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
Q

What do beta 2 receptors do when activated?

A

Vasodilate
Bronchodilator
Breakdown glycogen
Relax the uterus and bladder
Decrease secretions

26
Q

METOPROLOL
What kind of receptor blocker?
Treats?

A

-Beta 1 selective blocker
-HTN, reinfarction after MI, HR, angina
-IV and PO

27
Q

What are drugs called that are used to block the effects of acetylchoine?

A

Anticholinergics

28
Q

What do anticholinergics do?

A

Block the effects of parasympathetic nervous system
PARASYMPATHOLYTICs

29
Q

ATROPINE
TREATS

A

Anticholinergic / block only muscarinic
-Decrease secretions, bronchodilator, inhibit vagal responses in heart, relax GI and GU tracts, pupil dilation,

30
Q

What does the parasympthatic nervous system do?

A

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
Q

What does the sympathetic nervous system do?

A

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
Q

How do the following work
Chemical stimulants
BULK
OSMOTIC
LUBRICANTS

A

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
Q

BISMUTH SALTS (pepto)
MOA
TREATS

A

-Block stimulation of GI tract
TREAT- travelers diarrhea, prevent cramping and distention assoc with dietary excess and viral infections

34
Q

LOPERAMIDE
TREATS
ACTIONS
ADVERSE

A

-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
Q

PROTON PUMP INHIBITORS
DRUGS
MOA
TREATS
w/amoxicillin for

A

“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
Q

What do Alpha cells do?
Beta cells?
Delta cells?

A

Alpha - release glucagon
Beta - release insulin
Delta - somatostatin

37
Q

What does GLP-1 do?

A

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
Q

What is polyphagia and polydipsia?

A

Polyphagia - increased hunger
Polydipsia - increased thirst

39
Q

Signs of hyperglycemia?
<126

A

GRADUAL: Decreased consciousness, weak, lethargic, tachy, hypotension, rapid-deep breathing (kassmaul), nausea, vomit

40
Q

Signs of hypoglycemia?
>70

A

SUDDEN: Headache, blurred vision. weakness, spasms, tachy, palpitations, rapid shallow breathing, hunger, anxious, drunk

41
Q

What 2 insulins cannot be mixed with other drugs?

A

Insulin glargine and insulin detemir

42
Q

What are ways in which anti-infectives work?

A

-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
Q

How does bacteria aquire resistance to anti-infectives?

A

-develop an enzyme that deactivates the drug
-Change cellular permeability
-Alter binding sites
-Produce an antagonist

44
Q

How do superinfections occur?

A

When opportunistic pathogens have the opportunity to invade tissues

45
Q

Anti-anginal work in what 2 ways?

A

Dilate blood vessels
Decrease workload of heart

46
Q

What are the 4 classes of drugs that are antianginals?

A

Nitrates
Beta-blockers
Calcium channel blockers
Piperazine acetamide

47
Q

What 3 beta blockers are used for antianginal?

A

Metoprolol
Nadolol
Propranolol

48
Q

What is the MOA for the following
NITRATES
BETA BLOCKERS
CALCIUM CHANNEL BLOCKERS

A

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
Q

NITROGLYCERINE
Indications
Actions
Adverse

A

-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
Q

What are the drug classifications that affect blood pressure?

A

Renin-Angiotensin converting enzyme inhibitors
Angiotension II receptor blocker
Renin inhibitor
Calcium channel blocker
Vasodilator

51
Q

What area if the heart is the highest pressure?

A

Left ventricle during systole

52
Q

What area of the heart is lowest pressure?

A

Right atrium

53
Q

ACE INHIBITORS
MOA
DRUGS

A

-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
Q

ARBS / Angiotensin II blocker
MOA
DRUGS

A

Selectively bind with angiotension II in vascular smooth muscle to block vasoconstriction and release of aldosterone
“SARTAN”

55
Q

RENIN INHIBITOR
MOA
DRUG

A

Directly inhibits renin
ALISKIREN

56
Q

CALCIUM CHANNEL BLOCKERS
MOA
DRUGS

A

Inhibit movement of calcium in myocardial and arterial cells = blocking contraction
“DIPINE” & VErapamil

57
Q

VASODILATORS
MOA
DRUGS

A

Act directly on sm muscle to cause relaxation
Hydralazine, minoxidil, nitroprusside