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Pharm > Exam 1 Pharmacology > Flashcards

Exam 1 Pharmacology Flashcards

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1
Q

What are Prostaglandins?

A

Lipids made at the site of tissue injury.

These increase pain sensitivity, inflammation, and blood flow

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2
Q

Acetaminophen (Tylenol) MOA

A

Inhibits synthesis of prostaglandins in the CNS and works peripherally to block pain impulse generation

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3
Q

Acetaminophen (Tylenol) info and affects

A

Good at lower body temp

1st line of use in OA

No anti-inflammatory effects

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4
Q

Acetaminophen (Tylenol) ADRs

A

Hepatic necrosis at high doses

Not to be used w/ alcohol

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5
Q

APAP (Tylenol) overdose & Treatment

A

too much dose causes exhausts glutathione stores in the level, which neutralize toxic metabolites

TREATMENT
NAC (for overdose) - replenishes glutathione

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6
Q

NSAIDs MOA and Clinical use

A

MOA
- COX-1/2 inhibitor, decrease prostaglandin precursors

Clinical use
- pain/inflammation
- commonly combined w/ opioids

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7
Q

NSAIDs SE/ADR and risk factors

A

SE/ADR
GI bleeding, perforation, and kidney disease

Risk of bleeding due to decreased platelet

Fluid retention

Risk factors
Avoid w/ kidney/hepatic disease
caution w/ elderly (bleeding/kidney damage)

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8
Q

Characteristics that distinguish NSAIDs to Narcotics (Opioids)

A
  • Antipyretic (reduce fever)
  • Anti-inflammatory
  • Ceiling affect to analgesia(pain)
  • DO NOT cause tolerance
  • DO NOT cause dependence
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9
Q

COX-1 ADR w/ inhibition

A

GI
Peptic ulcers
GI Bleeding

Kidney
- Na/Water retention
- HTN
- hemodynamic acute kidney injury

Cardiovascular
- Vasoconstriction
- platelet aggregation

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10
Q

COX-2 inhibition SE/ADR

A

Kidney
- Na/Water retention
- HTN
- hemodynamic acute kidney injury

Cardiovascular
- Increase vasodilation
- inhibit platelet aggregation
- Stroke
- MI

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11
Q

What is Naproxen and what is its advantage

A

NSAID

BID (twice/day)

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12
Q

What is Meloxicam and what is its advantage

A

NSAID

once/day dosing

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13
Q

What is Ketorolac (Toradol)?

A

1st NSAID in U.S.

limited to 5 days due to ADRs (GI bleeding)

caution w/ renal insufficient pts.

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14
Q

What is Diclofenac

A

NSAIDs

has multiple dosage forms/names

Oral and Topical

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15
Q

What is Indomethacin (Indocin)

A

NSAID

Used for gout

Higher risk for GI bleeding compared to other traditional NSAIDs

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16
Q

What are Propionic acids?

A

Most commonly seen OTC NSAIDs like Ibuprofen

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17
Q

What are the chronic ADRs of NSAIDs

A

GI bleeding

Kidney damage

Fluid retention

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18
Q

Selective COX 1 vs COX 2 inhibition differences in ADR

A

COX-1
- GI ADR (Peptic ulcers and GI bleeds)

COX-2
- Cardiovascular ADR (Stroke/MI)

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19
Q

What is the only COX-2 inhibitor left on the market?

A

Celecoxib (Celebrex)

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20
Q

What are Salicylates?

A

Aspirin (ASA)

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21
Q

What is the MOA for Aspirin (ASA)?

A

Inhibits Cyclooxygenase which decreases prostaglandins

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22
Q

What are the ADRs for Aspirin (ASA)?

A

Tinnitus (first sign of toxicity) - ringing on the ear

GI bleeding

must avoid in children under 12

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23
Q

What are adjuvants?

A

meds that are meant to treat conditions that are not directly pain.

Fibromyalgia / neuropathic pain

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24
Q

What is the MOA of Adjuvants?

A

Effect 5-HT and NE

often used w/ opioids for greater pain relief

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25
Q

What are the 4 main types of adjuvants?

