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In Training Exam TL > ITE TL 2022-23 > Flashcards

ITE TL 2022-23 Flashcards

1
Q

Blood:gas coefficient

A

ratio of gas dissolved in the blood and the alveoli at equilibrium
-larger -> higher solubility in blood -> slower onsent of action

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2
Q

second gas effect

A

rapid uptake of nitrous oxide into the blood -> second gas inc in conc due to loss of volume of nitrous oxide -> more rapid uptaek of 2nd inhaled anesthetic (more concentrated)

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3
Q

B:G coefficient Des, iso, Nitrous oxide, sevo

A

Des: 0.42
Nitrous: 0.46
Sevo: 0.65
Iso: 1.46

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4
Q

Vecuronium metabolism

A

metab by liver w/ byproduct w/ 80% potency -> metabolite (3-desacetyl-vercuronium) can build up in pts w/ renal insuff or liver failure

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5
Q

Vecuronium onset/duration

A

onset: 3-4 minutes, duration: 25-50 minutes

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6
Q

Pancuronium metab

A

Active metabolite -> build up in hepatic/renal failure -> prolongation of NMB

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7
Q

Cisatracurium metabolism

A

Hofmann elimination and ester hydrolysis (spontaneous degradation in plasma) -> inactive metabolite

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8
Q

Mivacurium metabolism

A

metabolized by pseudocholinesterases into inactive metabolites

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9
Q

Rocuronium metabolism

A

excreted unchanged by biliary and renal systems
-small amount metabolized by liver -> 17-OH roc -> minimal NMB activity

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10
Q

Potentiating NMB w/ inhalational gases, which the most?

A

DES!
Des > Sevo > Iso > nitrous oxide

Does that gas potentiate the NMB? Yes it DES!

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11
Q

Perip fluid management peds

A

Healthy peds pts elective surgery: 20-40 cc/kg over 2-4 hours LR,NS, plasmalyte
12 hrs post-op: 2-1.05 cc/kg/hr if not tolerating PO

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12
Q

When to use glucose containing solutions in peds

A

neonates, infants <6 months old, malnourished children, undergoing cardiac solution 1-2.5% dextrose
-be sure to monitor glucose!

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13
Q

Digoxin MOA

A

Glycoside -> positive ionotropic and negative dromotropic and chronotropic effects
-inc myocardial contractility, inc phase 4 depolarizations, and shortens action potential
-dec AV node conduction velocity, and prolongs refractory period of AV node

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14
Q

Digoxin toxicity symptoms

A

nausea, vomiting, diarrhea, abd pain
-vision changes yellow -> green, blurry vision,
=vent tachyarrythmias, and atrial tachycardia w/ AV block
-EKG: ST depressions, dec QT interval, inc PR interval, T wave inversions (normal w/ digoxin, not necessarily toxicity)

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15
Q

Digoxin toxicity inc risk

A

advanced age, worsening renal function, hypokalemia, low body weight, med noncompliance

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16
Q

beta-blocker toxicity

A

bradycardia, hypotension, hypoglycemia, hyperkalemia, wheezing,
severe: sz, deliriuum, and coma

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17
Q

PONV guidelines

A

-if any risk factor -> multimodal ppx
-RF: female, hx of PONV or motion sickness, postop opioids, non-smoker
-volatile anesthetics, nitrous, GA, long duration, young, gastric, gyn, or laparoscopic surgery
-1-2 RF: 2 interventions
-3-4 RF: 3-4 interventions

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18
Q

Jugular bulb venous O2 saturation monitoring

A

-put a catheter in retrograde and measure mixed venous sats at the jugular venous bulb
-measure of GLOBAL cerebral oxygenation, not local
(no change in stroke b/c local ischemia)

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19
Q

global cerebral oxygen supply and demand

A

supply: CBF, arterial oxygen content, and Hgb
demand: CMRO2

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20
Q

Cardiac myocyte action potential phases

A

phase 0: Depolarization
-VG Na channels open -> influx of + Na => membrane -90 to +20

phase 1: early rapid repolarization
-Na channel inactive, K ions exit cell -> dec in membrane potential

phase 2: plateau
-Ca active, Ca moves intracellularly, balancing out K leaving -> slows rate of decline in AP

phase 3: repolarization
-Ca inactive, K permeability inc -> AP decline

phase 4: resting potential
-normal cell permeability restored, Na-K-ATPase pumps K in and Na out

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21
Q

post-heart transplant heart

A

Denervated -> isolated from recipient nervous system
-only resp to direct myocardial adrenergic -> isoproterenol, epi, dob
-no resp to atropine, no resp to hypovolemia, no reflex for phenylephrine
-resting HR: 90-110
-accelerated rate of atherosclerotic disease
-no angina b/c denervated

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22
Q

tingling lateral surface of lower leg and dorsum of feet and toes, weakness w/ eversion of foot, what n?

A

Common peroneal nerve
-likely due to lithotomy position -> to dec minimize pressure at fibular head

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23
Q

Tramadol metabolism

A

PRO-DRUG
-metab by cytochrome p450 2D6 and 3A4

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24
Q

Tramadol MOA

A

After metabolism (pro-drug)
+ enantiomer: mu opiod agonist
- enantiomer: SNRI ( serotonin and NE reuptake inh)

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25
Q

Stages of liver transplant

A

preanhepatic, anheptic, and neohepatic

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26
Q

Preanhepatic

A

incision to cross-clamping of protal v, hepatic a, IVC or hepatic v

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27
Q

Anhepatic

A

cross clamping -> anastomosis are made and perfusion starts

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28
Q

Neohepatic

A

Unclamping of portal v when reperfusion starts -> hepatic a, biliary duct anastomosis, and abd closure

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29
Q

Changes during ischemia of liver

A

-lack of ATP -> can’t maintain ion gradients -> swelling
-alterations in Ca homeostasis
-hepatic cell death
-dec in cytoprotective substances

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30
Q

Reperfusion of liver possible issues

A

-build up of ischemic products (lactate, H+, K+), preservation solution released
-blood through graft -> release of microemobli
-hypoTN or arrhythmias

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31
Q

Postreperfusion syndrome

A

First 5 minutes after reperfusion -> systemic hypoTN and pulm HTN
-ischemia-reperfusion injury b/c low ATP and glycogen -> Na/K pump failure -> extracellular Na ions move into cells and cause swelling
-vascular permeability inc -> dec ATP and adenylate cyclase activity dec

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32
Q

Blood alteration if IgA def

A

washed RBCs

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33
Q

Acute hemolytic transfusion reaction

A

IgM antigen-antibody complex activating complement

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34
Q

Standard deviation percentages

A

SD 1 68%, 2 95%, 3 99%

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35
Q

CBF changes with hypothermia

A

for every 1 degree decrease, CMRO2 dec by 6%, proportional dec in CBF

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36
Q

PaCO2 and CBF

A

1 mm Hg in PaCO2, CBF changes by 3%

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37
Q

CBF and PaO2

A

constant for PaO2 >50-60
-inc dramatically when below 50

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38
Q

CBF and MAPs

A

CBF constant b/w 50-150

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39
Q

Specificity

A

TN/ (TN + FP)
“rules in” a disease
-confirmatory test

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40
Q

Sensitivity

A

TP/ (TP+FN)
-screening test

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41
Q

Which coronary cusp

A

Non-coronary cusp
-is always located next to the inter-atrial septum

-LCC is next to the pulm artery
-RCC is anterior most and faces RV

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42
Q

Which coags go down/no change in pregnancy?

