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FINAL Flashcards

1
Q

NSAIDS
What are the 3 effects?
Therapeutic action?
Indications?

A

-Anti-inflammatory, analgesics, anti-pyretic
-Inhibit prostaglandin synthesis/block cox1&2
-Rheumatoid, osteoarthritis, mild-mod pain, primary dysmenorrhea, fever

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2
Q

Where is Cox 1 and 2 found?

A

Cox 1 - present in all tissues: blood clotting, stomach lining, maintaining sodium/water balance
Cox2 - active at site of injury

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3
Q

NSAIDS
are contraindicated in what conditions?

A

-Allergy to nsaid/salicylate, (celecoxib-allergy to sulfonamides). CV dysfunction/HTN, peptic ulcer/GI bleed/pregnancy

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4
Q

What are the adverse effects of NSAIDS?

A

Nausea, GI pain, Constipation, Diarrhea, headache, dizzy, bleeding, platelet inhibition, HTN, bone marrow depression/ anaphylactic reactions

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5
Q

What do NSAIDS interact with?

A

W/loop diuretics - decrease diuresis
w/Beta blocker - decreases anti-HTN effect
w/IBprofien - toxicity

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6
Q

What are the NSAID drugs

A

“Profen”
Naproxen, Oxaprozin
“Fenac”
“Olac” “dac”
Indomethacin
“Oxicam”
Celecoxib

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7
Q

What do MU and Kappa opioid receptors do?

A

MU - pain BLOCKING - respiratory depression, euphoria, decreased GI activity, pupil constriction, physical dependence.
KAPPA - analgesia, pupil construction, sedation

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8
Q

What are A FIBERS, A delta fibers, C fibers?

A

A FIBERS - LARGE diameter/assoc w/touch and temp
A DELTA FIBERS - SMALL diameter/assoc w/pain. QUICK
C FIBERS - unmyelinated slow fibers/ assoc w/ pain

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9
Q

What are narcotic agonists?
-Indicated
-Contraindicated
-Adverse
-Drugs

A

Drugs that react w/ opioid receptors to cause analgesia, sedation, euphoria
-Severe acute or chronic pain, pre-op med, analgesia during anesthesia
-Allergy. toxic poisons, after biliary surgery/surgical anastomosis, respir dysfunction, head injury, alcoholism
-Resp depression, cardiac arrest, shock, orthostatic, GI effects
-Morphine, codeine, fentanyl, hydrocodone/morphone, oxy, opium, tramadol

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10
Q

What are narcotic antagonists?
-Indications
-Contraindication
-Adverse
-Drugs

A

Drugs that bind strongly to opioid receptors but do not activate them
-Reverse effects of opioids
-Allergy
-Acute narcotic abstinence syndrome, nausea, vomit, tachy, HTN
-Naloxone, Naltrexone

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11
Q

What are the symptoms of acute narcotic absence syndrome?

A

Nausea, vomit, sweating, tachy, htn, anxiety

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12
Q

Ergot derivatives block?

A

alpha-adrenergic & serotonin receptor sites to cause vasoconstriction
*prevention or abortion of migraines

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13
Q

What do triptans block?

A

Bind to serotonin receptor sites to cause vasoconstriction
*used for treatment NOT prevention

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14
Q

What are narcotic agonist-antagonists
-MOA
-effects
-Drugs

A

Stimulate certain receptors and block others
-Analgesia, sedation, euphoria, hallucinations
Buprenorphine, butorphanol, nalbuphine, PENTZACINE

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15
Q

What do adrenergic antagonists do?
AKA

A

Block adrenergic receptors, which BLOCK response of sympathetic nervous system

*SYMPATHOLYTIC

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16
Q

What are the nonselective adrenergic blocking agents?
Effects?
Treats?

