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In Training Exam TL > ITE TL Block 3 > Flashcards

ITE TL Block 3 Flashcards

1
Q

Hydrophilic v hydrophobic opioids used in CSF

A

hydrophilic = easier absorption -> shorter duration faster onset ex: fent, sufent
hydrophobic = harder absorption -> longer duration, slower onset, and greater migration in CSF
ex: morphine, Dilaudid, meperidine

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2
Q

octanol/H2O partition coefficient

A

lipid solubility of opioids
-higher = more lipid solubility

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3
Q

first line therapy for pulm atresia w/ intact ventricular septum

A

Prostaglandin E1 -> keep the PDA open

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4
Q

Medication for PDA closure

A

Indomethacin

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5
Q

Most significant source of heat loss from body

A

Radiation
-heat from body travels to vasodilated surface capillaries

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6
Q

a pt status post tonic-clonic sz has a dec RR and is hypoxemic why

A

central resp depression so dec RR -> build up of CO2 -> inc partial P of CO2 -> inc arterial CO2 tension in alveoli -> cant effectively exchange gas in alveoli -> dec O2

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7
Q

Alveolar gas equation

A

PAO2 = FiO2 x (Patm - PH2O) - (PaCO2/R)
R: respiratory quotient

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8
Q

Status epilepticus

A

> 5 minutes of continuous sz activity or >2 consecutive sz w/o intervening recovery of consciousness

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9
Q

When using the term nitrogen handling in setting of liver damage what does that mean

A

metabolism of nitrogenous wastes, mainly ammonia
-if active GI bleed and breakdown and absorption of amino acids from Hg -> inc ammonia -> can overwhelm a cirrhotic liver to eliminate N compounds -> worsening hepatic encephalopathy

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10
Q

Tx for hepatic encephalopathy

A

Lactulose: laxative that prevents absorption of ammonia
Rifaximin: abx w/ bactericidal activity against ammonia-generating organisms in gut

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11
Q

25 YOM larygnospasm then in PACU 85-90% on room air w/ well controlled pain and normal RR why?

A

negative pressure pulm edema
-b/l fluffy infiltrates on xray
-tx: supportive w/ suppl O2, diuresis and PPV if severe

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12
Q

What causes overdamping in an art line

A

Factors that inc compliance or resistsance in circuit
-adding stopcocks, air bubbles or pliable tubing

-causing systolic BP to be lower than it actually is

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13
Q

Underdamping

A

-tubing should have a very high natural frequency -> if too low, resonance of the system will add to the pressure form -> underdamping

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14
Q

Controlled hypootension

A

MAP of 50-65 or 20-30% below baseline
-used for certain surgeries incl cranial aneurysm repair but risks must b econsidered
-done w/ CCB, direct vasodilators, BB and anesthesia

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15
Q

Renal test most reliable indicator of acute renal failure

A

Cr conc inc >100% from baseline

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16
Q

What causes artifical inc in BUN

A

reduced effective circulating blood volume
catabolic state: GI bleeding, steroid use
high protein diet
tetracycline use

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17
Q

Decrease in BUN

A

liver dx
malnutrition
sickle cell anemia
SIADH

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18
Q

If you give 2L NS what labs change immediately after

A

hyperchloremic metabolic acidosis
-bicarb dec
-Na inc
-K inc
dilutional dec in Hct and albumin

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19
Q

labs in hyperosmolar hyperglycemia

A

high glucose
low K
no acidosis
-osmotic diuresis due to elevated glucose

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20
Q

TURP blurred vision and minimally reactive pupils, whichh irrigation solution

A

glycine
(amino acid and Neurotransmitter)
-large amounts metabolized to ammonia

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21
Q

TURP with hyperglycemia, whichh irrigation solution

A

Mannitol

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22
Q

Lytes intracellular v extracellular

A

Majority of K is intracellular (157), so is Mg (20) comparatively
The other ions Cl, bicarb, Ca, Na higher extracellularly

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23
Q

Hyperk EKG changes

A

peaked T waves, prolonged PR interval and widened QRS

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24
Q

Rhabdo complications

A

DIC -> inc PTT, dec fibrinogen, dec plts
AKI (ATN from myoglobin)
Arrhythmias: hyperK

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25
Q

Normal AG met acidosis causes

A

normal: ~13
diarrhea, renal tubular acidosis, biliary drainage, large infusions of NS

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26
Q

CI to extracorporeal shock wave lithotripsy

A

Pregnancy (risk of harm to fetus)
Untreated bleeding d/o
active UTI

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27
Q

extracorporeal shock wave lithotripsy and AICD

A

not a CI, but should be shut off before with alternate defibrillator ready

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28
Q

Complications of enteric feeds

A

compl due to placement (aspiration)
long-term indwelling (sinusitis, otitis media)
hyperosmolar feeds cause diarrhea
obstruction from thick feeds
constipation
high gastric residual feeds

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29
Q

Lytes refeeding syndrome

A

HypoP
HypoMg
hypoK
hypoCa
-also skeletal m weakness: resp weakness, dysphagia, leg cramps, and constipation

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30
Q

What causes diarrhea w/ enteral feeds

A

hyperosmolar feeds
hypoalbuminemia
rapid administration
bacterial contamination of feeds

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31
Q

MC complication of enteral feeds

A
  1. high residual volumes
  2. constipation
  3. diarrhea
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32
Q

Three stages of liver transplant

A

preanhepatic
anhepatic
neohepatic

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33
Q

What happens post reperfusion in liver transplant

A

-large release of K and H+ into circuation w/ inc preload and inflammatory mediators-> cardiac arrhythmias, hypoTN, pulm HTN, and R heart strain
(can be postreperfusion syndrome)
-hypothermic
-coagulopathic (washout of tPA from organ)

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34
Q

tx of postreperfusion syndrome

A

pressor support
Na bicarb to neutralize the acid
Ca Cl to stabilize cardiac myocytes

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35
Q

What factors need Vit K to be active?

