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PHARMACOLOGY > EXAMS 3 DRUGS > Flashcards

EXAMS 3 DRUGS Flashcards

1
Q

Histamine2 Receptor Antagonists (H2RA) DRUGS

A

Cimetidine
Ranitidine
Famotidine
Nizatidine

  • All H2RAs are renally cleared and require dose adjustments in patients with renal impairment
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2
Q

WHAT ARE Histamine2 Receptor Antagonists (H2RA) DRUGS

A
  • A first-line treatment for PUD and GERD
  • Promote gastric healing by preventing acid secretion
  • All 4 agents equally effective
  • Serious adverse reactions uncommon
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3
Q

Cimetidine adverse effect

A
  • CNS effects
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4
Q

Cimetidine DDI

A

Inhibitor of CYP450 enzymes

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5
Q

Proton Pump Inhibitors (PPI) DRUGS

A

Omeprazole
Esmoeprazole
Lansoprazole
Dexlansoprazole
Rabeprazole
Pantoprazole

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6
Q

WHAT ARE PROTON PUMP INHIBITORS

A
  • Most effective drugs for inhibiting acid secretion
  • All agents equally efficacious
  • Well tolerated
  • Selection based on cost, preference, DDIs
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7
Q

PROTON PUMP INHIBITORS MECHANISM OF ACTION

A

Irreversible inhibition of proton pump

Short half-life
Long PD effects
New proton pumps must be created to overcome affects of drugs
EXCEPTION rabeprazole

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8
Q

ADVERSE EFFECTS OF PROTON PUMP INHIBITORS

A

↑ risk of pneumonia
- Fractures
- Hypomagnesemia
- Clostridium difficile infection

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9
Q

other effects of Proton Pump Inhibitors

A

promote bone resorption
decrease bone formation
decrease b12 absorption
= lead to risk of fall

decrease absorpiotn of mg and ca = less bone formation and collagen linkage

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10
Q

Sucralfate MOA

A
  • Undergoes polymerization and cross-linking in the stomach → sticky gel
  • Binds to ulcer
  • Blocks acid and pepsin from reaching tissue
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11
Q

Pharmacokinetics of sucralfate

A
  • Minimal systemic absorption
  • Duration of action ~6 hours
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12
Q

indication of sucralfate

A

Treatment and maintenance of pectic ulcer disease PUD

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13
Q

adverse effect of sucralfate

A

Constipation

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14
Q

sucralfate DDI

A
  • Minimal
  • May ↓ absorption of some medications
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15
Q

Nursing implications sucralfate

A
  • Give 1 hour before meals
  • Separate from other medications by ~2 hours
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16
Q

Misoprostol MOA

A
  • Analog of prostaglandin E1 (PGE)
  • Promotes PGE synthesis
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17
Q

Indication of misoprotol

A

Prevent ulcers in patients on chronic NSAID therapy

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18
Q

Adverse effects of misoprostol

A

Diarrhea
Abdominal pain

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19
Q

contraindications of misoprostol

A
  • Pregnancy – category X drug
    Precautions MUST be taken in women of child-bearing age
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20
Q

what are Antacids

A

Alkaline products that neutralize stomach acid

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21
Q

pharmakinetics of antacids

A
  • Poorly absorbed systemically
    ( Exception sodium bicarbonate )
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22
Q

Indication of antacids

A
  • PUD
  • Symptomatic relief in GERD
  • Potency based on acid neutralizing capacity (ANC)
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23
Q

Dosage of antacids

A
  • Lower doses for gastric ulcers.
  • Higher doses for duodenal ulcers
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24
Q

Antacid Compounds

A
  • Aluminum hydroxide
  • Magnesium hydroxide
  • Magnesium oxide
  • Calcium carbonate
  • Sodium bicarbonate
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25
Q

DDIs of ANTACIDS

A
  • decrease absorption of H2RA drugs. SEPARATE 1 HOUR
  • Interfere with sucralfate – separate by 1 hour
  • decrease absorption of other drugs due to binding – separate 2 hours
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26
Q