A

Amiodarone, carvedilol, labetalol
Effects: Lower BP, slower HR, increased renal perfusion w/ decreased renin levels
Treats: HTN assoc w/ pheochromocytoma/clonidine w/drawl

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17
Q

What are nonselective alpha-adrenergic blocking agents?

A

phentolamine
Vasodilation = decrease BP
*most freq used to prevent cell death after extravasion

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18
Q

What are alpha1 selective blockers?
MOA
DRUGS
TREATS

A

-Block smooth muscle receptors in prostate/urinary bladder
-Alfuzosin, doxasosin, prazosin, silodosin, tamsulosin, terazosin
-Treats BPH and HTN

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19
Q

What are nonselective beta blockers?
DRUGS
TREAT
MOA

A

Carteolol, metipranolol, nadolol, nebivolol, propranolol, sotalol, timolol
-MIgraine, CV problems, reinfarction after MI
-Decreased HR, contractility, c/o, o2 consumption, bp

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20
Q

What are the BETA 1 selective blockers?

A

Acebutolol, atenolol., betaxolol, bisprolol, esmolol, metoprolol
-HTN, angina, cardiac arrhythmias/perferred for ppts with asthma
-decreased HR, c/o, decreased intraocular pressure and treat open angle glaucoma

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21
Q

Where are the alpha 1 receptors?
Alpha 2?

A

Alpha 1 - blood vessels, iris, urinary bladder
Alpha 2 - Pre synaptic nerve membranes & pancreas

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22
Q

Where are Beta 1 receptors
Where are beta 2 receptors

A

BEta 1 - cardiac tissue, peripheral tissues
BEta 2 - blood vessels, bronchi, periphery, uterus

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23
Q

What do the alpha 1 receptors do when activated?

A

Vasocontrict
Pupil dilate
Close bladder
Pilo erection

24
Q

What do Beta 1 receptors do when activated?