A

SNOT
Seven
Nine
10
Two

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36
Q

Enzyme targeted by warfarin

A

Vitamin K epoxide reductase
-so Vit K dpt factors can’t be activated b/c active Vit K not being made so can’t act as cofactor

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37
Q

how is coag factor III produced

A

tissue factor/thromboplastin
-secreted by damaged vascular endothlium or plts
NOT liver

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38
Q

Citrate and lytes

A

HypoCa and hypoMg -> chelates both

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39
Q

which blood products have more citrate

A

FFP and plts

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40
Q

What inc rate of citric toxicity

A

hypothermia
liver dx/transplant
peds pts
hyperventilation (alk)
massive blood transfusion

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41
Q

When does Ca decrease from blood tranfusion?

A

6 units per hour (35 cc/min)

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42
Q

When does hyperK occur from blood transfusion?

A

120 cc/min or more

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43
Q

Citrate intoxication signs

A

hypoTN
narrow pulse pressure
inc VEDP
inc CVP

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44
Q

When does INR normalize post liver transplant if you’re a donor

A

post op days 5-7

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45
Q

INR trend post liver transplant for donor

A

w/ partial removal of liver -> loss of syn fxn, so inc peaking post op days 2-3 usually no higher than 2
-returns to normal post op 5-7

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46
Q

Liver metabolism of drugs depends on 3 facotrs:

A
  1. intrinisic liver fxn
  2. hepatic blood flow
  3. drug extraction ratio
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47
Q

Phase I biotransformation of drugs in liver

A

hydrolysis, oxidation or reduction
-goal to make more hydrophilic (so easier to eliminate)
-carried out by cytochrome p450

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48
Q

Phase II reactions in drug biotransformation

A

conjugation reactions, addition of a polar functional group
-continuing to make more hydrophilic

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49
Q

Extraction ratio for drugs and hepatic BF

A

ER: portion of drug removed from liver as it passes through
(100% -> all of drug that passes through liver in blood is removed)
-based on protein binding and efficiency of drug metabolism
-high ER more dpt on hepatic blood flow, low ER less dpt on hepatic blood flow

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50
Q

relationship b/w succ and obesity

A

need larger doses b/c
obese pts have inc in pseudocholinesterase activity and inc extracellular fluid volume

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51
Q

how to dose maintenance infusion dose of propofol

A

actual total body weight

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52
Q

how to dose succ

A

actual total body weight

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53
Q

how to dose thiopental

A

lean body weight

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54
Q

how to dose induction dose of propofol

A

lean body weight

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55
Q

how to dose fentanyl

A

lean body weight

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56
Q

how to dose rocuronium

A

ideal body weight

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57
Q

how to dose vecuronium

A

ideal body weight

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58
Q

volatile anestetics and hepatic BF

A

<1 Mac: all preserved
> 1 Mac: iso decreases HBF in dose dept

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59
Q

What IV anesthetic inc hepatic blood flow

A

Propofol

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60
Q

IV anesthetics and hepatic BF

A

neutral/small decrease: benzos, barbs, dex, etomidate
no change: ketamine
inc: prop

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61
Q

first-pass metabolism

A

before onset of drug
-breakdown or modification of drug or prodrug in GI tract or liver before systemic circulation
(why oral drugs have higher dosing than IV drugs)

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62
Q

Drug therapeutic index

A

ratio of the toxic dose (TD50) to effective dose (ED50)
-higher, safer drug

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63
Q

Adenosine and liver

A

Adenosine is a potent vasodilator
-it is a byproduct of the liver that is produced in the space of Mall (surrounds hepatic vasculature)
-washed out by portal v from space of Mall -> when flow dec, it builds up -> hepatic a dilation

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64
Q

Most sensitive lab test for acute changes in liver

A

PT
(synthetic fxn)

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65
Q

Measure excretory fxn of liver

A

alk phosphatase
gamma-glutamyl transferase (GGT)
bilirubin

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66
Q

measure of hepatocellular injury

A

AST, ALT
-ALT more liver specific, AST also found in heart, muscles, brain, and kidney

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67
Q

What is 2,3-BPG

A

2,3-diphosphoglycerate
-binds to Hg changing its conformation to allow O2 to leave, shifts O2 disassociation curve to the R
-higher in anemia and hypoxia

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68
Q

Body compensation for anemia

A

-inc cardiac output
-arteriolar vasodilation (inc nitric oxide from tissue hypoxia and acidosis)
-dec blood viscosity -> less shearing in microvasculature -> dec vascular resistance -> dec afterload
-inc 2,3 DPG and acidosis -> R shift of O2 curve

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69
Q

Where are the cell bodies of motor neurons located

A

ventral horn of the spinal cord

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70
Q

what’s at the dorsal horn of the spinal cord

A

first-order somatosensory afferent n terminate

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71
Q

dorsal root ganglion

A

cell bodies of somatosensory neurons

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72
Q

lateral horn

A

T1-L2
b/w dorsal and ventral horns
-cell bodies of the sympathetic NS

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73
Q

How n depolarize

A

ACh released from presynaptic n -> binds to nicotinic ACh receptor on postsynaptic membrane -> conformational change allow Na and Ca into cell -> miniature end-plate potential -> if several occur at once -> m depolarized -> action potential and m contraction

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74
Q

if you put iso in a sevo vaporizer

A

iso has a higher saturated vapor pressure -> in a sevo vaporizer a higher concentration will come out than intended

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75
Q

What color protective eyewear for neodymium:yttrium aluminum garnet laser

A

Nd:YAG
-green filter

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76
Q

what color filter for carbon dioxide laser

A

clear

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77
Q

what color filter for argon laser

A

orange

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78
Q

what color filter for potassium-titanyl-phosphate-Nd: YAG

A

orange-red

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79
Q

where is the sympathetic trunk

A

L1-L5 posterior to IVC on R and lateral and slightly posterior to aorta on L

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80
Q

What levels are the celiac plexus block

A

T5-12
-innervates all the abd organs

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81
Q

SE of lumbar plexus sympathetic blocks

A

-prob w/ ejaculation in men (esp if b/l)
back pain
accidental blockade of genitofemoral n or lumbar plexus in psoas m -> numbness in groin, thigh or quads -> neuralgia and burning pain