TREATMENT REGIMEN for h. pylori associated ulcers

A
  • Antibiotics
  • Minimum of 2 different agents
  • Up to 3 different agents
  • Do NOT use 1 antibiotic alone
  • Antisecretory agents
  • PPI or H2RA
  • Hasten healing and relieve symptoms
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27
Q

Ideal duration of therapy of TREATMENT REGIMEN for h. pylori associated ulcers

A

14 days

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28
Q

NSAID-induced Ulcers risk factors

A

Age > 60
History of ulcers
High-dose NSAID therapy

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29
Q

prophylaxis/prevention of NSAID-induced Ulcers

A

PPIs preferred
Consider misoprostol therapy

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30
Q

Treatment of NSAID-induced Ulcers

A
  • PPI or H2RA
  • Antacids and sucralfate NOT recommended
  • Consider discontinuing NSAIDs

Antacid and sucralfate provide more symptomatic control then fixing the cause

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31
Q

evaluation treatment of NSAID-Induced ulcers

A
  • Pain relief
  • NOTE: pain may subside before ulcer is fully healed
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32
Q

Non-drug Therapy of NSAID-Induced ulcers

A
  • Diet
    ‘Ulcer Diet’ does not accelerate healing
    Eat 5 to 6 small meals per day
  • Discontinue NSAIDs if possible
  • Avoid smoking, aspirin, -
    NSAIDs and alcohol
    Stress reduction
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33
Q

indications of drugs for constipation

A

Relieve constipation
Obtain stool sample
Evacuate bowel before procedure
Modify effluent from ileostomy or colostomy
Prevent fecal impaction in bedridden patients
Remove poisons

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34
Q

Laxatives

A

*Bulk-forming
*Surfactant (stool softner)
*Lubricant

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35
Q

Cathartics

A

*Stimulant
*Saline
*Osmotic

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36
Q

drugs for constipation

A

Laxatives
Cathartics
Other (*Lactulose
*Lubiprostone)

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37
Q

Contraindications of constipation drugs

A
  • Symptoms of intraabdominal infection
  • Acute surgical abdomen
  • Fecal impaction or bowel obstruction
  • Habitual use
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38
Q

CAUTION of constipation drugs

A

avoid use during pregnancy and lactation

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39
Q

drugs of Bulk-forming Laxatives

A

Methylcellulose (Citrucel)
Psyllium (Metamucil)
Polycarbophil (FiberCon)

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40
Q

Bulk-forming Laxatives MOA

A
  • Act like dietary fiber
  • Swell with exposure to water → form a gel → softens and ↑ fecal mass
  • Stimulates peristalsis
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41
Q

Indication of Bulk-forming Laxatives

A
  • Constipation
  • Modify effluent for ileostomy and colostomy
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42
Q

Bulk-forming Laxatives adverse effects

A
  • Flatulence and bloating
  • Esophageal obstruction
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43
Q

Bulk-forming Laxatives counseling points

A
  • Take with a full glass of water or juice
  • Contraindicated in patients with narrowing of the intestinal lumen or obstruction
  • May take 1 to 3 days to see effects
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44
Q

Surfactant Laxatives drugs

A

Docusate sodium
Docusate calcium

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45
Q

Mechanism of action surfactant laxatives

A
  • Alter stool consistency
  • Lower surface tension, allow more water penetration in feces
  • interact with intestinal wall
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46
Q

Surfactant Laxatives interaction with intestinal wall

A
  • Inhibit fluid reabsorption
  • Stimulate secretion of water and electrolytes into intestines
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47
Q

adverse effect of Surfactant Laxatives ( docusate sodium, calcium)

A

Minimal

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48
Q

Counseling Points for docusate sodium, calcium

A
  • Take with a full glass of water
  • May take 1 to 3 days to see effect
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49
Q

Lubricant Laxatives drug

A

mineral oil

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50
Q

Mechanism of action Lubricant Laxatives

A
  • Indigestible and poorly absorbed hydrocarbon
  • Lubrication
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51
Q