A

XI, XIII: down
II, V: no change
all the rest procoag inc, anticoag decrease

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43
Q

Major RF for PONV

A

female sex, motion sickness, postop opioids, hx of PONV

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44
Q

Tetanus toxin MOA

A

prevents release of inhibitory neurotransmitters
-SNARE cleaved by tetanus prevents vesicle fusion and prevents release of GABA and glycine

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45
Q

Autonomic symptoms tetanus

A

Autonomic dysfunction: sweating, vasoconstriction, severe tachycardia w/ HTN may rapidly alternate w/ bradycardia and hypoTN
-abnormally high epi and NE -> exagg symp NS
-major cause of morbidity and mortality

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46
Q

Where tetanus acts

A

travels via retrograde axons from peripheral ro central neurons
-prevents GABA release in synaptic cleft b/w inhibitory interneurons and motor neurons
-enters brainstem to affect SNS

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47
Q

Botulinum toxin

A

only affects peripheral motor neurons, and prevents release of ACh into NMJ -> flaccid paralysis

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48
Q

Kartagener syndrome

A

primary ciliary dyskinesia
-can be associated w/ situs inversus, recurrent sinusitis, bronchiectasis

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49
Q

Bronchiectasis

A

-issue w/ mucociliary clearance -> recurrent lung infxn and inflammation -> localized and irreversible dilation -> dialted bronchial malacia -> airway collapse and impair mucus clearance
-w/ progression can have dec FEV1/FVC ratio

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50
Q

Bronchiectasis tx

A

prevention w/ aggressive antimicrobials
-inhaled corticosteroids may dec sputum production and inflammation
-chest PT
-if hemoptysis or recurrnt PNA, lung resection can be indicated
**treat like COPD, lots of PEEP

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51
Q

Nerve agents

A

Inhibit AChE
-SLUDGE Mi: Salivation, Lacrimation, Urination, Defecation, GI Upset, Emesis, Miosis
-arrhythmias, typically bradycardia but can be any
-ACh at nicotinic rec at NMJ -> fasciculations, twitching, fatigue, and flaccid paralysis

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52
Q

Why hypothermia in OR?

A

Anesthetic induced impaired thermoregulatory control, internal redistribution, red in head development, cold OR

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53
Q

Pattern of heat loss

A

initial rapid decrease then slow, linear reduction, then stabilization and plateau

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54
Q

Consequences of hypothermia

A

-coag impaired -> defect in platelet fxn
-dec drug metabolism
-***wound infxn inc (impairs immune fxn and dec wound O2 delivery)
-shivering -> hypoxia and ischemia

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55
Q

Prevention of hypothermia from redistribution

A

preop pre-warming -> inc preipheral temp before vasodilation

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56
Q

heat loss radiation

A

radiates heat to surrounding environment, heat transfered to from core to subq vessels -> lost to environment
**major loss type

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57
Q

heat loss convection

A

thin layer of air adjacent to skin acts as an insulator -> since air exchanged every 15 min in OR -> loss of insulator

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58
Q

heat loss conduction

A

transmission of boy heat through conducting medium (contact w/ mattress)

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59
Q

heat loss evaporation

A

liquid -> vapor lowering of kinetic energy
-when sterile prep solutions applied

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60
Q

RF for postop hospital admission

A

age over 65, long op times (>120 min), ASA III or IV, OSA, vascular dx

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61
Q

Thyrotoxicosis

A

Hypermet state from high thyroid hormone
-sym: nervousness, irritability, tremors, tachycardia, arrhythmias, fever, vomiting, diarrhea

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62
Q

Tx of thyrotoxicosis

A

PTU and Methimazole: inhibit production of thyroid hormone
-PTU: prevents peripheral conversion of T4 to T3
-can be used as a therapy or bridge to tx w/ surgery or radioactive I

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63
Q

radioactive iodine

A

used to destroy thyroid gland
-SE: inc hyperthyroid sym the first few days b/c destroy gland -> hormone release
-pre treat w/ methimazole or propanolol
-CI: breast-feeding, pregnancy

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64
Q

Complications w/ periop hyperglycemia

A

-immunosuppression -> dec WBC fxn
-inc infections
-stim of sympatho-adrenergic activity
-osmotic diuresis
-red skin graft success
-inc catabolism in burn pts
-delayed wound healing
-delayed gastric emptying
-exacerbationo f brain, SC, and renal damage by ischemia
-increased mortality
-risk of postop cognitive dysfxn following CABG

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65
Q

What’s in cryoprecipitate

A

vWF, fibrinogen, fibronectin, factor VIII, and factor XIII

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66
Q

Indications for cryo

A

-microvascular bleedingw/ low fibrinogen (ex DIC)
-bleeding due to uremiathat is unresponsive to DDAVP
-factor XIII def
-ppx before surgery or tx of bleeding w/ congenital dysfirinogen, VW Dx, Hemophilia A (if factor concentrates unavailable)
-use in firbin sealant production

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67
Q

SE of high dose oxytocin

A

-Oxytocin mimics vasopressin -> dec urine excertion
-volume overload sensed by atria -> ANP -> natriuresis -> hypoNa
-hypoTN -> N/V

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68
Q

Normal fetal pH

A

7.32 to 7.38

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69
Q

Normal pregnant mother pH

A

7.43 -> chronic resp alk

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70
Q

Fetal ion trapping

A

low fetal pH
-crosses placenta in un-ionized form, accepts aH ion in more acidic environment -> drug accumulates and then b/c ionized can’t cross back

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71
Q

why does lidocaine accumulate w/ ion trapping

A

pKa is 7.8 -> once in pH lower than 7.8 it accepts a H ion

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72
Q

Determines if drugs cross placenta

A

-Size: drugs <500 Da cross easily, >1000 Da (heparin, protamine, insulin) don’t cross
-Degree of lipid solubility, ionized (succ, NDMR) don’t cross, lipophilic (fent) do
-Protein binding: highly protein bound less likely to cross
-Maternal drug conc: higher conc morel ikely to cross

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73
Q

Drugs that do NOT cross Placenta

A

He Is Going Nowhere Soon
Heparin
Insulin
Glycopyrrolate
NDMR
Succinylcholine

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74
Q

Reversal of MR in pregnant pts

A

Neo and atropine
-Neo crosses, glyo doesn’t -> fetal bradycardia

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75
Q

Lowest blood:gas coefficient

A

Des < N2O < Sevo < Iso

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76
Q

blood: gas partition coefficient

A

ratio of the concentration of inhaled anesthetics in blood to conc in alveoli at equilibrium
-Lower = faster onset

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77
Q

Why is nitrous faster than Des

A

Des has a lower blood: gas coefficient, but “concentration effect” -> nitrous has a bigger concentration

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78
Q

B:G coefficients

A

Des 0.42
nitrous 0.46
sevo 0.65
iso 1.46

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79
Q

Secondary HSV active gental wounds what to do

A

C/s
-no invasive fetal monitoring

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80
Q

Conn Syndrome: cause and tx

A

Primary hyperaldosteronism: excess secretion of aldosterone from adrenal adenoma
tx: Spironolactone, anti-HTN, supplemental K

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81
Q

Sym of primary hyperaldo

A

fatigue, m cramps, weakness, polyuria, HA
(from HTN and hypoK from excess aldo)

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82
Q

Midodrine MOA

A

alpha 1 rec agonist

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83
Q

Octreotide

A

Somatostatin analogue
-used in acromegaly (supp GH production)

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84
Q

Congenital Diaphragmatic Hernia

A

-L side more common, more common in females
-Triad: dyspnea, cyanosis, and dextrocardia
-assoc w/ congenital heart dx and intestinal malrotations

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85
Q

TEG parts

A

R time: clot initation
K and alpha angle: clot kinetics
MA: clot strength
Ly30: fibrinolysis, clot stability, breakdown

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86
Q

TEG R

A

t=0 to initial clot formation
-dpt on clotting factors
-tx: FFP

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87
Q

TEG K and alpha angle

A

strength of clot formation, alpha measures speed of clot formation
-dpt on fibrinogen
-tx: cryoprecipitate

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88
Q

TEG MA

A

strength of clot, and maximum width of TEG
-dpt on plt number, function, and fibrin cross linking
-tx: plts

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89
Q

Desmopressin uses

A

When fxnl issue w/ plts (dec MA on TEG)
-causes release of endothelial cell stoes of factor VII and vWF, inc plt glycoprotein expression
-used for uremic bleeding or vWD

