Keywords/TrueLearn Flashcards

1
Q

Acute vs Chronic Phenytoin on NDMB

A

Acute: prolonged
Chronic: resistance and shortened duration

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2
Q

Gentamicin + NDMB (why)

A

Interacts w/ Ca -> Disrupts ACh vesicle release

Depresses receptor sensitivity to ACh

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3
Q

NSAIDs on RBF (why)

A

Decreased - inhibit afferent R.A. dilation by PGs

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4
Q

Acoustic impedence equation

Which variable is more important?

Point of ultrasound gel?

A

Impedence (Z) = (medium density) x (propagation speed of sound)

Density is more important (propagation speed is similar in all body mediums)

Gel = reduce DENSITY between probe and skin

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5
Q

Ketamine emergence delirium: tx?

A

Barbs, benzos, propofol

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6
Q

Systemic local absorption: locations from most to least (8)

A
Tracheal
Intercostal
Caudal
Epidural
Brachial Plexus
Spinal
Femoral/Sciatic
SubQ
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7
Q

Leads for atrial dysrhythmias

Leads for myocardial ischemia

A

Atria: II > V1 (biggest P waves)
Ischemia: V5 alone (but II + V4 if can do 2 leads is best for both)

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8
Q

Bainbridge reflex

A

Atrial stretch -> inhibited vagus -> tachycardia

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9
Q

Hering-Breuer reflex

A

Lung stretch (PPV/CPAP) -> inhibited inspiration

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10
Q

4 causes of A-A instability

A

Downs
RA
Achondroplasia
Trauma

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11
Q

MC cause of mortality from blood transfusion

Pathophysiology?

A

TRALI (ALI w/in 6h of transfusion) - 5-10% mortality

Anti-leukocyte donor ABs attack pulm leukocytes

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12
Q

Does succ have increased aspiration risk? Why or why not?

A

NO - increased LES tone > increased intragastric tone

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13
Q

Spironolactone: electrolyte abnormalities?

A

Hyper-K, hypo-Na

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14
Q

Sensitivity and Specificity equations

A
Sensitivity = TP/TP+FN
Specificity = TN/TN + FP
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15
Q

How to monitor lovenox effect via lab?

A

Factor Xa activity

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16
Q

Signs of propofol infusion syndrome

A
Lactic acidosis
Cardiac failure
Rhabdo
Renal failure
Hyperkalemia
Hyper-TG
Hepatomegaly
Pancreatitis
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17
Q

Propofol + Lidocaine mixture –> ??

How to best avoid?

A

Small lipid droplets w/ possibility for embolic risk

20mg per 200mg propofol, and do it right before using

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18
Q

Chronic opioid use on endocrine?

A
  • Decreased HPA axis (low cortisol) and HPG axis (low testosterone/estrogen)
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19
Q

Ester vs amide local anesthetics: metabolism location

A

Ester: plasma cholinesterase
Amide: liver

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20
Q

Variable bypass vs Desflurane vaporizers: use at high altitude

A

Variable bypass: mostly compensates for decreased Atm
Des: constant CONCENTRATION but no change in partial pressure, therefore must increase percentage according to how low the Atm is

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21
Q

Hypoparathyroidism tx

A

Vit D and Ca++ supplementation 1st

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22
Q

How do NSAIDs cause renal dysfunction

A

Impaired vasodilation of AFFerent arterioles -> decreased RBF

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23
Q

Glucose/insulin management peri-op (Glc goal, IV vs SQ insulin, etc)

A
IV Insulin (short-acting, titratable) in acute situation or sx
Goal glc < 180 (stricter w/ CV or neuro sx)
SQ: variable peripheral vasodilation in sx = no consistent uptake -- OK in normal pre-op or pacu patient
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24
Q

Electrolyte/channel flow in phase 0-4 of cardiac myocyte AP

A

0: V-gated Na+, K outflow decreases
1: Na close, K open (transient outward)
2: Slow L-type Ca channels vs slow delayed K channels
3: Ca close, rapid K rectifier channels open
4: Na/K ATPase pumps Na out and K in, K gradient balance causes resting potential

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25
Q

Side effects of closed circuit ventilation

A
  • Increased PONV via re-breathing of acetone or CO

- Risk of hypoxia if enough O2 not supplied

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26
Q
  • Effect of temperature on CBF

