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
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
3
Q
Cimetidine adverse effect
A
- CNS effects
4
Q
Cimetidine DDI
A
Inhibitor of CYP450 enzymes
5
Q
Proton Pump Inhibitors (PPI) DRUGS
A
Omeprazole
Esmoeprazole
Lansoprazole
Dexlansoprazole
Rabeprazole
Pantoprazole
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
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
8
Q
ADVERSE EFFECTS OF PROTON PUMP INHIBITORS
A
↑ risk of pneumonia
- Fractures
- Hypomagnesemia
- Clostridium difficile infection
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
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
11
Q
Pharmacokinetics of sucralfate
A
- Minimal systemic absorption
- Duration of action ~6 hours
12
Q
indication of sucralfate
A
Treatment and maintenance of pectic ulcer disease PUD
13
Q
adverse effect of sucralfate
A
Constipation
14
Q
sucralfate DDI
A
- Minimal
- May ↓ absorption of some medications
15
Q
Nursing implications sucralfate
A
- Give 1 hour before meals
- Separate from other medications by ~2 hours
16
Q
Misoprostol MOA
A
- Analog of prostaglandin E1 (PGE)
- Promotes PGE synthesis
17
Q
Indication of misoprotol
A
Prevent ulcers in patients on chronic NSAID therapy
18
Q
Adverse effects of misoprostol
A
Diarrhea
Abdominal pain
19
Q
contraindications of misoprostol
A
- Pregnancy – category X drug
Precautions MUST be taken in women of child-bearing age
20
Q
what are Antacids
A
Alkaline products that neutralize stomach acid
21
Q
pharmakinetics of antacids
A
- Poorly absorbed systemically
( Exception sodium bicarbonate )
22
Q
Indication of antacids
A
- PUD
- Symptomatic relief in GERD
- Potency based on acid neutralizing capacity (ANC)
23
Q
Dosage of antacids
A
- Lower doses for gastric ulcers.
- Higher doses for duodenal ulcers
24
Q
Antacid Compounds
A
- Aluminum hydroxide
- Magnesium hydroxide
- Magnesium oxide
- Calcium carbonate
- Sodium bicarbonate
25
DDIs of ANTACIDS
- 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
26
TREATMENT REGIMEN for h. pylori associated ulcers
* 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
27
Ideal duration of therapy of TREATMENT REGIMEN for h. pylori associated ulcers
14 days
28
NSAID-induced Ulcers risk factors
Age > 60
History of ulcers
High-dose NSAID therapy
29
prophylaxis/prevention of NSAID-induced Ulcers
PPIs preferred
Consider misoprostol therapy
30
Treatment of NSAID-induced Ulcers
- PPI or H2RA
- Antacids and sucralfate NOT recommended
- Consider discontinuing NSAIDs
Antacid and sucralfate provide more symptomatic control then fixing the cause
31
evaluation treatment of NSAID-Induced ulcers
- Pain relief
- NOTE: pain may subside before ulcer is fully healed
32
Non-drug Therapy of NSAID-Induced ulcers
- 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
33
indications of drugs for constipation
Relieve constipation
Obtain stool sample
Evacuate bowel before procedure
Modify effluent from ileostomy or colostomy
Prevent fecal impaction in bedridden patients
Remove poisons
34
Laxatives
*Bulk-forming
*Surfactant (stool softner)
*Lubricant
35
Cathartics
*Stimulant
*Saline
*Osmotic
36
drugs for constipation
Laxatives
Cathartics
Other (*Lactulose
*Lubiprostone)
37
Contraindications of constipation drugs
- Symptoms of intraabdominal infection
- Acute surgical abdomen
- Fecal impaction or bowel obstruction
- Habitual use
38
CAUTION of constipation drugs
avoid use during pregnancy and lactation
39
drugs of Bulk-forming Laxatives
Methylcellulose (Citrucel)
Psyllium (Metamucil)
Polycarbophil (FiberCon)
40
Bulk-forming Laxatives MOA
- Act like dietary fiber
- Swell with exposure to water → form a gel → softens and ↑ fecal mass
- Stimulates peristalsis
41
Indication of Bulk-forming Laxatives
- Constipation
- Modify effluent for ileostomy and colostomy
42
Bulk-forming Laxatives adverse effects
- Flatulence and bloating
- Esophageal obstruction
43
Bulk-forming Laxatives counseling points
- 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
44
Surfactant Laxatives drugs
Docusate sodium
Docusate calcium
45
Mechanism of action surfactant laxatives