A

Antiepileptics
SNRIs
Local Anesthetics
TCAs

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26
Q

What do you use to treat neuropathic pain?

A

Antidepressants: Focus on 5-HT+NE
TCAs
SNRI
Antiepileptic drugs (AEDs)
Local/topical anesthetics

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27
Q

What is the main ADR for TCAs

A

Anticholinergic effects

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28
Q

What are anticholinergic effects?

A

Urinary retention

Increased HR

Blurry vision

Constipation

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29
Q

What are the two most common AEDs

A

Gabapentin and Pregabalin

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30
Q

What do Gabapentin and Pregabalin do?

A

Increase GABA inhibitory response

Decrease seizures/epilepsy

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31
Q

What is a ADR of using a drug that increases NE

A

vasoconstriction and increased HR

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32
Q

What is the short-term treatment of anxiety?

A

Benzodiazepines

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33
Q

What are the long-term treatments of anxiety?

A

Buspirone
SSRIs
SNRIs
TCA

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34
Q

What are the treatments for resistant anxiety?

A

Mood stabilizers and Beta blockers

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35
Q

What are Benzos MOA?

A

Bind to benzo receptors to enhance GABA.

Rapid relief and very effective

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36
Q

What are the Disadvantages of Benzos?

A

Tolerance, addiction, need to taper and only treat symptoms not actual cause

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37
Q

What are Xanax?

A

BENZO

intermediate onset w/ 12-15 hours t1/2

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38
Q

What are Klonopin?

A

BENZO

intermediate onset w/ 24-40 hr t1/2

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39
Q

What is valium?

A

BENZO

Rapid onset w/ 20-80 hr half life which makes it not good for the older pop.

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40
Q

What is Ativan?

A

BENZO

intermediate onset w/ half life 10-20 hr

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41
Q

What is the MOA for Buspirone?

A

Mid brain modulator, effects NE, ACh, DA, 5-HT, and GABA

basically affects all NTs

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42
Q

Adv and Disadv of Buspirone?

A

ADV
- non sedating and no dependence

DISADV
- no buzz, multiple doses per day, 2-6 wks for affect.

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43
Q

What is the SSRI MOA

A

Blocks reuptake of serotonin in CNS (increases serotonin)

Inhibits the p450 system

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44
Q

what are SSRIs

A

1st line of treatment for anxiety

used to control mood (serotonin)

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45
Q

What are the risks and ADRs for SSRI

A

Risk of overstimulation
INCREASES HR

inhibits p450 System

highly protein bound

can increase suicide ideation

sexual dysfunction

4-6 weeks for affect

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46
Q

What are Beta Blockers?

A

used for SITUATIONAL ANXIETY or PTSD

EX.
- Social anxiety
- public speaking

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47
Q

What are the ADRs of Beta Blockers?

A

Hypotension, Drowsiness, nausea, and diarrhea

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48
Q

What is Propranolol?

A

Non-selective beta blocker that is PRN

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49
Q

What is the MOA of Propranolol?

A

Blunts effects of NE + Epinephrine (decreases adrenaline)

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50
Q

What are mood stabilizers?

A

Used if 1st line agents are unsuccessful but have nasty ADRs

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51
Q

What is the duration of treatment for anxiety?

A

4-6 wks but typically require lifelong treatment

NOT BENZOS need to get off ASAP but tamper

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52
Q

What is a manic episode?

A

Irritable mood that last for at least 1 week

has 3 of the following symptoms
- inflated self esteem
- decreased need for sleep
- more talkative than usual
- racing thoughts
- distractibility
- decreased judgement

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53
Q

What is the etiology of Bipolar disorder?

A

UNKNOWN

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54
Q

What is the patho of BPD?

A

Changes in the limbic system, basal ganglia + hypothalamus

fluctuation in NE + DA and intracerebral Ca2+ lvls

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55
Q

What are the symptoms of BPD?

A

Overconfidence
change in sleep patterns
irrational decision making
grandiosity
increased activity
pressured speech

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56
Q

How do you treat BPD?

