Midterm Flashcards
(125 cards)
1
Q
1st generation H1 antagonist anticholinergic adverse effects
A
dry mouth, blurred vision, urinary retention, impotence
2
Q
1st generation H1 antagonist cardiovascular adverse effects
A
tachycardia, prolonged QTc, heart blocks, arrhythmias
3
Q
1st generation H1 antagonist CNS adverse effects
A
somnolence, diminished alertness, slowed reaction time, impaired cognitive function (take in PM)
4
Q
4 concepts of pharmacodynamics
A
absorption, distribution, biotransformation, elimination
5
Q
Additive effects
A
1+1=2 summation of drugs taken concurrently (same receptor)
6
Q
Antagonistic effects
A
1+1=0 one drug cancels/blocks effects of another
7
Q
Antagonistic effects
A
1+1=0 one drug cancels/blocks effects of another
8
Q
Are NSAIDs highly protein bound?
A
yes
9
Q
Benadryl is prescribed as:
A
antiemetic, sedative, antipruritic
10
Q
Benefits of benzos
A
less risk of tolerance and abuse, large margin of safety
11
Q
Benzos are used for:
A
antianxiety, sedatives, anticonvulsants, muscle relaxants
12
Q
Binding of glutamate to NMDA receptors allows
A
influx of Na and Ca
13
Q
Cardiovascular Adverse Effects of NSAIDs
A
HTN, HF exacerbation, thrombotic events
14
Q
Clearance
A
volume of plasma cleared of drug per unit time
15
Q
Clinical uses for SSRIs
A
depression, panic disorders, OCD, PTSD, social phobias
16
Q
Clonidine
A
selective partial alpha 2 agonist
17
Q
CNS adverse effects of NSAIDs
A
headache, aseptic meningitis, hearing disturbances
18
Q
conjugation
A
makes lipid soluble drugs water soluble (with glucoronic acid)
19
Q
conjugation leads to:
A
a more polar compound that is more highly ionized at physiologic pH and therefore more easily extractable by the kidney via glomerular filtration
20
Q
Consideration of patient taking lithium and anesthesia
A
decreased anesthetic requirements- may delay CNS recovery from barbiturates, response to NMBs may be prolonged
21
Q
contraindication of benzo use for anxiety
A
history of alcohol or other substance abuse
22
Q
Corticosteroids
A
naturally occurring from adrenal glands (hydrocortisone)
23
Q
dermatologic adverse effects of NSAIDs
A
urticaria, rash, erythema multiforme
24
Q
Does succinylcholine affect CP450?
A
no
25
Dosage of benzos for generalized anxiety
low dose, 2-5 mg (diazepam) up to 3 times daily
26
Effects of clonidine
antihypertensive, potentiate analgesic effects post-op induced by LA
27
End products of biotransformation are...
usually inactive and water soluble (easier excretion)
28
example of microsomal enzymes
cytochrome P450
29
Examples of 1st generation H1 antagonists
benadryl, chlorpheniramine, atarax
30
Examples of drugs that undergo zero order kinetics
alcohol, phenytoin (dilantin)
31
Examples of drugs that undergo zero order kinetics
alcohol, phenytoin (dilantin), fluoxetine, salicylates
32
Examples of H2 receptor antagonists
ranitidine, famotidine, nizatidine, cimeditine
33
Examples of MAOIs
phenelzine, tranylcypromine, isocarboxazid
34
Examples of SSRIs
fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram, escitalopram
35
First Order Kinetics
constant FRACTION of drug eliminated/unit time
36
First pass effect
drugs absorbed through GI tract enter portal venous blood and pass through liver before entering systemic circulation
37
GABA anion
chloride
38
GI adverse effects of NSAIDs
gastrophy, gastric bleeding, esophageal disease, pancreatitis
39
Goal lithium plasma concentration
1.0-1.2 mEq/L
40
GU adverse effects of NSAIDs
renal insufficiency (use with caution with renal disease), Na/fluid retention, papillary necrosis, interstitial nephritis
41
Half life
period of time required for the concentration/amount of drug to be reduced by half
42
hematologic adverse effects of NSAIDS
increased risk of intraop bleeding (platelet inhibition/dysfunction)
43
Hepatic clearance depends on
hepatic blood flow and hepatic extraction ratio
44
hepatic extraction ratio
drug removed from blood- limited by enzyme activity
45
How do benzos work?