Indication of lubricant laxatives

A

fecal impaction

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52
Q

adverse effects of lubricant laxative

A
  • Lipid pneumonia (aspiration)
  • Anal leakage
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53
Q

Counseling points:
lubricant laxatives

A
  • Taken PO or rectally
  • Most effective when administered rectally
  • Onset of effect is approximately 6 to 8 hours
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54
Q

Stimulant Cathartics drugs

A

Bisacodyl
Senna
Castor oil

Prompt fluid or semi-fluid evacuation of the bowel

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55
Q

Mechanism of action of, Bisacodyl, Senna, Castor oil

A
  • Irritate the GI mucosa
  • ↑ secretion of water and electrolytes into the intestine
  • Stimulates intestinal peristalsis
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56
Q

idications of Bisacodyl, Senna, Castor oil (stimulant cathartics)

A
  • Opioid-induced constipation
  • Constipation due to slow colonic transit time
  • Bowel prep for procedure
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57
Q

counseling points for bisacodyl

A
  • Tablets are enteric coated, do NOT crush or chew
  • Separate from milk and antacids by 1 hour
  • Suppositories may cause burning
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58
Q

Saline Cathartics MOA

A

Salts that are poorly absorbed in the intestines
Draw water into intestinal lumen
Stimulates peristalsis

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59
Q

adverse effects of magnesium salts (magnesium citrate, milk of magnesia).

SALINE CATHARTIC

A
  • Dehydration
  • Accumulation of Mg in renal impairment
  • Abdominal pain/ cramping
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60
Q

counseling points of magnesium salts (magnesium citrate, milk of magnesia)

A
  • Increase fluid intake during treatment
  • Use cautiously in renal impairment
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61
Q

Mechanism of action of osmotic cathartics (polyethylene glycol)

A

NON-ABSORBABLE compound, retains water in intestinal lumen
↑ fecal mass, softens feces
↑ peristalsis

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62
Q

Polyehtylene Glycol (Miralax) INDICATION

A

constipation

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63
Q

Polyehtylene Glycol (Miralax) adverse effects

A
  • Nausea
  • Abdominal bloating
  • Cramping
  • Flatulence
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64
Q

Counseling Points of Polyethylene glycol

A
  • Dissolve powder in water, juice, coffee, tea
  • May take 1 to 3 days for effects
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65
Q

Lactulose indication

A
  • Constipation
  • Hepatic encephalopathy
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66
Q

Semisynthetic disaccharide (galactose and fructose)

A

Lactulose

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67
Q

lactulose Mechanism of action:

A
  • Poorly absorbed
  • Metabolized by bacteria into compounds that cannot leave colon
  • Exerts osmotic effect, drawing water into colon
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68
Q

Adverse effects lactulose

A
  • Flatulence
  • Abdominal cramping
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69
Q

Lubiprostone (Amitiza) MOA

A
  • Selective chloride channel activator in intestines
  • ↑ chloride-rich fluid in intestines
  • Enhances peristalsis in small and large intestines
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70
Q

Indications lubiprostone

A
  • Chronic idiopathic constipation
  • Irritable bowel syndrome with constipation
  • Opioid-induced constipation
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71
Q

Adverse effects of Lubiprostone (Amitiza)

A
  • Diarrhea
  • Abdominal distention and pain
  • Flatulence
  • Vomiting
  • Chest tightness 30-60 minutes after the first dose
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72
Q

Counseling points for Lubiprostone (Amitiza)

A
  • Administered orally
  • Take with a full glass of water
  • Monitor for signs of chest tightness and dyspnea
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73
Q

causes of laxative abuse

A
  • misconception of “normal”
  • self-perpetuating cycle
74
Q

consequencies of laxative abuse

A
  • diminished defecatory reflexes
  • electrolyte imbalances, dehydration, colitis
75
Q

treatment of laxative abuse

A

stop laxatives use
patient education
dietary changes

76
Q

Catharsis effects

A

Prompt fluid or semi-fluid evacuation of the bowel

77
Q

Laxative effect

A

Produces soft, formed stool over 1 to 3 days

78
Q

pathogenesis of depression

A

Deficiency of serotonin, norepinephrine or both

79
Q

symptoms of deoression

A

(SIG E CAPS)