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82
Q

earliest sign that a lumbar symp plexus block is successful

A

vasodilation and temp changes

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83
Q

CMR and CBF of volatile anesthetics at MAC > 1.1

A

dec CMR with inc CBF “uncoupling”
b/c vasodilation from volatile anesthetic wins

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84
Q

nitrous oxide on CMR and CBF

A

both inc

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85
Q

ways to measure EtCO2

A

capnography, capnometry or mass spectroscopy
-and must have a low end-tidal CO2 alarm

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86
Q

ASA required monitors

A

EtCO2 w/ disconnection alarm
O2 analyzer w/ low O2 conc limit alarm
continuous EKG
continuous pulse ox w/ variable pitch pulse tone and low threshold alarm
BP monitored every 5 minutes
Temp if expecting changes

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87
Q

Recommended skin prep for central line placement

A

> 0.5% chlorhexidine w/ alcohol is BETTER than iodine or 70% alcohol

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88
Q

Brugada syndrome

A

inherited mutation in Na channels MC in southeast asian men
-high risk of ventricular arrythmias and sudden death
-ICD mainstay of therapy

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89
Q

EKG for brugada syndrome

A

pseudo RBBB (wide QRS, terminal R wave in V1, wide or exaggered S wave in V5-6) and ST elevations in V1-V3 with negative T wave

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90
Q

Anesthesia considerations for Brugada syndrom

A

-propofol infusions and bupivacaine are assoc w/ lethal arrythmias
-ICD
-high risk for lethal arrythmias
-avoid class I antiarryhtmic meds and beta blockers -> trigger or worsen arryhtmias

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91
Q

Delta wave and short PR interval on EKG indicates what?

A

Wolf-Parkinson White
-this short PR interval w/ delta wave -> widened QRS completed

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92
Q

Pt w/ known WPW and SVT tx

A

procainamide, ibulitide or cardioversion
NO Beta blockers

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93
Q

What causes a LBBB

A

aortic stenosis
dilated cardiomyopathy
LV MI
lyme carditis
aortic regurge
Pacing at RV

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94
Q

dx?

A

LBBB

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95
Q

dx?

A

RBBB

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96
Q

Def of long QT

A

> 480 ms

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97
Q

What happens to body when drowning in freezing water

A

hypothermia -> diving reflex: slowing of HR and constriction of peripheral arteries to shunt blood to heart and brain -> dec metabolic demand of tissues -> delaying hypoxia and acidosis
-breath holding and air hunger -> hypoxemia 2/2 laryngospasm and aspiration of water -> LOC and irreversible brain injury
-cardiac dysrhythmias -> sinus tach to brady to PEA to asystole
-asp fluid washes out surfactant -> pulm dysfxn

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98
Q

axillary n block view

A

A: median n
B: ulnar n
C: radial n
D: musculocutaenous n

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99
Q

when to use axillary block

A

fingers, hand, wrist and forearm surgery
-musculocutaneous not blocked
-if tourniquet is required, need to block intercostobrachial n

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100
Q

position for axillary n block

A

supine, abducted 90 degrees, externally rotated and elbow flexed at 90 degrees

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101
Q

when musculocutaenous n spared by axillary n, where to block it seperately?

A

b/c biceps brachii and coracobrachialis

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102
Q

Atrial natriuretic peptide

A

released by cardiac myocytes w/ inc atrial stretching (inc extracellular volume or volume overload)
-dec BP b/c vasodilator (inc cGMP)
-diuretic and natriuretic effects: suppresses effects of aldo, ADH and renin

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103
Q

Lung volume changes in pregnancy

A

dec FRC
dec ERV
dec RV
inc IRV
only slight dec in TLC

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104
Q

How does MV inc in pregnancy

A

progesterone inc TV w/ minimal inc in RR
-inc arterial O2 tension and dec CO2 arterial tension

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105
Q

P50 O2 curve

A

oxygen tension at which Hg is 50% saturated
normally: 26.7 mmHg

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106
Q

Causes of R shift of O2 curve

A

Dec pH
inc H+
inc 2,3 DPG (phosphate, so if low phosphate would go to the L)
inc temp
–> dec affinity of Hg for O2

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107
Q

How long is fetal Hg peristant?

A

2-4 months of age
-completely gone by 6 months

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108
Q

Cardiac changes w/ insufflation

A

inc in systemic and pulm vascular resistance
-pneumoperitoneum -> inc intraabd pressure -> compressed vessels in splanchnic vasculature -> inc in venous return -> inc preload and cacrdiac output
-hypoTN w/ insufflation + PPV
-vagal activation w/ pneumoperitoneum -> arrhythmias

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109
Q

how to minimize renal damage w/ abd insufflation

A

lower intraabd pressures and intravascular volume load

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110
Q

Type I hepatorenal syndrome

A

acute and rapid renal failure (Cr x2) assoc w/ precipitating cause (SBP, surgery, sepsis)
-responds to medical therapy and stabilizes after medical therapy is d/c
-w/o tx survival is 2-4 weeks

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111
Q

Type II hepatorenal syndrome

A

insidious onset of renal failure b/c of portal hypertension
-dec intravasc volumte from splanchnic dilation and ascites -> renal vasoconstriction -> activation of RAAS, sym act, and vasopressin
-survival is ~6 months

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112
Q

Terlipressin

A

vasopressin analogue

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113
Q

Tx for type II Hepatorenal Syndrome

A

Vasoconstrictors: midodrine, octreotide, NE, vasopressin analogues
Volume expanders: albumin
-definitive tx: liver transplant
-depending on how far gone, liver transplant will improve kidneys

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114
Q

Hemolytic Uremic Syndrome

A

thrombocytopenia, acute renal impairment, and microangiopathic hemolytic anemia
-plt microthrombi in small bllod vessels, nonimmune hemolytic anemia, thrombocytopenia, and clots get caught in kidneys
-usually post GI (E Coli) or resp (S pneumo)

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115
Q

What lab is the strongest predictor of periop outcomes in pts receiving TPN

A

serum albumin

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116
Q

Prolonged TPA causes what lab changes?

