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pharm exam 1 Flashcards

Srna

1
Q

non-competitive antagonist and EC50

A

irreversible binding to allosteric site, doesn’t change EC50 but lowers the Emax because it doesn’t matter how much agonist you give, it cannot reach its original Emax examples :
Aspirin, Phenoxybenzamine ( alpha 1 antagonist )

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2
Q

competitive antagonist

A

reversibly bind to the receptor site. it changes EC 50 curve to the right but it does not change Emax
examples: neuromuscular blockers, atropine

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3
Q

what does pharmacokinetics intel

A

Administration
Distribution
Metabolism
Elimination

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4
Q

propanolol

A

non selective Beta blocker

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5
Q

indirect antagonism

A

binding to the agonist and not to the receptor

example: protein binding to heparin

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6
Q

1+1=2

A

addition

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7
Q

1+1=3

A

synergism,effect of 1 drug is enhanced by a drug that has no effect on its own. 2 drugs

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8
Q

1+1=0

A

antagonism

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9
Q

ephedrine

A

Mephentermine, ephedrine, and metaraminol are mixed-acting drugs. Ephedrine increases blood pressure and has a positive inotropic effect. Because it does not have detrimental effects on uterine blood flow, ephedrine is widely used as a pressor in hypotensive parturient patients. As a result of its β1-adrenergic–stimulating effects, ephedrine is helpful in treating moderate hypotension, particularly if accompanied by bradycardia. It also has some direct β2-adrenergic–stimulating effects and has been used orally as a bronchodilator. The usual dose is 2.5 to 25 mg given intravenously.
**amphetamine works by being taken up by VMAT 2 (which takes up space in the vesicle instead of dopamine or NE) this increases dopamine and NE realease into the synapse; 2. amphetamine competes with with NE or DA for reuptake so less NE or DA is reuptake; 3 MAO is inhibited.

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10
Q

1+0=3

A

potentiation: only one drug is enhanced :: physostigmine and Ach

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11
Q

what makes the therapeutic index

A

Ed 50 and the LD 50

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12
Q

pharmacodynamic responses can be:

A

therapeutic, toxic or lethal

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13
Q

fundamental of pharmacokinetics

A

volume and clearance

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14
Q

7 factors that affect absorption:

A

blood flow, total surface area, time to arrival and contact time, solubility, chemical stability, lipid to water partition coefficient, and degree of ionization (Pka)

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15
Q

distribution depends on: (4)

A

Blood flow, Capillary permeability, Protein binding, Disease States

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16
Q

why os important to know the volume of distribution of a drug ?

A

to determine the drug’s dosing requirements

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17
Q

body mass %: VRG, muscle,

CO output %: VRG, muscle

A

10, 50, fat 20, poor 20

75, 20, fat 5, poor 0

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18
Q

formula of volume of distribution

A

Vd= amount of drug/ desired plasma concentration

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19
Q

volume of distribution is affected by 1.drug characteristics and 2. patient characteristics :

A
  1. molecular size, ionization, protein binding,

2. pregnancy and burns

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20
Q

clearance is 1. directly proportional and 2. is indirectly proportional to :

A
  1. blood flow, extraction ration and drug dose

2. half life and drug concentration in the central compartment

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21
Q

steady state is

A

giving and clearing from body at the same amount: rate of administration= rate of elimination
to keep a certain dose in body like dilantin you measure the level of the dose .

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22
Q

plasma concentration curve

A

alpha: distribution (1/t alpha) and beta: elimination from the central compartment (1/2t beta)

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23
Q

rank opioids potency 1 highest to 5 lowest

A
  1. sufentanyl 2. remifentanyl 3. fentanyl 4. alfentanyl 5.morphine 6. demerol
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24
Q

acid donates

A

H+

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25
Q

base donates

A

OH-

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26
Q

the amount of ionization depends on two things:

A

pH of the solution and the pKA of the drug

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27
Q

when the pKa and the pH are the same

A

50% of drug is ionized and 50% unionized

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28
Q

which creates the strongest gradient for passage of local anesthetic from mother to fetus?

A

alkalotic mother to acidotic fetus

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29
Q

what drugs bind to beta globulin proteins ? decrease? increase?

