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Prodigy > Prodigy Films A to F > Flashcards

Prodigy Films A to F Flashcards

1
Q

What hormones use cAMP?

A

Beta receptor catecholamines, PTH, Glucagon, TSH, FSH, LH

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2
Q

How is cAMP action terminated?

A

Phosphodiesterase

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3
Q

What is Adrenal outer-layer?

A

Zona Glomerulosa

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4
Q

Adrenal Glomerulosa secretes what?

A

Mineralocorticoids - aldosterone

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5
Q

Zona fasciculata secretes what?

A

Glucocorticoids

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6
Q

Zona reticularis secretes what?

A

androgens

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7
Q

what controls release of glucocorticoids?

A

ACTH

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8
Q

what controls release of mineralocorticoids ?

A

Renin/ Angiotensin system

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9
Q

drug potency determined by what?

A

determined by the affinity of the drug for its receptor

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10
Q

Desflurane at altitude, do you need to turn dial up or down?

A

At elevation ( high altitude), lower partial pressure (lower barometric pressure) so need to turn up Tec 6

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11
Q

amides vs esters lipophilicity and PB?

A

more lipophilic and more protein bound than esters

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12
Q

amides metabolized how and which are fast and which are slow and why?

A

CYP 450, prilocaine fastest, ropivacaine slowest

bupivacaine = enzyme activity, prilocaine = hepatic blood flow, metabolism altered by liver disease

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13
Q

Amide toxicity more or less likely than ester and why?

A

toxicity more likely with amide than ester, rely on hepatic clearance

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14
Q

Normal aortic valve area ?

A

2.5-3.5 cm2

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15
Q

Atrial Natriuretic Factor acts where and why, how does it work?

A

on collecting ducts of kidneys because of increased fluid in atria to inhibit water and sodium reabsorption, inhibits renin release

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16
Q

what is bilirubin and how is it broken down?

A

breakdown of heme metabolism, heme broken down to unconjugated bilirubin which is water insoluble @ high level neurotoxic, than uncog is delivered to liver bound to albumin, liver then metabolizes it with glucoronic acid and conjugates it and eliminates it thru bile

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17
Q

how is TBW composition made up?

A

60% is TBW, 40% intracellular , 20% extracellular, (extracellular than broken into plasma and interstitial)

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18
Q

what is anion ?

A

A -A N- negative ion ( mnemonic to remember it by)

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19
Q

Major intracellular cation and anion ?

A

Anion= Phosphate PO4, Cation = K+

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20
Q

Major extracellular anion and cation ?

A

anion = Chloride. cation = Na+

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21
Q

What is Bohr effect ?

A

describes how CO2 and decreased pH promote o2 release into tissues.
pH is lower, Temperature is higher, Increased CO2, O2HGB shift curve to RIGHT

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22
Q

What is Boyles Law?

A

pressure and Volume, P1V1 = P2V2, inverse relationship

as P up, volume down and vice versa,

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23
Q

which Bronchi leaves at less of an angle?

A

Right, why more likely to mainstem

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24
Q

how does calcium calmodulin system work?

A

once 3 calcium bind onto calmodulin receptors, the calmodulin then changes shape and is now able to bind to protein kinases that are able to exert an effect. it can activate myosin light kinases that are able to stimulate smooth muscle contraction

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25
Q

what do carcinoid peptides release?

A

histamine, serotonin, kinins

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26
Q

what are carcinoid symptoms?

A

hypo/HTN, flushing, diarrhea, bronchoconstriction

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27
Q

how does carcinoid syndrome affect the heart?

A

can cause fibrosis of right sided valves (TV & PV), (left sided valves not affected as lungs deactivate peptides

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28
Q

what is treatment of carcinoid syndrome?

A

octreotide & surgical excision of tumor

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29
Q

what is anesthesia keys to carcinoid syndrome ( what to avoid)?

A

avoid adrenergic stimulation (USE PHENYLEPHRINE), avoid histamine release - morphine, pancuronium, atracurium, & avoid increased RV work = hypoxia, hypercarbia, & light anesthesia

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30
Q

where is PMI and what is it?

A

point of maximal impulse, best place to listen to S1, heard at apex at 5th intercostal space midclavicular line

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31
Q

what is CO during labor? when does it peak? why is this important?

A

can be as high as 12-14 L/min,
peaks at 80% above baseline right after delivery
pt’s with cardiac hx at most risk for decompensation

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32
Q

how long until CO returns to normal after delivery?

A

2 weeks

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33
Q

what are cardiac changes at term?

A

diaphragm shifts heart up & left
increased risk of dysrhythmias (PACs, SVTs, Vent Dysrhythmias,
Left axis shift
Larger cardiac silhouette or CXR

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34
Q

How does pregnancy affect SVR, CO, DBP, MAP. . . ?

A

SVR decreases 20%, CO increases 40% mostly from 50% SV, diastolic BP decreases by 15 mm Hg and thus MAP can decrease

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35
Q

the supra-tentorial brain is composed of what

A

cerebral hemispheres and diencephalon

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36
Q

the infra-tentorial brain is made up of what?