A

trace metal depletioni: Zinc, copper, Mg

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117
Q

When d/c TPA what is likely to happen to labs?

A

Hypoglycemia (b/c inc insulin production 2/2 TPA)

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118
Q

Elemental diets v polymeric feeds

A

elemental diets are more expensive and may inc hospital length of stay and mortality

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119
Q

Enteric feeds w/ glucose and carbs dose this to body:

A

-red of gluconeogenesis and lypolysis
-stim insulin -> protein synthesis and dec lipolysis
-hyperglycemia

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120
Q

Why are lipid emulsions important in TPN

A

lipid oxidation is the predominant energy-prod pathway in stress (sepsis, burns, and surgery)
-adequate nutrition is key to healing

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121
Q

Complications of TPN

A

HypoMg
after d/c -> high insulin -> hypoglycemia, hypoK, hypoP
cholestasis due to a lack of enteric
**use enteric feeds whenever possible

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122
Q

When you decrease the glucose-to-lipid ratio

A

-dec risk of steatosis b/c dec carbs
-dec risk of hypoglycemia

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123
Q

Etomidate and liver

A

Decreases hepatic blood flow due to dec in hepatic arterial vascular resistance

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124
Q

Best IV anesthestic for concern w/ hepatic encephalopathy

A

Propofol: doesn’t dec hepatic blood flow, may increase due to splanchnic vasodilation
-midaz can accumulate, same w/ dex

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125
Q

Labs typical for DIC

A

inc D-dimer
dec factor VIII
dec fibrinogen
low plts

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126
Q

Best test for DIC in end stage liver dx

A

factor VIII (b/c d dimer elevated in ESLD anyway so hard to tell apart)

127
Q

clotting factors not produced by liver

A

factor III, IV and VIII

128
Q

What inc hepatic blood flow

A

Inc venous return (inspiration)
inc arterial bloood flow (inc CO)
inc portal blood flow by spanchnic vasodilation (after eating)

129
Q

What dec hepatic BF

A

dec venous return (PPV) and R heart failure
dec art BF (HF)
redistribution of splanchnic BF (exercise and catecholamine release)
dec BF (shock)

130
Q

Why hypoxia inc w/ laparoscopy

A

pneumoperitoneum causes shift of diaphragm (restricts lung expansion) cephalad -> dec lung expansion -> vent/perf mismatch -> intrapulm shunting

131
Q

In crisk of normal pt getting postop hepatic dysfxn

A

abd procedures (dec BF to liver), preop asymp elevation of liver enzymes
pre-exiting liver dx

132
Q

Autonomic dysreflexia

A

-Injury above T5-7 (takes wks to months)
-when stimulation below level of SC -> massive symp resp -> massive HTN, severe vasoconstriction below leevel of injury
-carotid sinus senses HTN -> severe bradycardia, heart block
-parasymp resp above injury: bradycardia, HA, flushing above injury

133
Q

Tx for autonomic dysreflexia

A

deepen anesthetic
stop stimuli
vasodilators: NG, CCB, hydralazine

134
Q

Carotid body v carotid sinus

A

body: senses composition of arterial BF: pH, CO2, temp, PaO2
sinus: baroreceptor by CN IX (glossopharyngeal) detect, respond and regulate BP
body-senses
sinus-BP

135
Q

When does sympathetic NS use ACh at NT?

A

at postgang sweat glands

136
Q

sym v parasymp stimulation at pulm vessels

A

sym: pulm constriction
parasym: pulm dilation

137
Q

parasym and symp at bladder: detrusor v trigone

A

trigone: area near urethra
detrusor: bladder muscle
parasym: trigone relax, detrusor contract
sym: trigone constrict, detrusor relax

138
Q

ciliary m in eyes symp v parasymp

A

sympathetic: relaxation for far vision
parasymp: contraction for near vision

139
Q

What levels artery of adamkiewicz

A

T9-12

140
Q

What tracts supplied by anterior spinal a

A

spinothalamic (pain and temp)
corticospinal (motor)
intermediolateral (autonomic)

141
Q

Inc risk of postop vision loss

A

Surgery: prolonged hypoTN, long duration of surgery, large blood loss, large volume of crystalloid, anemia/hemodilution, inc IOP from prone position

Pt: HTN, DM, atherosclerosis, obesity, male, tobacco

142
Q

Two types of postop vision loss

A

central retinal artery occlusion: unilateral vision loss, direct pressure on globe during surgery
ischemic optic neuropathy: prolonged duration of surgery, obesity, blood loss, hypoTN, male

143
Q

Duchenne Muscular Dystrophy: MOA, and cardiac implications

A

defect in dystrophin: pseudohypertrophy of m, m cells broken down and replaced by fat
-occurs in myocardium too -> dilated cardiomyopathy, regional wall abnormalities, vent arrhythmias
-X-linked recessive

144
Q

EKG Duchenne’s Muscular Dystrophy

A

sinus tach
inverted T waves
Q waves in precordial leads
tall R waves in R precordial leads

145
Q

highest risk of prob w/ ped sedation

A

Under 6 months of age
remote location (MRI)
developmental delays
invasive procedure: DL, endoscopy

146
Q

RF for optin n damange w/ retrobulbar blocks

A

myopic eye (axial length longer than 25 mm) -> longer eye lentgth -> RF for optic n damage or globe penetration

147
Q

Dedfinition of inc IOP

A

> 25 mmHg

148
Q

cataracts

A

opacification nof lens of eye

149
Q

retinal detachment and visual loss

A

no capillaries supply retina -> choroid layer provides O2 and nourishment -> retina detachment from choroid layer -> blindness

150
Q

Inc risk of relapse after training in substance use d/o

A

hx of major opioid use
IV admin of drugs
family hx of substsance abuse
psychiatric d/o dx

151
Q

periop fluids peds

A

20-30 cc/kg of isotonic fluid over 2-4 hrs (reduce ADH)
-if <6 mo, neonates, malnourished, cardiac surgery: give glucose-containing fluids

152
Q

Morphine hydrophobic or philic

A

Hydrophilic
-avoids first-pass uptake and retention by lungs, stays longer in SC

153
Q

opioids and lung uptake/retention

A

hydrophobic/lipophilic opioids taken up by lungs on first-pass -> will only be released when plasma conc decreases
-fent, sufent, and meperidine have a high first-pass uptake/retention
-morphine is hydrophilic so it does not

154
Q

Tx for digoxin OD

A

Digoxin-specific antibody fragments

155
Q

N/V/D, abd pain, anorexia, bradycardia, hx of afib, weakness dx?