Sleep disturbance (insomnia/ hypersomnia)
Interest ↓
Guilt
Energy ↓
Concentration ↓
Appetite ↓
Psychomotor retardation/ agitation
Suicidal ideation

80
Q

Drugs Used for Depression

A

Selective serotonin reuptake inhibitors (SSRIs)
Serotonin/norepinephrine reuptake inhibitors (SNRIs)
Tricyclic antidepressants (TCAs)
Monoamine oxidase inhibitors (MAOIs)
Atypical antidepressants

81
Q

Drug selection for depression

A

Patient specific
SSRIs, SNRIs, bupropion and mirtazapine tend to be preferred due to lower ADE profile

82
Q

Time course of response (treatment of depression)

A

Initial response in 1 to 3 weeks
Full response in up to 12 weeks
Take medication for at least 1 month before considering treatment failure

83
Q

Managing initial treatment:

A

Continue for 4 – 8 weeks to assess efficacy
Start low dose then, if ineffective consider:
↑ dose
Change to different drug in same class or different class
Add a second drug

84
Q

Suicide Risk with Antidepressants

A
  • All antidepressants carry a black box warning for risk of suicide
  • Suicide risk in increased early in therapy
85
Q

Selective Serotonin Reuptake Inhibitors (SSRIs) DRUGS

A

Fluoxetine
Citalopram
Escitalopram
Paroxetine
Sertraline

86
Q

SSRI mechanism of action

A

Selectively block neuronal reuptake of serotonin (5-HT)
Causes increased concentrations of serotonin in the synapse
Increased activation of post-synaptic serotonin receptors

  • NOTE: NO blockade of dopamine or norepinephrine with SSRIs
87
Q

ADVERSE EFFECTS OF SSRI DRUGS

A

Nausea
Insomnia
Weight gain
Sexual dysfunction
Hyponatremia
SEROTONIN SYNDROME

88
Q

Monitoring/ Counseling Points
for SSRI drugs

A

Monitor mood and for adverse effects
Counsel patient about onset of effects
Counsel patient on risk of suicide and how to proceed if they have suicidal ideation

89
Q

MAOI drugs and SSRI drug interactions

A
  • contraindicated when used together
  • MAOI must be stopped 2 weeks prior to starting SSRI
  • combination increases serotonin syndrome
90
Q

Antiplatelet and anticoagulants
interaction with SSRI drugs

A

SSRIs can displace these drugs from plasma proteins and increase their effects

91
Q

causes of Serotonin Syndrome

A

Accumulation of high serotonin levels

92
Q

serotonin syndrome is
Characterized by

A

Hyperreflexia
Rigidity
HYPERTHERMIA
Diaphoresis
Agitation

93
Q

Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) DRUGS

A

Venlafaxine
Desvenlafaxine
Duloxetine

94
Q

Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) MECHANISM OF ACTION

A

Selectively block neuronal reupdate of serotonin (5-HT) AND norepinephrine
Causes increased concentrations of serotonin and NE in the synapse
↑ stimulation of serotonin and NE receptors

95
Q

ADVERSE EFFECTS OF Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) DRUGS

A

Nausea
Headache
Nervousness
Constipation
Erectile dysfunction

96
Q

Monitoring/ Counseling Points
for (SNRIs)

A

Monitor for efficacy and adverse effects
Counsel patient on onset of effects
Counsel patient on increased risk of suicide
Counsel patient on signs and symptoms of serotonin syndrome

Avoid use with other drugs that ↑ serotonin
Contraindicated with MAOI therapy – hold MAOI for 14 days before starting SNRI

