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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
Q

calcium channel blockers antianginal

A

-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

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26
Q

peptic ulcer disease causes

A

-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)

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27
Q

gastroesophageal reflux disease (GERD)

A
  • 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”
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28
Q

GI disorder drugs: Histamine-2 antagonists

A

-block release of hydrochloric acid in response to gastrin
-famotidine (pepcid), cimetidine (tagmet)

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29
Q

Histamine 2 antagonists actions

A

-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

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30
Q

Histamine-2 antagonists indications

A

-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

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31
Q

GI disorder drugs: antacids

A

-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)

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32
Q

antacids indications

A

-relief of upset stomach due to hyperacidity
-hyperacidity associated with peptic ulcer, gastritis, peptic esophagitis, gastric hyperacidity, hiatal hernia

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33
Q

antacids adverse effects

A

-hypercalcemia and constipation
-milk-alkali syndrome (calcium)
-hypophosphatemia with aluminum antacids
-rebound acidity
-diarrhea (magnesium)
-fluid retention/heart failure, metabolic alkalois (sodium bicarb)

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34
Q

antacids drug drug

A

affect absorption of many drugs- separate from other meds by 2 hours at least

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35
Q

treatment of GI: proton pump inhibitors (PPIS)

A

-suppress the secretion of HCL into the lumen of the stomach
-pantoprazole (protonix), omeprazole, esomeprazole

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36
Q

PPI actions

A

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

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37
Q

PPI indications

A

-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

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38
Q

PPI adverse effects

A

-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

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39
Q

PPI drug drug interactions

A

-clopidogrel(plavix) avoid in combo PPIs can inferfere with antiplatelet activity

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40
Q

Helicobacter pylori

A

-clients with peptic ulcers who are postive for the bacteria get treated with antibiotics
-H.pylori is gram neg bacillus
-

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41
Q

h. pylori treatment meds

A

2 Antibiotics: clarithromycin, amoxicillin, metronidazole, tetracycline
PPI
Bismuth subsalicylate

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42
Q

treatment of GI disorders: GI protectants

A

-coat any injured area in the stomach to prevent further injury from acid
-sucralfate (carafate)

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43
Q

GI protectants action

A

-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

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44
Q

GI protectants indications

A

-short term treatment of duodenal ulcers
-maintenance of duodenal ulcers after healing
-treatment of oral and esophogeal ulcers due to radiation, chemotherapy, or sclerotherapy

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45
Q

Treatments of GI disorders: prostaglandins

A

-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)

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46
Q

prostaglandins (misoprostol) actions

A

-inhibits gastric acid secretion and increases bicarbonate and mucous production in the stomach- protects the stomach lining

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47
Q

prostaglandins (misoprostol) indications

A

-prevention of NSAID induced gastric ulcers in adults who are at high risk
-off label: termination of pregnancy

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48
Q

Prostaglandins (misoprostol) adverse effect

A

miscarriage

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49
Q

Digestive enzymes

A

-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

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50
Q

digestive enzyme actions

A

-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

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51
Q

laxatives: chemical stimulants

A

-chemically irritate the lining of the GI tract
- bisacodyl (dulcolax), castor oil, senna (senokot)

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52
Q

chemical stimulant laxative actions

A

begin working at the beginning of the small intestine and increase motility throughout the rest of the GI tract by stimulating the nerve plexus

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53
Q

chemical stimulation laxative indications

A

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

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54
Q

chemical stimulant laxative contraindications

A

acute abdominal disorders: obstruction, appendicitis, diverticulitis, ulceritve colitis
-increased motility could lead to rupture or further exacerbation of the inflammation

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55
Q

chemical stimulant laxative adverse effects

A

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

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56
Q

chemical stimulants drug drug

A

-separate from other medications by at least 30 minutes

57
Q

Laxatives: bulk forming agents

A

-cause fecal matter to increase in bulk
Fiber supplements: methylcellulose (citrucel), polycarbophil (fibercon), psyllium (metamucil)

58
Q

bulk forming agent laxative actions

A

-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
Q

bulk forming agent laxative administration

A

-separate from other meds and laxatives by at least 2 hours
-increase fluid intake to 3-4L a day

60
Q

osmotic laxatives

A

-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
Q

osmotic laxative actions

A

draw more water into GI tract via osmosis and stimulate GI motility

62
Q

osmotic laxative drug drug

A

seprate from other laxatives and drugs at least 30 minutes, some medications up to 2 hours

