pharm exam 3 Flashcards

1
Q

phase 0

A

the cell enters a point of stimulation
-Na+ (sodium) rushes into the cell and depolarization occurs

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2
Q

phase 1

A

short period when sodium ion channels close and decrease permeability of NA+
-repolarization as K+ potassium leaves the cell

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3
Q

phase 2

A

-permeability to K+ decreases and calcium enters the cell
-action potential lasts longer

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4
Q

phase 3

A

rapid repolarization period
-Ca2+ stops and K+ permeability increses rapid rush of potassium out
-membrane back to resting state

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5
Q

phase 4

A

cell is resting membrane potential
-sodium-potassium pump

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6
Q

class 1 antiarrhythmic

A

-blocks sodium channels in cell membrane
-depressed phase 0
-prolonged duration of action potential
-quinidine, procainamide 1a
-lidocaine 1b
-flecainide, propafenone 1c

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7
Q

lidocaine

A

-ventricular dysrhythmias
-bolus injection
-anesthetic agen

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8
Q

flecainide and propafenone

A

paraxysmal afib/flutter
-maintains normal sinus rythym

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9
Q

quinidine

A

-grapefruit juice interferes with metabolism causing toxic levels

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10
Q

class 2 antiarrhythmic

A

block beta receptors
-depressed phase 4
-esmolol, propranolol, adenosine

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11
Q

esmolol and propranolol

A

-avoid in asthmatic clients and cause bronchospasms

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12
Q

adenosine

A

-6mg rapid IV over 1-2 seconds
-can do 2nd dose 1-2 minutes later at 12mg x2
-converts SVT to sinus rhythm
-15 sec duration of action
-athmatic client caution
-flushing, headaches, dyspnea (short term)

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13
Q

class 3 antiarrhythmic

A

-block potassium channels and prolong phase 3 (potassium leaves slowly)
-amiodarone, dofetilide, sotalol, dronedarone, ibutilide

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14
Q

amiodarone

A

-treats life threatending vertricular dysrhythmias, ven. fib, pulseless ven. tachycardia
-drug of choice for cardiac arrest
-converts afib to normal sinus rhythm

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15
Q

amiodarone adverse effects

A

-QT prolongation
-bradycardia
-hypotension
-GI
-hepatotoxicity
-pulmonary toxic
-hyper/hypo thyroid
-blue-gray skin
-photosensitivity

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16
Q

class 4 antiarrhythmic

A

-calcium channel blockers
-block movement of Ca2+ across membrane in cardiac and smooth muscle cells
-depressing phases 1 and 2
-slows automaticity and conduction and ventricular rate
-non-dihydropyridines: diltiazem, verapamil

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17
Q

class 4 antiarrhythmic indications and adverse effects

A

indications: treats supraventricle dysrhythmias, supraventricle tachycardia, afib, a flutter, angina, and hyper tension
adverse : bradycardia, tachycardia, AV block

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18
Q

antianginal agents

A

-improve blood flow to the heart muscle (myocardium) by dilating vessels, increasing oxygen supply, and decreasing work of the heart
-nitrates, beta-adrenergic blockers, and calcium channel blockers
-used for all the anginas and STEMI/NSTEMI

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19
Q

ranolazine

A

-ranexa
-treats chronic angina

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20
Q

nitrates antianginal

A

-nitroglycerin
-directly on smooth muscle to relax and depress muscle tone
-relaxes and dilate veins, increasing blood flow through vessels and lowers BP because decrease in resistance
-decreases preload and afterload

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21
Q

nitroglycerin adverse effects

A

-headache, hypotension, dizziness, reflex tachycardia, syncope

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22
Q

nitroglycerin drug drug interactions

A

-heparin: decreases effect
-do not combine with phosphodiesterase type 5 PDE5
ihibitors like sildenafil (viagra), tadalafil, and vardenafil because it can cause serious hypotension

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23
Q

administering nitroglycerin

A

-1 tablet under tongue every 5 minutes PRN for a total of 3 tablets
-take BP before 1 dose and before any subsequent dose hold for hypotension

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24
Q

beta blockers antianginal

A

block sympathetic nervous system stimulation causing a decrease in cardiac output, myocardial oxygen consumption, excitability of the heart, and BP
-atenolol, metoprolol tartrate and succinate, propranolol, nadolol LOL

