q

FI O2 (fraction of O2 inspired from environment)

A

inspirator pressure of O2 of environment in atmosphere of 760mmhg over mar (21%)

PO2 200-300 @ full 100% oxgenation - can cause fibrosis pulmonar?? - we want to keep in normal range - modify FIo2 to get back to normal ranges

301
Q

most abundant element of environment

A

nitrogen 78%

others: ice, sulfur, - 1-2%

302
Q

gasometric changes

A
  1. 5 pH - alkalosis
  2. 3 - acidosis

ventilatory or metabolic - PCO2 tells you

if px has 40 PCO2  - not ventilatory problem - could be metabolic
indirectly proprtional ( up when pH descends and vice versa)

PCO2changes 10mmHg for every 0.1 change in Ph

bicarbonate is directly proprtional to CO2 changes (HCO3 up 2 for every q0 PCO2 up) - in ACUTE form not CHRONIC px (asthma, epoc, sedentary, intubated px) bicarbonate changes 4 for every 10 PCO2)

303
Q

normal HCO3

A

22-26 (24 average)

304
Q

deficit de base

A 
\+ or - 2
# of HCO3 lacking in px to evaluate values that px needs
....you wanted 26 and have 20 actually - deficit of 6

thats HCO3 your giving to compensate

resp acid - if nobase deficit - is pure

????

7.5 pH - alkalosis

PCO2 should be 30

HCO3 acute - should have gone dwn two so 22

basse deficit = 0

if px had HCO3 - 18
alk respwith base deficit of 4

if px had HCO3 - 30
px with alk resp with base excess of 8

…..

ph 7.3
PCO3 40 
not a ventilatory problem
hepatopata, pancreatic, renal px, too much saline solution
bicarbonate should be low in this px
305
Q

thyroiditis

A

not that common
hyperthyroid –> ey –> hypo –> total recuperation

heterogenous group of thyroid MC with in commun = inflammation even with diff etiology, MC, dx, tx

most are benign
some autolimited and others cause thyroid insuff that can be transitory or definitive

306
Q

classification of thyroiditis

A

etiology
pain?
evolution

307
Q

etiology thyroditis

A

autoimmune (linfocititca subaguda - sporadic or postpartum or…. linfocitica cronica = hashimoto, granulomatous)

infectious (viral bacterial

destructive (by radiation or trauma)

drug induced (amiodarone, cytokines)

308
Q

pain classification thyroii=tsis

A

pain - granulomatous subaguda

suparative or acute

radiation

trauma

the nonpainful
hashimoto, subacutere, drug induced, Riedel

309
Q

classification by evolution

A

acute
subacute
chronic (autimmune , hashimoto)

310
Q

thyroid phases of evolution

A

normal function –> follicles rupture (liberates preformed hormones increasing peripherla presence of thyroid hormones) –> hyperthyroid (usually insidious MC, subclinical)–> eythyroid –> hypothyroidism –> normal function

311
Q

acute thyroiditis

A

aka supurative, bacterial, pyogena

312
Q

cause of acute thyroiditis

A

hurt

due to inflammatory process from microbian agent

associated agents in adults - strep pyogenes and staph auresu

kids - strep alfa and beta hemolitico and anaerobes

circulation form distant infectious foci (GI, skin, resp traact), embryonic infeccted restos (cyst of tiroglose conduct, fistula of seno piriforme)

extension of neighboring infections like abscess mastoiditis otitis etc

unsual siutations from bad technique and accidental inoculation , bad fine needle aspiration or centra catheter, truama, esophageal rupture

main cause in kids seno piriform left infection infected from resp infection

68% bacteria
15% fungal
mycobact %9
parasite 5%
sifilitic 2%
313
Q

MC of acute thyroiditis

A

after an high resp infection cuadro

can have presexisiting disease, fisutla seno piriforme, persistent ting, PAAF biopsy

100% neck pain, dysphagia 91%, disfonia 80%, pain at palaption, fever 92%, erithema of skin 80%, concomitant faringits

314
Q

thyroid protective factors

A

capsule and muscles

blood and drainage

iodine

(but adjacent structures, from linfatic or hematogenous spread, or penetrating truama can still cause its infection)

315
Q

labs at acute thyroiditis

A

leucocytosis > 20-25000

high ERS

tyroid hormones usually normal (depends on phsase)

normal captation at gammagrpahy (if full inflammaed it will be low )

USG can see abcess or edema in area - encapsulation suggesting infection

+ hemoculture (90% + of dx) with MC (aggressive so give these px ATBs right away before waiting on culture)

