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Blue Anesthesia question book > Chapters 1-5 > Flashcards

Chapters 1-5 Flashcards

1
Q

What is the MOA of halothane effect on CV system?

A

Halothane interferes with Na-Ca exchange resulting in direct myocardial depression and decrease in MAP through a decrease in CO but it DOES NOT decrease SVR. It also blunts baroreceptor reflex.

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2
Q

How does isoflurane effect CV system?

A

Coronary artery vasodilation, decrease SVR, increase heart rate (baroreceptor activation from the decrease SVR). CO is maintained by increase in HR

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3
Q

What can cause compound A release?

A

Halothane or sevo

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4
Q

What are risk factors for compound A?

A

long duration, low fresh gas flow, higher absorbant temperatures and dessication

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5
Q

How does desflurane effect CV system?

A

No coronary artery vasodilation (this is ONLY iso), decreased MAP, decreased SVR, increase HR. Near normal CO from increase rise in HR.

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6
Q

how long do you have to wait to use nitrous oxide on a patient that had eye surgery and use air bubble?

A

5 days

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7
Q

how long do you have to wait to use nitrous oxide on a patient that had eye surgery and used sulfur hexafluroide bubble?

A

10 days

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8
Q

What is the pathway for SSEP monitoring?

A

electrical stimulation to posterior tib, median nerve or ulnar nerve.
Electrical stimulation –> posterior column –> medial lemniscus pathway –> scalp

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9
Q

How is desflurane treated to improve specificity of its vaporizer output?

A

Desflurane vapor pressure is 660 mmHg which is close to sea level (760 mm Hg) so small changes in pressure or temperature can have a huge impact on amount the vaporizer releases.

Desflurane is heated to 39 degrees celcius and partial pressure of des is 1500 mmHg at that point which allows for accurate administration of des

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10
Q

If you are at higher altitude with desflurane what do you need to do to give appropriate depth of anesthesia?

A

because You are higher your patient must be higher too! because there is a decrease in the partial pressure of the anesthetic gas delivered.

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11
Q

What is the key factor for delivering inhalational anesthesia? Percentage or partial pressure

A

partial pressure!

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12
Q

What what percent does MAC change per decade?

A

6%

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13
Q

What is 1 MAC of nitrous oxide?

A

105%

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14
Q

By what percent are all of the gases metabolized? Des/Sevo/Iso/Halothane

A

Des-

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15
Q

What can metabolism of enflurane cause?

A

high concentration of fluoride ions leading to high output renal failure.

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16
Q

Full tank of O2 pressure and volume in L?

A

2000 psi and 625 L

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17
Q

Full tank of nitrous oxide pressure and volume in L?

A

750 psi and 1600 L

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18
Q

Once you see the pressure in the nitrous oxide tank falling, what is the approximate volume in liters remaining?

A

200-400 or 25%

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19
Q

What enzymes does nitrous oxide effect and what are the effects?e

A

it irreversibily oxizes the cobalt atom in vitamin B12.

Enzymes/Use
Thymidylate synthetase/ DNA synthesis
methionine synthetase/ myelin

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20
Q

What type of metabolism does halothane undergo?

A

oxidative- trifluoacetic acid

reductive- fluoride ions

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21
Q

Which volitile prolongs NMB the longest?

A

desflurane

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22
Q

What is ischemic preconditioning? When it is effective for volitiles?

A

Ischemic preconditioning describes short episodes of ischemia prior to a larger insult will confer protection to the tissues and delay necrosis.

Effective 1-2 hours and then again 24-3days

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23
Q

What is the MOA of ischemic preconditioning of volatile anesthetics?

A

ATP-sensitive potassium channels are activated

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24
Q

What is critical temperature?

A

The temperature of a substance at an dabove which vapor of the substance cannot be liquefied no matter how much pressure is applied.

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25
Q

In the setting of a shunt (endobronchial intubation) how will it affect induction with inhaled anesthetics?

A

Slows induction with insoluble agent > soluble agent because the soluble agent will have uptake that will partially compensate for the dilutional effect

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26
Q

What effects do you see with a left to right shunt on speed of inhalation induction?