- Alter stool consistency
- Lower surface tension, allow more water penetration in feces
- interact with intestinal wall
46
Surfactant Laxatives interaction with intestinal wall
- Inhibit fluid reabsorption
- Stimulate secretion of water and electrolytes into intestines
47
adverse effect of Surfactant Laxatives ( docusate sodium, calcium)
Minimal
48
Counseling Points for docusate sodium, calcium
- Take with a full glass of water
- May take 1 to 3 days to see effect
49
Lubricant Laxatives drug
mineral oil
50
Mechanism of action Lubricant Laxatives
- Indigestible and poorly absorbed hydrocarbon
- Lubrication
51
Indication of lubricant laxatives
fecal impaction
52
adverse effects of lubricant laxative
- Lipid pneumonia (aspiration)
- Anal leakage
53
Counseling points:
lubricant laxatives
- Taken PO or rectally
- Most effective when administered rectally
- Onset of effect is approximately 6 to 8 hours
54
Stimulant Cathartics drugs
Bisacodyl
Senna
Castor oil
Prompt fluid or semi-fluid evacuation of the bowel
55
Mechanism of action of, Bisacodyl, Senna, Castor oil
- Irritate the GI mucosa
- ↑ secretion of water and electrolytes into the intestine
- Stimulates intestinal peristalsis
56
idications of Bisacodyl, Senna, Castor oil (stimulant cathartics)
- Opioid-induced constipation
- Constipation due to slow colonic transit time
- Bowel prep for procedure
57
counseling points for bisacodyl
- Tablets are enteric coated, do NOT crush or chew
- Separate from milk and antacids by 1 hour
- Suppositories may cause burning
58
Saline Cathartics MOA
Salts that are poorly absorbed in the intestines
Draw water into intestinal lumen
Stimulates peristalsis
59
adverse effects of magnesium salts (magnesium citrate, milk of magnesia).
SALINE CATHARTIC
- Dehydration
- Accumulation of Mg in renal impairment
- Abdominal pain/ cramping
60
counseling points of magnesium salts (magnesium citrate, milk of magnesia)
- Increase fluid intake during treatment
- Use cautiously in renal impairment
61
Mechanism of action of osmotic cathartics (polyethylene glycol)
NON-ABSORBABLE compound, retains water in intestinal lumen
↑ fecal mass, softens feces
↑ peristalsis
62
Polyehtylene Glycol (Miralax) INDICATION
constipation
63
Polyehtylene Glycol (Miralax) adverse effects
- Nausea
- Abdominal bloating
- Cramping
- Flatulence
64
Counseling Points of Polyethylene glycol
- Dissolve powder in water, juice, coffee, tea
- May take 1 to 3 days for effects
65
Lactulose indication
- Constipation
- Hepatic encephalopathy
66
Semisynthetic disaccharide (galactose and fructose)
Lactulose
67
lactulose Mechanism of action:
- Poorly absorbed
- Metabolized by bacteria into compounds that cannot leave colon
- Exerts osmotic effect, drawing water into colon
68
Adverse effects lactulose
- Flatulence
- Abdominal cramping
69
Lubiprostone (Amitiza) MOA
- Selective chloride channel activator in intestines
- ↑ chloride-rich fluid in intestines
- Enhances peristalsis in small and large intestines
70
Indications lubiprostone
- Chronic idiopathic constipation
- Irritable bowel syndrome with constipation
- Opioid-induced constipation
71
Adverse effects of Lubiprostone (Amitiza)
- Diarrhea
- Abdominal distention and pain
- Flatulence
- Vomiting
- Chest tightness 30-60 minutes after the first dose
72
Counseling points for Lubiprostone (Amitiza)
- Administered orally
- Take with a full glass of water
- Monitor for signs of chest tightness and dyspnea
73
causes of laxative abuse
- misconception of "normal"
- self-perpetuating cycle
74
consequencies of laxative abuse
- diminished defecatory reflexes
- electrolyte imbalances, dehydration, colitis
75
treatment of laxative abuse
stop laxatives use
patient education
dietary changes
76
Catharsis effects
Prompt fluid or semi-fluid evacuation of the bowel
77
Laxative effect
Produces soft, formed stool over 1 to 3 days
78
pathogenesis of depression
Deficiency of serotonin, norepinephrine or both
79
symptoms of deoression
(SIG E CAPS)
Sleep disturbance (insomnia/ hypersomnia)
Interest ↓
Guilt
Energy ↓
Concentration ↓
Appetite ↓
Psychomotor retardation/ agitation