facilitating actions of GABA (y-aminobutyric acid)- major inhibitory NT of nervous system
46
How long does it take for lithium to be effective?
several weeks
47
hydrolysis
split apart with water
48
In 1st order kinetics, rate of drug elimination is ? to drug plasma concentration
proportional (rate increases as drug concentration increases)
49
In order to be eliminated by the kidneys, can the drug still be bound to proteins?
no- must be non protein bound to cross into glomerular filtrate
50
In zero order kinetics, the rate of drug elimination is ? of drug plasma concentration
independent (rate does not increase as drug concentration increases)
51
ionized
charged, not lipid soluble
52
Lithium plasma concentrations should be drawn no sooner than ? after dosage change
5 days (unless toxicity suspected)
53
Mechanism of action of glucocorticoids
decrease production of inflammatory mediators (alter pain perception), inhibition of phospholipase A2, glucocorticoid receptor activation
54
Mild lithium toxicity
1-1.5 mEq/L lethargy, irritability, weakness, tremor, slurred speech, nausea
55
Moderate lithium toxicity
1.6-2.5 mEq/L confusion, drowsiness, restlessness, unsteady gait, coarse tremor, dysarthria, fasciculations, vomiting
56
Molecular size
the smaller, the better it crosses membrane
57
Most common side effects of lithium:
polydipsia, polyuria, hypothyroidism, tremor
58
nonionized
no charge, lipid soluble - usually pharmacologically active
59
Nonionized vs ionized, lipid or water soluble?
nonionized= lipophilic (easier to get in) ionized= hydrophilic
60
NSAIDs
ASA and COX inhibitors
61
NSAIDs should be used with caution with...
renal and liver disease
62
Oxidation
lose electron, gain oxygen
63
pharmacologic interactions (NSAIDs)
displace albumin bound drugs and can potentiate effects (warfarin)
64
phase 1 reactions
oxidation, reduction, hydrolysis
65
phase 2 reaction
conjugate
66
Phase 2 reactions- a drug or metabolite is conjugated with an endogenous substrate such as...
glucuronic, sulfonic, or acetic acid
67
Phases of 1st order kinetics
alpha- initial rapid decline in concentration (redistribution) beta- elimination of drug central compartment
68
Plasma proteins and what they bind to
-albumin- acidic -alpha 1 glycoprotein- basic beta globulin- basic
69
Plasma proteins and what they bind to
-albumin- acidic -alpha 1 glycoprotein- basic beta globulin- basic
70
Prohibited drugs for MAOIs
cyclic antidepressants, fluoxetine, cold/allergy medications, nasal decongestants, sympathomimetic drugs, opioids (ESPECIALLY MEPERIDINE)
71
Protein binding
-if drug is protein bound, it is not available for site of action -bind is usually weak -protein binding prevents meds from leaving bloodstream to site of action
72
Protein binding and lipid solubility are ? proportional
directly
73
Re-distribution
alpha phase of the two compartment model- initial rapid decline in plasma concentration (redistribution of drug from central to peripheral compartment)
74
Reduction
electron gain
75
respiratory adverse effects of NSAIDs
nasal polyps, rhinitis, dyspnea, bronchospasm, angioedema, asthma exacerbation
76
Samter's triad
where an individual has asthma, sinus inflammation with recurring polyps, and sensitivity to ASA and other NSAIDs (severe reaction- upper and lower respiratory symptoms)
77
SE of Trazodone
nausea and vomiting, sedation, orthostatic hypotension
78
Severe lithium toxicity
\>2.5 mEq/L coma, delirium, ataxia, extrapyrimidal symptoms, seizures, impaired renal function
79
skeletal adverse effects of NSAIDs
inhibit bone growth/healing/formation
80
Synergistic effects
1+1=3 effect of drug is enhanced by another (different receptors)
81
Tachyphylaxis
rapid decrease in response to repeated doses over a short period of time- see this with ephidrine boluses
82
Trazodone
SSRI- used for depression and insomnia
83
trazodone considerations
should not be taken with MAOIs, has brief half life
84
Use of clonidine reduces the need for what?