A

minimal

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27
Q

What effect do you see if you change CO on speed of inhalation induction?

A

Decrease CO = increase speed of induction
Increase CO = decrease speed of induction
***greater effect on soluble agents

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28
Q

What is the MOA of change in HR and BP seen with rapid changes of desflurane?

A

release of catecholamine

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29
Q

What is the second gas effect?

A

uptake of one gas enhances rate of rise of alveolar partial pressure of another gas that is administered at the same time.

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30
Q

What is the concentrating effect?

A

absorption of 1 gas into the blood results in concentrating a second gas into the alveoli because the loss of the first gas causes an overall decrease in alveolar volume

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31
Q

What is the concentration effect?

A

inspired partial pressure of anesthetic gas is so high that is causes the alveolar concentration of the gas to rise quickly

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32
Q

What are the vapor pressures of the commonly used volatile anesthestics?

A

DHIESM

D- 670
H- 244
I- 240
E- 172
S- 160
M- 23
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33
Q

What is the affinity differences between O2 and CO for hemoglobin?

A

230 x stronger CO than O2 for hemoglobin

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34
Q

What are the important pulse oximeter wave lengths and what do they absorb?

A

940 nm- deoxyHgb

660 nm-COHgb and oxyHgb

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35
Q

What does isoflurane do that no other volatiles do in terms of neuro positive effects?

A

increase CSF absorption

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36
Q

Which volatile is the worst for MH?

A

Halothane

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37
Q

What is the usual volume of FRC for adults?

A

35 mL/kg

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38
Q

What is hysteresis?

A

compliance of lung is greater during deflation than during inflation. More than expected pressure to inflate a lung and less than expected recoil pressure. Due to surfactant.

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39
Q

What is LaPlaces Law and when do we consider it clinically?

A

Pressure= 2(wall tension)/ radius

Alveoli and cardiac oxygen demands

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40
Q

What is Poiseuille’s Law and when do we consider it clinically?

A

describes the flow rate of a liquid in a straight circular tube. Resistance = 8viscositylength/ pi*radius^4

consider it for flow rates for IV, airway pressures

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41
Q

What is the alveolar gas equation?

A

PaO2 = FiO2 x [Barometric pressure ((760)) - water pressure ((47))] -(PaCO2/R)

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42
Q

What is the Bohr Effect?

A

change in hemoglobins affinity for oxygent with changes in PCo2 and pH. Affinity increases with decrease in PCo2 and increase in pH.

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43
Q

When you shift the Oxygentation curve to the right what happens to the P50?

A

p50 increases

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44
Q

What happens to pH in chronic respiratory acidosis?

A

increase 0.03 U

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45
Q

In the medulla the dorsal respiratory group is responsible for what?

A

pacemaker of the respiratory system. Effects the CO2

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46
Q

In the medulla, the ventral respiratory group is responsible for what?

A

coordinates expiration

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47
Q

What can you use to calculate dead space to tidal volume ratio and what is the equation

A

Bohr equation

Vd/Vt= (PaCO2 - PeCO2)/ PaCO2

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48
Q

When can you have hypoxia without having a change in the A-a gradient?

A

hypoventalation from either obesity hypoventilation syndome OR opiate induction hypoventalation OR elevated altitude

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49
Q

What are the West Zone levels?

A

Zone 1 = apex = Alveolar pressure > pulm arterial pressure> venous pressure

Zone 2= Pulm art pressure > alveolar pressure > venous pressure

Zone III = pulm artery pressure > pulm venous pressure > alveolar pressure

Zone IV = bottom of lung that has decreased pressure from increased interstial pressure

50
Q

What pharmacologic effect is seen in patient with liver failure that has decreased portal flow?

A

decreased first pass metabolism

51
Q

What pharmacologic effect is seen in patient with liver failure that has hypoalbuminemia?

A

Increased free drug fraction

52
Q

What pharmacologic effect is seen in patient with liver failure that has ascietes and Na and H20 retension?

A

increased Vd

53
Q

What pharmacologic effect is seen in patient with liver failure that has encephalopathy?