A

basic drugs

nothing , nothing

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30
Q

what drugs bind to alpha1 acid glycoprotein? what lowers ? increase?

A

basic drugs

  • pregnancy, and neonates
  • surgical , stress, MI , advanced age , chronic pain, and RA
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31
Q

what drugs bind to albumin ? decrease? increase?

A

acidic blood:

  • advanced age, malnutrition, pregnancy, liver and kidney disease
  • nothing
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32
Q

protein binding % fo propofol, diazepam, midazolam, dexmedetomidine, lorazepam, barbiturates, etomidate, ketamin ?

A 
propofol 98%
diazepam 98%
midazolam 94%
dexmedetomidine 94%
lorazepam 90%
barbiturates 85% 
etomidate 75%
ketamin 15%
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33
Q

examples for zero oder drugs?

A

logarithmic. there’s more drug the enzyme, linear.

aspirin, dilantin, alcohol, heparin, warfarin and theophylline

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34
Q

examples of first order drugs?

A

there is the less amount of drug than enzyme. no saturation. a drug can change from 1st order to zero

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35
Q

pharmacokynetic age difference between newborns and older people?

A

newborns:
- Tend to metabolize drugs more slowly
-Exception is theophylline (more rapidly)
-Digoxin (similarly metabolized)
older people:
-Altered drug distribution
-Lean body weight to fat ratio.
-Metabolic activity of liver.
-Principally P450 enzymes.

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36
Q

metabolism is affected by? (6)

A
  • Age
  • Sex
  • Liver function
  • Nutrition
  • Environment
  • Genetic factors
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37
Q

phase 2 of metabolism : common substrates are? (4)

A

glucoronic acid, glycine, acetyl acid , sulfuric acid, or a methyl group

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38
Q

enterohepatic recirculation medication example?

A

diazepam

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39
Q

how is lidocaine and succinylcholine metabolized in phase one?

A

hydrolysis

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40
Q

enzyme induction ?

A

Dilantin Rifampin Barbiturates (phenobarbital) Ethanol Tobacco Carbamazepime

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41
Q

enzymes inhibitors?

A

Ciprofloxacin Cimetidine INH Erythromycin Grapefruit juice Omeprazole SSRIs Ketoconazole (Diego’s can’t see their fungus)

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42
Q

Disulfiran

A

antabuse; Disulfiram is an oral drug used for treating alcoholism. Alcohol is converted in the body into acetaldehyde by an enzyme called alcohol dehydrogenase. Another enzyme called acetaldehyde dehydrogenase then converts acetaldehyde into acetic acid. inhibiting acetaldehyde dehydrogenase causes hangover effect . also a Dopa-beta hydroxyls inhibitor

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43
Q

Acetazolamide (diamox)

A

it makes urine basic therefore excreting acidic drugs

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44
Q

pseudocholinesterase breaks down

A

succ, local anesthetics (tetracaine, procaine chloroprocaine, cocaine -also hepatic)

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45
Q

non specific esterases

A

remifentanyl, esmolol, etmoidale (also hepatic) atracurium (also in Hoffman)

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46
Q

non specific esterases breaks down:

A

remifentanyl, esmolol, etmidate (also hepatic) atracurium (also in Hoffman)

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47
Q

alkaline phosphatase breaks down :

A

fospropofol

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48
Q

Hoffman elimination is

A

cisatrucurium, atracurium (plasma esterase)

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49
Q

Children exhibit different pharmacokinetics from adults because

A

of their altered protein binding, larger volume of distribution (Vd), smaller proportion of fat and muscle stores, and immature renal and hepatic function

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50
Q

old people and metabolism

A
  • decrease albumin, decrease in blood volume by 20-30%^, ^ in body fat (^ reservoir) , decrease in muscle mass, 60% of the GFR of that of a young adult.
    Vecuronium will last 45 mins instead of 16 (young adult)
    diazepam will last 72 hr instead of 24 hr (young adult)
    Fentanyl will last 925 mins instead of 250 mins ( Y.A.)
    versed will last 4.3 hrs instead of ( 72 hr)
    inhalation agents decrease linearly with older age
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51
Q

enantiomer drugs that are racemic mixture are ?