316
Q

complications of actue thyroiditis

A 
sepsis thromboembolism septic
abcess rupture
obstruction of airway
larynx edema
traqual estenosis
tirotoxicosis
317
Q

tx acute thyroiditis

A

EV antibiotics, hospitalize and drain lesion
(CS1gen, and aminoglycoside
pen anti st with aminoglycoside
amoxi with clavulinic acid or ampi and sulbactam
quinolones or C3g

drain lesion

318
Q

subacute de quervain thyroiditis

A

autolimited viral infalmation

with genetic prediposition HLA-35, B27 in summer and fall

more in women between 30-50yrs

eneterovirus incidence coorelates

319
Q

non specific signs of quervain

A

myalgia
atralgia
fatique low grade fever

320
Q

specific sign of quervain

A

thyroid pain
exquisto ini palapation

irradiates to mandible and ear

321
Q

phases of thyoridis quervain

A

pain predominates , manifestation s of tirotoxicosis 50%
pain irradiates retro acular

3-6wk

MC of infallmamtion and hyperthyroidism remit for 6-12months
px can be euthyroid

finally can or not have hypothyroidism
5-15% permanent

322
Q

querviain lab

A 
ERS high 50-100mm/h
elevated tiroglobulin
high PCR
high thyroid hormones
low iodine captation
anti TPO and anti TG normal

USG - hipoecogenic areas without mass formation and without vascular flow (CUZ OF INFLAMMATION IOU CANT SEE CIRCULATION)

323
Q

dx quervain

A

thyroid pain
high ERS and TG
USG and gamma

324
Q

PAAF in quervain

A

not alaways

can have varies depends on stage of process
beginning inflammation and disorganzied folicular arquitecture
infiltration of PMN and lymphcytes and macrophages

most cx accumualtion f giant cells and with granoulomous image

coloid ceenter of granulomas

coloidophageia

formation of microabcesses

follicular disrption

325
Q

tx quervain

A

AINES
glucocorticoids start with 30mg of prednisone and go decreasing by .2
betablockers (propanolol)
levotyroxine

326
Q

other subacteute thyroidistis

A

sporadic silent thyroiditis (autimmune with infiltraiotn more in iodine deficient women, with small painless bocoi in 50% inflmamatory so transitory

5-20% have h=thyoroid rofile altered
anti TPO + 50% low cpatation
evolution occurs in less than a year
10% of recurrence

pos partum
same as sporadic = autommune
can be 1yr postpartum
5-10% of px 30-50yr

HLA DR3/DR4/DR5

clinca: similar to sporadic and postpartum
doest hurt
25-30% can have permanent hypothyroidism
give propanolol to tx symptoms, most thyrodisits are tranistory

phases of hyperthyroidism (TSH supprsed and high T3, T4) tiroglobulin can be up, positive antibodies, captation low)

327
Q

meds thyroiditism

A

cytotocixc effect on follicles

litio lesioins cells

cytokines - interferon a tx and IL2

amiodarone causes lesion type I (increases synthessi) or II (rupture)

328
Q

tx thyroitidis

A

betablockers of MC of tirotoxicosis and tx hipotyroidism/TSH > 20mU/L (in pure thyroiditis, but if subclinical > 10 treat as well, could be hashimoto or thyroid has been taken out - other wise wait till 20 because transitory)

DONT tx sublicinical hypothyrodisim except (preg ladies and px with other coomorbilities that will also improve - recent infraction, cardiac insuff III,IV - oldies)

amiodarone - only suspend in type I
manage with glucocorticoides 0.5-1.25 mg/kg 3-6wk

329
Q

meds thyroiditism

A

cytotocixc effect on follicles

litio lesioins cells

cytokines - interferon a tx and IL2

amiodarone causes lesion type I (increases synthessi) or II (rupture)

330
Q

tx thyroitidis

A

betablockers of MC of tirotoxicosis and tx hipotyroidism/TSH > 20mU/L (in pure thyroiditis, but if subclinical > 10 treat as well, could be hashimoto or thyroid has been taken out - other wise wait till 20 because transitory)

DONT tx sublicinical hypothyrodisim except (preg ladies and px with other coomorbilities that will also improve - recent infraction, cardiac insuff III,IV - oldies)

amiodarone (used to tx arrytmia) - only suspend in type I
manage with glucocorticoides 0.5-1.25 mg/kg 3-6wk
at type II dont necessarily suspend but manage with above

331
Q

hashimoto thyroditis presentation

A

ddifuse bocio , symmetrical, firm, atrophic in 10%

332
Q

hashimoto function

A

normal or elevated
RF of hypothyrodism

no genetic direct associttion (we think tho)

333
Q

hashimoto asoociated

A

other autoimmune pathologies (Grave, AAddison, premature ovarian failure)

334
Q

hashimoto linfoma

A

fast growing nodules in px with hashimoto

infiltration, encapsulate and form linfoma

335
Q

riedal thyroiditis

A

painless hard lenoso o petreo, unilateral slow growing bocio

lots of compressive MC disphagia, disfonia, disnea, estridor

ERS normal or high, AC poitive, or normal thyroid function

can invade other neighboring strcutures

336
Q

dx reidal

A

low captation
ERS and thyroid profile normal or altered
PAAF necessary - fibroinflmmation (disscart tumor)