A

exaggerated sedation effects

54
Q

What induction aduvent drugs are safe to used in a patient with liver failure?

A

Lorazepam, remifentanil

55
Q

Describe some alterations of the hemostatic system that cause impairment of hemostasis in patients with liver disease

A

thrombocytopenia, platelet function defects, enhanced production of NO, low levels of factors, Vit K deficiency, low levels of alpha 2 antiplasmin, low levels of factor XIII, elevated tPA

56
Q

Describe some alterations of the hemostatic system that cause a liver patient to be hypercoagulable.

A

Elevated levels of vWF, Decreased levels of ADAMTS-13, decreased protein C and S, decreased levels of plasminogen

57
Q

What is the SAAG and what cutoff points are signifiant and what do they mean?

A

Serum and ascitic albumin gradient

Low SAAG 1.1 g/dL= transudate = cirrhosis, CHF, myxedema, Budd-Chiari syndome, portal vein thrombosis

58
Q

How does cirrhosis influence CO, HR, PVR and fluid retention?

A

1) cirrhosis causes portal hypertenion
2) portal hypertension causes hepatocellular dysfunction that leads to portosystemic shunting
3) the portosystemic shunting leads to increased production of vasodilators
4) increased amount of vasodilators in the systemic systems leads to spalanchnic arteriolar dilation -> increased CO, decreased SVR, decreased MAP
5) Leads to activation of arterial barorectors –> increased HR and further increased in CO
6) Leads to activation of SNS RAAS to increase HR and CO and cause renal vasoconstriction and sodium and water retention

59
Q

What are predictors of difficult mask ventilation?

A 
Age >55
BMI >26
Edentulous
Beard
Snoring history
60
Q

Which drugs should be based on IBW for obese patients?

A

Propofol, roc and vec, remi and sufenta, epidural lidocaine

61
Q

Which drugs should be based on TBW for obese patients?

A

Benzos, maintenance of propofol, sux, cisatra and atracurium, fentanyl

62
Q

What triggers ADH to be released in response to hypoosmolarity?

A

Osmoreceptors in the hypothalamus regulate release of ADH from pituittary

63
Q

What are the types of heat loss seen in anesthesia and what are examples?

A

Redistribution- heat from central goes to periperhy
Convection- loss by currents (drafts and cold fluids)
Radiation- heat lost from one surface to another (2nd most important method of heat loss under anesthesia)
Conduction- heat lost from skin to cold OR table
Evaporation

64
Q

What are examples of fixed obstruction in respiratory system and what does it look like on flow volume curves?

A

Can be EITHER intra or extrathoracic

  • large goiter
  • causes plateaus in BOTH inspiration and expiration
  • looks like loaf of bread
65
Q

What are examples of variable extrathoracic obstruction and what does it look like on flow volume curve?

A

ex: vocal cord paralysis, neoplasm in neck
- only the inspiratory limb plateaus
- looks like sailboat

66
Q

What are examples of variable intrathoracic obstruction and what does it look like on a flow volume curve?

A

ex: endobronchial lesion, tracheomalacia
- only the expiratory limb plateaus
- looks like an iceberg

67
Q

What does hyperthryoidism cause in terms of CPK levels

A

decreases them…can be used to DDx MH from thryoid storm

68
Q

Why should ASA not be used to treat thyroid storm?

A

it displaces thyroid hormone from binding proteins and increases level of free thyroid hormone

69
Q

When should iodide therapy by used during treatment of thyroid storm?

A

Delayed until after beginning antithyroid drug therapy. Antithryoid drugs reduce the secretion and production of thyroid hormone and prevent iodide from binding.

70
Q

Which is the preferred beta blocker for treatment of thyroid storm and why

A

Propranolol impairs the peripheral conversion of T4 to T3 over 1-2 weeks; allows for reduction of excessive sympathetic stimulation

71
Q

Why would you use guanethidine for thyroid storm?

A

inhibits catecholamine release

72
Q

Why would you use Iodide for thyroid storm?

A

inhibition of thyroid hormone synthesis

73
Q

Why would you use reserpine for thyroid storm?

A

depletion of catecholamine stores

74
Q

Which side are pheochromocytomas usually on?

