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Pharm. Final Review > Previously Tested exams 1-3 > Flashcards

Previously Tested exams 1-3 Flashcards

0
Q

Define: Potency

A

measurement of how much drug is needed to produce the effect (determined by affinity & intrinsic activity)

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1
Q

What legislation established regulations for the use of opium, opiates, and cocaine (marijuana added in 1937)

A

Harrison Narcotic Act 1914

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2
Q

Describe schedule 2 drugs

A
  • High abuse potential
  • Currently accepted for clinical use under severe restrictions (no phone in or refills
  • Abuse may lead to psychological or physical dependence
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3
Q

Define tachyphylaxis

A

development of tolerance with only a few doses

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4
Q

Define: affinity

A

degree to which molecule is attracted to receptor

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5
Q

What is “intrinsic activity”

A

degree to which a molecule performs its actions at a receptor

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6
Q

Define: synergistic effect

A

two drugs interact to produce greater effect equal to a mathematical equations

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7
Q

What’s ED50

A

Dose at which desired effect will occur in 50% of individuals

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8
Q

What determines the concentration of drug required?

A

Receptor affinity

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9
Q

What type of bond is strong, non-reversible?

A

Covalent bond

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10
Q

Define: down regulation

A

When receptors are bombarded/ overwhelmed with stimuli they decrease in numbers

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11
Q

What is “up regulation”

A

When stimuli os down receptors increase in an attempt to respond maximally

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12
Q

What is a ligand-gated ion channel

A

A channel opens/ closes in response to binding of the signaling molecule (ligand)

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13
Q

Define a racemic mixture

A

When 2 molecules exist in equal (50:50) proportions in a substance

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14
Q

What is a competitive antagonist

A
  • Binds ,REVERSIBLY, to same site as the agonist

- Can be overcome by increased amounts of agonist

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15
Q

What’s a “Non-competitive antagonist”

A
  • Binds IRREVERSIBLY to receptor via covalent bonds.
  • Not displaced by increased amounts of agonist
  • Duration of action depends on turn over of receptors more than elimination of drug
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16
Q

Describe First Pass Hepatic Effect

A

Some of the drug absorbed from GI enters the portal venous blood thereby passing through liver before entering systemic circulation

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17
Q

Define “High Hepatic extraction ratio”

A

Drugs that are extensively extracted into liver (1st pass effect)

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18
Q

Which parts of the rectum are & aren’t subject to first pass effect & why/ why not

A
  • Proximal rectum is subject to 1st pass r/t venous supply from the superior hemorrhoidal veins which drain into portal venous supply
  • Distal rectum has no 1st pass effect because it’s absorbed into systemic circulation via the IVC
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19
Q

The movement of a drug from the central compartment to the peripheral compartment is termed:

A

Distribution

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20
Q

How much of cardiac output goes to the central compartment (Highly perfused tissues)

A

75%

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21
Q

Define volume of distribution (Vd)

A

MAthematical expression of amount of drugs in the compartments

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22
Q

Formula for figuring out the Vd (Volume of distribution)

A

Vd= the amount of drug in the body divided by the concentration in blood

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23
Q

What is the Volume of Distribution a reflection of?

A

Reflects the balance between binding tissues, which decreases plasma concentrations and makes apparent volume larger, and binding to plasma proteins which increases plasma concentration & makes volume of distribution smaller

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24
Q

Most acidic drugs bind to________ where as most basic drugs bind to______

A

Most acidic drugs bind to ALBUMIN where as most basic drugs bind to AAG

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25
Q

How is volume of distribution related to protein binding

A

Vd is INVERSELY related to protein binding

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26
Q

What happens when highly protein bound drugs are altered

A

The amount of drug available increases & the Vd increases

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27
Q

Define pKa related to pH

A

the pKa is the pH @ which the drug is 50% ionized

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28
Q

Environment that acidic & basic drugs are most highly ionized

A
  • Acidic drugs are most highly ionized in an alkaline environment
  • Basic drugs are most highly ionized in an acidic environment
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29
Q