Suicidal ideation
80
Drugs Used for Depression
Selective serotonin reuptake inhibitors (SSRIs)
Serotonin/norepinephrine reuptake inhibitors (SNRIs)
Tricyclic antidepressants (TCAs)
Monoamine oxidase inhibitors (MAOIs)
Atypical antidepressants
81
Drug selection for depression
Patient specific
SSRIs, SNRIs, bupropion and mirtazapine tend to be preferred due to lower ADE profile
82
Time course of response (treatment of depression)
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
Managing initial treatment:
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
Suicide Risk with Antidepressants
- All antidepressants carry a black box warning for risk of suicide
- Suicide risk in increased early in therapy
85
Selective Serotonin Reuptake Inhibitors (SSRIs) DRUGS
Fluoxetine
Citalopram
Escitalopram
Paroxetine
Sertraline
86
SSRI mechanism of action
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
ADVERSE EFFECTS OF SSRI DRUGS
Nausea
Insomnia
Weight gain
Sexual dysfunction
Hyponatremia
SEROTONIN SYNDROME
88
Monitoring/ Counseling Points
for SSRI drugs
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
MAOI drugs and SSRI drug interactions
- contraindicated when used together
- MAOI must be stopped 2 weeks prior to starting SSRI
- combination increases serotonin syndrome
90
Antiplatelet and anticoagulants
interaction with SSRI drugs
SSRIs can displace these drugs from plasma proteins and increase their effects
91
causes of Serotonin Syndrome
Accumulation of high serotonin levels
92
serotonin syndrome is
Characterized by
Hyperreflexia
Rigidity
HYPERTHERMIA
Diaphoresis
Agitation
93
Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) DRUGS
Venlafaxine
Desvenlafaxine
Duloxetine
94
Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) MECHANISM OF ACTION
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
ADVERSE EFFECTS OF Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) DRUGS
Nausea
Headache
Nervousness
Constipation
Erectile dysfunction
96
Monitoring/ Counseling Points
for (SNRIs)
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
Tricyclic Antidepressants DRUG INTERACTIONS
Monoamine oxidase inhibitors
Anticholinergic agents
98
Monoamine Oxidase Inhibitors DRUGS
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
monoamine oxidase inhibitors Mechanism of action:
Inhibit MAO
Increase amount of neurotransmitter available for release
Intensifies transmission of signal
100
MOAIs drugs adverse effects
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
Drug interactions of MAOI's
TCAs
SSRIs/SNRIs
102
Bupropion (atypical antidepressants) adverse effects
seizures
103
Mirtazapine (atypical antidepressants) adverse effects
Weight gain
Sedation
Pts experiencing insomnia may benefit from mirtazapine
104
Trazodone ( Atypical Antidepressants) effects
excessive sedative effects
105
Bipolar Disorder
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
drug selection for manic episodes
Lithium
Valproate
Lithium or valproate
107
drug selection for depressive episodes
Lithium or Valproate
Antipsychotic
Lithium or Valproate
108
drug selection for Long-term Preventative Therapy
Lithium
Valproate
109
Antiepileptic Drugs
- 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
Benefits of antiepileptic drugs compared to lithium:
Higher therapeutic index (less monitoring or levels)
Faster onset
Better side effect profile
111
Adverse effects of (Divalproex Sodium/Valproaic acid/ Valproate)
ANTIEPILEPTIC DRUG
Hepatotoxicity
Pancreatitis
Enhance gaba and block v-gated na channels
112
Adverse effects of Carbamazepine (antiepileptic drug)
Hyponatremia
Visual disturbances
Headache
113
monitoring points for Carbamazepine (antiepiletic drug)
MOOD STABILIZERS
Start doses low and titrate up
Narrow therapeutic index
114
Antipsychotic Drugs
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
o Which COX inhibitor is used for PDA closure in neonates
indomethacin
116
Which COX inhibitor can only be used for 5 days maximum?
Ketorolac (PO IV IM)
117
Which COX inhibitors are available IV?
Indomethacin
Ketorolac
118
Which COX inhibitors are available IM?