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90
Q

Normal TEG values

A

Rule of 6’s
R time: 6 minutes
alpha angle: 60 degrees
MA: 60mm
Ly30 6%

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91
Q

location of landmark interscalene block

A

behind the lateral border of SCM at level of cricoid cartilage

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92
Q

Coverage for interscalene block

A

Ventral rami of C5-C7, and supraclav (C1-3)
-100% block ipsilateral phrenic nerve -> hemidiaphgramatic paralysis
-covers shoulder and proximal upper extremity -> ulnar spared so no forearm or hand

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93
Q

Interscalene block landmark technique w/ n stim

A

at level of cricoid cartilage, posterolateral to SCM, in interscalene groove, insert needle, move caudad -> until movement of deltoid, triceps, biceps or pectoralis gets a response
-make sure stim at 0.4 mA, if stim at < 0.2 mA intraneural, pull back

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94
Q

hyperparathyroid and NMB

A

thought is hyperparathyroid -> inc Ca and inc in ACh rec -> hyposens to NDMR but resp is variable and unpredictable

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95
Q

Gold standard for core temp

A

pulmonary artery via pulm artery catheter

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96
Q

Acceptable alternatives for core temp

A

nasopharynx, distal esophagus, tympanic membrane

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97
Q

Pregnancy factor level changes

A

INCREASE: factor I (fibrniogen), factor VII, smaller inc in others
DECEASE: anticoag: antithrombin III, and protein S

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98
Q

Normal coags in pregnancy labs

A

20% decreasein PT, PTT
-dilutional effect on plts dec

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99
Q

Gestational thrombocytopenia

A

plts < 150k

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100
Q

Which factors procoag DEC in pregancy

A

XI, XIII

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101
Q

Pregnancy TEG

A

dec R time, K, alpha angle, MA
hypercoag

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102
Q

TX for congenital long QT syndrme

A

BB: propranolol, nadolol

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103
Q

QT prolongation leads to

A

syncope, cardiogenic sz, MI, sudden cardiac death -> all from polymorphic tachyarrhthmia, torsades

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104
Q

Tx for QT prolongation causing torasades

A

unsynchronized cardioversion and 2g Mg sulfate

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105
Q

Myasthenia Gravis risk for postop ventilation

A

-Diagnosis > 6 years
-Vital capacity < 2.9 L
-Daily dose > 750mg
-chronic respiratory illness

secondary:
-EBL >1L
-BMI >28
-advanced stage of MG
-hx of MG crisis
-Anti-ACh titer > 100 nmol/mL
-pronounced decremtanl resp (18-20%) on low freq repetitive n stim

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106
Q

Myasthenia gravis and NMB

A

-very sensitive to NDNMB
-resistant to succ

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107
Q

Change for CBF and temp

A

6-7% change by 1degree C in temp

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108
Q

Hypothermia body changes

A

-dec in speed of chemical and enzyme rxns -> less metabolism
-peripheral vasoconstrictin -> inc SVR and inc BP
-if <32 cardiac conduction slows -> bradycardia
-diuresis -> contraction of blood volume -> inc Hct and viscosity
-leukocyte and plt fxn dec
-dec in insulin sensitivity and secretion -> hyperglycemia
-arterial partial P of O2 and CO2 dec b/c soluble in blood

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109
Q

inhalational agents and fetus

A

cross placenta esaily b/c higher lipid solubility and low molecular weight

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110
Q

Possible SE of inc intra abbd pressure from repairing gastroschisis

A

-abd compartment syndrome
-compress IVC -> hypoTN
-compress liver and kidney -> altered drug metabolism
-prevent diaphragm excusion -> red lung compliance -> inc peak and plateau pressures
-inc in ICP (inc in intrathoracic pressure reduces cerebral venous return)

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111
Q

Inc in peak pressue w/o inc plateua pressure

A

inc in airway resistance -> bronchospasm, ETT obstruction, mucous plugging, kink in circuit, retrained secretion

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112
Q

Inc in peak and plateau pressure

A

PTX, pulm edema, ARDS, PNA

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113
Q

Labetalol half life, effect on BP

A

1/2 life: 6 hours
effect on BP: 16-18 hours

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114
Q

Labetalol MOA

A

antagonism to alpha 1: arteriolar vasodilation
antag to beta 1: dec HR and dec contracility
antag to beta 2: arteriolar vasodilation

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115
Q

Labetalol metabolism

A

hepatic glucuronide conjugation w/ excretion via urine and feces

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116
Q

Esmolol half life

A

9 minutes

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117
Q

Esmolol metabolism

A

metabolized by RBC estereases -> short 1/2 life
-useful to tx acute tachycardia => dose dpt response
-used for DL to attenuate symp response

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118
Q

Abx that do NOT affect NMB

A

PCN and cephalosporins

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119
Q

Abx that inc NMB

A

aminoglycosides (Gentamycin), polymixins, lincosamides: clindamycin
-gluoroquinolones and tetracyclines

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120
Q

Prolong NMB

A

-inh gas: des most
-Lithium (activates K inhibit ACh release)
-Mg (block Ca)
-CCB
-acute antepileptics

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121
Q

Chronic antiepileptic drugs and NMB

A

inc conc of serum glycoproeins and postynatpic nAChR -> more rapid clearance and shorter duration of action

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122
Q

What’s blocked in adductor canal block

A

vastus medialis is the ONLY muscle, remaining sensory block (saphenous on)

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123
Q

boundaries of adductor canal

A

vastus medialis laterally, sarterius anteriorly (roof), adductor longus (superior) or magnus (inferior)

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124
Q

Fascia iliaca block

A

Blocks femoral and LFCN
-large volume

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125
Q

Zero-order kinetics

A

Will eliminate a constant amount of drug per unit time, regardless of plasma conc
-ethanol, cisplatin, phenytoin, high dose salicylates

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126
Q

First order kinetics

A

eliminate a constant fraction of drug per unit time (decreases exponentially)
-higher conc, faster clearance

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127
Q

LFCN

A

L2-L3 n roots, sensory innervation to anterolateral aspect of thigh
-blocked for surgeries w/ femoral neck or skin grafting on thigh, or muscle biopsies of lateral thigh

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128
Q

LFCN location

A

emerges from lateral border of psoas, crosses iliacus m toward ASIS, behind/through inguinal ligament, in front of sartorius

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129
Q

LFCN block

A

ASIS, -1 cm medical and 1-2 distal, advanced until pierces fascia lata

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130
Q

Meraglia paresthetica

A

d/o LFCN -> pain, parethesia, hypesthesia in anterolateral thigh assoc w/ n compression
-LFCN n block is diagnostic

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131
Q

Intravascular injxn of caudal anesthesia symp

A

inc in 25% or more in T-wave amplitude
inc HR and BP (T waves more reliable b/c not guaranteed when under GA)

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132
Q

Layers to femoral block

A

Skin, subq, fascia lata, and fascia iliacus

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133
Q

Temp and CMRO2

A

each degree C < 37, CMRO2 dec by 6-7%

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134
Q

gold standard of cerebral temp

A

jugular bulb venous temp

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135
Q

Oxygenator arteial outlet temp

A

measures temp of the arterial blood leaving CPB circuit and entering body via aortic cannula

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136
Q

NG and dec myocaridal demand

A

preferentially dilates Venules -> dec preload
v > a

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137
Q

NG onset and 1/2 life

A

onset: 1-3 minutes, 1/2 life 2-3 minutes
metab by liver

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138
Q

NG MOA

A

smooth m: activates guanylyl cyclase to inc cGMP -> inh Ca into cells -> smooth m relaxation

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139
Q

Artery of Adamkiewicz supplies

A

anterior 2/3 of SC T9-T12 -> loss of motor fxn of lower extermities, loss of pain and temp 1 level below lesion, sexual dysfxn, urinary and fecal incont
-proprioception and vibration intact (posterior a)

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140
Q

spinal n

A

anterior: motor, posterior: sensory root

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141
Q

Anatomical landmarks for dermatomes

A
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142
Q

Dermatomes

A
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143
Q

surgery post DES

A

elective is 6 months

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144
Q

surgery post bare metal stent

A

30 days

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145
Q

anatomy near stellate ganglgion

A

carotid a anterior to at level of C6
anterior to neck of the first rib and C7 transverse processes
lateral: scalene muscles
posterolateral: vertebral arteries