A

rupivacain and levobupivacaine

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52
Q

weak base are meds morphine, thiopental, ephedrine, metohexital (pick 2)?

A

morphine and epinephrine

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53
Q

autonomic nervous system is part of what division ?

A

motor division

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54
Q

preganglionic fibers are

A

myelinated and Fiber B

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55
Q

postganglionic fibers are

A

unmyelinated and fiber C

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56
Q

blocking T4 will cause

A

Bradycardia and hypertension

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57
Q

acetylcholine is terminated by :

A

cholinesterase

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58
Q

norepinephrine is terminated by:

A

reuptake into the nerve terminal, diffusion out of the synaptic cleft, metabolic transformation by the MAO, or COMT by the liver

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59
Q

epinephrine terminated by

A

COMT

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60
Q

membrane bound receptors

A

Ion Channels
G-Protein Coupled Receptors
Enzyme Linked Receptors
Intracellular Receptors

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61
Q

example of enzyme linked receptors

A

insulin

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62
Q

example of intracellular receptors

A

steroids, and thyroid hormone

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63
Q

cAMP functions?

A

activates protein kinase, phosphorylates 3 reactions–> Ca+ channels, myosin like chain kinase MLCK, phopholamban

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64
Q

cAMP functions?

A

in the cardiac muscles : phosphorylates protein kinase and increases intra cellular Ca+ therefore increase contractility and phospholyrates phopholamban.
in the vascular smooth muscle: cAMP inhibits myosin like chain kinase MLCK causing vasodilation and decreasing SVR

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65
Q

phospholamban

A

protein that regulates the Ca+ pump in the SR in cardiac muscles so it bring the Ca+ back into the SR. so it causes lusitropy.

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66
Q

MLCK

A

myosin like chain kinase:

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67
Q

alpha 2 receptors are located

A

presynaptic, postsynaptic, and platelet

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68
Q

Dexmedetomidine is a centrally acting alpha-2 agonist reducing:

A

reduces SNS tone and causes sedation, MAC reduction, bradycardia, and vasodilation

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69
Q

Alpha 2 in my spinal cord will

A

cause analgesia, anti-shrivering

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70
Q

thiophyllin is

A

non selective PDEI

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71
Q

primacor (Milrinone)

A

PDE3i

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72
Q

cAMP reactions

A

cardiovascular: increase lusitropy and increase inotropy

vascular muscle: relaxation , and vasodilation

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73
Q

activation of PKA

A

lypolysis , glycogenolysis and protein synthesis somewhere else

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74
Q

Inodilators are also known as

A

PDE3i

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75
Q

rate limiting stop

A

tyrosine hydroxyls

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76
Q

what is the primary mechanism of NE removal?

A

reuptake into the presynaptic nerve

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77
Q

final metabolite oo Ne

A

vanillylmandelic acid VMA

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78
Q

how do you know if a person has pheocromocytoma?

A

VMA in urine

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79
Q

Preganglionic neurons

A

between segments T1 and L2 – lateral gray horn of spinal cord

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80
Q

Sympathetic chain ganglia

A

paired. visceral effectors , thoracic cavity, head, body wall , and limbs

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81
Q

3 types of sympathetic ganglia

A

(sympathetic chain) Paravertebral, (collateral ganglion) prevertebral, and adrenal medulla

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82
Q

(collateral ganglion) prevertebral

A

unpaired, visceral effectors in abdominal pelvic cavity.
-Preganglionic fibers will pass through the sympathetic chain without synapsing then Preganglionic fibers will synapse within collateral ganglia. -Splanchnic nerves will synapse on one of the four collateral ganglions

83
Q

adrenal medulla

A

paired. through release of hormones in the circulation and organs and systems throughout body.

84
Q

Sympathetic gives rise to the fibers through ?

A

ventral roots give rise to myelinated white ramus that Leads to sympathetic chain ganglia (Segments T1-L2)

85
Q

Some fibers will form sympathetic nerves that will innervate thoracic organs, which ganglion is this?

A

paravertebral chain .