A

digoxin toxicity
-vision changes (yellow or green) MC
-hyperK
-hyperCa -> proarrythmic -> premature contractions

155
Q

N/V/D, abd pain, anorexia, bradycardia, hx of afib, weakness dx?

A

digoxin toxicity
-vision changes (yellow or green) MC
-hyperK
-hyperCa -> proarrythmic -> premature contractions

156
Q

when can you give activated charcoal

A

1-2 hours of suspected OD

157
Q

Antidote for Beta blocker OD

A

Glucagon

158
Q

CBF and PaCO2

A

w/i 25-75
1-2 cc/100g/min for each 1 mmHg
-if above or below, resp is diminished
-if hypoTN, responsiveness is reduced

159
Q

region from soft palate to epiglottis

A

oropharynx

160
Q

region from base of skull to cricoid

A

pharynx

161
Q

region b/w epiglottis and cricoid cartilage

A

larygnopharynx or hypopharynx

162
Q

skull base and soft palate region

A

nasopharynx
posterior to nasal cavity

163
Q

Why hypoxia when you place mobidly obese pts supine

A

Dec FRC -> closing capacity above FBC -> small airways closing, V/Q mismatch, R to L shunting

164
Q

Miosis and Mydriasis symp v parasymp

A

Miosis: parasymp activation
Mydriasis: symp activation

165
Q

Why inc in MAP and SVR w/ abd insufflation

A

CO2 absorption -> symp response
-dec in renal BF -> activation of renin, angiotensin, aldosterone system
-AT II causes a direct vasoconstriction effect
-vasopressin causes a vasoconstriction effect and causes an inc reabsorption of water
vasopressin level inc is the primary inc in SVR and MAP, dec venous return is NOT directly responsible

166
Q

Metabolic resp to surgical stress

A

immunosuppresion
-release of epi, NE, cortisol
-breakdown of glycogen stores
-insulin resistance in tissues -> hyperglycemia
-m catbolism and proteolysis (cortisol)
-lipolysis

167
Q

which are cutting and not cutting needles spinals

A

cutting: Quincke
not cutting: Whitacre, Sprotte

168
Q

Parkland formula for resuscitation after burns

A

Replacement = TBSA burned (%) x weight (kg) x 4
-1/2 over 1st 8 hours
`1/2 over next 16 hours
**leave % as a whole number not a decimal

169
Q

supraclav n block
-supclavian a and first rib view -> brachial plexus tranks in relation to artery?

A

lateral

170
Q

what level does infraclav block target?

A

level of cords next to axillary artery does block axillary and musculocutaneous n
-level of cords

171
Q

TAP block between what layers

A

internal oblique and transversus abdominis

172
Q

What n does the TAP block block?

A

anterior rami of the thoracolumbar spinal segment n from T7-L1
-subcostal, ilioinguinal and iliohypogastric blocked
***somatic postop pain, not visceral

173
Q

What n provides sensory inervation over the sole of foot?

A

posterior tibial n
-behind medial malleolus

174
Q

what innverates skin over dorsum of foot

A

superficial peroneal

175
Q

what innervates lateral ankle and foot

A

sural n
-inject behind lateral malleolus

176
Q

ankle block

A
177
Q

possible complications for TAP block

A

LAST: large volume **calculate*
peritoneal puncture
bowel perf
liver/spleen lac
retroperioneal hematoma

178
Q

what n block is phrenic n paralyis a complication

A

interscalene

179
Q

What n block is PTX a complication

A

supraclav and infraclav

180
Q

symp blockade is a complication of what n block

A

thoracic paravertebral block

181
Q

ilioinguinal/iliohypogastric n block

A

-used in orhidopexy and hydrocele repair in kids
-ASIS located
-needle b/w internal oblique and transversus abdominis m

182
Q

which eye block causes more chemosis

A

peribulbar

183
Q

which eye block is faster with greater analgesia

A

retrobulbar

184
Q

which eye block as a higher risk of retrobulbar hemorrhage, subarachnoid injxn, eyelid hematoma, globe perforation

A

retrobulbar

185
Q

sub-tenon block

A

eye block -> quick onset but akinesia variable
-blunt cannula inserted via incision in the conjuctiva and tenonn capsule
-dec risk of perforation and subarachnoid injxn (b/c blunt)
-but inc risk of chemosis
-CI: eye infxn

186
Q

what n injured during proximal humerus fx

A

axillary n

187
Q

axillary n block anatomy

A

muscles surrounding: latissmus dorsi, biceps muscle, coracobrachialis muscle

188
Q

deep peroneal n sensation

A

first web space of the foot

189
Q

deep peroneal n relative to extensor hallicus longus tendon

A

n is lateral to tendon

190
Q

post single shot caudal pt hypoTN needing pressors, post emergence apneic, weakness, fixed dilated pupils, dx?

A

total spinal blockade

191
Q

Signs of intravascular injxn instead of cadual

A

peaked T waves
inc in heart rate
inc in BP

192
Q

why total spine w/ caudal higher in infants ?

A

dural sac extends to S3-4, so close to puncture site (adults S1-2)

193
Q

Rectus sheath block b/w what layers

A

rectus abdominis and posterior rectus sheath

194
Q

where does probe go for interscalene block

A

level of cricoid cartilage (C6)
-SCM medial, and middle scalene laterally

195
Q

interscalene block anesthetizes what?

A

ventral rami of C5-C7

195
Q

interscalene block anesthetizes what?