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146
Q

Obesity changes on lung volumes

A

Dec compliance -> shallow breaths, inc WOB, and limited max VC
-dec FRC (dec ERV), dec TV, dec TLC
-RV unaffected
-FEV1 and FVC slightly decreased, ratio preserved or slightly inc
-nc O2 consumption and CO2 production due to inc adipose tissue

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147
Q

NG MOA

A

enters endothelial cells from the bloodstream and are converted to nitric oxide intracellularly -> smooth m relaxation (incl uterine smooth m)
-nitric oxide -> cGMP -> sequesters intracellular Ca

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148
Q

SE of NG

A

tachycardia, hypoTN, flushing, and HA

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149
Q

Mg Sulfate preterm labor

A

tocolytic and neuroprotection
-blocks intracellular Ca

150
Q

Terbutaline MOA

A

selective beta 2 activation -. beta 2 rec complex is Gs coupled -> activation of adenylyl cyclase and inc cAMP

151
Q

COA NG

A

PDE 5 inh (sildenafil, tadalafil, vardenafil)
-potentiate nitrates b/c prolongation of cGMP activation -. hypoTN

152
Q

cardiac arrest pulseless v fib post cardiac surgery, next?

A

defibrillation x3 prior to any compressions (w/i 10 days after cardiac surgery)
-if no change w/ defib rec to repeat sternotomy for direct cardiac massage (external compressions associated w/ fatal complications)
-if using epi dec doses to avoid HTN

153
Q

Affects the level of spinal

A

primary: dextrose content (hyperbaric more influenced by gravity), total drug dose
others: volume of local anesthetic, pt position, pt height, pt age, CSF volume, intra-abd pressure, injxn site, needle bevel direction

154
Q

clonidine spinal

A

inc analgesic properties (alpha 2 stimulation)

155
Q

Epinephrine spinal

A

inc duration of action of local anesthetic and quickens speed of onset

156
Q

Morphine spinal

A

inc analgecis properties, esp visceral pain
-minimally enhance block height

157
Q

Diagnosis

A

B-lines
pulm edema

158
Q

Diagnosis

A

PTX
-no lung sliding, so when on M mode -> barcode sign

159
Q

Dx

A

Normal u/s
-on M mode you see lung sliding: “seashore sign”

160
Q

Diagnosis

A

pleural effusion
-M mode: sinusoid sign
-area of fluid b/w visceral pleura and parietal pleura

161
Q

Dermatome innervates the skin over the lateral malleolus

A

S1

162
Q

Dermatome medial aspect of thigh, knee, calf

A

L3

163
Q

Dermatome anterior knee and medial malleolus

A

L4

164
Q

Dermatome dorsal and lateral foot, toes 2-4

A

L5

165
Q

Which local anesthetic has a duration of action that would be prolonged LEAST by addition of 1:200,000 epi

A

Bupivacaine: more readily absorbed from epidural space indepent of epi vasospasm which negates epi impact

Epi adds a benefit with alpha 1 stimulation, dec bleeding, red toxicity, prolonged duration of action
-epi benefits more pronouned w/ short or intermediate acting local anesthetics

166
Q

sodium bicarb as a block additive

A

increases local pH -> inc rate of onset, facilitating nonionized local anesthetic into neurons

167
Q

LMWH

A

bind and potentiates antithrombin III, but more selective inhibition of factor Xa w/ minimal inhibition of thrombin
-not reversed w/ protamine
-risk of HIT but lower than UFH

168
Q

Cardiac effects of isoflurane

A

dec SVR, dec MAP, dec contracility, prolonged QT interval, inc HR

169
Q

Which inhaled anesthetics prolong QT interval

A

sevo, iso, des

170
Q

Inc in K after succ in normal healthy people

A

0.5 mEq/L

171
Q

ppx for postop myalgias due to succ

A

pretreament with NSAIDs: ASA, diclofenac

172
Q

Boundaries of adductor canal

A

lateral: vastus medialis
superior: adductor longus
inferior: adductor magnus
anterior: sartorius
-deep to sartorius is aponeurosis: vasoadductor membrane

173
Q

UFH MOA

A

indirectly inhibits thrombin and factor Xa by bing to ATIII -> enhanced degradation of thrombin and factor Xa

174
Q

Renal adjustments for UFH v LMWH

A

LMWH metabolized 40% by kidneys, needs adjustment
UFH does not require renal adjustment dosing

175
Q

UFH monitoring

A

PTT or ACT

176
Q

Emergence from nitrous oxide anesthesia

A

-high conc N2O exits tissue and blood and enters alveoli -> w/i first 5-10 min after discontinuing, inc N2 in alveoli causes less O2 in alveoli -> hypoexemia
-enahnced washout of CO2 as well, causing hypocarbia and dec resp drive

177
Q

second gas effect

A

N2O concentrating effect
-due to rapid uptake of N2O in blood, second gas inc in concetration due to loss of volume of nitrous oxide -> more rapid uptaek of second higer conc volatile anesthetic

178
Q

Airway anatomy

A
179
Q

only complete cartilaginous ring in upper airway

A

cricoid cartilage

180
Q

trachea cartilage

A

C-shaped rings of hyaline, open end opposing esophagus

181
Q

bronchi/bronchioles and carilage

A

bronchi: complete circular cartilage rings
bronchioles lack cartilaginous structures

182
Q

site of carina landmark

A

5th thoracic vertebra

183
Q

what level disc herniation?

A

L5-S1
-L5 nerve root could be affected

184
Q

acute normovolemic hemodilution

A

occurs before significant blood loss
-whole blood removed from pt while giving back crystalloid or colloid (3:1 for every 1 cc blood removed), blood stored in citrate-containing solution, and stored at room temp for 8 hours or 24 if 4C
-when bleeding occurs, number of RBCs los is lower
-blood transfused back to pt in reverse order of collection (1st unit has highest conc of plts, Hg)

185
Q

Indication for Acute normovolemic hemodilution

A

-likelihood of blood transfusion >10%
-preop Hg is >12
-no significant renal, pulm, liver, or conoary dx
-no severe HTN
-no infxn

186
Q

Body compensation for ANH

A

inc cardiac output
-in HR b/c anemia
-SV inc due to dec in SVR and afterload
-dec blood viscosity -> dec in shear stress in microvasculature inc flow and venours return to heart
-mild tissue hypoxia and acidosis -> ateriolar vasodilation red afterload
-if Hct <25, 23DPG inc causing R Hg curve shift

187
Q

When to use cell salvage

A

Anticipated blood loss of >20% of estimated blood volume
-crossmatch compatible blood not available
-pt refuses allogeneic blood transfusion but agrees to cell salvage
-more than 1 pRBCs is expected

188
Q

opioids and sz threshold

A

do not alter sz threshold unless pt has renal failure (accumulate toxic metabolites)
-and no EEG sz activity even if m rigidity or shivering is present

189
Q

Why muscle rigidity w/ opiods

A

inhibit GABA release and inc DA production in CNS (like Parkinsons)

190
Q

morphine and renal failure

A

inc morphine-3-glucuronide -> neuroexcitation and sz when accumulated after repeat doses

191
Q

meperidine and renal failure

A

Normeperidine accumulates -> sz

192
Q

GI SE of opioids why?