86
Q

Celiac ganglion

A

part of collateral ganglion. innervates stomach, liver, gall bladder, pancreas, spleen

87
Q

Superior mesenteric ganglion

A

part of collateral ganglion. Postganglionic fibers innervates small intestine and initial portion of large intestine

88
Q

Inferior mesenteric ganglion

A

part of collateral ganglion. Postganglionic fibers innervate the final portion of large intestine.

89
Q

Inferior hypogastric ganglion

A

part of collateral ganglion. Postganglionic fibers innervates urinary bladder , sex organs

90
Q

medulla gland secretes?

A

Medulla: Secretes Catecholamines
Cortex: Secretes glucocorticoids, mineralocorticoids, and androgens

91
Q

greater splanchnic, lesser splanchnic, and lumbar splanchnic innervate?

A

collateral ganglions

92
Q

inferior cervical ganglion fuses with the first thoracic ganglion to form?

A

stellate ganglion

93
Q

SNS stimulation causes hepatocytes to release?

A

glucose and potassium into the systemic circulation

94
Q

Phases to K+ response?

A
  1. Initial K+ release from the liver causes increase K+ concentration.
  2. SNS stimulation– Adrenal medulla releases EPI, binds to bets-2 on skeletal muscle and erythrocytes activating Na+/K+ pump and shifts K+ into the cell.
95
Q

bring potassium into cell?

A

Alkalosis, beta-2 agonist ( Albuterol, ritodrine, epi), methylxanthine (theophylline), insulin (activates Na+/K+ pump), hypothermia

96
Q

takes potassium out of the cell?

A

rewarming phase ,hyperosmolarity, succinylcholine (nicotinic-m agonism), acidosis (activates H+/K+ pump), burns (receptors are sensitive) , any trauma like cell lysis (rhabdomyolysis)

97
Q

Preganglionic neurons located in the nuclei of the brainstem form:

A

cranial nerves III, VII, IX, X

98
Q

CN III (ocular motor)

A

innervates ciliary ganglion –> target organs are intrinsic eye muscles

99
Q

CN VII (facial)

A

innervates pterygopalatine and submandibular ganglion–> target organs: lacrimal, salivary

100
Q

CN IX (glossopharyngeal)

A

innervates otic ganglion–> target parotid glands

101
Q

CN X

A

innervates intramural ganglion–> target organs visceral organs of neck, thoracic cavity, and most of the abdominal cavity

102
Q

S2-S4

A

innervates intramural ganglion–> inferior muscle of the abdominopelvic cavity

103
Q

what nerve provides 75% of the parasympathetic outflow?

A

vagus nerve

104
Q

parasympathetic Postganglionic fibers of the upper 4 ganglia (ciliary, otic, pterygopalatine, submandibular, intramural) travel through what nerve?

A

trigeminal

105
Q

where is the Ach synthesized?

A

nerve terminal

106
Q

where is acetyl coA produced?

A

mitochondrial?

107
Q

what enzyme forms acetylcholine?

A

choline acetyl transferase

108
Q

which nervous system is more precise ?

A

parasympathetic . it’s rapidly metabolized to have precise control and the post ganglia is closer to the effector organ!

109
Q

in case you have too much acetylcholine , what receptor presynaptically do you have to regulate it (negative feedback)?

A

M2

110
Q

reactivation of acetylcholinesterase medication?

A

pralidoxime

111
Q

what are the sites of actions of cholinergic antagonist?

A

ganglonic (Nn–> causes profound vasodilation aka preganglionic global blockers) muscarinic, and Nm

112
Q

indirect cholinergic agonist medications?

A

Neostigmine, physostigmine, edrophonium, echothiophate,

113
Q

what PNS receptor does the bladder have?

A

M3 are the ones responsible for the parasympathetic detrusor contraction

114
Q

why is the ANS so important ?

A

because it maintains cardiovascular, metabolic, thermal, and gastrointestinal homeostasis.

115
Q

central control of the ANS is primarily in?

A

medulla oblongata and hypothalamus

116
Q

what is bethanechol?

A

it helps with urinary retention by agonizing muscarinic 3 receptors therefore contracting the muscle and post op GI depression .

117
Q

why do we care about DM with ANS?