Rule of thumb for acidic/ basic drugs r/t administering to patients

A
  • acidic drugs into acidic patients

- basic drugs into less acidic (basic) patients

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30
Q

Define drug “Redistribution”

A
  • movement of drug away from vessel rich group
  • As plasma concentrations drop below tissue concentrations in vessel rich group, drug leaves vessel rich group to less perfused sites like muscle
  • DOES NOT MEAN ELIMINATION
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31
Q

Define “Zero Order Kinetics”

A
  • Constant amount of drug eliminated PER UNIT of TIME. Occurs when plasma concentrations of drug exceeds capacity of metabolizing enzymes.
  • Rate of metabolism is not increased by higher concentrations (ex. ETOH, will eliminated over same time no matter what the plasma level is)
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32
Q

Define “First order of Kinetics”

A
  • Rate of amount of drug metabolized is proportional to the concentration of drug in plasma
  • (How fast metabolized depends on how much in plasma)
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33
Q

Define hydrolysis (drug)

A
  • involves non-microsomal enzymes
  • Hydrolysis often at ester bond
  • CP450 not involved
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34
Q

The time it takes to eliminate 50% of drug from the BODY is defined as:

A

Elimination half LIFE

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35
Q

The time needed to eliminate 50% of drug from the plasma is defined as:

A

Elimination half TIME

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36
Q

Define “Context sensitive half time”

A

Time needed for plasma concentration of drug to reach 50% after discontinuation of a CONTINUOUS IV infusion

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37
Q

Where are most drugs metabolized

A

Liver

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38
Q

What organ is responsible for the elimination of most drugs

A

Kidneys

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39
Q

How does cardiac output effect onset of anesthesia in the brain

A

Decreased CO> increase alveolar concentration> increase of anesthesia onset in brain

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40
Q

Define MAC

A

The inspired concentration (%) at 1atm that prevents skeletal muscle movement in response to painful stimuli (surgical incision) in 50% of individuals

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41
Q

What does “Thoracolumbar outlow” refer too?

A

Nerves arising from T1-L2 segments of spinal cord

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42
Q

Describe the PNS results in the lungs

A
  • Pulmonary arteriole relaxation

- Smooth muscle contraction

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43
Q

What neurotransmitter is released by all preganglionic neurons

A

ACh

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44
Q

What is released by all PNS postganglionic neurons

A

AcH

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45
Q

What is released by all MOTOR neurons to SKELETAL muscle

A

AcH

46
Q

Course Catecholamine synthesis (the synthesis of epinephrine/ EPI)

A

TYROSINE (converted by tyrosine hydroxylase)> DOPA (converted by decarboxylase)> DOPAMINE (enters vessicle & converted by dopamine-beta-hydroxylase)> NE (converted by phenylethanolamie-N-methyltransferase) > EPI

47
Q

What is the “rate limiting step” to catecholamine synthesis?

A

( Tyrosine ) Tyrosine hydroxylase

48
Q

How & when is Norepinephrine released? What ion is essential for its release?

A

Released by exocytosis through a CALCIUM ion dependent mechanism in response to an action potential

49
Q

What is responsible for the NE being metabolized in extra nodal tissue?

A

catechol-methyltransferase (COMT)

50
Q

Is COMT inhibited pharmologically?