A

Increase HR
Increase contraction
Lipolysis = energy

25
What do beta 2 receptors do when activated?
Vasodilate Bronchodilator Breakdown glycogen Relax the uterus and bladder Decrease secretions
26
METOPROLOL What kind of receptor blocker? Treats?
-Beta 1 selective blocker -HTN, reinfarction after MI, HR, angina -IV and PO
27
What are drugs called that are used to block the effects of acetylchoine?
Anticholinergics
28
What do anticholinergics do?
Block the effects of parasympathetic nervous system PARASYMPATHOLYTICs
29
ATROPINE TREATS
Anticholinergic / block only muscarinic -Decrease secretions, bronchodilator, inhibit vagal responses in heart, relax GI and GU tracts, pupil dilation,
30
What does the parasympthatic nervous system do?
REST and DIGEST Constricts pupils; causes salivation; slows down the heart rate; tightens the bronchi in the lungs; enacts digestion; releases bile; makes the bladder contract
31
What does the sympathetic nervous system do?
FIGHT OR FLIGHT dilate blood vessels, increase blood pressure, contract muscles, secrete sweat from sweat glands, dilate bronchi for more oxygen exchange and contraction of heart
32
How do the following work Chemical stimulants BULK OSMOTIC LUBRICANTS
CHEMICAL STIM - stim nerve plexus in the intestinal wall (bisacodyl, cascara, castor oil, senna) BULK - stretch (methycellulose, polycarbophil, psyllium) OSMOTIC - pull fluid (Magnesium ones, polyethylene glycol) LUBRICANTS - (docusate, glycerin, mineral oil
33
BISMUTH SALTS (pepto) MOA TREATS
-Block stimulation of GI tract TREAT- travelers diarrhea, prevent cramping and distention assoc with dietary excess and viral infections
34
LOPERAMIDE TREATS ACTIONS ADVERSE
-Short term treat of diarrhea assoc w/ diet and IBS and viral infections -Inhibits intestinal peristalsis through direct effect on longitudinal and circular muscles of intestinal wall -Ab pain, distention, dry mouth, nausea, constipation, dizzy
35
PROTON PUMP INHIBITORS DRUGS MOA TREATS w/amoxicillin for
"PRAZOLE" -Suppress gastric secretion by inhibiting hydrogen-potassium adenosine triphosphatase enzyme system on surface of gastric cells / blocks final step in acid production = lowering acid levels in stomach -Short term treatment of GERD, erosive esophagitis, benign gastric ulcer -W AMOCILLIN for H PYLORI
36
What do Alpha cells do? Beta cells? Delta cells?
Alpha - release glucagon Beta - release insulin Delta - somatostatin
37
What does GLP-1 do?
Produced in GI tract in response to food -increases insulin release and decreases glucagon in prep for food to be absorbed -Slows GI emptying & stims satiety center in brain to decrease desire to eat
38
What is polyphagia and polydipsia?
Polyphagia - increased hunger Polydipsia - increased thirst
39
Signs of hyperglycemia? <126
GRADUAL: Decreased consciousness, weak, lethargic, tachy, hypotension, rapid-deep breathing (kassmaul), nausea, vomit
40
Signs of hypoglycemia? >70
SUDDEN: Headache, blurred vision. weakness, spasms, tachy, palpitations, rapid shallow breathing, hunger, anxious, drunk
41
What 2 insulins cannot be mixed with other drugs?
Insulin glargine and insulin detemir
42
What are ways in which anti-infectives work?
-interfere with the biosynthesis of cell wall -interfere with ability to divide -Interfere with protein synthesis -Interfere with DNA synthesis -Alter permeability of cell membrane
43
How does bacteria aquire resistance to anti-infectives?
-develop an enzyme that deactivates the drug -Change cellular permeability -Alter binding sites -Produce an antagonist
44
How do superinfections occur?
When opportunistic pathogens have the opportunity to invade tissues
45
Anti-anginal work in what 2 ways?
Dilate blood vessels Decrease workload of heart
46
What are the 4 classes of drugs that are antianginals?
Nitrates Beta-blockers Calcium channel blockers Piperazine acetamide
47
What 3 beta blockers are used for antianginal?
Metoprolol Nadolol Propranolol
48
What is the MOA for the following NITRATES BETA BLOCKERS CALCIUM CHANNEL BLOCKERS
NItrates - act on smooth muscle to cause relaxation Beta-blockers - block beta receptors in heart and juxtaglomerular Calcium channel - Inhibit movement of calcium = blocking contraction
49
NITROGLYCERINE Indications Actions Adverse
-treatment of acute angina, prophylaxis, pre-op htn, HF assoc w/ MI, controlled hypotensions during surgery -Relax vascular sm muscle = decreased in venous return and decreased in BP -Hypotension, headache, dizzy, tacy, rash, flush, nausea, chest pain
50
What are the drug classifications that affect blood pressure?
Renin-Angiotensin converting enzyme inhibitors Angiotension II receptor blocker Renin inhibitor Calcium channel blocker Vasodilator
51
What area if the heart is the highest pressure?
Left ventricle during systole
52
What area of the heart is lowest pressure?
Right atrium
53
ACE INHIBITORS MOA DRUGS
-act in lungs to prevent ACE from converting angiotensin 1 to angiotensin II = decrease in BP and aldosterone secretion _"PRIL" *also used in conjunction with digoxin
54
ARBS / Angiotensin II blocker MOA DRUGS
Selectively bind with angiotension II in vascular smooth muscle to block vasoconstriction and release of aldosterone "SARTAN"
55
RENIN INHIBITOR MOA DRUG
Directly inhibits renin ALISKIREN
56
CALCIUM CHANNEL BLOCKERS MOA DRUGS
Inhibit movement of calcium in myocardial and arterial cells = blocking contraction "DIPINE" & VErapamil
57
VASODILATORS MOA DRUGS
Act directly on sm muscle to cause relaxation Hydralazine, minoxidil, nitroprusside

Pharm (16 decks)

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