A

ventral rami of C5-C7

196
Q

what change in anatomy does cricoid pressure cause

A

lateral displacement of esophagus

197
Q

consequences of cricoid pressure

A

dec LES tone
poorer laryngoscopic view
longer time from induction to intubation

198
Q

anatomy

A

A: middle scalene
B: anterior scalene
C: carotid
D: SCM
roots seen: C5-C7

199
Q

Types of regional that is inhibited w/ recent use of apixaban

A

neuraxial blocks and paravertebral blocks

200
Q

PEC I and II blocks

A

PECs I: injxn only b/w pec major and minor
PECS II: 2 locations, between pec minor and serratus anterior and second pec major and pec minor

201
Q

Why is bupivacaine the most cardiac toxic

A

stronger affinity for resting and inactivated Na channels in myocardium

202
Q

cardiac-to-CNS dose toxicity ratio

A

normally LA cause CNS toxicity before cardiac
-cardiotoxicity is related to potency and higher lipid solubility
-bupivacaine has the highest

203
Q

u/s of the neck carotid a relative to v position

A

v is lateral and superficial (superior) to artery

204
Q

what muscles does the external branch of the superior laryngeal n innervate?

A

cricothyroid muscle
-affects voice pitch

205
Q

What muscle sit he primary abductor of the VC?

A

posterior cricoarytenoid m
-RCLN innervation

206
Q

what keeps LA around the femoral N?

A

fascia iliaca

207
Q

gag reflex afferent/efferent in posterior pharynx

A

afferent: CN IX
efferent: CN X

208
Q

pupillary light reflex afferent, efferent

A

afferent: CN II
efferent: CN III

209
Q

First 2 reflexes lost during gerenal anesthesisa

A

oculocephalic (doll’s eyes): eyes open and head turned briskly and held -> normal is eyes move to opposite direction, abrnoaml, eyes follow rurning
corneal

210
Q

Why does spinals last longer w/ older age

A

Dec CSF volume
N more sensitive to lcoal anesthetics

211
Q

Absolute CI to spinal

A

pt refusal
infxn at site
severe coagulation problem
inc ICP due to mass lesion

212
Q

presenting sign of subcutaneous emphysema after abd insufflation

A

extensive hypercarbia and crepitus
-no assoc w/ high inspiratory pressures

213
Q

RF for subq emphysema

A

longer opeartive times
greater number of prots
higher insfflation pressures
retroperitoneal laparoscopy
lower BMI
older age

214
Q

post spinal anesthesia, have discomfort aching pian in lower back that radiates down leg, no longer neuro sym
dx and tx?

A

transient neurologic symptoms (exact not known, possibly trauma to local structures, drug tox, and n root irritation)
NSAIDs -> opioids 2nd line

215
Q

SE of loop diuretics

A

hypoNa
hypoK
hypoMg
hypoCa
sulfonamide hypersentivity (abx)
ototoxicity

216
Q

eplerenone MOA

A

K sparing diuretics

217
Q

Furosemide MOA

A

inhibitor of Na-K-2Cl cotransporter in thick ascending loop of Henle

218
Q

recurrent laryngeal n monitoring during neck surgery

A

specialized ETT -> doesn’t need a neuromonitoring tech
-doesn’t require TIVA
-can’t use muscle relaxants
-no definitive decrease in injury been shown

219
Q

which NMB has same metabolism similar to succ

A

mivacurium

220
Q

if you give roc first then succ, any changes to succ dosing?

A

succ dose must be increased

221
Q

hypoP and Hg dissociation curve

A

L ward shift (dec 2-3 biphosphoglycerate)

222
Q

Ca and phosphate repletion

A

replenishing phos can cause hypoCa b/c P binds Ca -> despositio in tissues

223
Q

Phos and granulocytic phagocytosis and chemotaxis

A

severe low Phos diminished ability of immune system to have energy to move it’s cells -> inc infxn risk

224
Q

how does ventilation affect phos?

A

hypervent -> resp alkalosis -> inc pH -> activates phosphofructokinase stimulating glycolysis and consuming ATP
(makes sense, breaking too fast, need energy to keep it up)

225
Q

why is hyperglycemia assoc w/ worse outcomes w/ cerebral ischemia

A

worsens lactic acidosis (anaerobic resp w/ hyperglycemia -> inc production of lactate)
inc cortisol resp w/ hyperglycemia -> stress resp worsening ischemia
enhanced glu-Na exchnage

226
Q

Part of primary pattern generator for neural initiation of phasic respiration

A

subparabrachial nucleus
parabrachial nucleus in the pons
ventrolateral medullary complex
rostral and caudal ventral respiratory groups in the medulla
-cause rhythmic ventilation through reciprocal inhibition and modulate according to chemoreceptors, wakefulness and anesthesia

227
Q

why is digoxin toxicity occur in hypoK

A

binds at the Na, K ATPase jate the same site as K -> when K is low, less competition and toxicity potentiated

228
Q

dromotropic

A

affects conduction speed

229
Q

mixed venous O2 in sepssis

A

high due to increase dcardiac output

230
Q

what type of shock:
hypotension, high cardiac ouptu, low SVR

A

septic

231
Q

what ppx helps succ myalgias

A

NSAIDs

232
Q

fects w/ succ

A

pretx w/ anticholinergics

233
Q

atracurium metabolism

A

ester hydrolysis and hofmann elimination (same as cisatracurium)

234
Q

which inhaled anesthetics produced fluoride

A

des iso and sevo in liver via cytochorome p450 2E1
-highest in sevo***, lowest in des

235
Q

Bezold-Jarish reflex

A

reduced preload sense low ventricular pressure -> inc vagal tone -> dec HR

236
Q

MC assoc w/ severe bradycardia after spinal (HR < 40)

A

male gender
baseline bradycardia (,60bpm)

237
Q

Assoc w/ bradycardia after spinal (HR <50)

A

male
baseline bradycardia
younger age
nonemergent surgery
beta-blockers
longer operative duration

238
Q

Lithium and surgery

A

d/c 24 hours prior
prolonged NMB (reduces release of ACh)
lower anesthetic requirements (reduced release of NE, epi, DA)
-hypoNa and NSAID cause lower excretion -> inc risk of toxicity