A

No, not like MAO (Monomineoxidase)

51
Q

Describe the synthesis of acetylcholine (Ach)

A

AcCoA (acetyl coenzyme A) + Choline (w/ choline acetyltransferase as a catalyst)= Acetylcholine

52
Q

What must be present in extracellular fluid for acetylcholine to be released iin response to an action potential

A

Calcium

53
Q

Are Alpha 2 receptors pre or post synaptic

A

both

54
Q

function of alpha 2 post synaptic receptors

A
  • Sedation

- hyper polarization of CNS cells (Decrease MAC), platelet aggregation

55
Q

function of alpha 2 pre synaptic receptors

A

-inhibition of NE release (negative feedback loop)

56
Q

Define allodynia

A

pain evoked by a non-noxious stimulus

57
Q

in which laminae do afferent C fibers terminate

A

in dorsal horn in laminae 2 & 3

58
Q

Clonidine analgesic characteristics

A
  • Alpha 2 agonist
  • Analgesic properties after a single dose
  • Sedation, bradycardia, or hypotension can be seen
  • Useful to augment morphine analgesia, & L.A blocks
59
Q

Result of opiate receptor activation

A
  • inhibition of adenylyl cyclase

- Presynaptic inhibition of neurotransmitter release block Ca channels causing decrease cAMP

60
Q

Kappa, K-1 is responsible for what type of analgesia

A

spinal analgesia

61
Q

kappa, K-3 subset is responsible for what type of analgesia

A

-Supraspinal analgesia, may elicit sedation/ dysphoria (doesn’t contribute to dependence)

62
Q

Binding properties of Sufentanil.

A

-Extensive protein binding (92.5%) therefore smaller vD than fentanyl therefore shorter elimination half life & shorter context sensitive half time

63
Q

How is remifentanil affected by pseudocholinesterase deficiency?

A

It’s not

64
Q

How is remifentanil’s pharmacokinetics affected by renal or hepatic failure

A

It is uneffected

65
Q

Dose of Naloxone (Narcan)

A

0.05-0.1mg increments to effect

66
Q

Relative potency

A

MsO4 1
Alfentanil x10
Fentanyl x100
Sufentanil x1000

67
Q

Where does acetylcholine work

A

-muscarinic receptors

68
Q

Effect of glutamate

A

excitatory

69
Q

Effects of dopamine & seratonin

A
  • inhibitory

- (serotonin can be excitatory @ some subsets)

70
Q

How should Thiopental be prepared ?

A

as a 2.5% solution

71
Q

How should Methohexital solution be prepared

A

1%^ solution

72
Q

What is the awakening of Thiopental a result of?

A

Rapid redistribution

73
Q

MOA of barbiturates

A

-Thought to act through interaction of GABA (decrease rate of dissociation of GABA from receptor thereby depressing RAS)

(speed GABA leaves receptor is slowed down by Ca++ channel staying open longer> cell stays more negative> inhibitory response)

74
Q

What is given to manage an intrarterial injection?

A

Phenoxybenzamine (vasodilator to avoid ischemia)

75
Q

What is the chemical make up of Propofol

A

1% solution in aqueous solution of 10% soybean oil, 2.25% glycerol, 1.2% egg phosphatide

76
Q

How long can Propofol be kept at rm. temp

A

-12 hours thought to be ok, but 6 hours is current thinking

77
Q

Induction dose of propofol

A

2.0-2.25 mg/kg

78
Q

Propofol cardiovascular effects

A
  • INHIBITS BARORECEPTOR reflex

- myocardial depression, (decrease CO, SVR, HR, B/P)

79
Q

What side neuro-effect is unique to Etomisate

A
  • Myoclonus (common occurrence as high as 87%)
  • Caused by a central effect, disinhibition of subcortical structures responsible for suppressing extrapyramidal motor activity
80
Q

Where does Precedex work?

A

Alpha-2 agonist pre & post (primarily pre-synaptic)

81
Q

Ketamine is a derivative of what substance

A

Phencylidine

82
Q

at what receptor does Ketamine interact

A

interacts at N-methyl-D-asparate (NMDA) receptor

83
Q

Cardiovascular effects of Ketamine

A
  • Think SNS stimulation

- Increase HR, PAP, CO, Myocardial MRO2 (Myocardial oxygen consumption)

84
Q

Does Droperidol increase or decrease SVR? How so?