A

There is NO CURE

drug therapy is likely lifelong w/ the goals of controlling symptoms and reducing the frequency of cycles

BZDs and antipsychotics are used or non-pharm treatment

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57
Q

What are the acute BPD treatment options?

A

Benzo (short-term), lithium, valproic acid, carbamazepine, antipsychotics

58
Q

What are the maintenance BPD treatment options?

A

Monotherapy (one drug) but not likely

lithium
valproic acid
lamotrigine

59
Q

What are the treatment options for depressive BPD?

A

anti-depressants cautiously due to possible flip into mania

60
Q

What is the MOA of lithium?

A

effects anion exchange and sodium transport in nerves which normalizes transmission of NE, 5-HT, and DA

100% renally eliminated

61
Q

What are the ADRs of Lithium?

A

ACUTE
Polyuria, polydipsia, tremor, and anthimeria

LONG-TERM
hypothyroidism, EKG changes, and increased WBC

62
Q

What is lithium?

A

GOLD STANDARD of Mood Stabilizers

takes 5-10 days for benefit but has a long t1/2

63
Q

What is the MOA of Valproic acid?

A

Increase GABA

onset in 3-5 days

64
Q

What is valproic acid used for?

A

Good for rapid cyclers and mixed episodes but need baseline labs first to reduce ADRs

65
Q

What is the MOA for Carbamazepine?

A

Increase the GABA system and block Na channels

Mood Stabilizer

Metabolized hepatically

1-2 wk onset

66
Q

What is Lamotrigine?

A

Used as a last resort or add on therapy.

Mood Stabilizer

67
Q

What are atypical antipsychotics?

A

1st line agents for depression

68
Q

What is the MOA for atypical antipsychotics?

A

DA antagonist, 5-HT partial agonist/antagonist

69
Q

What is the biogenic amine hypothesis?

A

Depression is caused by reduction of multiple NTs (DA, 5-HT, and NE)

70
Q

What parts of the brain and what NTs are involved w/ Depression?

A

Limbic system and hypothalamus most involved.

NE, 5-HT, and DA

71
Q

What are antidepressants?

A

Restore NT balance

all work 60-70% of the time no matter the agent (generic or not)

onset takes wks for benefit but quicker for ADRs

72
Q

What are SSRIs used to treat?

A

Depression

73
Q

What is the MOA of TCAs?

A

Inhibit reuptake of NE + 5-HT

74
Q

What are the ADRs of TCAs?

A

Anticholinergic effects
lowers threshold for seizures
cardiovascular risks

75
Q

What do TCAs put elderly people at a higher risk for?

A

Sedation and orthostatic hypotension

all things to increase fall risk

76
Q

TCAs

A

Antidepressant (1st generation SNRIs)

used in combo w/ SSRIs to help sleep

Fetal in overdose (20mg/kg)

77
Q

What are monoamine Oxidase Inhibitors?

A

SUCK

78
Q

What is the MOA of MAO?

A

impair degradation of NE, 5-HT, DA. These would increase NT concentration

increases risk of HTN

79
Q

What is the MOA of Desyrel?

A

inhibits serotonin reuptake (increase 5-HT)

80
Q

What is the MOA of wellbutrin?

A

mild dopamine reuptake inhibitor only (no affect on other NTs)

81
Q

ADRs of wellbutrin?

A

minimize alcohol use

don’t use w/ seizure pts

no cardio, sexual, or anticholinergic effects

weight loss, insomnia, headache, and nausea

82
Q

What are the ADRs of Remeron?

A

sleepiness
dizziness
increased appetite
increased cholesterol
orthostatic hypotension
HALLUCINATIONS

83
Q

what is the MOA of SNRI

A

blocks reuptake of 5-HT and NE which means an increase in 5-HT and NE

may cause BP risk in HTN pts.

84
Q

What are the ADRs for fetzima?

A

serotonin syndrome
increased BP
hyponatremia

85
Q

What is serotonin syndrome?

A

Too much serotonin
which can cause peristalsis
which will cause bad diarrhea

86
Q

What is the definition of schizophrenia?