A

spasming of smooth muscles -> constipation, biliary colic and delayed gastric emptying
-esp morphine which dec peristalsis, and b/c moving slowly, inc in water absorption
-inc tone of pyloric sphincter, ileocecal valve and anal sphincter

193
Q

sym/parasympathetic changes w/ aging

A

inc baseline sympathetic activity -> why such big blood pressure lability during surgery
-dec resp to alpha and beta stimulation
-dec parasym activity

194
Q

heart changes w/ aging

A

stiffening of myocardium, arteries and veins -> HTN
-conudction changes: blocks and loss of SA node cells
-defective ischemic preconditioning
-baroreflex dec due to dec in HR
-stiff aorta, more stroke volume stays in aorta -> waves back to heart -> inc work of LV -> LVH impairs diastolic filling -> diastolic dysfxn -> so reliant on atrial kick

195
Q

Pulmonary changes w/ aging

A

inc stiffness of chest wal and dec stiffness of lung
-inc curve of diaphgram -> harder to generate negative pressure -> inc work of breathing
-dec elastin so lung tissue less stiff, easier to inflate but inc collapsing -> inc closing capacity
-dec response to hypercapnia and hypoxia
-inc risk of upper airway obstruction due to loss of muscle mass, impaired swallowing and dec coughing

196
Q

Definition of larynx

A

epiglottis to inferior border of cricoid cartilage (C6) ie start of trachea

197
Q

Nasopharynx

A

anterior: nasal cavity
superior: base of skull
posterior: posterior pharyngeal wall
inferior: soft palate

bordered by oral cavity

198
Q

oropharynx

A

b/w soft palate and hyoid bone

199
Q

hypopharynx

A

pharynx below hyoid bone
-connects oropharynx to esphogus and larynx

200
Q

Desflurane Boiling point and vapor pressure

A

BP: 24C
VP 669
-b/c BP is near room temp -> why requires closed storage container and a pressurized and heated vaporizer to allow predictable responses

201
Q

Isoflurane BP and VP

A

BP: 49
VP 238

202
Q

Sevoflurane BP and VP

A

BP 59
VP 157

203
Q

what happens if you put isoflurane in a sevo vaporizer?

A

Iso has a HIGHER vapor pressure: 241 (I) to 160 (S)
-PV is the pressuer exerted by the gas phase on walls of container
-b/c iso’s VP is higher, it’s vapor concentration is higher, so at 1atm: iso 241/760 = 32% vapor concentration
-more iso in gas form than sevo -> so if iso in sevo vaporizer -> actual output conc will be higher than indicated by the dial

204
Q

Nitrous oxide BP and VP

A

BP: -88 C, which is why it’s a gas at room temp
VP: 38,770

205
Q

Advantages to postop epidural analgesia

A

-superior pain control
-red periop inflammation and sensitization of pain pathways\
-red GI hypomotility
-improved visceral BF -> dec MI and bowel ischemia
-dec postop pulm comp (PNA)
-vascular surgery improved mortality

206
Q

Disadvantages to epidural postop analgesia

A

-CI: inc ICP, coagulopathy, high risk of infxn
-inc hypoTN intraop
-epidural failure up to 25%
-SE of anesthestic-opioid: pruritis, nausea, urinary retention
-small risk of major compl: hematoma, abscess,
-lower exremity m otor blocks, uncommon but delay mobilization

207
Q

nasopharynx innervation

A

maxillary branch of trigeminal nerve

208
Q

oropharynx innervation

A

glossopharyneal nerve

209
Q

superior laryngeal nerve external branch

A

motor innervation to cricothyroid

210
Q

airway innervation

A
211
Q

Pharmacokinetic compartment models

A

Movement of drugs b/w tissues w/i body
-central compartment (where drugs get injected to and where they get eliminated/metabolized)
3 phases:
-a step, rapid phase (slow and fast equilibrating compartments take the drug up from the central compartment)
-intermediate phase (fast equilibrated w/ central, but slow stil taking up the drug)
-flat slow elimination phase: all compartments equilibrating toward central compartment as it eliminates

Vd: sum of all the compartment volumes at equilibrium w/ drug

212
Q

CYP2D6 inhibitors

A

SSRI: escitalopram, fluoxetine, or paroxetine, SNRIs, Histamine antag (Cimetidine), Chlorpromazine, amiodarone, quinidine
-dec conversion of codeine to morphine

213
Q

Methadone MOA

A

racemic mixture w/ opioid analgesic and NMDA antagonist, also SNRI

214
Q

Cause of malignant hyperthermia

A

mutation in the RYR1 gene coding for the ryanodine receptor (Ca channel)
-mutation causes abnormal, unregulated release of Ca iosn

215
Q

muscle rigidity (masseter rigidity), inc O2 production

A

Malignant hyperthrmia

216
Q

MH labs

A

lactic acidosis, rhabdomyolysis, inc CK, hyperK, myoglobinuria

217
Q

Cyproheptadine

A

Tx for serotonin syndrome
-blocks serotonin and histamine receptors

218
Q

Rigidity, hyperthermia, myoclonus, hyperreflexia

A

Serotonin syndrome
-also get nausea, vomiting, diarrhea

219
Q

hyperthermia, rigidity, dysautonomia, mental status change

A

Neuroleptic malignant syndrome
-can tell apart from serotonin syndrome by hyperreflexia (in SS but not NMS)

220
Q

Inc risk of Mg toxicity w/ pregnancy and preeclampsia

A

Renal insufficiency
-skip or lower loading dose in renal insuff

221
Q

Inc risk of Mg toxicity w/ pregnancy and preeclampsia

A

Renal insufficiency
-skip or lower loading dose in renal insuff
-renal insuff if Cr > 1.1

222
Q

Therapeutic range for Mg tx in preeclampsia

A

5-9 mg/dL

223
Q

Mg toxicity symptoms if Mg < 7

A

Nausea, HA, lethargy, diminished deep tendon reflexes

224
Q

Mg sym if Mg 7-12

A

-somnolence
-bradycarida, hypoTN
-EKG: prolonged PR, QRS and QT
-absent DTR

225
Q

Sym if Mg > 12

A

muscle paralysis, resp failure, complete heart block

226
Q

Sym if Mg > 15

A

cardiac arrest

227
Q

Papilledema caused by what electrolyte disturbance

A

severe hypoCa

228
Q

ST elevations caused by what electrolyte disturbance

A

severe hyperCa

229
Q

acceleromyography

A

Quantitative nerve monitoring technique
-TOF ratio >.9 to .95 is considered full reversal
-most sensitive compared to qualitative and clinical maneuvers

230
Q

Mechanomyography

A

Quantitative NM monitoring
-gld standard for measurement of blockage, but primarily used for research

231
Q

how do BB slow disease progression in HRrEF

A

prevention of catecholamine cardiotoxicity
-HF -> dysregulated symp NS w/ inc circulating catecholamines -> adrenergic cardiotoxicity -> cardiac remodeling
-BB interrupt this vicious cycle

232
Q

Hydralazine MOA, effect on HF

A

MOA: directly relaxes venous and arterial smooth muscle
-reduces afterload and myocardial work

233
Q

Sacubitril MOA

A

Neprilysin inhibitors
-prevents breakdown of natriuretic peptides

234
Q

Sacubitril effect on HF

A

Reduce sodium, volume retention, adverse cardiac remodeling

235
Q

Dapagliflozin MOA

A

Sodium-glucose cotransporter 2 inhibitors
-promotes glucosuria and natriuresis

236
Q

EKG changes hyperMg

A

prolonged PR, QRS duration, and QT interval

237
Q

HypoK EKG changes

A

Flat or inverted T waves, U waves

238
Q

HyperCa EKG changes

A

shortening of ST segment, can also in a few cases mimic MI w/ ST elevations

239
Q

HyperCa EKG changes

A

shortening of ST segment

240
Q

electrolyte abnormality

A

hypoK

241
Q

Normal CBR

A

50 mL/100g/min
gray matter 80%
white 20%

242
Q

Hyperthermia on CBF

A

b/w 37-42 CBR inc
>42 marked reduction in CBF b/c reduction in CMR

243
Q

CO2 BP and CBF

A

25-75 CBR inc linearly w/ PaCO2 when normotensive
-when MAP is low, resp to PaCO2 attenuated, and w/ severe hypoTN no changes for PCO2

244
Q

Infant cyanotic and HR 80 what next?