Ketorolac
119
Which COX inhibitors are available TOPICALLY
Diclofenac
120
What drugs interact with COX inhibitors?
Aspirin
NSAIDs
Anticoagulants
Glucocorticoids
ACE-I
ARBs
121
List the second-generation COX inhibitors (HINT! There is only one)
celecoxib
122
Why are celecoxib not preferred compared to first generation COX inhibitors?
increased risk of MI and stroke
123
For what indications (diseases) are COX inhibitors used? (Think about their therapeutic effects)
Mild-moderate pain
Fever
Rheumatoid arthritis
Osteoarthritis
Closure of PDA in neonates (indomethacin)
124
mechanism of COX 1 (good)
Beneficial processes
GI tract: decreases gastric acid, increases bicarbonate and mucus
Platelets: platelet aggregation
Kidney: vasodilation
125
mechanism of COX-2 (‘bad’)
Tissue injury: inflammation and pain
Brain: fever and pain
Kidney: vasodilation / renal impairment
126
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?
dysmenorrhea and suppression of platelet aggregation
127
Why is aspirin avoided in children less than 16 years of age?
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
What are signs/symptoms of salicyism?
- aspiring levels slightly above therapeutic levels
- symptoms include tinnitus , sweating, headache dizziness
- result in increased respiration leading to respiratory alkalosis
129
why should aspiring be avoided in pregnancy
risk to fetuses
anemia and post-partum hemorrhage
130
What are signs and symptoms of aspirin overdose
non-specific at first
respiratory alkalosis( hyperventilation )
hyperthermia, sweating
electrolyte imbalances
coma
131
treatment of aspirin overdose
supportive care
external cooling
sodium bicarbonate infusion
132
What are the available dosage forms for aspirin overdose
lethal dose in adults - 20 to 35 grams
lethal dose in children 4 gram
133
acetaminophen MOA
inhibits COX enzymes but ONLY IN CNS
134
adverse effect of acetaminophen
well tolerated
anaphylaxis (very rare)
steven johnson syndrome
INDICATION: well tolerated, anaphylxis (rare) and steven johnsons syndrome
OVERDOSE TREATMENT: N-acetylcysteine (IV/PO)
135
routes of acetaminophen
oral rectal and IV
136
How is acetaminophen overdose treated?
N-acetylcysteine IV or PO
i’m overdose glutathione is depleted leading to build up hepatotoxicity and liver failure
137
When is acute management used in gout treatment
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
When is gout preventive therapy used
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
first line NSAID ( indomethacin/naproxen ) MOA and When should they be started
reduce inflammation through cox inhibition
MUST START THERAPY AT FIRST SIGN OF ATTACK
140
adverse effect of NSAID ( indomethacin, Naproxen )
GI ulceration
impaired renal function
fluid retention
increased risk of CV events
141
second line therapy for acute gout attacks (GLUCOCORTICOIDS= prednisone, triamcinolone acetate
typically reserved for patients who cannot take NSAIDS or for people that NSAIDS are ineffective
142
MOA of glucocorticoids ( prednisone and triamchinolone acetate
anti inflammatory and immunomodulatory effects
143
prednisone adverse effect and counseling points
- increases blood glucose levels levels
- take with food or after meal
- take in the morning
144
triamcinolone acetate adverse effect and counseling point
(ROUTE: intra-articular)
- pain at inject site
- shake well to suspend product prior to injection into the joint
145
COLCHICINE INDICATIONS
- acute gout attacks (last line)
prophylaxis (preventing of gout attacks)
146
MECHANISM OF ACTION: COLCHICINE
- prevents infiltration of joint space by leukocytes
- disrupts microtubules needed for cellular functions and motility
DONT USE IN PREGNANCY
147
adverse effects of colchicine (do not take with grape juice)
- diarrhea
- nausea vomiting
- myelosuppresion
- myopathy
148
Xanthine Oxidase (XO) inhibitors ( allopurinol and febuxostat)
first line THERAPIES FOR GOUT PREVENTION OF GOUT ATTACKS
149
XANTHINE OXIDASE (allopurinol and febuxostat) inhibitors MOA
inhibits xanthine oxidase which i need to make uric acid
BOTH DRUGS HAVE EQUAL EFFECTS but ALLOPURINOL is less expensive
150
What types of drugs have a drug-drug interaction with xanthine oxidase inhibitors (allopurinol and febuxostat ?