- Effect of pO2 on CBF

A
  • Each 1 degree C drop in temp = 6% drop in CBF

- CBF maintained despite pO2 until <50, then CBF rises precipitously

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27
Q

Effect of myasthenia gravis on NDMBs and Succ

A

MG: sensitive to NDMBs, resistant to succ but not dangerous

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28
Q

Effect of prolonged NDMBs on Succ use

A

Prolonged NDMBs -> increased NAChRs -> Succ dangerous

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29
Q

Effect of pyridostigmine and chronic steroids on muscle relaxation

A

Both cause resistance, therefore must monitor twitches

Pyridostigmine –> more ACh around to combat the NDMB
Steroids –> remember that NDMBs are steroidal, so maybe some increased resistance to steroids over time if chronic

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30
Q

Lab abnormalities of excess mannitol (before diuresis)

A
  • Hypervolemic dilutional hyponatremia
  • Dilutional hypo-HCO3 = metabolic acidosis
  • Hyperkalemia (via solvent drag and leak from increased intracellular K+ stores due to loss of H20)
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31
Q

Lab abnormalities of excess mannitol (after diuresis)

A

Hypovolemic hypernatremia, hypokalemia, alkalosis (loss of Na and hence K and H+ in the urine)

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32
Q

6 indications for FFP transfusion

A
  • MTP dilutional coagulopathy
  • Factor deficiency(s)
  • AT3 deficiency
  • TTP
  • Hepatic insufficiency coagulopathy
  • Warfarin reversal
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33
Q

Why is FFP frozen for storage?

A

Factors V and VIII will degrade above 4 degrees C

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34
Q

Meperidine in renal dysfunction

A

Normeperidine -> seizures

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35
Q

MAC aware and MAC-BAR levels

A

MAC aware = 0.3-0.5 MAC (loss of recall, voluntary reflexes)

MAC BAR = 1.7-2 MAC

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36
Q

Side effects of magnesium toxicity

A
  • Weakness -> loss of DTRs -> flaccid paralysis and respiratory arrest (reduced acetylcholine/catecholamine release)
  • EKG changes (long PR and QRS) -> nodal block -> cardiac arrest
  • Sedation (loss of neurotransmitter release)
  • Warm/flushed (hypotension, vasodilation)
  • N/V (hypotension, etc)
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37
Q

Cause of magnesium side effects

A

Inhibition of Na/K - ATPase

  • Loss of release of neurotransmitters -> weakness, hypotension, sedation
  • Direct inhibition of vasoconstriction and vasoconstrictors
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38
Q

Effects of neuraxial on PFTs, cough, forced exhale, etc

A
  • Greatly reduced cough and forced exhalation pressure due to abdominal muscle weakness
  • Small reduction in VC and FEV1
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39
Q

Reason for dyspnea in neuraxial anesthesia (assuming no high spinal)

A

Loss of proprioception to chest wall and abdominal muscles, thus loss of feeling of breathing (psychiatric)

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40
Q

Reasons to avoid cephalosporins with prior penicillin reaction

A
  • Penicillin reaction < 10 years ago AND/OR…
  • IgE reaction (bronchospasm, angioedema, anaphylaxis)
  • Severe non-IgE (SJS, TEN, organ failure/damage, DRESS)
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41
Q

Gas law that explains why high altitude results in under-dosing of volatile

A

Dalton’s law:

P(x) = [ P(b) - P(h2o) ] * F

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42
Q

Gas law that explains why hypercarbia results in hypoxia

A

Alveolar gas equation:

PaO2 = PIO2 - (PaCO2 / R) + correction factor

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43
Q

Gas law that explains why increasing the volume percentage of a volatile increases the speed of induction

A

Henry’s law:
C = P x solubility
Increased partial pressure (P) -> increased concentration in the blood (and hence the brain)

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44
Q

Gas law that explains why V1/T1 = V2/T2

A

Charles Law (King Charles is under constant PRESSURE)

45
Q

Gas law that explains why P1V1 = P2V2

A

Boyles Law (Water boyles at constant TEMPERATURE)

46
Q

Gas law that explains why P1/T1 = P2/T2

A

Gay-Lussac Law

47
Q

Describe standard error of the mean

Equation?