A

1st. warming, drying, stimulation
2nd. supplemental O2, suction and open airway
3rd. PPV, pulse ox 60-65% at 1 min, 85-95% by 10 minutes
4th. HR less than 60bpm compressions
5th Epi if no changes

245
Q

what HR in infants do you start chest compressions

A

less than 60 bpm

246
Q

breathing ratio in infants

A

3 compressions to 1 breath

247
Q

when to use epi in newborn resuscitation

A

PPV, intubation, and chest compressions -> epi

248
Q

APGAR score

A

HR, resp effort, reflex irritability, muscle tone, color

249
Q

MOA HCTZ

A

inhibits Na/Cl transport in distal convoluted tubule

250
Q

Chlorthalidone MOA

A

inhibits Na/Cl transport in distal convoluted tubule
-thiazide diuretic

251
Q

HCTZ electrolyte changes

A

hypoNa, hypoCl alk, hypoK, hyperCa, and Hyperglycemia

252
Q

What is phosgene

A

Phosgene is a chemical warfare agent that is regarded as a potential terrorist threat
-initially attacks type one and two pneumocytes ~> free radical release
-Secondary attack includes release of inflammatory mediators -> Prostaglandins cause vasoconstriction and platelet issues, bradykinin causes increased capillary permeability, thromboxane causes vasoconstriction, and compliment activating enzymes lead to attraction of leukocytes.

253
Q

Phosgene treatment

A

Supportive therapy with steroids beta-2 agonist and prophylactic antibiotics (risk of secondary infection)
-Leuokotriene inhibitors and glutathione may lesson respiratory damage

254
Q

How does phosgene act?

A

Colorless gas that dissolves slowly in water to form carbon dioxide and hydrochloric acid
-When liquid released, turns into gas stays close to ground and spreads rapidly
-allows phosgene to enter respiratory tissue without significant upper airway damage
-necrosis follows inflammation and airways and alveoli
-alveolar capillary leak produces pulmonary edema
-Can get hypoxia from intense laryngeal or bronchospasm

255
Q

Blood and oxygen supply to the liver

A

-hepatic artery provides 25% of blood supply and 50% oxygen supply
-Hepatic vein provides 75% blood supply and 50% oxygen supply

256
Q
A
257
Q

TEE mid SAX view

A

transfastric midpapillary short axis view

258
Q

blood supply in 4 chamber view

A
259
Q

Which papillary muscle rupture is the most common

A

Postero medial papillary muscle because of single blood supply from right coronary or LAD
- Anterolateral papillary muscle rapture is less common because of dual blood supply from L a D and left circumflex artery

260
Q

Effects of spinal anesthesia

A

Mostly from removal of sym innervation and unopposed parasym
-Cardiac: v and a dilation -> dec in preload and afterlaod
-renal: red in renal perfusion, urinary retention, give fluids
-GI: hyperperistalsis -> N/V and hypoTN to chemoreceptor trigger zone, and red in hepatic blood flor

261
Q

Myosin – actin interaction with skeletal muscle contraction

A
  1. Myosin release from Actin
  2. Myosin extending attaching to actin through conversion of ATP to ADP (site must be open from calcium binding to troponin)
  3. Power stroke. ADP released from myosin causing myosin to rotate and move along Actin
  4. Actin relaxes
262
Q

CHF and med changes

A

A. Furosemide
B. ACE inh or NG
C. Milrinone
D. Epi/NE

263
Q

Medical direction versus supervision for medicare reimbursement

A

Direction: higher reimbursement than supervision
To meet qualifications for direction you must
-preanesthesic exam/eval
-anesthetic plan
-participate in most demanding procedures of anesthesia
-ensure procedures done by qualified individual
-monitor admin at frequent intervals
-be physically present and available for emergencies
-post anesthtic care
-ratio of CRNAs max 1:4
-can leave to go to OB epidural
-all can be done by different members of anesthesia team

-CANNOT leave to go to ED

264
Q

when to use epi in PEA arrest

A

ASAP, w/i 1-3 minutes is ideal

265
Q

when to use epi in shockable rhythms

A

defib then 2 min CPR then defib then EPI

266
Q

IV PCA v on request

A

inc pt satisfcation, inc quality of analgesia, inc total opioid requirement, inc pruritis, equal resp depression (w/o continuous infusion)

267
Q

Glucagon what is it and what does it affect

A

secreted by alpha-cells of pancreas in resp to hypoglycemia and inc alanine, inc epi and cortisol
-CAUSES: gluconeogenesis, glycogenolysis, lipolysis, and inhibits glycogenesis

268
Q

Glucagon as a treatment for what toxicity

A

beta blockers
-inc cAMP -> inc intracellular Ca -> inc contractility and HR

269
Q

What is deep hypothermic circulatory arrest and when to use it

A

Deep hypothermic circulatory arrest: cooling pt to 15C to 22C and global arrest of blood flow (w/o flow for CPB circuit)
-used for neuroprotection during operations of aortic arch or pulm thromboendarterectomy

270
Q

when to use retrograde cardioplegia

A

obstructive CAD, aortic insufficiency, or procedures incolving manipulation/distortion of aortic valve or coronary ostia

271
Q

Why use leukoreduced blood

A

decrease risk of alloimmunization (host antigens, important to avoid if need transplant), allergic rxns (soluble antigens in transfused blood cause mild allergic rxns), dec febrile non-hemolytic rxns, and dec risk of CMV (if immunocompromised)

272
Q

MG and need for mechanical ventilation postop RF

A

-Disease > 6 years
-chronic resp illness
-pyridostigmine dose > 750 mg/day
-Vital capacity < 2.9L

RF for minimally invasive approach
-BMI > 28
-adv MG (bulbar involvement, slurred speech)
-prior myasthenic crisis
-assoc w/ pulm resection

Regardless of approach
-EBL >1L
-anti-ACh receptor tite > 100nmol/mL
-pronouned decremtal resp (18-20%) on low freq repeated n stimulation

273
Q

“birds beak” appearance on pressure-volume loop

A

lungs are overdistended and further inc in pressure will not inc TV

274
Q

detect venous air embolism in peds crani

A

precordial doppler ultrasound
-doppled probe placed over or R of sternum at 4th IC space, if prone b/w scapulae

275
Q

detect venous air embolism in adults

A

TEE/TTE

276
Q

EtCO2 venous air embolism

A

Moderate sensitivity
-consider dx if sudden drop in EtCO2 -> dec b/c air blocked blood flow and reflex pulm vasoconstriction
-wills tart to have physiological changes before EtCO2

277
Q

treatment of venous air embolism

A

communicate to surgical team, rapid flood the field w/ saline
-reposition pt supine
-100% O2, d/c Nitrous oxide, give fluids

278
Q

SE of TURP syndrome w/ glycine

A

transient blindness
-b/c glycine is inh NT in brainstem/cranial nerves
-breakdown into ammonia -> encephalopathy, N/V

279
Q

normal saline and TURP

A

electrical current dispersion b/c balanced salt solution

280
Q

TURP and sorbitol/mannitol

A

Sorbitol -> hyperglycemia
Mannitol ->intravsscular fluid expansion
both cause osmotir diuresis

281
Q

MetHg pulse ox

A

85% b/c absorbs light at 660 nm and 930 nm equally

282
Q

Pulse ox nm absorbion

A

660 nm deoxy absorbs
930 nm ox absorbs

283
Q

MetHg tx w/ and w/o G6PD def

A

w/o: methylene blue
w/: Vitamin C (ascorbic acid)

284
Q

What causes MetHg

A

Prilocaine, Benzocaine, Metochlopramide, nitrites (nitric oxide, NG)
-aniline dyes, benzene
-fhloroquine, dapsone, suflonamides

285
Q

Methylene blue change in pulse ox

A

65% transiently for ~10 minutes

286
Q

What pulse ox should be used in MetHg

A

Multi-wavelength co-oximetry

287
Q

Composition of 1.8% Hetastarch

A

Na 308, Cl 308
(NS is 154 of each)

288
Q

What’s only in plasmalyte and none of the otehr fluids

A

Acetate and gluconate
-acetate oxidized by liver, m and heart into bicarbonate
-gluconate converted to glucose