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25
calcium channel blockers antianginal
-decrease preload and after load, which reduces cardiac workload and oxygen consumption -dihydropyridines: amlodipine, nifedipine (lower BP) -non-dihydropyridines: diltiazem, verapamil (lower HR, BP) -prinzmetal angina, chronic angina, exertional angina
26
peptic ulcer disease causes
-bacterial infection :helicobacter pylori -Nsaid usage (COX1) -acute physiological stress which activates the SNS and decreases flow to GI leading to erosion of stomach lining (trauma, burns, illness)
27
gastroesophageal reflux disease (GERD)
- digestive disorder that affects lower esophogeal sphincter -stomach acid flows back into esophogus and can irritate the lining -symptoms: heartburn, dysphagia, chest pain, regurgitation, "lump in the throat"
28
GI disorder drugs: Histamine-2 antagonists
-block release of hydrochloric acid in response to gastrin -famotidine (pepcid), cimetidine (tagmet)
29
Histamine 2 antagonists actions
-block histamine-2 receptor sites in the parietal cells of the stomach that are responsible for secretion of gastric acid -increase PH of stomach acid
30
Histamine-2 antagonists indications
-GERD -short term- peptic ulcer -prohylaxis (prevention) of stress induced ulcers, GI bleeds, and NSAID ulcers -relieves symptoms of heartburn and indigestions -uclers caused by H.pylori
31
GI disorder drugs: antacids
-interact with acids at the chemical level to neutralize them -sodium bicarbonate -calcium salts (oystercal, Tums) -magnesium salts (milk of magnesia, maalox) -aluminum salts (amphojel)
32
antacids indications
-relief of upset stomach due to hyperacidity -hyperacidity associated with peptic ulcer, gastritis, peptic esophagitis, gastric hyperacidity, hiatal hernia
33
antacids adverse effects
-hypercalcemia and constipation -milk-alkali syndrome (calcium) -hypophosphatemia with aluminum antacids -rebound acidity -diarrhea (magnesium) -fluid retention/heart failure, metabolic alkalois (sodium bicarb)
34
antacids drug drug
affect absorption of many drugs- separate from other meds by 2 hours at least
35
treatment of GI: proton pump inhibitors (PPIS)
-suppress the secretion of HCL into the lumen of the stomach -pantoprazole (protonix), omeprazole, esomeprazole
36
PPI actions
suppress gastric acid secretion by specificially inhibiting the hydrogen-potassium adenosine triphosphatase enzyme system on the secretory surface of gasric parietal cells -block the final step of acid production, lowering acid levels in the stomach
37
PPI indications
-short term treatment of peptic ulcer, gerd, erosive esophogatis, begnign gastric disease -maintenance therapy for healing erosive esophogitis, and ulcers -used in combo with amoxicillins and clarithromycin to treat H. pylori infection
38
PPI adverse effects
-superinfections: CDIFF -long term usage: hypomagnesemia, and bone loss with decrease calcium (risk for osteoporosis and fractures) -rebound acid hypersecretions can occur when stopping, therefor short term, low doses should be used
39
PPI drug drug interactions
-clopidogrel(plavix) avoid in combo PPIs can inferfere with antiplatelet activity
40
Helicobacter pylori
-clients with peptic ulcers who are postive for the bacteria get treated with antibiotics -H.pylori is gram neg bacillus -
41
h. pylori treatment meds
2 Antibiotics: clarithromycin, amoxicillin, metronidazole, tetracycline PPI Bismuth subsalicylate
42
treatment of GI disorders: GI protectants
-coat any injured area in the stomach to prevent further injury from acid -sucralfate (carafate)
43
GI protectants action
-from an ulcer adherent complex at duodenal ulcer sites, protecting the sites against acid, pepsin, and bile salts -prevents further breakdown and promotes ulcer healing
44
GI protectants indications
-short term treatment of duodenal ulcers -maintenance of duodenal ulcers after healing -treatment of oral and esophogeal ulcers due to radiation, chemotherapy, or sclerotherapy
45
Treatments of GI disorders: prostaglandins
-inhibit the secretion of gastrin and increase the secretion of the mucous lining of the stomach, providing a buffer -synthetic prostaglandin E1 analogue: misoprostol (cytotec)
46
prostaglandins (misoprostol) actions