97
Q

Tricyclic Antidepressants DRUG INTERACTIONS

A

Monoamine oxidase inhibitors
Anticholinergic agents

98
Q

Monoamine Oxidase Inhibitors DRUGS

A

Phenelzine
Isocarboxazid (PO)
Selegiline (transdermal)

second- or third-line therapy
High risk of adverse effects
Highest risk of hypertensive crisis which can be triggered BY FOOD
Significant interactions with SSRI, SNRIs, and TCAs

99
Q

monoamine oxidase inhibitors Mechanism of action:

A

Inhibit MAO
Increase amount of neurotransmitter available for release
Intensifies transmission of signal

100
Q

MOAIs drugs adverse effects

A

CNS stimulation
Orthostatic hypotension
Hypertensive crisis from tyramine
Inhibition of neuronal MAO, ↑ NE levels in neurons
Inhibition of intestinal and hepatic MAO, ↑ circulating tyramine
Tyramine stimulates release of accumulated NE

101
Q

Drug interactions of MAOI’s

A

TCAs
SSRIs/SNRIs

102
Q

Bupropion (atypical antidepressants) adverse effects

A

seizures

103
Q

Mirtazapine (atypical antidepressants) adverse effects

A

Weight gain
Sedation

Pts experiencing insomnia may benefit from mirtazapine

104
Q

Trazodone ( Atypical Antidepressants) effects

A

excessive sedative effects

105
Q

Bipolar Disorder

A

Imaging studies have shown areas of brain atrophy associated with prolonged mood disorders.
Mood stabilizing drugs may contribute to prevention or reversal of neuronal atrophy and restoration of those pathways

106
Q

drug selection for manic episodes

A

Lithium
Valproate
Lithium or valproate

107
Q

drug selection for depressive episodes

A

Lithium or Valproate
Antipsychotic
Lithium or Valproate

108
Q

drug selection for Long-term Preventative Therapy

A

Lithium
Valproate

109
Q

Antiepileptic Drugs

A
  • Divalproex Sodium/Valproaic acid/ Valproate
    = higher thera index than lithium, faster onset, better side effect profile
    =ADV EFFEC: hepatoxicity and pacreatisis
  • CARBAMAZEPINE
    = start low doses and titrate up/ Narrow therapeutic index
    = ADV EFFE: hyponatremia, visual disturbances, headache
110
Q

Benefits of antiepileptic drugs compared to lithium:

A

Higher therapeutic index (less monitoring or levels)
Faster onset
Better side effect profile

111
Q

Adverse effects of (Divalproex Sodium/Valproaic acid/ Valproate)

ANTIEPILEPTIC DRUG

A

Hepatotoxicity
Pancreatitis

Enhance gaba and block v-gated na channels

112
Q

Adverse effects of Carbamazepine (antiepileptic drug)

A

Hyponatremia
Visual disturbances
Headache

113
Q

monitoring points for Carbamazepine (antiepiletic drug)

MOOD STABILIZERS

A

Start doses low and titrate up
Narrow therapeutic index

114
Q

Antipsychotic Drugs

A

Aripiprazole
Olanzapine
Ziprasidone

All are effective when used alone or in combination with lithium or valproate for management of acute symptoms but generally these will be combined with lithium or valproate.

115
Q

o Which COX inhibitor is used for PDA closure in neonates

A

indomethacin

116
Q

Which COX inhibitor can only be used for 5 days maximum?

A

Ketorolac (PO IV IM)

117
Q

Which COX inhibitors are available IV?

A

Indomethacin
Ketorolac

118
Q

Which COX inhibitors are available IM?

A

Ketorolac

119
Q

Which COX inhibitors are available TOPICALLY

A

Diclofenac

120
Q

What drugs interact with COX inhibitors?

A

Aspirin
NSAIDs
Anticoagulants
Glucocorticoids
ACE-I
ARBs

121
Q

List the second-generation COX inhibitors (HINT! There is only one)

A

celecoxib

122
Q

Why are celecoxib not preferred compared to first generation COX inhibitors?