A

With larger populations, different groups of samplings would have different means. SEM is the standard deviation of all those sample means over all possible samples drawn from that population

SEM = SD / square root of n
Example: n = 100, SD = 10 –> SEM = 10/10 = 1

48
Q

Result of giving succ after neostigmine

Why?

Same as with pyridostigmine or edrophonium?

A

Prolonged phase 1 duration

Unsure exactly why, but possibly due to decreased plasma cholinesterase activity and/or direct interaction with succ

Not nearly as much, not sure why

49
Q

Possible side effects of bicarb administration

A
  • Conversion to CO2 -> worsened acidosis if not exhaled
  • CO2 into brain -> cerebral vasodilation, increased ICP/CBF
  • Binding of Ca –> transient hypocalcemia -> impaired CV function
  • Alkalosis -> K driven intracellularly -> hypo-K
  • Loss of acidosis -> loss of peripheral/pulmonary vasoconstriction -> hypotension
50
Q

When should FFP not be used? (4)

A
  • Vitamin K deficiency that can be corrected w/ vit K
  • Primary volume expander
  • To replace a factor if the specific recomb. factor is avail.
  • INR < 1.8 w/o bleeding
51
Q

Factors that increase closing capacity

A

ACLS-S

  • Age
  • COPD/Chronic bronchitis
  • Left ventricular failure (increased pulm blood volume)
  • Smoking
  • Surgery
52
Q

Factors that decrease FRC

A

PANGOS

  • Pregnancy
  • Ascites
  • Neonate
  • General anesthesia
  • Obesity
  • Supine
53
Q

MetHb treatment

G6PD?

A

Methylene blue (Met = Met)

Ascorbic acid (met blue causes hemolysis)

54
Q

COHb treatments

A

B12, sodium thiosulfate

55
Q

Cause of bradycardia after succ

A

Activation of mAChR’s at SA node (more in kids b/c higher vagal tone)

56
Q

When would you expect phase 2 block w/ succ

When would you NOT?

A
  • Prolonged continuous administration
  • Very large dose
  • NOT: after 2 regular doses spread apart
57
Q

How to adjust neo/glyco drugs in CRF?

A

No adjustment - drug excretions are prolonged but in equal doses there are no significant toxicities after 1 dose - maximal doses still apply as normal

58
Q

Normal P50 of oxyHb

A

27

59
Q

Effect of hypophosphatemia on SaO2

When is this likely to be seen

A

Decreased (low 2,3-DPG maybe?)

Critical care patients (maybe refeeding?)

60
Q

Is doxorubicin toxicity limited to cardiotoxicity?

A

NO - affects just about every organ system and is cumulative

61
Q

Effects of benzos and opioids on inhalational induction

A

Benzos - improved induction

Opioids - worsened induction (apnea risk)

62
Q

Low dose vs high dose ketamine - receptor interaction

A
Low dose (<50 mg) - NMDA non-competitive inhibitor in midbrain
High dose (1-2 mg/kg) - opioid receptors (can be altered by naloxone)
63
Q

Explain alfentanil CSHT curve

A
  • Long to start (<1-2 hours) b/c low plasma clearance

- Low plateau after 2 hours

64
Q

Alfentanil metabolism

A

Patient-specific hepatic CYP clearance

65
Q

Metabolism of different benzos (w/ significance)

A

Lorazepam, oxaz, temaz (LOT): glucuronidation (no active metabolites, less susceptible to CYP-altering agents)

Midaz, Diaz: oxidation -> active metabolites

66
Q

Definitions of data types:

  • Nominal
  • Ordinal
  • Interval

Test types for each

A

Nominal: distinct result categories
Ordinal: A range of data where difference between each is variable (pain score, mild/mod/sev, etc)
Interval: numerical structured range of data (1,2,3)

Nominal = chi-squared / McNemar / logistic regression
Interval = t-test / ANOVA
Ordinal = chi-squared / Wilcoxon-Mann-Whitney / Friedman / Kruskal-Wallis
67
Q

Why does hypercalcemia cause polyuria?

Initial treatment?

A

1) calcium salts damage renal parenchyma
2) extra calcium inhibits ADH activity

Initial tx = SALINE INFUSION

68
Q

Can opioids be used as the primary sedative/hypnotic for general anesthesia? Why or why not?