63
Q

osmotic laxative lactulose inidcation

A

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
Q

osmotic laxative polyethylene glycol electrolyte solution (golytely)

A

-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
Q

osmotic laxative sodium picosulfate with magnesium oxide and citric acid

A

provide combination of stimulant laxative and bulk forming laxative
-cleanse the colon before colonoscopy

66
Q

lubricant laxatives

A

help the intestinal contents that soft and slippery

67
Q

lubricants: docusate sodium (colace)

A

-has a detergent action on the surface of the intestinal bolus, increasing the admixture of fat and water, making a softer stool

68
Q

lubricant: glycerin (sani-supp)

A

-hyperosmolar laxative used in suppository form to gently evacuate the rectum without system effects higher in GI tract

69
Q

lubricant: mineral oil (agoral liquid)

A

-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
Q

opioid antagonist laxatives

A

block the effects of opioids on the GI tract by selectively binding to opioid receptors
-alvimopan, methylnaltrexone, noloxegol, nalemedine

70
Q

antidiarrheal drugs

A

block stimulation of the GI tract form symptomatic relief of diarrhea

71
Q

antidiarrheal : bismuth subsalicylate

A

–pepto bismol
–direct action on the lining of the GI tract to inhibit local reflexes

72
Q

antidiarrheal loperamide

A

-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
Q

antidiarrheal opium derivatives

A

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
Q

antiemetics

A

-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
Q

centrally actin antiemetics

A

phenothiazines: prochlorperazine, chlorpromazine, promethazine
nonphenothiazines: metoclopramide
serotonin (5-HT3) receptor blockers: ondansetron (zofran)

76
Q

antiemetic: phenothiazines

A

-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
Q

phenothiazine: indications

A

-nausea and vomiting associated with anesthesia
-intractable hiccups: chlorpromazine

78
Q

phenothiazines: adverse

A

CNS: dizziness, weakness, tremors, headache
extrapyramidal symptoms
-promethazine: extravasation of the drug can cause severe tissue injury including gangrene with IV admin

79
Q

metoclopramide

A

-used as a GI stimulant or an antiemtic agent

80
Q

metoclopramide actions

A

-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
Q

metoclopramide indications

A

-relief of GERD
-prevention of postoperative nausea and vomiting or after chemotherapy
-relief of symptoms of chronic diabetic gastroparesis

82
Q

metoclopramide adverse effects

A

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
Q

serotonin (5-HT3) receptor blockers

A

-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
Q

serotonin receptor blockers indications

A

treatment of postoperative nausea and vomiting
-treatment of n/v associated w chemo and radiation

85
Q

5-Ht3 receptor (serotonin) blockers adverse

A

-pain at injection site
-hypotension
-urinary retention
-serotonin syndrome
-QT prolongation
-stevens johnson syndromo and toxic epidermal necrolysis (TEN)

86
Q

serotonin syndrome

A

-excessive accumulation of serotonin in the body
-key risk factor is exposure to a serotonergic drug

87
Q

serotonin syndrome signs

A

-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
Q

serotonin treatment syndrome

A

stop the drug
-administer benzodiazapines, IV fluids, oxygen, medications to control HR and BP
-can cause death

89
Q

central nervous system

A

-brain and spinal cord

90
Q

peripheral nervous system

A

-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
Q

autonomic nervous system

A

-sympathetic nervous system: flight or flight
-parasympatheric nervous system: rest, digest, see, and pee best

92
Q

nerve synapse

A

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
Q

neurotransmitter: acetylcholine

A

-communicated between nerves and muscles
-stimulate cholinergic receptors (musclarinic and nicotinic)

94
Q

neurotransmitters: norepinephrine and epinephrine

A

-catecholamines released by nerves in sympathetic system
-stimulate adrenergic receptors (alpha and beta 1s and 2s)

95
Q

neurotransmitter: dopamine

A

-involved in the coordinatinon of impulses and responses

96
Q

neurotransmitter: gamme-aminobutyric acid (GABA)

A

-inhibits nerve activity and in important in prevent over exitablity or stimulation like a seizure

97
Q

neurotransmitter: serotonin

A

-important in arousal and sleep and in preventing depression and promoting motivation