-inhibits gastric acid secretion and increases bicarbonate and mucous production in the stomach- protects the stomach lining
47
prostaglandins (misoprostol) indications
-prevention of NSAID induced gastric ulcers in adults who are at high risk -off label: termination of pregnancy
48
Prostaglandins (misoprostol) adverse effect
miscarriage
49
Digestive enzymes
-substances produced in the GI tract to break down foods into usable nutrients -saliva substitute: aquoral, moi-stir, mouth kote, salivart, etc.. -pancrelipase: creon, prancreaze, pertzye, viokace, zenpep
50
digestive enzyme actions
-saliva substitutes contain electrolytes and carboxymethylcellulose to act as a thickening agent in dry mouth conditions (make the flood bolus easier to swallow) - clients with stroke, radiation therapy, chemotherapy, sjogren syndrome, etc... - pancreatic enzymes are replacement enzymes that aid in the digestion and absorption of fats, proteins, and carbohyrdates-- clients with cystic fibrosis, pancreatic insufficiency and malabsorption syndromes -ADMINISTER WITH MEALS AND SNACKS
51
laxatives: chemical stimulants
-chemically irritate the lining of the GI tract - bisacodyl (dulcolax), castor oil, senna (senokot)
52
chemical stimulant laxative actions
begin working at the beginning of the small intestine and increase motility throughout the rest of the GI tract by stimulating the nerve plexus
53
chemical stimulation laxative indications
short-term treatment of constipation -prevention of constipation and straining after GI surgery, MI, and obstetrical delivery -part of a colon preparation prior to elective surgeries or procedures (barium enema, colonoscopy)-- used as an adjunct to other agents (such as Go-lytely) to evacuate the colon
54
chemical stimulant laxative contraindications
acute abdominal disorders: obstruction, appendicitis, diverticulitis, ulceritve colitis -increased motility could lead to rupture or further exacerbation of the inflammation
55
chemical stimulant laxative adverse effects
GI: diarerhea, cramping, nausea CNS: dizziness, headache, weakness Cathartic dependence castor oil: blocks absorptions of fats and fat-soluable vitamins and may lead to mal nutrition if used chronically
56
chemical stimulants drug drug
-separate from other medications by at least 30 minutes
57
Laxatives: bulk forming agents
-cause fecal matter to increase in bulk Fiber supplements: methylcellulose (citrucel), polycarbophil (fibercon), psyllium (metamucil)
58
bulk forming agent laxative actions
-increase motility of GI tract by increasing size of fecal material which helps to pull more fluid in the intestinal contents-- stimulates local stretch receptors and activates local GI activity -similar to dietary fiber -nondigestable and absorb water from intestines from a glutinous mass that adds bulk to stool -production of soft, formed shit in 1-3 days
59
bulk forming agent laxative administration
-separate from other meds and laxatives by at least 2 hours -increase fluid intake to 3-4L a day
60
osmotic laxatives
-pull more solute/water into the GI tract -lactulose (constilac) -magnesium sulface (epsom salts) -magnesium citrate -magnesium hydroxide -polyethylene glycol (miralax) -polyethylene glycol electrolyte solution (go lytley) -sodium picosulfate with magnesium oxide and citric acid (clenpiq)
61
osmotic laxative actions
draw more water into GI tract via osmosis and stimulate GI motility
62
osmotic laxative drug drug
seprate from other laxatives and drugs at least 30 minutes, some medications up to 2 hours
63
osmotic laxative lactulose inidcation
saltless osmotic laxative that pull fluid out of venous system and into the lumen of the small intestine --short term treatment of constipation and treatment of hepatic encephalopathy (decrease serium ammonia levels)
64
osmotic laxative polyethylene glycol electrolyte solution (golytely)
-hypertonic fluids containing many electrolytes that pull fluid out of intestinal wall to increase bulk -used for bowel evacuation prior to GI diagnostic tests
65
osmotic laxative sodium picosulfate with magnesium oxide and citric acid
provide combination of stimulant laxative and bulk forming laxative -cleanse the colon before colonoscopy
66
lubricant laxatives
help the intestinal contents that soft and slippery
67