239
Q

nitrous oxide and cobalamin

A

cobalamin = B12
-B12 cofactor for homocysteine to methionine -> methionine involved in the synthesis of DNA, RNA
-in adults nitrous oxide -> megaloblastic anemia
-anemia rare in healthy pts, but in seriously ill pts -> bone marrow changes w/i 2-6 hours

240
Q

HypoNa and MAC

A

decreased MAC b/c hypoNa causes CNS depression

241
Q

HypoNa and MAC

A

decreascocaine and MACed MAC b/c hypoNa causes CNS depression

242
Q

HypoNa and MAC

A

decreased MAC b/c hypoNa causes CNS depression

243
Q

HypoNa and MAC

A

decreascocaine and MAC acute and chroniced MAC b/c hypoNa causes CNS depression

244
Q

acidosis and MAC

A

decreased MAC
(makes sense, hypovent assoc a/ acidosis -> likely neuro off, dec MAC_

245
Q

melanocortin-1 receptor gene MAC

A

inc MAC
seen in pts w/ red hair

246
Q

Mg and anesthetic requirements

A

TIVA + Mg = less anesthesia
Mg + gas -> incMAC req

247
Q

RF for transient neurological symptoms

A

lithotomy position
lidocaine use
adding phenyleprhine to 0.5% tetracaine
outpt procedures

248
Q

phenytoin and NMB

A

acute: longer NMB
chronic: reduced blockade

249
Q

carbamazepine and NMB

A

reduced blockade

250
Q

what metabolite of morphine accumultes in renal dysfxn and causes rep depression

A

morphine-6-glucuronide
3 looks like a brain, 6 is a g upside down -> assoc w/ lungs

251
Q

morphine metabolite that accumulates and causes neuroexcitation

A

morphine-3-glucuronide
3 looks like a brain, 6 is a g upside down -> assoc w/ lungs

252
Q

Oxymorphone

A

metabolite of oxycodone
-metabolized by cytochrome P450 2D6
8x more potent

253
Q

termination of succ

A

diffusion away from NMJ
degraded by pseudocholinesterase in blood away from NMJ

254
Q

HyperCa and EKG

A

prolonged PR interval
shorted QT interval
-Ca extends depolarization when you think about Ca acting w/i Na current, but high Ca leads to contraction of heart -> shorter QT

255
Q

HyperK EKG

A

peaked T waves
prolonged PR interval
wide QRS

256
Q

HypoCa EKG

A

shortened PR interval
prolonged QT

257
Q

HypoCa EKG

A

shortened PR interval
prolonged QT

258
Q

Where to look for U waves

A

V4-6 -> vectors monitoring thicker parts of the heart
(hypoK and hypoMg)

259
Q

what causes PR prolongation

A

hyPeR
hyPeR-kalemia, calcemia, magnesemia leads to PRolongation of the PR interval
-and opposite happens to QT interval

260
Q

When should you monitor/check labs for someone on enoxaparin

A

morbid obesity (BMI >40)
altered GI anatomy (post gastric bypass)
possible drug-drug interaction
-concern over drug adherence

lab: anti-factor Xa activity or drug plasma concentration to assess for proper absorption

261
Q

What fluid should you be careful of in acute liver failure?

A

Lactate b/c metabolized in liver to bicarb

262
Q

Inhaled anesthetics effect on resp system

A

dec TV
blunt resp to hypercarbia and hypoxia
inc RR
bronchodilation
dec FRC

263
Q

why does nitrous have a faster onset than des despite blood:gas coefficients

A

concentration effect

264
Q

oil:gas coefficient

A

lipophilicity, and related to anesthetic potency
iso has the highest

265
Q

what is fent metabolized by

A

CYP3A4

266
Q

if a pt almost OD’d on coedine what other meds would be a problem?

A

oxycodone -> if ultrametabolizer will create more oxymorphone (results of metabolism by CYP2D6) -> more potent opioid than oxycodone
tramadol -> prodrug like codeine metabolized active by CYP2D6

267
Q

Nitrous oxide MOA

A

noncompetitive inhibition of NMDA receptors

268
Q

Effects of nitrous oxide on body

A

cardiac: may cause myocardial depression, but stim symp NS -> inc SVR and CO
resp: dec TV but inc RR
inc CBF and inc ICP

269
Q

Sevo MOA

A

enhancement of GABA on GABA-A receptor

270
Q

ACE inhibitors effects

A

prevent conversion of ATI to ATII
-dec in vasoconstriction -> dec BP
-dec in aldo -> red water and Na absorption, limit K wasting -=> hyper K
-dilation of renal arterioles
-inc arachidonic acid metabolites -> inc vasodilation -> dec BP
***hyperK inc in renal dx, DM, or K sparing diuretic use w/

271
Q

teratogenic effect of ACEinh on pregnant ladies

A

renal malformations

272
Q

When do you commonly see Bezold-Jarisch reflex

A

post-spinal (otherwise symp usually outshine)
-dec preload -> bradycardia

273
Q

which is which

A
274
Q

Confidence interval equation

A

sample statistic +/- confidence factor *(standard error)
standard error = standard deviation / (square root of sample size)

275
Q

how to decrease confidence interval

A

sample statistic +/- confidence factor *(standard error)
standard error = standard deviation / (square root of sample size)
-lower confidence interval
-inc sample size
-dec standard deviation
-dec variation of the sample

276
Q

GI changes in full term pregnant women

A

-if NOT laboring -> gastric emptying is NORMAL
-progesterone dec LES tone
-cephalad movement of esophagus -> dec competence of LES, inc risk of regurge, aspiration
-inc gastrin -> more acidic gastric fluids

277
Q

epidurals and GI pregnant women

A

epidurals w/ opioids will delay gastric emptying -> preserved if only local anesthetic

278
Q

what to give pregnant women pre GA

A

prior to induction, metochlopramide and antacid

279
Q

When does aspiration risk inc in laboring pts

A

after 20 weeks
-gravid uterus -> displacement
-hormonal changes

280
Q

Epi dosing for anaphylaxis

A

Epi 1 mcg/kg
-max dose is code dose of 0.01 mg/kg
-adult dosing typically 50-100 mcg IV

281
Q

Tx for anaphylaxis

A

-reduce contact w/ offending agent
-d/c all meds that could cause anaphylaxis
-intubate if needed
-maintain airway and 100% O2
-IVF 25 cc/kg (up to 50)
-Epi 1 mcg/kg
-d/c all anesthetic agents

282
Q

if you have allergies to tropic fruits or chestnuts what are you at high risk of being allergic to?