A

cerebellum and brainstem

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37
Q

what are 4 lobes of brain

A

frontal, parietal, temporal and occipital (temporal over ear, Parietal over bald-spot area)

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38
Q

what is diencephalon made up of?

A

thalamus and hypothalamus

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39
Q

what does hypothalamus do

A

relay for sensory and and motor information, connected to pituitary, does endocrine and autonomic functions

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40
Q

what makes up limbic system & what is it responsible for

A

hippocampus, amygdala, and part of cortex,

for cognition, memory and emotion

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41
Q

what makes up brainstem & what is it responsible for

A

Midbrain, Pons & medulla,

responsible for consciousness, respiratory and cardiac control & many reflexes

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42
Q

what is cerebellum function for?

A

proprioception and maintaining posture and gait

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43
Q

discuss cerebral metabolism % (#’s bodyweight, )2 & glucose consumption)

A

makes up 2% of body weight
20% of O2 consumption
25% of glucose consumption

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44
Q

what is normal cerebral metabolism CMRO2, glucose & % CO ( #’s)

A

3-4 mL/100g/min
glucose consumption 5g / 100 g / min
15% of CO or 750 ml / min

45
Q

when is MAP autoregulated values?

A

between a MAP of 60-160 mm Hg

46
Q

what is CPP formula (cerebral)?

A

MAP - ICP (CVP)

47
Q

how does ventilation affect CBF?

A 
hypoventilation = increases CBF & increases CO2
Hyperventialion = decreases CBF & decreases CO2
48
Q

how do Volatiles affect CMRO2, CBF?

A

cause cerebral vasodilation
impair CBF auto-regulation
decrease CMRO2
minimal increase CBF at low doses

49
Q

how does Nitrous affect CMRO2 & autoregulation (important for brain & heart cases which is when we avoid it)

A

causes cerebral vasodilation
potentially increases CMRO2
preserves autoregulation with propofol
impairs autoregulation with VA

50
Q

what is Charles’ Law?

A

V1T2 = V2T1,

direct relationship like a hot air balloon

51
Q

what are examples of weak drug bonds?

A

hydrogen bonds, ionic bonds & van der Waals bonds (weakest, distant dependent )

52
Q

examples of strong bonds?

A

covalent bond, permanent bond, ASA & COX

53
Q

what is the chemical structure of inhaled anesthetics

A

VA are ethers, meaning R-O-R structure,

54
Q

what are iso, des and sevo chemical structures

A

Iso 5 F, Des 6 (like tec 6), Sevo 7 (seven Sevo)
Isoflurane has Cl
adding fluorines increases potency as does heavier halogens
adding halogens increases arrhythmias

55
Q

how does fluorine affect flammability and metabolism

A

adding more F ions decreases flammability and metabolism (even tho sevo 2%, iso 0.2 & Des 0.02%)

56
Q

describe liver cirrhosis

A

increase in resistance to blood flow from fibrous tissue = portal HTN

57
Q

what are dangers of portal HTN?

A

cardiac, renal and pulmonary disorders
hemostasis alterations
ascites and varices
hepatic encephalopathy

58
Q

what are cardiac effects of cirrhosis

A 
hyperdynamic state
Decreased SVR
Decreased BP
Increased HR
Increased CO
59
Q

what are systemic effects of cirrhosis

A 
hyponatremia
anemia
thrombocytopenia
hyperbilirubinemia
hypoalbuminemia
60
Q

how is cirrhosis scored

A

MELD score - provides 3 month mortality risk

Child Pugh score as well

61
Q

what is a critical incident

A

powerful and overwhelming event that lies outside the range of human experience

62
Q

what is an adverse event

A

an unintended patient injury, harm or complication that results in a prolonged hospitalization, disability or death

63
Q

what is a medical error

A

the failure to take a known & planned action or using the wrong plan of action to achieve an outcome

64
Q

what is closing capacity

A

closing volume + residual volume

65
Q

what is FRC

A

volume left in lungs at end of normal exhalation

66
Q

what factors lower FRC

A

obesity
sedation
supine position

67
Q

what is closing capacity at 45 & 65

A

CC at 45 = supine

CC at 65 = sitting position

68
Q

what factors increase closing capacity

A

COPD,
Asthma
pulmonary edemas

69
Q

CO2 and blood brain barrier

A

CO2 + H20 —> H2CO3
H2CO3 —> H + HCO3
CO2 INDIRECTLY influences ventilation as H can’t cross BBB but CO2
H+ DIRECTLY influences ventilation

70
Q

Describe CO2 ventilatory curve

A

its a linear relationship from 20-80 mm Hg

71
Q

Combined Spinal EPidural benefits

A

Spinal fast on

Epidural long term pain control that can be converted to surgical anesthesia if needed

72
Q

Opioid only spinal advantage

A

produces no motor block, good in aortic stenosis and preload dependent conditions

73
Q

give example of Competitive antagonism

A

NDMR (ROC) compete with acetylcholine at NMJ

Shifts effective dose curve RIGHT ONLY

74
Q

Describe noncompetitive antagonism

A

binds permanently

Shifts effective dose curve RIGHT & DOWN

75
Q

What is Tort

A

civil wrongdoing,

Negligence & malpractice

76
Q

What must plaintiff prove (4 things)

A

Duty
Breach of Duty
Causation
Damages

77
Q

what is acceptable standard

A

reasonable & prudent manner must be demonstrated

78
Q

WHat is proving proximate cause

A

‘But for’ Test

Substantial Factor Test

79
Q

what is Res Ipsa Loquitur

A

Only occurred due to negligence
Factors only under CRNA control
Can’t be attributed to the patient
Evidence more accessible to the CRNA

80
Q

What are the damages seen in court?