lubricants: docusate sodium (colace)
-has a detergent action on the surface of the intestinal bolus, increasing the admixture of fat and water, making a softer stool
68
lubricant: glycerin (sani-supp)
-hyperosmolar laxative used in suppository form to gently evacuate the rectum without system effects higher in GI tract
69
lubricant: mineral oil (agoral liquid)
-not absorbed: forms a slippery coat on the contents and causes less absorption of water out of the bolus -frequent use of mineral oil can effect absorption of vitamins ADEK
70
opioid antagonist laxatives
block the effects of opioids on the GI tract by selectively binding to opioid receptors -alvimopan, methylnaltrexone, noloxegol, nalemedine
70
antidiarrheal drugs
block stimulation of the GI tract form symptomatic relief of diarrhea
71
antidiarrheal : bismuth subsalicylate
--pepto bismol --direct action on the lining of the GI tract to inhibit local reflexes
72
antidiarrheal loperamide
-imodium A-D -direct effect on muscle layers of GI tract to slow activity -slows peristalsis (decreases intestinal motility) and allows increased time for absorption of fluid and electrolytes
73
antidiarrheal opium derivatives
paregoric: acts on CNS centers that cause GI spasm and slowing -crofelemer: works in the inner lining of gi tract to block specific chloride channels-- less water loss as diarreah
74
antiemetics
-decrease or prevent nausea and vomiting -work locally to decrease the local response to stimuli that are being sent the medulla to induce vomit -work centrally to block the chemoreceptor trigger zone or to suppress vomit center directly
75
centrally actin antiemetics
phenothiazines: prochlorperazine, chlorpromazine, promethazine nonphenothiazines: metoclopramide serotonin (5-HT3) receptor blockers: ondansetron (zofran)
76
antiemetic: phenothiazines
-change the responsiveness or stimulation of the chemorecptor trigger zone -most work as dopamine receptor antagonists taht can be used to treat psychiatric disorders
77
phenothiazine: indications
-nausea and vomiting associated with anesthesia -intractable hiccups: chlorpromazine
78
phenothiazines: adverse
CNS: dizziness, weakness, tremors, headache extrapyramidal symptoms -promethazine: extravasation of the drug can cause severe tissue injury including gangrene with IV admin
79
metoclopramide
-used as a GI stimulant or an antiemtic agent
80
metoclopramide actions
-blocks dopamine receptors and makes the GI cells more sensitive to acetylcholine which stimulates parasympathetic activity -leads to increased GI activity and rapid movement of food through the upper GI tract
81
metoclopramide indications
-relief of GERD -prevention of postoperative nausea and vomiting or after chemotherapy -relief of symptoms of chronic diabetic gastroparesis
82
metoclopramide adverse effects
extrapyramidal symptoms: -dystonia: involuntary muscle contractions results in abnormal posturing or repetitive movements (tongue, neck, back legs) -tardive dyskinesia: abnormal muscle movements such as lip smacking, tongue darting, chewing movements, and slow aimless arm and leg movements -pseudoparkinsonism: muscle tremors, cogwheel rigidity, drooling, shuffling gait, slow movements -akathisia: subjective feeling of internal restlessness and a compelling urge to move -neuropathic malignant syndrome
83
serotonin (5-HT3) receptor blockers
-ondansetron (zofran) -block the serotonin receptors associated with nausea and vomiting the CTZ and on the nerve terminals of the vagus nerves that innervate the stomach and small intestines
84
serotonin receptor blockers indications
treatment of postoperative nausea and vomiting -treatment of n/v associated w chemo and radiation
85
5-Ht3 receptor (serotonin) blockers adverse
-pain at injection site -hypotension -urinary retention -serotonin syndrome -QT prolongation -stevens johnson syndromo and toxic epidermal necrolysis (TEN)
86
serotonin syndrome
-excessive accumulation of serotonin in the body -key risk factor is exposure to a serotonergic drug
87
serotonin syndrome signs
-Clonus! involuntary and rhythmic muscle movements and hyperreflexia other: agitation, confusion, anxiety, tremors, muscle jerking, shivering, sweating, headache, tachycardia, hypertension, rigidity less common: hyperthermia, diarreah, diaphoresis, flushing, dilated pupils, goosies