A

right side

75
Q

What is MEN IIA?

A

medullary carcinoma of thyroid, parathyroid hyperplasia, pheo

76
Q

What is MEN IIB?

A

medullary carcinoma of the thryoid, pheo and neuromas of the oral mucosa

77
Q

What is the target and duration of phenoxybenzamine?

A 
duration= 24-48 hours
Target = noncompetitive alpha 1 and alpha 2 blocker by irreversibly alkalating the receptors
78
Q

What is the MOA of alpha-methyl-paratyrosine?

A

inhibition of tyrosine hydralase which is the rate limiting step for making catecholamine from tyrosine–> dopamine

79
Q

What is the most specific sign of MH?

A

generalized muscle rigidity

80
Q

What is the most sensitive sign of MH?

A

hypercarbia

81
Q

What is the MOA of dantrolene?

A

direct skeletal muscle relaxant– binds the RYR1 receptor and blocks the release of Ca from the SR

82
Q

Which mediations do you need to be vary of if you have an HIV patient on protease inhibitors?

A

midazolam and fentanyl because protease inhbitors cause cyto 3A4 inhibition and cause prolonged effects of midazolam and fentanyl

83
Q

What is MOA of fenoldopam?

A

Dopamine 1 agonist= decreases SVR and increases blood flow

84
Q

What is the definition of the diagnosis of bronchopulmonary dysplasia?

A

1) born before 32 weeks, needing O2 for >28 days
- then reassess as 36 weeks gestation as mild (room air) moderate (30% O2)
2) born after 32 weeks, needing O2 after 56 days

85
Q

What is the mutation in patients with Sickle Cell?

A

Inherited hemoglobinopathy of beta-globulin with single AA substitution of valine for glutamine at 6th AA of beta chain

86
Q

What are general recommendations for sickle cell patients undergoing surgery?

A

avoid dehydration, hypoxemia, hypothermia, acidosis or stasis of blood (tourniquet)

87
Q

What is the HABR mechanism of the liver

A

Hepatic arterial buffer response

  • intrinsic mechanism in which a decrease of blood flow from portal vein causes an increase in blood flow from the hepatic artery.
  • relies on the synthesis of adenosine in the portal system which is a vasodilator that will decrease the hepatic artery resistence during periods of low portal flow and be washed away during period of high portal flow
  • *There is NO autoregulation of liver flow
88
Q

What receptors are found in the hepatic artery?

A

alpha1, alpha 2 and beta 2 receptors (target for nadolol, propranolol by blocking the vasodilatory effects of B2 in the hepatic artery)

89
Q

What receptors are found in the portal vein?

A

alpha1 and alpha 2 receptors

90
Q

Which anesthetic agents abolish the HABR response

A

halothane

91
Q

What is the HBeAg signify?

A

active viral replication of hepatitis B virus

–if HBsAg and HBeAg are positive= high risk of infectivity

92
Q

What is the “window” period during hepatitis C infection and what should you look for?

A

HBsAg is negative and anti-HBs is not yet detectable

Look for IgM and IgG antibodies to the HBC core antigen –Anti-HBc

93
Q

For Hepatits C what can you look for with acute infection?

A

Elevation of AST/ALT. Seroconversion takes weeks to develop Anti-HCV.

94
Q

How is rocuronium excreted?

A

biliary excretion = 66%

kidney excretion = 33%

95
Q

How is vecurion action terminated?

A
  • Vec can metabolized to 3-desacetylvecyluronium (12% of the clearance is by deacetylation) 3-desacetvecuronium has 80% potency of vec and is dependent on kidney for elimination.
  • vec can also by excreted as parent compound in the liver
  • Vec is excreted 25% by kidney and 75% by liver.
96
Q

How is pancuronium eliminated?

A

mainly kidney, 15% by liver

97
Q

Describ the the more severe form of halothane liver toxicity.

A

Immune-mediated auses massive centrilobular hepatic necrosis.