A

increased risk of MI and stroke

123
Q

For what indications (diseases) are COX inhibitors used? (Think about their therapeutic effects)

A

Mild-moderate pain
Fever
Rheumatoid arthritis
Osteoarthritis
Closure of PDA in neonates (indomethacin)

124
Q

mechanism of COX 1 (good)

A

Beneficial processes
GI tract: decreases gastric acid, increases bicarbonate and mucus
Platelets: platelet aggregation
Kidney: vasodilation

125
Q

mechanism of COX-2 (‘bad’)

A

Tissue injury: inflammation and pain
Brain: fever and pain
Kidney: vasodilation / renal impairment

126
Q

How does aspirin’s mechanism differ from the other first-generation COX inhibitors? What unique indication does this give aspirin that the other COX inhibitors do not have?

A

dysmenorrhea and suppression of platelet aggregation

127
Q

Why is aspirin avoided in children less than 16 years of age?

A

reye syndrome: a rare but serious adverse event in children less than 16 years old
- happens when taking aspiring whiles infected with influenza or chicken pox
- encehepalopathy and fatty liver degeneration

128
Q

What are signs/symptoms of salicyism?

A
  • aspiring levels slightly above therapeutic levels
  • symptoms include tinnitus , sweating, headache dizziness
  • result in increased respiration leading to respiratory alkalosis
129
Q

why should aspiring be avoided in pregnancy

A

risk to fetuses
anemia and post-partum hemorrhage

130
Q

What are signs and symptoms of aspirin overdose

A

non-specific at first
respiratory alkalosis( hyperventilation )
hyperthermia, sweating
electrolyte imbalances
coma

131
Q

treatment of aspirin overdose

A

supportive care
external cooling
sodium bicarbonate infusion

132
Q

What are the available dosage forms for aspirin overdose

A

lethal dose in adults - 20 to 35 grams
lethal dose in children 4 gram

133
Q

acetaminophen MOA

A

inhibits COX enzymes but ONLY IN CNS

134
Q

adverse effect of acetaminophen

A

well tolerated
anaphylaxis (very rare)
steven johnson syndrome

INDICATION: well tolerated, anaphylxis (rare) and steven johnsons syndrome

OVERDOSE TREATMENT: N-acetylcysteine (IV/PO)

135
Q

routes of acetaminophen

A

oral rectal and IV

136
Q

How is acetaminophen overdose treated?

A

N-acetylcysteine IV or PO

i’m overdose glutathione is depleted leading to build up hepatotoxicity and liver failure

137
Q

When is acute management used in gout treatment

A

given for a short time to relieve symptoms: USED FOR INFREQUENT FLARE UPS

TREATMENT
- NSAIDS 1st line (indomethacin: naproxen)
- glucocorticoids (predisnone, triamicinolone acetate)
- colchicine

138
Q

When is gout preventive therapy used

A

treatments of hyperuricemia and prevents acute attacks: USED for chronic gout

TREATMENT:
- decrease uric acid (UA) production
- enhance UA excretion
- convert UA to allantoin
-

139
Q

first line NSAID ( indomethacin/naproxen ) MOA and When should they be started

A

reduce inflammation through cox inhibition

MUST START THERAPY AT FIRST SIGN OF ATTACK

140
Q

adverse effect of NSAID ( indomethacin, Naproxen )

A

GI ulceration
impaired renal function
fluid retention
increased risk of CV events

141
Q

second line therapy for acute gout attacks (GLUCOCORTICOIDS= prednisone, triamcinolone acetate

A

typically reserved for patients who cannot take NSAIDS or for people that NSAIDS are ineffective

142
Q

MOA of glucocorticoids ( prednisone and triamchinolone acetate

A

anti inflammatory and immunomodulatory effects

143
Q

prednisone adverse effect and counseling points

A
  • increases blood glucose levels levels
  • take with food or after meal
  • take in the morning
144
Q

triamcinolone acetate adverse effect and counseling point

A

(ROUTE: intra-articular)