98
Q

anxiety

A

-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
Q

sedation

A

loss of awareness and reaction to environmental stimuli

100
Q

hypnosis

A

extreme sedation resulting from further depression and sleep

101
Q

classes for treatment of anxiety

A

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
Q

benzodiazepines

A

-alprazolam (xanax), diazepam (valium), lorazepam (ativan), chlordiazepoxide (librium), midazolam (versed), clonazepam (klonopin)

103
Q

benzodiazapine actions

A

-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
Q

benzodiazepines black box

A

-concomitant use with opiods can result in profound sedation, respiratory depression, coma, or death
-CNS depression when taken with alcohol

105
Q

benzodiazepines indications

A

-anxiety
-first line agent for alc withdrawl
-hyperexitability and agitation
-preoperative relief
-seizures
-emergency treatment of status epilepticus
-insomnia

106
Q

benzodiazepines adverse

A

sedation, lethargy, “sleep driving”, hypotension, respiratory depresion
-confusion and delerium in older adults avoid using

107
Q

nursing interventions with benzodiazpines

A

-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
Q

barbiturates actions

A

-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
Q

barbituates: indications

A

relief of anxiety (no longer mainstay treatment, sedation, insomnia, pre-anesthesia, seizures

110
Q

barbiturate adverse

A
  • bradycardia, hypotension, and respiratory depression, CNS depression
    -physical dependency, exitement (hallucinations, anxiety, laryngospasms
    -increase in CNS effects with alcohol, antihistamines, and other tranquilizers
111
Q

antihistamines

A

-promethazine and diphenhydramine (benedyrl)
-postoperative and preoperative medication to decrease need for narcotics

112
Q

buspirone

A

-reduces s/s of anxiety without severe CNS and adverse
-no sedative or muscle relaxant properties
-binds to serotonin and dopamine

113
Q

dexmedetomidine

A

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
Q

eszopiclone (lunesta)

A

-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
Q

zaleplon (sonata) and zolpidem (ambien)

A

-short term treatment of insomnia
-selectively binds to specific GABA receptors
-associated with sleep depriving

116
Q

depression

A

affective disorder in which individuals experience sadness that is much more severe and longer lasting than the event that precipitated it

117
Q

classes of antidepressants

A

-tricylic antidepressants
-monoamine oxidase inhibitors
-serotonin norepinephrine reuptake inhibitors
-others

118
Q

actions of antidepressant therapy

A

-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
Q

tricyclic antidepressants (TCAS)

A

-inhibit presynaptic reuptake of neurotransmitters
-amines: amitriptyline, clomopramine, imipramine, trimipramine
secondary amines: desipramine, nortriptyline, protriptyline

120
Q

tricyclic antidepressant indications

A

-relief of depression symptoms
-sleep disorders
-enursis bed wetting over 6yo
-chronic pain
-migraine prevention
-obsessive compulsive disorder

121
Q

TCA black box

A

increased risk of suicide, especially in children

122
Q

TCA’s adverse

A

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
Q

monoamine oxidase inhibitors

A

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
Q

MAOIS indications

A

-depression treatment for clients who dont tolerate safer treatment

125
Q

MAOIs black box

A

suicide in younger populations

126
Q

MAOIs adverse

A

CV effects: fatal hypertension, cardiac dysrhythmias, angina

127
Q

MAOIs drug drug

A

-other antidepressants
-serotonin syndrome with SSRIs

128
Q

MAOIs food interactions

A

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
Q

selective serotonin reuptake inhibitors (SSRIs)

A

-block the reuptake of serotonin with little to no effection on Norepinephrine
-fluoxetine (prozac), citalopram (celexa), escitalopram (lexapro), paroxetine (paxil), sertraline (zoloft)

130
Q

SSRI indications

A

-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
Q

SSRIs black box

A

suicide in young

132
Q

SSRI adverse

A

CNS: drowsiness, dizziness, anxiety, insomnia, agitation, tremor, seizures, mania
serotonin syndrome
-sexual dysfunction
-decrease sodium and fluid retention

133
Q

SSRI drug drug

A

MAOI
TCAs

134
Q

serotonin norepinephrine inhibitors (SNRIs)

A

-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
Q

SNRIs indications

A

-major depressive disorder
-generalized anxiety, social anxiety, addictive behavior
-treatment of neuropathic pain (duloxetine)

136
Q

bupropion

A

-treatment of depression in adults
-smoking cessation
-blocks reuptake of NE and dopamine

137
Q

trazodone

A

-depression in adults and children 6-18yo
-blocks 5-HT and some 5HT precursor reuptake

pharm (5 decks)

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