289
Q

Considerations for anterior mediastinal masses

A

-NMB avoided -> maintain spontaneous ventilation (neg intrathoracic pressure helps keep everything open)
-use rigid bronch/ have 911 equipment available
-px ECMO cannulation in high risk pts
-sitting/semirecumbent positions improve vent mechanisms (avoid supine)

290
Q

Type II error

A

Incorrect acceptance of the null hypothesis
-More likely to happen when the alpha value is decreased
-Also known as beta error
-Conventional set to 10% (because power is set to 90%)
-Decreased by increasing the sample size, increasing the expected effect size, and increasing the precision of a measurement, increasing power

291
Q

Power experiment

A

1- beta (type II error), conventionally 90%
-if you increase, decreases type II error

292
Q

Clomipramine MOA

A

Tricyclic antidepressant

293
Q

Desipramine MOA

A

Tricyclic antidepressant

294
Q

Doxepin MOA

A

Tricyclic antidepressant

295
Q

TCA toxicity

A

-blocks Ca channels widening QRS (100ms or greater predicative of Vent arrhythmia)
-anticholinergic (tachycardia, mydriasis, hyperthermia), hypoTN, sz

296
Q

treatment of TCA OD w/ EKG cahnges

A

sodium bicarb: perserve physiologic Na channel activity
-infuse continuously until QRS narrows
-IV lidocaine/Mg 2nd line

297
Q

tx of TCA sz

A

Benzos
-b/c TCA inh GABA receptors -> benzos help potentiate GABA

298
Q

what does the external branch of the superior laryngeal n innervate

A

cricothyroid muscle: tenses VC

299
Q

laryngospasm reflex afferent and efferent

A

afferent: internal branch of the SLN
efferent: RLN

300
Q

Phase I reactions (pharm)

A

oxidation, reduction, and hydrolysis
-goal is to make functional groups thatcan undergo phase II reactions
ex: cytochrome P450 aledhyde and alcohol dehydrogenase
-slower than phase II (if a drug does both, time for elimination dpt on phase I)
-nonsynthetic rxn
-MC occurs in liver

301
Q

synthetic rxn()Phase II reactions (pharm)

A

use conjugating enzymes and result in formation of metabolites w/ inc mass (synthetic rxn)
-conjugation rxns using glucuronyl transferase, sulfotransferase, methylases -> form metabolite w/ increased affinity for aqueous environment (inc water-to-lipid partition coefficient)-> eliminated out of body
-faster than phase I
-MC occurs in liver

302
Q

Des + dessicated CO2 absorbent makes

A

carbon monoxide and heat
-sevo, iso, and des all make CO, des makes the most) sevo makes the most heat

303
Q

When is maternal cardiac output the highest

A

immediately after delivery (2.5x prepregnancy)
-less vena cava compression, uterine contraction causes autotransfusion, and less demand for blood flow to uterus

304
Q

cardiac ouput and pregnancy

A

1st trimeser: HR inc, inc in CO by 40%
2nd and 3rd: SV inc, inc in CO by 50%
onset of labor: 110% inc in CO
highest: immediately after delivery
co inc 10% by 2 weeks postpartum
normal 24 weeks postpartum

305
Q

what to avoid in methylenetetrahydrofolate reductase def

A

nitrous oxide
-b/c inhibits methionine synthetase -> homocysteine rises -> thrombosis and coronary events

306
Q

Propofol and mitochondria

A

Propofol inhibits mitochondrial fxn so avoid in mitochondrial dx
-reason for propofol-related infusion syndrome

307
Q

etomidate inhibits

A

11-beta-hydroxylase

308
Q

cervical spine injury, HR to 22 w/ larygnoscopy why

A

unopposed vagal tone
-cardiac accelerators T1-T4 -> if injury above neurogenic shock -> severe bradycardia and hypoTN

309
Q

Bainbridge reflex

A

stretch receptors in RA wall sense inc pressure -> inh parasympathetic activity -> inc HR

(if you’re crossing a bridge and a big wave is coming, rush the people faster trying to get them out of the way)

310
Q

Hering-Breuer reflex

A

When subject to excessive stretching (CPAP/PEEP), pulm stretch receptors trigger the reflex -> prevents inspiration and allows expiration to occur
-no effect on HR

311
Q

Autonomic hyperreflexia and SC

A

2-3 weeks after injury
-occurs when stimulation below level of spinal cord injury -> uninhibited symp stimulation
(above T5)

312
Q

Treatment for acute dystonia reaction after metochlopramide + prochlorperazine

A

25-50 mg diphenhydramine
1-2mg benztropine

313
Q

Net ATP production of aerobic and anaerobic respiration

A

Aerobic: 32
Anaerobic: 2

314
Q

Aerobic Respiration Steps

A

Aerobic glycolysis: Glucose -> pyruvate + 2 ATP
-Pyruvate enters mitochondria to generate NADH -> oxidative phosphorylation in ETC to generate 30 ATP
-O2 final electron acceptor

315
Q

Anaerobic resp
-where and steps

A

Cells that don’t have mitochondria (erythrocytes)
-Glycolysis -> pyruvate + 2 ATP
-Pyruvate converted to lactate for continued glycolysis to regenerate NAD+
- Can only occur for a limited time due to build-up of lactic acid and acidotic environment
**cannot do ETC b/c location or b/c O2 is final electron acceptor and is limited or absenti n anaerobic

316
Q

Blood supply for anterolateral papilary muscle

A

LAD and LCx

317
Q

LAD supplies blood to what part of the heart

A

1/2 of LA and LV (anterior aspect)

318
Q

Branches off RCA

A

R marginal artery, PDA (R dom), AV nodal artery and sinoatrial artery

319
Q

R marginal artery supplies what part of the heart

A

laterval RV and cardiac apex

320
Q

PDA supplies what part of heart

A

posterior 1/3 of intraventricular septum, posterior inferior aspect of the heart and the posteromedial papillary muscle

321
Q

ST elevations in I, aVL, and V5-V6 which artery issue?

A

L Cx or diagonal branch of LAD

322
Q

Activation of which pathway causes bronchoconstriction

A

Act of M3 muscarinic receptors on airway smooth muscle
-influx of intracellular ionized Ca -> inc in smooth m tone and force -> bronchoconstriction

323
Q

Predisposing factors to develop bronchospasm

A

hx of asthma, heavy tobacco smoking, active bronchial infxn (bronchitis)

324
Q

Airway smooth muscle innervation and reflexes

A

Autonomic N system, basal tone is parasympathetic nerves in vagal centers, cholinergic neurons, M3 muscarinic receptor
-occasional nonadrenergic noncholinergic mechanisms activated by bronchopulm sensory C fibers (include tachykinis, vasoactive intestinal peptide) -> rare, minimal
-pure reflexive vagal stimuli -> bronchoconstriction is larger airways and more central
-beta 2 receptor important in relaxation: efflus of ionized Ca from cell -> SR relax muscles

325
Q

What is responsible for the determination of dynamic airway resistance

A

Caliber of the small airways of the lung

326
Q

Why does nitrous oxide cause air-containing spaces to expand?

A

Nitrous oxide diffuses from the blood to air-containing spaces faster than nitrogen can diffuse back out -> expansion

327
Q

When ok to use nitrous oxide in laproscopic surgery

A

if case is short, no effect on surgical visualization

328
Q

Nitrous oxide PONV

A

does not increase risk when used for less than 1 hour

329
Q

Metabolism in volatile anesthetics

A

Oxidation mediated biotransformation by cyto CYP2E1 renal and hepatic
Sevo 5% > Iso .2% > Des .02%
-Des/Iso have highly reactive intermediates that bond w/ hepatic proteins -> Ab form against metabolite-hepatic protein complex -> on 2nd exposure Ab activate and cause destruction of liver (still less than halothane)
-Sevo has a 4-6x higher rate of release of fluoride ions during metabolism -> still nopostop renal dysfxn
-nitrous oxide is not metabolized

330
Q

Nitrous oxide and metabolism

A

not metabolized, no significant biotransformation in the body
-inhibit methionine synthase by oxidizing cofactor B12 -> hematologic and neuro dysfxn -> inc homocysteine -> vasc inflammation and inc risk of thrombosis

331
Q

Partial pressure of gases w/ ABG syringes at higher of lower than room temp

A

-As temp decreases, partial pressure of O2 and CO2 will decreases
-if pt is hypothermic and blood gas is warmed -> ABG will have a higher partial pressure of O2 and CO2
-if pt is hyperthermic and blood gas is cooled -> results will be a lower partial pressure of O2 and CO2

332
Q

Complication of decrease phosphorous level

A

Decreased O2 delivery to tissues
-dec P -> dec 2,3-DPG -> L shift of Hg curve -> dec O2 delivery to tissues
-dec in diaphragmatic contraction (dec ATP stores) -> resp compromised and difficulty in weaning off vent (dec FVC)
-profound (<1) -> RBC membrane not stable -> hemolytic anemia, cardiac failure, nero symp b/c dec ATP stores

333
Q

How does CO2 exist in the body? majority is in what form?