A

autonomic neuropathy . blood pressure is labile, gastroparesis, possible prolonged QT interval (because of the imbalance on the right and left stallion ganglion), risk for developing preoperatively cardiac complication. painless myocardial ischemia, arrhythmia. resting tachycardia is a feature of DM neuropathy and a HR between 90-100 bpm is a feature of cardiac autonomic disfunction.

118
Q

epinephrine low, intermediate and high doses effects?

A

-low dose: non selective beta effect predominate (0.01 - 0.03 mcg/kg/min)
beta 1 ^ HR and contractility while b2 mediates vasodilation in the skeletal muscle therefore decrease SVR and increase CO.
-intermediate 0.03-0.15 mcg/kg/min : mixed alpha and beta
- high doses >0.15 mcg/kg/min - alpha effect prevail and bp rises - SVTs are common, and this limits the uses of high dose of epi

119
Q

which of the following MOST accurately describes the affinity to dopamine to adrenergic receptors?

A

dopamine>beta>alpha

120
Q

Dopamine low, intermediate and high doses effects?

A

-low 1-2 mcg/kg/min - renal . selective for DA1 postsynaptic and DA2 presynaptic . in the kidney, DA 2 inhibits release of NE from presynaptic nerve terminals. this augments the vasodilating effects of DA1 receptor in the renal vasculature. the net effect is ^ renal blood flow and urine output. 25% of CO output got to kidneys and low dose DA creates renal validation–> BP may decrease and small reflex tachycardia may be observed
-intermediate 2-10 mcg/kg/min cardiac:
activate beta receptors which ^ contractility, HR and CO . BP is usually unchanged. this is an ideal dose for CHF.
-high doses 10-20 mcg/kg/min vasopressor : dopamine resembles high dose norepinephrine, alpha effects over shadow the dopamine and beta effect .

121
Q

uses for isoproterenol ?

A

Cor pulmonale , bronchoconstriction, heart transplant, chemical pacemaker for Brady and unresponsive to atropine .. DOES NOT WORK ON ALPHA ! just B1 and B2

122
Q

yohimbine

A

alpha 2 antagonist - increases sympathetic tone by ^ NE release from the presynaptic nerve terminal. used to tx orthostatic hypotension . OD leads to tachycardia and hen

123
Q

prazosin

A

alpha 1 antagonist

124
Q

what does methyl blue cause on the vessels?

A

it inhibits NO pathway, which causes wide spread vast constriction . do not exceed 7mg/ kg

125
Q

what is vasoplegia?

A

refractory hypotension

126
Q

central anticholinergic syndrome symptoms?

A

sedation, stupor, coma,. seizure , restlessness, anxiety, hallucinations, and delirium.
other signs of antimuscarinic symptoms: dry mouth , flushed, mydriasis, blurred vision, fever

127
Q

whats another way of saying membrane stabilizing properties?

A

that the drug has local anesthetic-like effects

128
Q

Beta 1 selective antagonist examples?

A

atenolol, acebutolol, betaxolol, esmolol and metropolol

129
Q

non selective beta antagonist examples?

A

cervedilol, labetalol, nadolol, propanolol, timolol

130
Q

cholinergic intervention sites-precursor transport blockade example?

A

Hemicholineum, blocks choline from going into the nerve terminal

131
Q

what can inhibit the choline acetyltransferase enzyme?

A

no clinical example

132
Q

what promotes the Ach transmitter release?

A

choline and black widow spider venom (latrotoxin)

133
Q

what prevents the Ach transmitter release?

A

botulinum toxin

134
Q

what prevents the storage of Ach?

A

Vesamicol

135
Q

cohlinesterase inhibitor?

A

Neostigmine, physostigmine

136
Q

M1 are found in?

A

Neural, gastric parietal cells, hippocampus, cerebral cortex, striatum,

137
Q

M2 are found in?

A

cardiac cells , smooth muscles

138
Q

M3 are found in?

A

bladder, exocrine, smooth muscle

139
Q

Nm(N1) agonist and antagonist?

permeable to what cations?

A

located in skeletal muscular junction
agonist-acetylcholine, succinylcholine and nicotine
antagonist- atracurium, vecuronium, pancuronium, tubocurarine
permeable to K+ and Na+

140
Q

Nn (2) agonist and antagonist ?
permeable to what cations?
and where are they located?