337
Q

riedel tx

A

elminante cpmreession with resection

steroids for inflmmation

replace with levothyroxinve

TABLE flow chart

338
Q

types of thyroid CA

A 
papilar - 80-85%
folicular ca - 10% (hurthe)
medular ca - 5%
anaplasic ca - 3%
miscelaneous 1% ( linfoma, fibrosarcoma, hemangioendotelioma maligo, teratoma)
339
Q

riedel tx

A

elminante cpmreession with resection

steroids for inflmmation

replace with levothyroxinve

TABLE flow chart

340
Q

types of thyroid CA

A

papilar - 80-85%
folicular ca - 10% (hurthe) - good but most metsastaiss
medular ca - 5%
anaplasic ca - 3%
miscelaneous 1% ( linfoma, fibrosarcoma, hemangioendotelioma maligo, teratoma)

can be follicular or parafolicular (type C which make calcitonin - medular from this one :() cells and tis is how they are differentiated

341
Q

epi of thyroid ca

A

PCT in women betwen 30-50yrs

folicular CA more common in women between 40-60yrs

differentiated carcinomas have 100% survical at 5yrs if detected on time

342
Q

papilar CPT

A

firm cold on gammagraphy solid in US nodule

7% microcalcinomas

in BMN dominating nodules is usually carcinoma

in kids usually in 20-50% linfatic

usually intraglandular extension

slwo growth can delay dx

343
Q

follicular CFT

A

small follicles and poor presence of coloid formation

diff from adenomas of follicles because present invation of vessels and capsular

metastasize to LNs anf through hematogenous reaching lung and bone more than CPT

secrete Tg

344
Q

tx ca

A

TABLES

after total thryoid ablation tx with L,4 (2.5 mcg/kg/d)

at 3 motnshs during tx with L4 mesure TSH and Tg (glucoprotein with receidos de tirosina if + something in there is producing)

at 6-12hr conretirada of L4 measure TSH and Tg and do a RCT with 2-5mCi of I 131

RCT negative measure Tg ……………

345
Q

riedel tx

A

elminante cpmreession with resection

steroids for inflmmation

replace with levothyroxinve

TABLE flow chart

346
Q

types of thyroid CA

A

papilar - 80-85%
folicular ca - 10% (hurthe) - good but most metsastaiss
medular ca - 5%
anaplasic ca - 3%
miscelaneous 1% ( linfoma, fibrosarcoma, hemangioendotelioma maligo, teratoma)

can be follicular or parafolicular (type C which make calcitonin - medular from this one :() cells and tis is how they are differentiated

347
Q

epi of thyroid ca

A

PCT in women betwen 30-50yrs

folicular CA more common in women between 40-60yrs

differentiated carcinomas have 100% survical at 5yrs if detected on time

348
Q

papilar CPT

A

firm cold on gammagraphy solid in US nodule

7% microcalcinomas

in BMN dominating nodules is usually carcinoma

in kids usually in 20-50% linfatic

usually intraglandular extension

slwo growth can delay dx

349
Q

follicular CFT

A

small follicles and poor presence of coloid formation

diff from adenomas of follicles because present invation of vessels and capsular

metastasize to LNs anf through hematogenous reaching lung and bone more than CPT

secrete Tg

350
Q

differentiated thyoi ca

A

papilar and follicular

agressive cariants

columnar cells
diffuse sclerosante
insular

351
Q

bethesda

A

I - …….repeat FNA - no dx , unsatisfactory

II - benign 0-3% risk of malignancy - follow clinic

III - atypucal of uncertain significanse, follicular lesion incertain - 5-15% - repeat FNA

IV - follicular neoplasia 15-30% - lobcomy/tiroidectomy

V - suspect malignity 6-75% - almost total thyroidectomy or lobectomy

VI - malignant 97-99% - total thyroidectomy

TABLe

352
Q

medular CA

A

from parafolicular cells

sporadic 75-80%
hereditary 25-20%

3-4% of all thyroid neoplasias

secrete CT and CEA

seen in MENs

353
Q

sporadic medular

A 
66-75%
RET gene somatic
more unicentric
alone nodule
LN metastasis 80%
also to liver, skeleton, lung with calcitonin > 5000pg/mL
354
Q

hereditary medualr

A

RET
part of MEN2
lesion in hyperplasia of cel C, diffuse or nodular
multifocal
any age
metastasis to local ganglio, higdao pulnon, hueso

355
Q

MEN 2a

A

80% MTC hereditary multicentric
feocromocitoma 50% bilateral or unilateral
hyperparathyroidism primary…..pic

356
Q

Men 2b

A

[pic

357
Q

dx CMT

A

history PE
anatopathological exploration
immunohistoquimica
tumor markters

358
Q

tx CMT

A

1st group - localized sisease, < 500 calctonin can cure

2nd group - neck metastasis - possible to cure

3rd - mestastssis to distance - deadman

359
Q

1st grou p tx

A

tiroidectom total
dissection of LNs
25% cure

360
Q

2nd gorup tx

A

total tiredoicotmy and GL dissection

361
Q

3rd group

A

same as second ,

resecar identified disease

ORTHO (9 decks)

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