A

Majority: Bicarbonate ions
-other: dissolved CO2 and with protein as carbamino compounds

334
Q

MOST likely to predict for difficult intubation

A

Class 3 upper lip bite test (can’t bite their upper lip w/ their lower teeth at all) >60% likelihood of difficult intubation
-short hyomental distance, impaired neck mobility and high mallampati are only moderate predictors, ULBT was better

335
Q

What happens if using too much NS in a kidney transplant

A

hyperK (b/c of non-AG hyperchloremic metabolic acidosis)
-coagulopathy (dilutional plus acidosis worsens)
-dec renal and gastric perfusion

336
Q

Eaton-Lambert Syndrome cause and symp

A

Ab: presynatpic VG Ca channels
sym: proximal m weakness, autonomic dysfxn, constipation, dry mouth, erectile dysfunction, dec sweating, orthostatic dysregulation

337
Q

Eaton-Lambert and NMB

A

Sensitive to BOTH dep and nondepolarizing paralytics
-no response to cholinesterase inhibitors

338
Q

Lambert assoc w/ what disease

A

Small cell lung carcinoma

339
Q

Myasthenia Gravis Ab and symp

A

Ab: postsynaptic ACh receptors
-extraocular m weakness (ptosis, diplopia, blurred vision), bulbar m weakness, proximal m weakness, resp weakness

340
Q

MG and resp to NMB

A

resistant to dep (use 1.5-2 mg/kg)
sensitive to nondep

341
Q

MG and assoc dx

A

Thymoma

342
Q

paresthesia in thumb and lateral surface of forarm and upper arm, weakness w/ flexion and supinatio of forearm, external rotation of arm, abduction of arm, and wrist extension. Where is the injury?

A

brachial plexus neuropathy

343
Q

midback pain, sudden, severe, point tenderness over vertebrae
most likelyl dx and imaging?

A

Compression fx
initial: lateral radiography of thoracic and lumbar spine

344
Q

Why 4 hours NPO time for breast milk and 2 hours for clear liquids

A

higher gastric residual volume w/ breast milk than clear liquids
**why NPO guidelines are the way they are, ALWAYS gastric residual volumes

345
Q

postoperative vision loss causes and which is MC

A

retinal artery occlusion, ischemic optic neuropathy, acute glaucoma
-ischemic optic neuropathy is MC

346
Q

RF for postop vision loss

A

prone positioning, long surgical length (5 hours or more), obesity, male sex, significant blood loss, external ocular compression, wilson frame use (looks like a half circle under your torso)
-hypoTN alone is not, hypoTN due to blood loss >1L can be

347
Q

anterior v posterior ischemic optic neuropathy

A

anterior: common post cardiac surgery
posterior: more common post prone surgeries

348
Q

If you put an iso vaporizer on the top of a mountain, what will change in output and what wont’?

A

won’t change: partial pressure of iso (what vaporizer is set to)

will: inc in volume % conc of inhaled anesthetic leaving vaporizer, inc volume of iso entrained by 100 mL of O2, barometric pressure decreases

349
Q

Des vaporizer and altitude changes

A

Dual gas blender vaporizer: constant conc of vapor output and not constant partial pressure -> at higher altitudes, will need to inc des vaporizer to maintain same partial pressure

350
Q

BIS: GA target, burst suppression, sedation

A

sed: 80
GA: 40-60
BS: 20
0: flatline EEG

351
Q

BIS & temp

A

BIS goes down 1.12 units for each 1 C red in body temp (dec CRMO2)

352
Q

What meds cause BIS to increase

A

ketamine, nitrous oxide

353
Q

RF for PPH

A

c/s, induction of labor, augmented labor, multiple gestations, macrosomia, polyhydramnios, prolonged labor, adv maternal age, HTN or DM in mother, tocolytic meds

354
Q

SE of oxytocin

A

powerful vaso constriction in umbilical arteries, veins, and coronary vessels
-hypoTN, tachycardia, and coronary vasoconstriction -> MI

355
Q

Options for uterine atony and SE

A

oxytocin: hypoTN, tachycardia, coronary vasoconstriction
methylergonovine: HTN
misoprostol (prostaglandins): bronchospasm

356
Q

What types of births should oxytocin be given to postpartum?

A

all of them (ppx for uterine atony)

357
Q

Cardiovascular effects of ECT

A

-initial parasymp resp: transient bradycardia -> symp resp from sz: tachycardia and HTN
-sym surge can inc myocardial O2 demand -> MI in some pts
-EF dec for 6 hours following ECT

358
Q

ECT and CNS effects

A

inc CMRO2, inc CBF, inc ICP
-MC: disorientation, impaired attention and memory deficits

359
Q

Lusitropy

A

rate of active myocardial relaxation
-if POSTIVE lusitropy -> inc LVEDV for a given EDP
(more compliant ventricle w/ greater rate of relaxation)
-shift to A is POSTIVE, shift to B is NEGATIVE

360
Q

Inotropy def and PV loops

A

myocardial contractility
-slope of the end-systolic pressure-volume relationship
-POSTIVE is D, NEGATIVE is C

361
Q

normal EDV and ESV, SV

A

EDV: 120, ESV: 40-50 mL
SV: 70-80 mL (normal EF is 60-67%)

362
Q

factors that inhibit hypoxic pulm vasoconstriction

A

Vasodilator (NG and nitroprusside)
Acetazolamide
phosphodiesterase inhibitors (sildenafil, tadalafil)
ACE inh
metabolic alkalemia
Hypocarbia, hypothermia
Infxn
SEVOFLURANE (modestly by dilating pulm vascular beds at > 1 MAC) usually not clinically relevant

363
Q

Cistatracurium degradation

A

spontaenously degrades in plasma by Hofmann elimination and ester hydrolysis
onset 4-6 min, duration 20-50 min

364
Q

Mivacurium degradation

A

butrylcholinesterase or plasma cholinesterase or pseudocholinesterase

365
Q

Succinylcholine degradation

A

butrylcholinesterase or plasma cholinesterase or pseudocholinesterase

366
Q

ASA basic physiologic standard monitors

A

oxygenation: O2 analyzer w/ low O2 conc limit alarm, pulse ox
ventilation: EtCO2 w/ audible alarm, disceonnection alarm
circulation: ECG continously, BP q5mins
temp: when temp changes are anticipated

367
Q

Normal CVP waveform

A

a: atrial contraction
c: tricuspid valve elevation into the R atrium
x: downward movement of the contracting RV
v: back pressure wave from blood filling the right atrium
y: tricuspid valve opens in early ventricular diastole

368
Q

what change in CVP waveform for pt w/ a fib

A

loss of a wave and prominent c wave
-contractions less effective b/c not synchronized w/ ventricular activity

369
Q

when do you get a loss of x descent in CVP

A

tricuspid regurgitation
-due to abnormal systolic filling of RA

370
Q

When is y descent lost

A

tricuspid stenosis
-atrial emptying impaired

371
Q

MOA of gabapentin

A

binds to calcium channel alpha 2 delta subunit of VG Ca channels
-decrease glutamate release -> dec production of substance P

In Training Exam TL (11 decks)

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