A

Heterogenous syndrome of disorganized and bizarre thoughts of delusions, hallucinations, disorganized speech/behavior, and impaired psychosocial function.

87
Q

What are the structural changes that happen w/ schizophrenia?

A

Increased ventricular size
reduction of medial temporal lobe and hippocampus

88
Q

what is the patho of schizophrenia?

A

DA is hyperactive in limbic system and hypo functioning in prefrontal cortex

89
Q

What are positive vs negative symptoms of schizophrenia?

A

Positive
- things that schizophrenia pts have that normal people would not
- easier to treat w/ drug therapy

Negative
- that that normal people have but pts w/ schizophrenia do not.
- hard to treat w/ drug therapy

90
Q

Examples of positive symptoms of schizophrenia?

A

hallucination
delusion

91
Q

Examples of negative symptoms of schizophrenia?

A

Alogia
flattened affect
avolition
anhedonia
attentional impairment

92
Q

What is the MOA of schizophrenia treatment?

A

block DA receptors in mesolimbic area which will reduce hyperactivity

D2 for antipsychotics

D1 responsible for EPS symptoms

93
Q

What are the classes of antipsychotics?

A

Typicals (1st class)

Atypical 2nd class

94
Q

What are the common ADRs w/ antipsychotics?

A

Weight gain and Type 2 diabetes

95
Q

What happens when DA is affected?

A

relief of psychosis and can cause EPS

96
Q

What happens when serotonin is affected?

A

suppresses DA and protects from EPS

Can have weight gain

97
Q

What happens when Alpha 1 is affected?

A

adrenaline

orthostatic hypotension and dizziness

98
Q

what happens when M1 is affected?

A

anticholinergic SE but may protect against EPS

99
Q

What happens when H1 is affected

A

weight gain and drowsiness

100
Q

What is the treatment algorithm for schizophrenia?

A

Atypical

different atypical or typical

clozapine

add atypical or typical to clozapine

101
Q

What is clozapine?

A

1st atypical and a mixed antagonist

typically used only in pts who have failed other agents due to its strict monitoring of WBC affects that can lead to agranulocytosis

102
Q

What are the ADRs for Clozapine?

A

NO EPS, NO Tardive dyskinesia (TD), NO effect on prolactin

Hypersalivation
weight gain
hypotension
sedation

103
Q

What is Olanzapine?

A

Atypical and mixed antagonist
worst anti-psychotic

high metabolic impact
weight gain
orthostatic hypotension

104
Q

What is Quetiapine?

A

atypical and mixed antagonist

DOC for Parkinson’s since it only blocks D2 receptors

105
Q

What are the ADRs of Quetiapine?

A

low risk of EPS and TD

sedation
mild hypotension
weight gain
headache

SE less severe than clozapine and Olanzopine

106
Q

What is Risperidone

A

2nd atypical and SDA

good if trying to stay away from Benzos

107
Q

What are the ADRs of Risperidone?

A

not good for EPS

low dose very sedating

108
Q

What is Geodon (ziprasidone)?

A

Atypical and SDA

has cardiac risk (prolonged QT interval)

109
Q

What is invega (paliperidone)

A

Atypical and SDA

active metabolite of risperidone

110
Q

What are the ADRs of invega?

A

less risk of EPS
more prolactin elevation

sedation and orthostatic hypotension

111
Q

What is lurasidone?

A

Atypical

good but very expensive

112
Q

What is ABILIFY?

A

Atypical and DA partial Agonist/ 5-HT Antagonist

SHOULD BE FRONT LINE (used alot)

Blocks D2 when DA is high and activates D2 when DA is Low

VERY CLEAN (minimal ADRs)

113
Q

What are the typical adverse effects of antipsychotics?

A

Extrapyramidal Symptoms

BIGGEST W/ RISPERODONE

114
Q

What does Benztropine (Cogentin) do?

A

Blocks ACh

anticholinergic effects

115
Q

What are Extrapyramidal effects?