88
serotonin treatment syndrome
stop the drug -administer benzodiazapines, IV fluids, oxygen, medications to control HR and BP -can cause death
89
central nervous system
-brain and spinal cord
90
peripheral nervous system
-cranial nerves, spinal nerves, autonomic nervous system -sensory receptors bring info to the CNS -motor nerves carry info away from CNS to facilitate response
91
autonomic nervous system
-sympathetic nervous system: flight or flight -parasympatheric nervous system: rest, digest, see, and pee best
92
nerve synapse
nerve communicate with other nerves or effectors at the nerve synapse -presynaptic nerve: releases a neurotransmitter into the synaptic cleft -synaptic cleft: junction between nerve and effector -postsynaptic effector cell: neurotransmitter reacts with specific receptor site on the postsynaptic cell to cause reaction
93
neurotransmitter: acetylcholine
-communicated between nerves and muscles -stimulate cholinergic receptors (musclarinic and nicotinic)
94
neurotransmitters: norepinephrine and epinephrine
-catecholamines released by nerves in sympathetic system -stimulate adrenergic receptors (alpha and beta 1s and 2s)
95
neurotransmitter: dopamine
-involved in the coordinatinon of impulses and responses
96
neurotransmitter: gamme-aminobutyric acid (GABA)
-inhibits nerve activity and in important in prevent over exitablity or stimulation like a seizure
97
neurotransmitter: serotonin
-important in arousal and sleep and in preventing depression and promoting motivation
98
anxiety
-feeling of tension, nervousnes, apprehension, or fear that usually involves unpleasant reactions to a stimulus whether actual or unknown -often comes with: sweating, tachycardia, rapid breathing, evelated BP
99
sedation
loss of awareness and reaction to environmental stimuli
100
hypnosis
extreme sedation resulting from further depression and sleep
101
classes for treatment of anxiety
benxodiazapines antidepressants: serotonin reuptake inhibitors are now the first line treatment for anxiety -anticonvulsant -antipsychotic agents -antihistamines -selective mediation that act on autonomic nervous system
102
benzodiazepines
-alprazolam (xanax), diazepam (valium), lorazepam (ativan), chlordiazepoxide (librium), midazolam (versed), clonazepam (klonopin)
103
benzodiazapine actions
-act in limbic system and the reticular activating system (RAS) -make GABA more effective: causes interference with neurons firing and stablizes postsynaptic cell -lower doses assit with anxiety -high doses cause sedation and hypnosis
104
benzodiazepines black box
-concomitant use with opiods can result in profound sedation, respiratory depression, coma, or death -CNS depression when taken with alcohol
105
benzodiazepines indications
-anxiety -first line agent for alc withdrawl -hyperexitability and agitation -preoperative relief -seizures -emergency treatment of status epilepticus -insomnia
106
benzodiazepines adverse
sedation, lethargy, "sleep driving", hypotension, respiratory depresion -confusion and delerium in older adults avoid using
107
nursing interventions with benzodiazpines
-do not abruptly withdraw can cause nausea, headache, vertigo, malaise, and nightmares + Withdrawal SEIZURES -taper dose gradually especially in epileptic clients over 2 weeks -administer IV slowly because of hypotension, bradycardia, and cardiac arrest -bed rest for at least 3 hours -for overdose give flumazenil (romazicon)
108
barbiturates actions
-CNS depression, inhibit neuronal impulse conduction in the ascending RAS, depress the cerebral cortex, depress motor output -butabarbital, pentoabarbital, phenobarbital -cause: sedation, hypnosis, anesthesia, and possible coma
109
barbituates: indications
relief of anxiety (no longer mainstay treatment, sedation, insomnia, pre-anesthesia, seizures
110
barbiturate adverse
- bradycardia, hypotension, and respiratory depression, CNS depression -physical dependency, exitement (hallucinations, anxiety, laryngospasms -increase in CNS effects with alcohol, antihistamines, and other tranquilizers
111
antihistamines
-promethazine and diphenhydramine (benedyrl) -postoperative and preoperative medication to decrease need for narcotics
112
buspirone
