Random3 Flashcards

1
Q

what two classes of meds SHORTEN NDMB

A
anticonvulsants (phenytoin, carbamazepine)
cholinesterase inhibitors (neostigmine)
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2
Q

which beta blockers are non-specific?

A

after m

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3
Q

prophylaxis for dentist for heart patients

A

only consider procedures with gingival, bronch, skin manipulation

heart transpant with residual valvular abnormalities
previous IE
prosthetic valves

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4
Q

aspirin overdose symptoms

A

initially nonspecific - n/v/tinnitus

at first, hyperventilate -> stimulates medullary respiratory area. (resp alk) THEN metab acid

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5
Q

metabolic effects of respiratory alkalosis

A

hypoCa (H ions taken off albumin, which now sucks up Ca -> tingling), hypoK, hypophos)

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6
Q

Fick equation

A

SvO2 = SaO2 - [VO2 / (CO x Hgb x 1.36)]

VO2 = total body oxygen consumption

SO things that decrease SvO2

  • MI = less CO
  • decreased arterial oxygen saturation
  • decrease o2 carrying capacity
  • increased consumption (pain, shivering, hyperthermia)
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7
Q

what does the recurrent laryngeal nerve do?

A

abducts and adducts vocal cords. Provides motor function to all muscles of larynx EXCEPT cricothyroid. Sensation to larynx BELOW glottis. Comes from Vagus nerve

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8
Q

what does the superior laryngeal nerve, internal brnach do?

A

sensory above glottis

SIME = sensory internal, motor external

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9
Q

what does SLN, external branch do?

A

cricothyroid muscle, adducts VC

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10
Q

when is Succs contraindicated and why?

A

in patients >24 hours from burn, trauma, neuromuscular disorders, prolonged immobility 2/2 upregulation of extrajunctional nicotinic ACh receptors. Can raise K by 3.5 as opposed to 0.5 normally

also usually avoided in peds population

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11
Q

signs and symptoms of nitroprusside toxicity

A

AGMA, CNS depression, arrythmias, elevated mixed venous oxygenation

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12
Q

average stroke volume?

A

60-100ml/beat

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13
Q

how do we make the diagnosis of carbon monoxide poisoning?

A

co-oximetry (VBG/ABG)
elevated levels of COHgb (>15)

Tx: high FiO2
hyperbaric chamber only IF COhgb >30 or severe symptoms (obtunded, delirium, bradyarrythmias)

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14
Q

Fa/Fi - soluble agents - decreased CO or increased MV

A

both cause faster induction and rise of FA/FI

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15
Q

does HCO3- buffer H+?

A

NO! But it facilitates transport of H+ intracellularly where intracellular processes (proteins, phosphates, hgb) do actual buffering

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16
Q

why do liver patients have thrombocytopenia?

A

splenic sequestration and reduced thrombopoetin production by liver

platelet count can informally be used for progression of portal hypertension

17
Q

why are factor 8 and vwf increased in liver disease?

A

produced in endothelium, NOT liver

18
Q

why don’t liver patients spontaneously bleed?

A

increase in BOTH pro AND anticoagulant factors

19
Q

low fibrinogen in a liver patient can indicate what?

A

DIC - fibrinogen is dysfunctional and usually INCREASED in liver patients.

20
Q

power of a study

A

1-B
B is usually 10-20%
power = chance of correctly rejecting null hypothesis (no treatment effect) when alternative hypothesis is true

21
Q

what measures the partial pressure of O2 requiring a voltage source?

A

clark electrode

22
Q

sanz electrode is used to measure

A

pH of blood

23
Q

severinghaus electrode is used to measure

A

Co2

based on the fact that pH and CO2 change in a linear fashion with temperature

24
Q

all about doxorubicin

A

cardiomyopathy, pulm, hepatic, renal
dose-dependent
ekg used for acute toxicity monitoring

25
how does magnesium work
calcium channel antagonist, intra and extracelullarly tocolysis by smooth muscle relaxation muscle weakenss from decrease release of ACh (presynpatic Ca channel blockade) LESS NDMB needed hypotension and bradycardia: 5-6 EKG changes: 6-12 heart block: 18 tx: IV Calcium
26
most accurate measure of central tendency?
median (minimizes effect of outliers)