A

NO - ceiling effect of MAC, cannot reach 1 MAC and obviously have significant side effects at high doses

69
Q

How does sepsis affect SvO2?

A

Sepsis can cause EITHER increased OR decreased SvO2

  • Increased: high C.O., peripheral blood shunting
  • Decreased: increased O2 consumption from sick tissue
70
Q

Effect of C.O., cyanide, and MetHb on SvO2

A

INCREASED – decreased O2 utilization by tissues

71
Q

Anterior vs Posterior ischemic optic neuropathy - MC cause

A

AION: cardiac sx
PION: spine sx (prone)

72
Q

Airway closure vs emptying in lung locations during forced exhalation

A

Closure: base (thus can’t empty)
Emptying: apex (b/c airways still open)

73
Q

Esophageal detector device: ETT placement confirmation in code (no perfusion) state

A

Squeeze bulb, will not get air return if in esophagus b/c walls will collapse

74
Q

Ideal wait time after DES

When can 180 days after DES be ignored?

A

365 days

Emergency surgery (risk of no sx > risk of thrombosis)

75
Q

See varying side effects of barbiturates

A

Flagged in TL (test 21)

76
Q

Highest to lowest LA absorption by block

A
ICEBaLLSS
Intercostal
Caudal
Epidural
Brachial plexus
Lower limb
SubQ
77
Q

Type 2 DM:

  • Insulin resistance vs deficiency
  • Is insulin deficiency reversible?
  • Degree of hyper-glc vs degree of deficiency
A
  • Resistant –> loss of beta cell mass (deficient)(burnout)
  • Reversible PARTIALLY w/ improved glc
  • More severe high-glc -> more severe deficiency
78
Q

Vasopressin levels in septic shock

After surgery, how long to vasopressin levels stay elevated for?

A

Initial burst –> depletion

A few days

79
Q

Bezold-Jarisch reflex

What else might you see in this situation?

A

Depleted preload in ventricle –> reflexive bradycardia and decreased inotropy –> hypotension

Carotid baroreceptor -> tachycardia and increased inotropy (is generally slower to kick in when drop in preload is very quick)

80
Q

How do PPIs and H2 blockers decrease gastric volume AND increase gastric pH?

A

Decrease SECRETION of acid, thus stomach empties over time and becomes more alkalotic

Does not directly stimulate gastric emptying

81
Q

Garlic as supplement: use?

Concern?

A

Prevent atherosclerosis (lower BP/TGs/thrombus/plt agg)

Irreversible platelet inhibition (d/c 7d b4 surgery)

82
Q

Ginkgo as supplement: uses?

Concern?

A

Several (vasoregulation, antioxidant, modulate neurotransmitters, alter PAF)

Inhibit platelet activating factor (d/c 36h b4 surgery)

83
Q

Ginsing as supplement: uses?

Concerns?

A

Several

  • Inhibit platelet aggregation and prolong PT/PTT in vitro
  • Hypoglycemia (lower post-prandial blood glucose)
  • D/c at least 1d (prefer 7d for platelet inhibition)
84
Q

Saw palmetto: use?

Concern?

A

BPH

Excessive bleeding (unknown cause, no rec’s)

85
Q

Learn about digoxin interactions

A

Flagged test 21

86
Q

QT interval in hypo vs hypercalcemia?

A

Hypo: prolonged QT
- Less Ca-mediated K-channel opening causes
prolonged repolarization
Hyper: shortened QT

87
Q

Learn all the EKG changes w/ electolyte anomalies

A

88
Q

Recommended IO locations

A
  • Proximal humerus (3rd best)
  • Proximal (best) and distal (2nd best) (not mid - variable bone thickness) tibia
  • Manubrium (uncommon now)
89
Q

Why is IO better than central line in emergency? (4)

A
  • Higher 1st success rate
  • Lower infection rate
  • Faster than central line placement
  • Equivalent for fluid administration
90
Q

Is fat/marrow embolism common in IO placement?

A

Yes (40-90%) - but no evidence of PaO2 changes or morbidity

91
Q

Look up Bayes theorum

A

92
Q

What is in cryo?

A
  • VIII:C
  • VIII:vWF
  • Fibrinogen
  • XIII
  • Fibronectin
93
Q

MetHb -> change in SvO2?