A

Pain & suffering
Special damages: actual expenses due to the injury
Punitive damages : from CRNA Fault, rare in medical malpractice, could lose CRNA license

81
Q

What is vicarious liability?

A

this affects the employer

respondeat superior - the employer has a duty for the reasonable oversight of the employee

82
Q

what is concentration effect

A

inhaled partial pressure (PI) influences alveolar partial pressure (PA)
Higher the PI than faster PA approaches PI

83
Q

WHat is Conn Syndrome

A

Primary hyperaldosteronism

84
Q

What does aldosterone do

A

Increases Na reabsorption & K excretion in DCT / CT

85
Q

What are s/s of Conn Syndrome

A

Fluid volume excess / HTN - from Inc Na levels
Hypokalemic metabolic alkalosis - K excretion
Muscle weakness - K excretion
Decreased renin levels - From HTN feedback loop

86
Q

WHat is treatment of Conn’s syndrome?

A

Spironolactone/ Eplerenone (get rid of Na & retain K)

Tumor removal as most likely from adrenal tumor

87
Q

What is conscientious objection?

What do you do about it?

A

unwilling to provide care because of advanced directive - consult ethics committee

  • transfer care to another CRNA
  • honor pt’s decision and deliver care
  • Cannot remove self if result in harm of breach of duty
88
Q

what is countercurrent mechanism?

WHat part of kidney is in cortex vs medulla?

A

how kidney concentrates urine
cortex - DT, PCT, Glomerulus
medulla - Loop of Henle, CD

89
Q

What are cardiovascular effects of VA?

What about N20?

A

Decrease MAP, CO, CI mainly from decreased SVR

exception is N20 = increases sympathetic stimulation, increases SVRM CVP and arterial pressure

90
Q

What are HR effects of VA & N20?

A

HR increases with VA & N20
Seen more with rapid dose increase like Des
Sevo least effect on HR

91
Q

What are Desflurane CI effects?

A

maintains CI more effectively than ISO / Sevo - likely due to increased HR

92
Q

how to VA affect Myocardial contractility

A

all produce dose dependent decrease

does not affect myocardial functional reserve

93
Q

How do VA affect RAP?

A

ISO/DES/N20 all increase RAP

Sevo does not affect RAP (right atrial pressure)

94
Q

what is diabetic ketoacidosis triad?

A

more common in Type 1

-Hyperglycemia, ketonemia, acidosis

95
Q

what are DKA s/s?

A 
Elevated Anion Gap
Hyperosmolarity
Glucose 250+
Electrolyte depletion
lethargy/ Kussmaul breathing
96
Q

what factors affect diffusion?

A

of molecules,
opening in membrane
molecular velocity

97
Q

What are regulatory proteins?

A

proteins that control gene expression

targeted by hormones and drugs such as antineoplastic agents

98
Q

ESRD and drug pharmacokinetics

A
  • ESRD pt’s have less proteins, so highly protein bound drugs may require a lower dose due to higher free fraction of the drug
  • ESRD pt’s are acidoic which can change drug ionization & pKa
  • renally excreted metabolites can prolong duration of action
99
Q

what is the ED50 vs LD50?

A

ED50 - dose that produces the desired response in 50% of patients
LD50 - dose tha tis lethal in 50% of patients

100
Q

why is ED50 important?

A

ED50 is used to compare potency, lower ED50 the greater the potency, yes lower ED50 increased potency

101
Q

What is LD50/ED50?

A

therapeutic index

102
Q

how do you calculate Safety margin of a drug?

A

LD1 - ED99 / ED99 x 100 = safety margin

103
Q

what is first order kinetics

A

half drug eliminated per half life

104
Q

how long until a drug is completely eliminated from system?

A

4 half lifes (only 5% remains then)

105
Q

how are half life and clearance and Vd related?

A

Half life is inversely proportional to clearance.

directly proportional to volume of distribution

106
Q

What are ester local anestehtics & how are they metabolized

A

one i in name - procaine, tetracaine, cocaine. . .

metabolized by plasma and tissue cholinesterase’s (except cocaine which is metabolized in liver)

107
Q

Ester metabolites & metabolism

A
  • PABA and thus allergy more common,
  • cross sensitivity more common within esters
  • impaired metabolism with liver disease and elevated BUN, pregnancy, chemo agents & atypical plasma cholinesterase
108
Q

what is an example of a variable extra-thoracic obstruction

A
  • unilateral vocal cord paralysis

- on flow volume loop shows normal expiraotyr pattern but inspiratory pattern is chopped off

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