  • pain at inject site
  • shake well to suspend product prior to injection into the joint
145
Q

COLCHICINE INDICATIONS

A
  • acute gout attacks (last line)
    prophylaxis (preventing of gout attacks)
146
Q

MECHANISM OF ACTION: COLCHICINE

A
  • prevents infiltration of joint space by leukocytes
  • disrupts microtubules needed for cellular functions and motility

DONT USE IN PREGNANCY

147
Q

adverse effects of colchicine (do not take with grape juice)

A
  • diarrhea
  • nausea vomiting
  • myelosuppresion
  • myopathy
148
Q

Xanthine Oxidase (XO) inhibitors ( allopurinol and febuxostat)

A

first line THERAPIES FOR GOUT PREVENTION OF GOUT ATTACKS

149
Q

XANTHINE OXIDASE (allopurinol and febuxostat) inhibitors MOA

A

inhibits xanthine oxidase which i need to make uric acid

BOTH DRUGS HAVE EQUAL EFFECTS but ALLOPURINOL is less expensive

150
Q

What types of drugs have a drug-drug interaction with xanthine oxidase inhibitors (allopurinol and febuxostat ?

A

allopurinol inhibits some hepatic enzymes substrates of COX

151
Q

What adverse effects might be expected with these Xanthine Oxidase Inhibitors ( allopurinol, febuxostat )

A

increases gout attacks initially for both

ALOPURINOL- hypersensitivity syndrome, nausea, vomiting, diarrhea

FEBUXOSTAT- well tolerated and increased LFTs

152
Q

Probenecid MOA

A
  • prevents reabsorption of uric acid from renal tubules
  • increases excretion of uric acid
153
Q

What are the indications for probenecid?

A

prevents gout attacks
prolong the effects of penicillin and cephalosporin antibiotics

154
Q

cautions of using probenecid

A

DO NOT START PROBENECID DURING AN ACUTE GOUT ATTCK

  • STAY HYDRATED!!
155
Q

adverse effects for probenecid

A
  • well tolerated
    -mild nausea and or vomiting
    hypersensitivity (4%)
  • renal injury

DDI - aspiring, indomethacin

156
Q

what is abortive therapy for headaches

A
  • taken when migraine starts, first sign of migraine
  • this suppresses associated symptoms before it happens
  • route is based on associated symptoms
    LIMIT USE TO 1 to 2 days/week
157
Q

preventive therapy for headaches

A
  • reduces frequency, intensity and duration
  • increases response to abortive medications
  • indicated for frequent attacks, very sever and non responsive
    BENEFITS IN 4 to 6 WEEKS
158
Q

drugs of preventive therapy migraines

A
  • beta blockers ( Propranolol and metoprolol)
    BETA ARE THE FIRST LINE. EFFECT IN ABOUT 2 WEEKS!!

side effects: nausea and extreme tiredness
- tricyclic antidepressants (amitriptyline and nortriptyline)
- antiepileptic drugs( topiramate and divalproex)

159
Q

drugs for abortive therapy of migraines/headaches

A
  • non specific analgesic (mild to moderate pain) = ASPIRIN-LIKE DRUGS
    Agents (oral):
    Aspirin
    Acetaminophen
    Naproxen
    Diclofenac
    Combination therapy
  • migrane specific ( moderate severe pain) = OPIOID
    Meperidine (oral)
    Butorphanol (intranasal)
    Used for severe pain
160
Q

Serotonin 1B/1D Receptor Agonists (ALL ENDS IN - TRIPTANS)

A

first line agent for TERMINATING MIGRANE HEADACHE

  • relieve pain through vasoconstriction
  • possible coronary vasospasm
161
Q

mechanism of action 5-HT1B/1D SEROTONIN

A

selective for 5-HT1B/1D

NO BINDNG TO 5-HT2 or 5-HT3
NO BINDING TO ADRENERGIC, DOPAMINERGIC, MUSCARINIC or HISTAMERGIC RECEPTORS

Binds to 5HT1B/ID receptors on blood vessels causing VASOCONSTRICTION
then it binds o 5HT1B/ID on trigermimla sensory nerves which decreases inflammatory peptides =PAIN RELIEF