A

Decreased: changed Hb Fe causes impaired O2 binding –> functional anemia and decreased SaO2 –> decreased SvO2

94
Q

Sepsis -> change in SvO2?

A

Increased: microvascular shunting in acidotic tissue leads to decreased O2 utilization + increased cardiac output from decreased SVR, etc

95
Q

CO poisoning -> change in SvO2?

A

Increased: decreased O2 utilization

96
Q

Asthma + nasal polyps…think what?

A

ASA/NSAID-induced asthma

97
Q

Succ in asthma?

A

Succ IS associated w/ histamine release BUT has not been shown to cause bronchoconstriction

98
Q

Beta-1 selective beta blockers

A

BEAM

  • Bisoprolol
  • Esmolol
  • Atenolol
  • Metoprolol
99
Q

How to calculate total AMOUNT of dissolved O2…

How to calculate total PERCENTAGE of O2 that is dissolved…

A

Amount = 0.003 * PaO2

% = Amount / CaO2
CaO2 = (Hb * 1.36 * SaO2) + (0.003 * PaO2)
100
Q

Cyanide poisoning -> change in O2 delivery?

Dilutional anemia -> change in O2 delivery?

A

Increased delivery to compensate for decreased usage ability

Decreased delivery due to decreased Hb molecules per second (body compensates by increasing C.O.)

101
Q

TEG values/meanings…

  • R
  • K
  • Alpha angle
  • Max amplitude (MA)
  • Teardrop shape of curve?
A

R = time to start clotting (nml 5-10 min) = coag factors or heparin admin (tx = FFP)

K = time from initial clot formation to 20mm amplitude of curve (1-3 min) = fibrinogen (tx = cryo)

Alpha angle = slope/speed of clot formation (nml = 50-70 degrees) = fibrinogen (tx = cryo)

MA = maximal width of clot strength (nml = 50-70 nm) = platelets

Teardrop shape = too fast fibrinolysis = anti-fibrinolytics (TXA, etc)
- Normal fibrinolysis by 30 min = 0-8%

102
Q

Morphine epidural vs addition of clonidine

  • Length
  • Strength
  • Side effects

What about adding it to fentanyl?

A
Longer, stronger (clonidine longer than morphine)
Less PONV (less morphine needed, less catecholamine release)
Less morphine-related pruritis, etc 2/2 less needed
More hypotension (resolved w/ fluid)

NOT added benefit w/ fentanyl

103
Q

Why is alfentanil so short-onset?

A

Lowest pKa (6.5) = very high non-ionized fraction at physiologic pH (89%) – so very fast onset despite only moderate lipid solubility (sufenta > fent > alfent > morphine)

104
Q

Ankylosing spondylitis…mask, intubation, neuraxial

A
Difficult mask (TMJ)
Difficult intub (c-spine)
Difficult neuraxial + increased hematoma risk from multiple attempts
105
Q

Neuraxial and Lovenox rules:

  • How long after last dose
  • How long to restart after doing
  • How to restart while catheter is in
  • How long to restart after catheter removal
A

Therapeutic - 24h (before doing AND to restart)
Prophylactic - 12h (before doing AND to restart)
While catheter is in - 1x/day prophylactic 12h later
4h to restart after removal of catheter

106
Q

Blood transfusion + abdominal/chest/flank/back pain, hypotension, bronchospasm, hematuria, shock, pulmonary edema, renal failure, shock

Tx?

A

Acute hemolytic transfusion reaction (ABO)

  • Stop transfusion
  • Maintain UOP (fluids, diuretics) w/ possible alkalinization to prevent hemoglobin deposits
  • Support BP
  • Bronchodilators as needed
  • Check for hematuria
107
Q

Blood transfusion 24h ago –> fever, hemolytic anemia, jaundice

Cause?

Tx?

A

Delayed (2nd exposure) hemolytic transfusion reaction

Non-major RBC antigens (Kell, Kidd, Duffy, etc)

Usually nothing, may need some support if very anemic or renal failure

108
Q

2 causes of febrile non-hemolytic transfusion reactions

Tx?

Prevention?

A
  • Cytokines from WBCs
  • Recipient antibodies against donor WBCs or platelets

Tx = tylenol/benadryl

Prevention = leukoreduction

109
Q

GVHD - cause

A

Donor WBCs against immunocompromised host who cannot fight back