A

located on the autonomic ganglia and renal medulla
Na+ and K+
agonist: nicotine, Ach and epibatidine
antagonist: trimethapan, mecamylamine, hexamethonium ,

141
Q

whats inonotropic ?

A

its a ligand.-gated ion channels

142
Q

Choline Esters examples? (muscarinic agonist)

A

Acetylcholine (works on muscarinic and nicotinic), Methacholine, Bethenechol , Carbachol (direct/indirect muscarinic and nicotinic) (MBC)

143
Q

Alkaloids examples? (muscarinic agonist)

A

Muscarine (found in certain mushroom), Pilocarpine (use for glaucoma) (PM)

144
Q

diagnosis for belladonna poisoning?

A

belladonna is too much atropine (M receptor); methacholine (agonist muscarinic) acts like acetylcholine

145
Q

metyrosine

A

blocks the tyrosine hydroxilase

146
Q

emergency drug for glaucoma

A

pilocarpine which is an muscarinic agonist topical .

147
Q

cholinesterase inhibitor examples ?

A

Slowly Reversible: Neostigmine, Physostigmine
(BBB can be given for atropine OD)
Rapidly Reversible: Edrophonium
Non Reversible: chemical warfare agents, insecticides-atropine is the tx

148
Q

dobutamine acts on what receptors

A

B1>B2>a1

149
Q

general anesthesia

A

It is a controlled state of unconsciousness, accompanied by partial or complete loss of protective reflexes, including the inability to independently maintain an airway or respond purposefully to verbal command

150
Q

conscious sedation

A

It is a state of mind obtained by IV administration of combination of anxiolytics, sedatives and hypnotics &/or analgesic that render the patient relaxed, yet allows the patient to communicate, maintain patent airway and ventilate adequately.

151
Q

Deep sedation

A

It is a depressed level of consciousness with some blunting of protective reflex, although it remains possible to arouse the patient.

152
Q

IATRO

A

A general term used for any technique of anxiety reduction in which no drugs are given
Relief of anxiety through the doctor’s behavior - it is one of the form of psychosedation

153
Q

Fluorination

A

less potent (^ MAC), less intermolecular pressure (^ intermolecular pressure), less metabolism (^ resistance to metabolism) less TFA risk of immune mediated hepatitis ,

154
Q

mechanism of anesthesia

A

facilitates Gaba-a, Glycine; and inhibits NMDA

155
Q

amnesia

A

hippocampus and amygdala

156
Q

consciousness

A

pass and thalamus

157
Q

general anesthesia

A
  1. unconsciousness
  2. amnesia
  3. Immobility
158
Q

Fresh gas flow is determined by ?

A

vaporizes, and flowmeters settings

159
Q

what’s Fi?

A

concentration leaving the circuit not the machine ! (1) FGF (2) breathing circuit volume (3) circuit absorption

160
Q

what’s FA?

A

fraction concentration of gas in alveoli ; (1) uptake (2) ventilation (3) the concentration effect and the second gas effect

161
Q

pharmacokinetics of Inhaled Anesthetics

A 
Affected by Aging:
decreased lean body mass & increased fat 
decreased hepatic function
decreased pulmonary exchange
decreased cardiac output.
162
Q

pharmacokinetics of Inhaled Anesthetics

A 
Affected by Aging:
decreased lean body mass & increased fat 
decreased hepatic function
decreased pulmonary exchange
decreased cardiac output.
Opposite effects in very young
163
Q

what’s Fa ?

A

the arterial gas pressure is determined by ventilation and perfusion

164
Q

what’s vapor pressure?

A

The pressure of the vapor over the liquid at equilibrium

165
Q

what law is for volatile of anesthetics?

A

Henry’s slaw: states that for a given solvent at a given temperature, the amount of gas dissolved in solution is directly proportional to the partial pressure of the gas

166
Q

what are partition coefficients or partition ratios?

A

Partition coefficient = conc of dissolved gas in one solvent/ concentration of gas in gaseous state at equilibrium

167
Q

how is partial pressure controlled ?.

A

Vaporizer → Circuit → Alveoli → Arterial → Brain

We indirectly regulate PBR by adjusting vaporizer

168
Q

what is PA used as an index of?