162
Q

What are common drug interactions of serotnin1B/1D receptor agonists

A

other TRIPTANS
ergot alkaloids
MAOI
SSRI
SNRI

163
Q

adverse effects of serotnin1B/1D receptor agonists

A

avoid use in patients with CAD = coronary vasospasm
avoid in pregnancy (teragenesis)

164
Q

Which drugs of SEROTONIN 1B/5D are available intranasally?

A

remember they all ends in PITANS and available in PO

SUMATRIPTAN (SQ/IN) AND ZOLMITRIPTAN = INTRANASALLY

IN= 15-20 mins
SQ= 10-15 mins
ORAL= 30-120 mins

165
Q

Ergot alkaloids ( ERGOT in the names )
NON SELECTIVE

A

second line agent for TERMINATING MIGRAINE HEADACHE

  • risk of physical dependence
    higher adverse effect profile than TRIPTANS
166
Q

ERGOT ALKALOIDS MOA

A

NON SELECTIVE

  • binds to 5H1B/1D, dopaminergic adrenergic receptors on blood vessel resulting in VASOCONSTRICTION
  • binds to 5HT1B/1D on trigerminal sensory which DECREASES release of inflammatory peptides
167
Q

What are common adverse effects of ERGOT ALKALOIDS

A

nausea, vomiting
weakness in legs
myalgia
tingling sensation in fingers and toes
angina-like pain
tachycardia or bradycardia

168
Q

What are common drug interactions of ergot alkaloids

A

TRIPTANS
other ergot alkaloids
CYP3A4 inhibitors

169
Q

Who should not use ergot alkaloid drugs and why?

A

hepatic or renal impairment
CAD
peripheral vascular disease
uncontrolled HTN
pregnancy

170
Q

What are signs/symptoms of ergotism? Who is at risk?

A

significant ischemia
extremes cold pale and numb. eventually leading to gangrene
HIGHEST RISK- CAD PVD sepsis, renal and hepatic impairment

171
Q

What are signs/symptoms of physical dependence? How can this risk be minimized?

A

characterized by withdrawal syndrome
nausea vomiting headache restlessness
RISK CAN BE MINIMIZED BY COUNSELING PATIENTS TO ABOID DIALY USE

172
Q

ERGO DRUGS ROUTE

A

Ergotamine - PO or PR
dihydroergotamine: IM SQ IN IV

173
Q

OTHER PROPHYLACTIC/PREVENTIVE THERAPIES

A

estrogen gel and patch
- calcium channel blockers
- botulinum toxin
ACE-i or ARB
Supplements
- riboflavin
- coenzyme Q-10
butterbur

174
Q

Which of the drugs for preventative therapy are a good option for pregnant patients?

A

X

175
Q

How can we manage medication overuse headache once it occurs?

A

stop all abortive HA medications
HA will increase for short period
resolve in days to weeks

176
Q

drugs for anxiety

A

short time : benzodiazepines
long term: SSRI, SNRI, TCA

177
Q

first line non drug treatment of insomnia

A

sleep hygiene ( first line)

178
Q

Which drugs are used for mild insomnia?

A

melatonin
antihistamines

OVER THE COUNTER DRUGS

179
Q

drugs for severe insomnia

A

benzodiazepines
benzodiazepines-like drugs
ramelteon
others

180
Q

Benzodiazepines mechanism of action

A

binds to have reception and potentials the action of gaba

GABA is an inhibitory neurotransmitter

181
Q

drugs if benzodiazepines

A

HINT: ends in ZEPAM, ZPAM

CHLORDIAZEPOXIDE

182
Q

What drug can be used to reverse a benzodiazepine overdose?

A

flumazenil (IV)

PHARMACOLOGY (7 decks)

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