allopurinol inhibits some hepatic enzymes substrates of COX
151
What adverse effects might be expected with these Xanthine Oxidase Inhibitors ( allopurinol, febuxostat )
increases gout attacks initially for both
ALOPURINOL- hypersensitivity syndrome, nausea, vomiting, diarrhea
FEBUXOSTAT- well tolerated and increased LFTs
152
Probenecid MOA
- prevents reabsorption of uric acid from renal tubules
- increases excretion of uric acid
153
What are the indications for probenecid?
prevents gout attacks
prolong the effects of penicillin and cephalosporin antibiotics
154
cautions of using probenecid
DO NOT START PROBENECID DURING AN ACUTE GOUT ATTCK
- STAY HYDRATED!!
155
adverse effects for probenecid
- well tolerated
-mild nausea and or vomiting
hypersensitivity (4%)
- renal injury
DDI - aspiring, indomethacin
156
what is abortive therapy for headaches
- 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
preventive therapy for headaches
- 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
drugs of preventive therapy migraines
- 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
drugs for abortive therapy of migraines/headaches
- 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
Serotonin 1B/1D Receptor Agonists (ALL ENDS IN - TRIPTANS)
first line agent for TERMINATING MIGRANE HEADACHE
- relieve pain through vasoconstriction
- possible coronary vasospasm
161
mechanism of action 5-HT1B/1D SEROTONIN
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
What are common drug interactions of serotnin1B/1D receptor agonists
other TRIPTANS
ergot alkaloids
MAOI
SSRI
SNRI
163
adverse effects of serotnin1B/1D receptor agonists
avoid use in patients with CAD = coronary vasospasm
avoid in pregnancy (teragenesis)
164
Which drugs of SEROTONIN 1B/5D are available intranasally?
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
Ergot alkaloids ( ERGOT in the names )
NON SELECTIVE
second line agent for TERMINATING MIGRAINE HEADACHE
- risk of physical dependence
higher adverse effect profile than TRIPTANS
166
ERGOT ALKALOIDS MOA
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
What are common adverse effects of ERGOT ALKALOIDS
nausea, vomiting
weakness in legs
myalgia
tingling sensation in fingers and toes
angina-like pain
tachycardia or bradycardia
168
What are common drug interactions of ergot alkaloids
TRIPTANS
other ergot alkaloids
CYP3A4 inhibitors
169
Who should not use ergot alkaloid drugs and why?
hepatic or renal impairment
CAD
peripheral vascular disease
uncontrolled HTN
pregnancy
170
What are signs/symptoms of ergotism? Who is at risk?
significant ischemia
extremes cold pale and numb. eventually leading to gangrene
HIGHEST RISK- CAD PVD sepsis, renal and hepatic impairment
171
What are signs/symptoms of physical dependence? How can this risk be minimized?
characterized by withdrawal syndrome
nausea vomiting headache restlessness
RISK CAN BE MINIMIZED BY COUNSELING PATIENTS TO ABOID DIALY USE
172
ERGO DRUGS ROUTE
Ergotamine - PO or PR
dihydroergotamine: IM SQ IN IV
173
OTHER PROPHYLACTIC/PREVENTIVE THERAPIES
estrogen gel and patch
- calcium channel blockers
- botulinum toxin
ACE-i or ARB
Supplements
- riboflavin
- coenzyme Q-10
butterbur
174
Which of the drugs for preventative therapy are a good option for pregnant patients?
X
175
How can we manage medication overuse headache once it occurs?
stop all abortive HA medications
HA will increase for short period
resolve in days to weeks
176
drugs for anxiety
short time : benzodiazepines
long term: SSRI, SNRI, TCA
177
first line non drug treatment of insomnia
sleep hygiene ( first line)
178
Which drugs are used for mild insomnia?
melatonin
antihistamines
OVER THE COUNTER DRUGS
179
drugs for severe insomnia
benzodiazepines
benzodiazepines-like drugs
ramelteon
others
180
Benzodiazepines mechanism of action
binds to have reception and potentials the action of gaba
GABA is an inhibitory neurotransmitter
181
drugs if benzodiazepines
HINT: ends in ZEPAM, ZPAM
CHLORDIAZEPOXIDE
182
What drug can be used to reverse a benzodiazepine overdose?
flumazenil (IV)