A
  1. Depth of anesthesia
  2. Recovery from anesthesia
  3. Anesthetic equal potency (MAC)
169
Q

Pbr or PA equals

A

Input into alveoli (input) – arterial blood uptake (loss of the drug from alveoli into arterial blood)
PA is a balance between delivery of drug to the
alveolus and uptake of that drug into the blood
-PA= input ( delivery) – uptake (loss)

170
Q

input (Delivery) transfer from anesthesia machine to alveoli depends on?

A
  1. Inspired partial pressure (PI) (concentration of agent by vaporize Fi)
  2. Alveolar minute ventilation [-increase ↑volume → slower induction (dilution of anesthetic gases)
    - TV
    • RR
    • Dead Space
    • FRC]
  3. Characteristics of the breathing system [time constant of delivery system= fresh gas flow= ↑ FGF → ↑ speed of induction & recovery) and circuit volume(Absorption by the breathing circuit)]
  4. FRC
  5. Anatomical dead space-(Absorption by the breathing circuit)

Concentration Effect & Second Gas Effect

171
Q
  1. Anesthetic loss (uptake) = Transfer of the inhaled anesthetic from alveoli to arterial blood
  2. Anesthetic loss (uptake) = Transfer from arterial blood to brain
A
  1. a. Blood: gas partition coefficient
    b. Cardiac output
    c. Alveolar-to-venous pp difference
    (gradient between alveolar gas and
    mixed venous blood)
    2.
    a. Brain: blood partition coefficient
    b. Cerebral blood flow
    c. Arterial-to-venous partial pressure difference
    PA Pa  Pbr
172
Q

High blood-gas partition coefficient =

A

slow rate of rise of FA to meet FI

173
Q

the rate of rise is directly proportional to

A

to the Fi

174
Q

what is the most important concept of Fi ?

A

FA/FI ratio because We can measure/monitor both FA & FI

We cannot directly measure other compartments directly

175
Q

what does Increased alveolar ventilation results in ?

A

faster increase in alveolar partial pressure by constantly replacing the inhalation agent taken up by the pulmonary blood flow.

176
Q

what does a larger FRC do to the inspired concentration of the gas?

A

dilutes the inspired concentration of gas resulting initially in a lower alveolar partial pressure and therefore slower onset of anaesthesia

177
Q

how do you Increase input of agent to alveoli?

A

High vaporizer %, alveolar ventilation and FGF.

178
Q

how do you Increase output of agent from alveoli?

A

Low venous agent, high solubility, high CO

179
Q

The higher the blood / gas partition coefficient (solubility); what happens to the Fa/Fi ratio?

A

the greater the uptake from the alveolus and The slower the rise of FA to met FI.
Minute ventilation, CO, FGF, and venous agent PP also affect rise of FA to meet FI.

180
Q

what are the Factors that affect increase of PA ?

A

Volume of breathing system
Solubility of gas into the plastic components of the circuit
Gas inflow from anesthesia machine

181
Q

example of time constant and what does it mean ?

A

If 10 L box ( lungs) is initially filled with O2 & nitrogen at 5 L/min into the box (lungs), the t = volume/flow

Thus, t = 10/5= 2 minutes = 1 Time constant

Or, we say the nitrogen concentration at the end of 2 minutes is 63 %
1t 63%
2t 86%
3t 95%
4t 98%

182
Q

what does the concentration effect impact?

A

The impact that FI has on the rate of rise of PA of an inhaled anesthetic agents is the concentration effect
The higher the FI the more rapidly the PA approaches the FI. The rate of rise of alveolar end tidal concentration is dependent upon and accelerated by high initial inspired concentration of anesthetic gas,

183
Q

what its second gas effect

A

Reflects the ability of high-volume uptake of one gas (first gas) to accelerate the rate of rise of PA of a concurrently administered companion gas (second gas)

184
Q

how do we measure solubility ?

A

blood: gas partition coefficient.
the larger the number , the more soluble in the. blood.
Higher BGPC= increased uptake in blood = slower rise in PA(slow induction)
Ex: BGPC of .42 means each 1mL of blood holds .42 times as much agent as a 1mL of alveolar gas does.

185
Q

how do you measure potency of gas?