-reduces s/s of anxiety without severe CNS and adverse -no sedative or muscle relaxant properties -binds to serotonin and dopamine
113
dexmedetomidine
selective alpha 2 adrenergic agonist : continours infusion mg/kg/hr -sedation of clients in ICU- does not supress respiratory -used as an adjunct to benzodiazepine in alcohol withdrawal
114
eszopiclone (lunesta)
-treatment of insomnia -though to react with GABA sites to prolong sleep and decrease awakening -associated with sleep depriving and othr behaviors like next day sedation, sleepiness, memory loss, and loss of coordination
115
zaleplon (sonata) and zolpidem (ambien)
-short term treatment of insomnia -selectively binds to specific GABA receptors -associated with sleep depriving
116
depression
affective disorder in which individuals experience sadness that is much more severe and longer lasting than the event that precipitated it
117
classes of antidepressants
-tricylic antidepressants -monoamine oxidase inhibitors -serotonin norepinephrine reuptake inhibitors -others
118
actions of antidepressant therapy
-inhibit effects of monoamine oxidase, an enzyme that remove neurotransmitters from the neuron synaptic cleft, leading to increase norepinephrine or serotonin -block reuptake of neurotransmitters by releaseing nerve, leading to incresed neurotransmitter numbers in synaptic cleft -regulate receptor sites and breakdown of neurotransmitters, leading to an accumulation of neurotransmittrs in the synaptic cleft
119
tricyclic antidepressants (TCAS)
-inhibit presynaptic reuptake of neurotransmitters -amines: amitriptyline, clomopramine, imipramine, trimipramine secondary amines: desipramine, nortriptyline, protriptyline
120
tricyclic antidepressant indications
-relief of depression symptoms -sleep disorders -enursis bed wetting over 6yo -chronic pain -migraine prevention -obsessive compulsive disorder
121
TCA black box
increased risk of suicide, especially in children
122
TCA's adverse
sedation, drowsiness -sleep distrubances -antocholinergic effects: blurred vision, urinary retention, dry mouth, decrease salivation, nausea, vomiting, constipation, tachycardia, hypertension -WITHDRAWAL: nausea, vomiting, vertigo, headache, nightmares
123
monoamine oxidase inhibitors
isocarboxazid, phenelzine, tranylcypromine -irreversibly inhibits MAO, an enzyme found in nerves and other tissues, that breaks down biogenic amines, dopamine and serotonin -allows NE, serotonin and dopamine to accumulate in synaptic cleft
124
MAOIS indications
-depression treatment for clients who dont tolerate safer treatment
125
MAOIs black box
suicide in younger populations
126
MAOIs adverse
CV effects: fatal hypertension, cardiac dysrhythmias, angina
127
MAOIs drug drug
-other antidepressants -serotonin syndrome with SSRIs
128
MAOIs food interactions
tyramine- containing foods can increase blood pressure -aged cheese, pepperoni, salami, processed meats (corn beef, hotdogs, bologne, bacon), red wines, tap or home beers, avocados, soy and teriyaki sauce
129
selective serotonin reuptake inhibitors (SSRIs)
-block the reuptake of serotonin with little to no effection on Norepinephrine -fluoxetine (prozac), citalopram (celexa), escitalopram (lexapro), paroxetine (paxil), sertraline (zoloft)
130
SSRI indications
-major depresion, OCD, panic disorder, bulimia nervosa, PMDD, PTSD, social phobias, social anxiety -a period of 4 weeks is necessary to see effects -clients may respond to one and not the other
131
SSRIs black box
suicide in young
132
SSRI adverse
CNS: drowsiness, dizziness, anxiety, insomnia, agitation, tremor, seizures, mania serotonin syndrome -sexual dysfunction -decrease sodium and fluid retention
133
SSRI drug drug
MAOI TCAs
134
serotonin norepinephrine inhibitors (SNRIs)
-desvenlafaxine, duloxetine, venlafaxine -decrease neuronal reuptake of both serotonin and norepinephrine, more weakly inhibit dopamine -often wont have therapeutic effects for 4-6 weeks
135
SNRIs indications
-major depressive disorder -generalized anxiety, social anxiety, addictive behavior -treatment of neuropathic pain (duloxetine)
136
bupropion
-treatment of depression in adults -smoking cessation -blocks reuptake of NE and dopamine
137
trazodone
-depression in adults and children 6-18yo -blocks 5-HT and some 5HT precursor reuptake