opioids
85
Use of glucocorticoids (steroids)
reduce inflammation (most powerful steroid)
86
vessel intermediate compartment
muscle, fat, skin
87
Vessel poor compartment
bone, ligament, cartilage
88
Vessel rich compartment
brain, heart, liver, kidney, endocrine glands -receive 75% of cardiac output
89
volume distribution of NSAIDs is?
low
90
What % of protein binding is considered highly protein bound?
\>90%
91
What are H1 antagonists used for?
allergic rhinoconjuctivitis, protection against bronchospasm, pruritis, acute anaphylaxis
92
What are H2 antagonists used for?
inhibition of H2 receptor mediated gastric acid secretion
93
What are some conditions that decrease plasma proteins?
renal failure, liver failure, malignancies, trauma, infection, malnutrition
94
What can caused increased reabsorption of lithium?
sodium depletion (dehydration)- sodium restriction/wasting
95
What cases are clonidine commonly used for?
labor epidural- no effects on fetal HR, etc.
96
What disorder is lithium used for?
bipolar disorder
97
what do NSAIDs inhibit?
biosynthesis of prostaglandin
98
What do phase 1 reactions do?
converts drug into polar metabolites
99
What do phase 2 reactions do?
couple/conjugate drug into polar end product
100
What do SSRIs do?
block reuptake of serotonin
101
What do we use for skeletal muscle rigidity associated with MAOIs?
dantrolene
102
What does lithium do to the neurons?
depletes second messengers, dampens signal transmission
103
What drugs should patients avoid while on lithium?
NSAIDs and diuretics (increases plasma levels)
104
What foods should be avoided when taking MAOIs?
cheese, liver, fava beans, avocados, chianti wine
105
What happens if a patient has a reduction in plasma proteins?
highly protein bound drugs will have a greater clinical effect (more circulating drug available)- but rate of elimination will also increase
106
What increases half time of lithium?
renal disease, old age
107
What is a ligand?
drug or neurotransmitter
108
What is a safer alternative to NSAIDs in the perioperative setting?
coxibs (less platelet dysfunction and GI toxicity)
109
What is another route that clonidine is administered?
Epidurally- prolongs sensory and motor blocks
110
What is the largest compartment in the compartment model?
vessel poor
111
What is the ligand for NMDA receptors?
glutamate
112
What route is most subject to the first pass effect?
oral
113
What tricyclic antidepressants are good for chronic pain like fibromyalgia?
amitriptyline, imipramine
114
When should lithium levels be drawn?
10-12 hours after last oral dose
115
Where are hepatic microsomal enzymes located?
smooth endoplasmic reticulum
116
Which drug has a black box warning for prolonged QTc and torsades?
droperidol
117
Which route may or may not be subject to the first pass effect?
rectal
118
Which routes completely bypasses the first pass effect?
IV, topical (including buccal), sublingual
119
Zero order kinetics
constant AMOUNT of drug eliminated per unit time (once you saturate enzymes, eliminated at constant rate)
120
Half life table
121
First order vs zero order graph
122
4 Types of target proteins
receptors, ion channels, enzymes, carrier molecules (transporters)
123
Specificity
specific for that receptor (will key fit into lock)
124
Affinity
how well/avidly drug binds to receptor
125
Intrinsic activity
magnitude of the effect of the drug once it is bound (how well the key turns)