A

Oil: Gas Partition Coefficient: Reflects anesthetic requirements. Describes the lipid solubility of an IA

186
Q

Why might lipid solubility be related to the potency of the volatile and gaseous agents?

A

Because IA depend on lipid solubility to cross the CNS to exert their effect and this requires for them to cross the blood- brain barrier. Only lipid soluble drugs can gain acces to the brain.

187
Q

what is Alveolar-Venous Gradient affected by?

A

Tissue-blood partition coefficient (tissue solubility)
Tissue blood flow
Tissue anesthetic concentration
-Gradient depends on tissue uptake
Tissue uptake depends on tissue solubility, tissue blood flow, partial pressure diff betⁿ arterial blood & tissue

188
Q

Vessel rich group (VRG):

A

Brain, heart, liver, kidney & spinal cord
Perfusion is 75ml/min/100gm.
Small vol. of tissue (10% of body mass) relative to perfusion (75% of C.O)
Time constant for anesthetic equilibration between these organs, only few minutes

189
Q

low hepatic ER

A 
rocuronium 
diazepam 
lorazepam
methadone
thiopental 
thephyllin
phenytoin
190
Q

intermediate hepatic ER

A

midazolam vecuronium alfentanyl methohexital

191
Q

high hepatic ER

A

morphine, FENTANYL, ketamine, propofol, metoprolol propanolol, LIDOCAINE, diltiazem, naloxone

192
Q

medications metabolized by pseudocholinestarase

A

PROcaine, TETrAcaine, , Chloroprocaine, Cocaine (+hepatic) SUccx

193
Q

medications metabolized by other non specific esters

A

Esmolol, Etomidate, Remifentanyl, Atracurium

194
Q

Hoffman elimination

A

(Cisa) Cistracurium, and Atracurium (+non specific esterases)

195
Q

neonates and term babies pharmacokynetics

A

more water weight, less protein, less muscle, less fat, kidneys and liver not fully developed

196
Q

older people pharmacokynetics

A

Decreased circulating levels of drug-binding serum proteins
Protein binding is less effective
Co-administered drugs may interfere with the ability of anesthesia agents to bind to available serum protein binding sites
Certain disease states exaggerate this phenomenon
Loss of skeletal muscle (lean body mass)
Increase in the percentage of body fat
Greater reservoir
20-30% decrease in blood volume occurs by 75 yrs of age
Drugs administered into a contracted volume (increased concentration)
glomerular filtration rate that in old age is only 60 percent of that found in younger individuals.

197
Q

volume of distribution is inversely proportional to ?

A

protein binding

198
Q

racemic mixtures

A

ephedrine, ketamine, and desflurane

199
Q

Mac is Inversely proportional to and Indirectly related to

A

Inversely proportional to anesthetic potency

Indirectly related to anesthetics oil: gas partition coefficient

200
Q

MAC awake:
MAC 95%:
MAC intubation:
MAC-BAR

A

MAC allowing voluntary response to command in 50% of patients(0.15 – 0.5 MAC)

  • MAC that prevents movement in 95 % of patients (1.2-1.3 MAC or +25% of MAC)
  • MAC that allows intubation without muscle relaxant, coughing or bucking in 50% of patients.
  • 1.7-2.MAC or +50% of stand. MAC), which is the concentration required to blockautonomic reflexes tonociceptive stimuli.
201
Q

factors decreasing MAC?

A 
Increasing age
Hypothermia
Hyponatremia
Hypotension (MAP<50mmHg)
Pregnancy
Hypoxemia (<38 mmHg)
O2 content (<4.3 ml O2/dl)
Metabolic acidosis
Narcotics 
Ketamine
Benzodiazepines
alpha2 agonists
LiCO3
Local anesthetics
ETOH (acute)
202
Q

factors increasing MAC?

A 
Hyperthermia
Chronic ETOH abuse
Hypernatremia
Increased CNS transmitters
MAOI
Amphetamine
Cocaine 
Ephedrine
L-DOPA
203
Q

factors that do not influence on MAC?

A 
Duration of anesthesia
Sex
Alkalosis
PCO2
Hypertension
Anemia
Potassium
Magnesium
And others

pharm exam 1 (12 decks)

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