  • occurs 5-7 days after halothane exposure
  • the oxidative metabolism of halothane to create TFA (trifluroacetyl mebolite by CYP2E1) binds to liver proteins causing hapten-protein adduct that is immunogenic and subsequent exposure to halothane cuses cytotoxic T cell response
98
Q

If you get halothane toxicity will you have problems with other inhaled anesthetics?

A

The antibodies created by the halothane can cross react; however NOTE sevoflurane DOES NOT cause TFA!.

99
Q

What are the stages acute renal failure by RIFLE and AKIN criteria?

A

Risk= Cr increased 1.5x or 4 weeks
End stage = need for dialysis > 3 months

AKIN (acute kidney injury network)
Stage 1= Cr increased 1.5x or increased Cr by 0.3 or 4 with 0.5 increase OR

100
Q

What is the carcinoid triad?

A

diarrhea, flushing & carcinoid heart disease (right sided fibrosis causing regurg or stenosis)

101
Q

What does somatostatin do in treatment of carcinoid?

A

reduced hormone production with half life of 3 min

102
Q

What does octreotide do in the treatment of carcinoid?

A

somatostatin analog with half life of 3 hours

103
Q

What are the important MSO4 metabolites?

A

M3G- most abundant & inactive

M6G- 5-10% of metabolism, active metabolite

104
Q

What is myotonic dystrophy?

A

autosomal dominant disorder with myotonia( sustained contracture after muscle contraction or elective stimulation) that causes progressive muscle weakness and wasting due to abnormal calcium metabolism.

105
Q

What are anesthetic considerations for myotonic dystrophy?

A

pulmonary complications including central and peripheral hypoventilation, cardiomyopathy, conduction abnormalities, abnormal response to anesthetic drugs including increased somnolence to benzos and opioids, poor gastric motility leading to aspiration

106
Q

What are triggers for myotonic dystrophy?

A

hypothermia, shivering, mechanical and electric stimuli

107
Q

Which drugs should be avoided to prevent myotonic reactions?

A

Etomodate, propofol, methohexital and neostigmine

108
Q

What is the classic triad of Parkinson’s disease?

A

resting tremor, bradykinesisa, muscle rigidity (cogwheel)

109
Q

What is the purpose of carbidopa in treatment of parkinsons?

A

peripheral decarboyxlase inhibitor that decreases the side effects of levodopa (dopamine precursor)

110
Q

What is the purpose of seligiline in treatment of Parkinsons?

A

type B MAO - not associated with hypertensive crisis in patients taking type A MAOI

111
Q

What is the purpose of taking Bromocriptine in treatment of Parkinsons?

A

dopamine receptor agonist

112
Q

What is the name of primary hyperaldosteronism and what are the symptoms?

A

Conn syndrome,; find low levels of renin (renin is increased in 2ndary hyperaldosteronism) hypertension and hypokalemia (remember licorice can look like this too!)

113
Q

What is treatment for Conn syndrome?

A

spironolactone- aldosterone antagonist that requires 1-2 weeks to work

114
Q

How does a burn effect muscle relaxants?

A

sux- increased sensitivity

nondepolarizers- decreased sensitivity

115
Q

How do patients with MG respond to muscle relaxants?

A

resistance to sux because decrease in number of acetylcholine receptors. Effects may be PROLONGED if on pyridostigmine (blocks psuedocholinease too) OR if getting plasmaporesis from loss of pseudocholinesterase.

Sensitive to nondepolarizers

116
Q

What is the pathophysiology of MG?

A

postsynaptic anti- nAChr antibodies that leads to decrease in AChr receptors on postsynaptic membrane

117
Q

What is the pathophysiology of ELS?

A

Eaton-lambert syndrome if antibodies to presynaptic voltage-gated Ca channels resulting in decreased ACh release from presynaptic neuron

118
Q

What does exercise do in both MG and ELS?

A

MG- weaker

ELS- stronger

119
Q

In patients with ELS, how do they respond to NMB?

A

sensitive to BOTH sux and nondepolarizers. ELS patients are more sensitive to nondepolarizers than MG patients.

120
Q

What is the pathway of the oculocardiac reflex?

A

ciliary nerves of eye–> trigeminal nerve (opthalmic division)–> gasserian ganglion –> motor nucleus of vagus nerve

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