A

Happen from all typicals and some atypicals

related to blockage of D1 DA receptors

Acute dystonia
Pseudoparkinsonism
Akathsia
Tardive dyskinesia

Metabolic changes w/ atypicals

116
Q

What is Acute dystonia and how to treat?

A

Twisting repetitive motions

Treated w/ benedryl and cogentin but will have anticholinergic effects

these restore effects of DA and ACh

117
Q

What is Pseudoparkinsonism and how to treat?

A

Presents w/ Parkinson’s s/s

DA blockage causes imbalance of DA and ACh

treatment is to block ACh or to reverse blockage of DA

118
Q

What is Akasthisia and how to treat?

A

Inner restlessness

treated by decreasing dose of drug causing issues
also by adding a beta blocker and/or BZDs (Ativan)

119
Q

What is Tardive dyskinesia and how to treat?

A

This is the biggest limitation of typicals

central movements (blinking, lip smacking, involuntary central movements)

NO EFFECTIVE TREATMENT
-cogentin makes worse w/ anticholinergic affects

120
Q

What is Neuroleptic Malignant syndrome?

A

must have 5 of the following
- change in mental status
- incontinence
- tachycardia
- CPK elevation
- Leukocytosis
- tremor
- tachypnea or hypoxia

MUSCLE RIDGITY is the HALLMARK sign

121
Q

How to treat NMS?

A

Atypicals w/in 7 days

use muscle relaxors (Dantrium) and DA agonists

fluid replacement
temp reduction
supportive care

122
Q

What are the signs of Metabolic syndrome?

A

Any of the 3
- abdominal obesity
- HTN
- Impaired fasting glucose
- Decreased HDL
- Elevated Triglycerides

123
Q

What is Bioavailability (BA or F)?

A

Total amount of drug that reaches circulation

anything above 70% is considered good

124
Q

What is bioequivalence?

A

same everything

Generic band vs brand

125
Q

What is Clinical/therapeutic equivalence?

A

Same drug outcome but doesn’t have to get to the outcome the same way.

126
Q

What is potency?

A

amount of med needed to achieve pharmacodynamic response

used in toxicity

ONLY SIGNIFICANT if fewer SE w/ more potent agent or admin less often

127
Q

What does pharmacokinetics mean?

A

What the body does to the drug

128
Q

What does Pharmacodynamics mean?

A

Effects of drug on the body

129
Q

What is absorption?

A

Time required for dose to reach circulation

bypassed by IV

130
Q

What is distribution?

A

Time required for dose to arrive at desired site of action

131
Q

What characteristics does a drug need to penetrate the BBB?

A

small molecule size
low pH
non-protein binding
balance of fat solubility

132
Q

What does protein binding have to do w/ drugs?

A

drugs bind to proteins in the blood

low protein = more free drugs in circulation = ADRs

133
Q

What is the normal Albumin levels?

A

3.5-4.5

134
Q

What is biotransformation (metabolism)?

A

way of getting drug ready for elimination

kidney or liver(99%)

Source of a lot of drug interaction

135
Q

What is the cyt p450 system?

A

system in liver responsible for most all metabolism

major site of drug interaction

136
Q

What is a metabolite?

A

Transformed molecule during metabolism

aren’t always less active
can be more active than parent drug

137
Q

What is a half life t1/2?

A

time required for 1/2 dose to be eliminated

requires 6-7 t1/2 to be out of system

138
Q

What is steady state?

A

amount of drug admin = amount of drug eliminated

only time a pt can be objectively assessed

requires 5-6 t1/2 to achieve ss

139
Q

How is absorption affect in the elderly?

A

Delayed gastric emptying
decrease splanchnic blood flow
elevated gastric pH
impaired intestinal motility

140
Q

How is distribution affected in the elderly?

A

influenced by age

increased t1/2
decreased protein binding = more free drug in circulation

141
Q

How is renal excretion affected in the elderly?

A

50% decline by 70 y.o.

BUN good predictor (5-25)

142
Q

What drugs can be life-threatening if stopped cold turkey?

A

Benzos
Opiates (Opioids)
CNS stimulants
Most psychoactive meds

Pharm (1 decks)

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