A

latex

283
Q

Anaphylaxis 4 grades

A

I: cutaneous-mucous signs
II: mild cutaneous-mucous features, may be assoc w/ cardiovascular and/or resp signs
III: cardiovascular collapse or bronchospasm
IV: cardiac arrest

284
Q

if concerned about an anaphylactic reaction what lab do ou send?

A

tryptase level
-peak 15-60 minutes then decline
-if increased, suggestive of mast cell activation
-get a 2nd sample 24 hours later to compare to baseline

285
Q

Equation for total arterial oxygen content in blood

A

O2 content = (1.34 x Hg x O2 saturation (in decimal)) + (0.0031 x PaO2)

286
Q

ERAS goal-directed fluild management

A

-as pt and procedure complexity inc -> more intense modalities to monitor fluid responsiveness
-fluid management when analyzed solo as part of an ERAS protocol does not have any actual impact, but we still do it anyway
-fluid management ALONE outside of ERAS protocol has been shown to decrease ileus and length of hospital stay

287
Q

cause of adrenal insuff in critical illness in ICU

A

functional adrenal insuff
-b/c chronic stress, system depleted in the HPA axis and adrenal glands
-def: no obvious structural defects in HPA

288
Q

Exogenous glucocoritcoids is causes what type of adrenal insuff

A

tertiary adrenal insuff

289
Q

How long after taper of steroids does it take for the adrenals to fully recover

A

6-12months

290
Q

What medication should NOT be given in thyroid storm

A

Salicylates = Aspirin
-b/c competes w/ T3 and T4 for thryoid-binding globulin -> inc circulating free hormones

291
Q

Tx of thyroid storm

A

-Beta blockers for heart
-coiling blankets, acetaminophen fo rfevers
-PTU for hormonal control (prevents peripheral conversion unlike methimazole, so PTU > methimazole)
-dexamethasone (relative adrenal insuff 2/2 extreme hypermetabolic state)

292
Q

Bronchopulm dysplasia

A

most likely to occur in neonates < 32 weeks
-RF: O2 toxicity, sepsis, inflammation, ifxn, barotrauma
-long-term consequence of respiratory distress syndrome
-chronic dx of airways and lung parenchyma

293
Q

anesthesia considerations of bronchopulm dysplasia

A

desat fast (lack of reserve and poor lung compliance)
airway reactivity
hyperinflation

294
Q

resp distress syndrome and bronchopulm dysplasia

A

RDS –> bronchopulm dysplasia
-b/c when you have resp distress syndrome (implies shorter = syndrome), iif not fixed, will chronically lead to bronchopulm dysplasia (dysplasia = longer Duration)

295
Q

Expiration in emphysema

A

alveolar walls and small distal airways are destroyed -> when intrathroacic pressure positive during expiration, can’t stay open as long as normal lungs -> premature closure -> air trapping and hyperinflation
-occurs in smallest airways and thinnest

296
Q

expiration in dpt and non-dpt lung regions

A

-dpt lungs will have small airway closure before non-dpt b/c greater pleural pressure in dpt-lung regions (positive P during nexpiration)
-dpt lung regions closer to bottom, non-dpt at top of lungs

297
Q

resistance to airflow and radius

A

radius to the 4th power
-so as radius inc, R decreases to 4th power

298
Q

peak pressure and plateua pressure and statis anc dyanmic compliance

A

static compliance -> measured during zero airflow = plateau pressure (has to do w/ volume of lung and lung compliance, less volume of lung ventilated, dec lung compliance, dec static compliance)
dynamic compliance = peak pressure-plateua pressure (resistance in airways)
-inc in peak pressure = decreased dynamic compliance

299
Q

Dec static compliance caused by

A

-dec volume of lung ventilated, reduced chest wall compliance
-requires greater plateau pressures to maintain similar lung volumes
PTX
pulm edema
PNA
pneumonectomy
endobronchial intubation
abd insufflation
abd distention
thoracic deformities

300
Q

Endobronchial intubation static and dyanmic compliance

A

dec static compliance (inc plateau pressure)
no change in dynamic compliance (b/c no inc airway resistance)

301
Q

PNA static and dynamic compliance

A

dec lung for ventilation, dec lung volume for a given pressure -> dec statis compliance
inflammation and ractivity in small airways -> inc bronchiolar resistasnce -> dec dynamic compliance

302
Q

Pulm embolism on static and dyanmic compliance

A

does not affect gas flow -> no change in either

303
Q

Dynamic compliance determined by

A

resistance to airflow through small airways of the lung

304
Q

Static compliance determined by

A

ability of lung to expand inn setting of static positive airway pressure admin

305
Q

How to determine dyanmic compliance

A

difference b/w peak pressure and plateu pressure

306
Q

Static compliance estimated

A

diff b/w plateau pressure and PEEP

307
Q

HypoCa QT

A

prolonged QT
-less Ca in SR -> slows Ca-activated K current -> slows repolarization and lengths QT

308
Q

Tx for hyperCa due to hyperparathyroid intraop

A

hydrationn w/ Normal saline
diuresis w/ furosemide to dec Ca levels to < 14

309
Q

Eaton-Lambert Syndrome sensitivity to succ and NDNMB

A

INCREASED to both

310
Q

hypokalemic periodic paralysis and NMB

A

link b/w malignant hyperthermia and hypoK PP -> avoid succ
inc sensitivty to NDNMB

311
Q

Digoxin ionotropic, dromotropic, chronotropic

A

POSTIVE ionotrope (inc contractility)
NEGATIVE dromotropic (conduction speed), chronotropic (HR)

312
Q

Nitrous O2 and ETT and pulm a catheters

A

at 75% a cuff can double or triple on volume -> pressure on tracheal mucosa
-in pullm artery cathetrer can double w/i 10 minutes

In Training Exam TL (11 decks)

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