A

by alpha 1 antagonist effects

85
Q

What are Benzodiazepines effect on memory?

A

-they cause antegrade amnesia (from time of drug forward)

86
Q

Benzodiazepine proposed occupancy

A 
20%= anxiolysis
30-50%= sedation
>60%= loss of consciousness
87
Q

Effects of benzodiazepines are dependent upon what

A

rate of occupancy

88
Q

What are the active metabolites of Diazepam?

A
  • Desmethyldiaepam

- oxazepam

89
Q

How does Midalozam effect EEG

A
  • Unable to get isoelectric EEG like barbiturates

- Decrease CMRO@ & CBF but a ceiling effect exists

90
Q

What type of receptors will cause an increase in potassium?

A

extrajunctional

91
Q

Anticholinesterase on a phase 1 block

A

block is augmented not reversed

92
Q

Cardiac effects of Succinylsholine

A
  • Bradycardia
  • Hyperkalemia may be result of proliferation of extrajunctional cholinergic receptors in nerve damage or denervated states providing sites for K+ to leak from cells during depolariztion
93
Q

Onset of Succs

A

30-60 sec

94
Q

DOA of Succs.

A

4-6 minutes

95
Q

How much of receptors can be occupied before evidence of blockade?

A

70%

96
Q

What are the cardiac side effects of Pavulon?

A

-Increased HR r/t may block cardiac muscarine receptors

97
Q

Non-Depolarizing Neuromuscular blocking drugs can be enhanced by what main drugs (on last exam)

A
  • Magnesium

- antibiotics (aminoglyceride)

98
Q

How is potency of neuromuscular blocking drugs determined

A

-potency comparisons are made by the amount of drug needed to produce a 95% block when given with barbiturate, opiate, and N2O

99
Q

Effects of NMBD on diaphragm compared to small, rapidly moving muscles

A

Affect small rapidly moving muscles before diaphragm (may take 2x the dose)

100
Q

How much blockade noted with 2 twithces on TOF

A

80%

101
Q

How many TOF twitches necessary prior to reversal

A

1-2

102
Q

Vecuronium undergoes what type of excretion?

A

30% renal & 40-70% biliary

103
Q

Which 2 muscle relaxations can be used for RSI

A

Succinylcholine & Rocuronium

104
Q

What med. is used to treat Atropine toxicity (post op delirium)

A

Physostigmine

105
Q

Signs & symptoms of Atropine toxicity (post op delirium)

A
  • Increased temp,
  • Dry mouth (dehydration)
  • Tachycardia
  • red, flushed skin
  • NO HTN!!!
106
Q

Atropine doses for SB/ ACLS, preop, and reversal

A
  • SB/ACLS 0.5-1.0mg
  • Preop 0.5-1.0mg
  • reversal 0.015mg/kg (1mg for 70kg), with Neo 0.05mg/ kg or Enlon 0.5-1.0mg/ kg
107
Q

Which anticholinergic has the greatest antisialoguge effect?

A

Glycopyrulate

108
Q

Neostigmine (prostigmine) dose

A
  • 0.05mg/ kg (max 5mg)

- with Atropine 0.015mg/ kg or Glycopyrrulate 0.01mg/ kg

109
Q

Edrophonium (Enlon, Tensilon) dose

A
  • 0.5-0.1mg/ kg (max 40mg)

- with Atropine 0.015mg, kg or Glycopyrrolate 0.01mg/kg

110
Q

Pyridostigmine doses

A
  • 0.25mg/ kg (30mg max)

- with Atropine 0.015mg/ kg or Glycopyrrolate 0.1mg/ kg

111
Q

If your patient has 4 twitches on TOF and spontaneously breathing should you still give full reversal dose

A

YES!!!

112
Q

Cardiovascular effects of Anticholinesterase reversal drugs

A

Profound bradycardia

Pharm. Final Review (1 decks)

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