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Pharmacology 1 > Final Review MOA > Flashcards

Final Review MOA Flashcards

1
Q

Ethacrynic Acid
Bumetamide
Torsemide,
Furosemide,

A

Loop Diuretic, MOA To prevent the active reabsorption of NaCl by 20% at the ascending loop of henle

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2
Q

spironolactone (more hormonal)

A

aldosterone antagonists,
MOA Aldosterone Antagonists work by blocking the effects of aldosterone, (selective blockade of aldosterone receptors)

the net effect is less sodium potassium pump production,

they retain k and excrete Na

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3
Q

eplerenone (less hormonal)

A

aldosterone antagonists,
MOA Aldosterone Antagonists work by blocking the effects of aldosterone, (selective blockade of aldosterone receptors)

the net effect is less sodium potassium pump production,

they retain k and excrete Na

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4
Q

triamterene

A

non-aldosterone antagonist

MOA- block sodium potassium pumps

USES- electrolyte benefits

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5
Q

amiloride

A

non-aldosterone antagonist

MOA- block sodium potassium pumps

USES- electrolyte benefits

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6
Q

Mannitol

A

Osmotic Diuretic,

Theraputics: prophalaxis of renal failure,
intracranial pressure

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7
Q

HCTZ

A

Thiazide diuretic-

MOA works at the distal convoluted tubule,
blocks 10% of sodium and water from being reabsorbed.

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8
Q

Diuretic therapy:

MOA-

A

General diuretics prevent active NaCl reabsorption and by doing this, it will limit the passive reabsorption of water through the concentration gradient.

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9
Q

Loop diuretics

A

work by preventing the reabsorption of 20% of solute.

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10
Q

ace inhibitors

A

MOA- decreases levels of angiotension 2 thus dilating the vasculature

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11
Q

(sartans)
telmisartan
losartan

A

Angiotension 2 receptor blocker

no accumulation of bradykinin

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12
Q

(prils)
Lisinopril
Caropril

A

ACE Inhibitor

MOA- decreases levels of angiotension 2 thus dilating the vasculature

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13
Q

metolazone

A

thiazide diuretic
MOA works at the distal convoluted tubule,
blocks 10% of sodium and water from being reabsorbed.

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14
Q

sodium polystyrene sulfate

A

.

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15
Q

Tubocurarine and atracurium

A

Block nic m receptors

Does not effect cns

Antidote is physostigmine

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16
Q

Albuterol

A

Beta 2 agonist

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17
Q

Bethanechol

A

Cholinergic agonists

MOA: Reversibly binds to muscarinic receptors

Makes muscarinic man: <3 decreased, sweaty, snotty, drool,reflux, wheeze, congestion, poopy, peeing, pupils dilated, boner,

Their competition is acetylcholine

Use in chronic constipation
Urinary retention
Xerostomia
Glaucoma

Atropine is antidote

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18
Q

Rapid Acting NOVALOG- (Aspart)

A

Shorter acting insulin- take right before you eat!

Administration- bolus insulin,( fast acting, in and out quickly)

Purpose Prandial or bolus insulin always used in combo with basal to match carbohydrate intake

Continuous infusion for basal and bolus for prandial in PUMPS.

Also used for sliding scale

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19
Q

Regular Insulin

A

SLOWER ACTING- clear

Regular-clear insulin- short duration, can be given iv, available in U-100 or U500

Route- sc, or IV, inhaled (EXUBERA) no longer available

Purpose- prandial insulin

Timing of injections: works 30-40 min before you eat

20
Q

NPH (HUMULIN)-

A

INTERMEDIATE ACTING- cloudy

protamine suspension (mixed with regular) . Protamine retards absorbtion of RHI-> delays onset of action- makes insulin last longer

Onset 1-2 hrs

*******Peak- 8-10 hrs- give 2x a day

Purpose: basal insulin with some prandial properties at peak. Typically dosed BID.

Appearance- cloudy

Mixing- Dose at breakfast and at bedtime, clear before cloudy, roll it in your hands to agitate it.

21
Q

Insulin Detmir (LEVIMIR)

A

INTERMEDIATE ACTING

dose dependant pharmacodynamics- tweener- between NPH and Lantus.

Once or 2 x a day.

Basal insulin- Cant mix with other insulins.

Peak 18 hrs

Purpose basal insulin

22
Q

Insulin Glargine

A

LONG DURATION insulin

long acting, no peak, dosed at bedtime, 24 hr coverage,

clear like reg insulin

Purpose basal insulin (Peakless)

Inject only SC

DO NOT mix with other insulins

23
Q

What are Sulfonylureas and how do they work

A

1st oral agents

A1c reduction-large 1-2%- cost effective

MOA-stimulates beta islet cells to release insulin

Therapeutic use- type 2 diabetics only- bc type 1 diabetics don’t have islet cells

24
Q

Glypizide
glyburide
glimepiride

A

2nd generation sulfonylureas

ADE-hypoglycemia. Caution is severe sulfa allergy

Do not take if you have a sulfa allergy

Anything that works through insulin pathway can cause hypoglycemia

Pregnancy-avoid- teratogenic in animals- Avoid if breastfeeding as well

25
Q

Nateglinide (STARLIX)

Repaglinide (Prandin)

A

MOA-stimulates beta islet cells to release insulin

Dosing: prior to each meal

Adverse effects: hypoglycemia, wt gain

26
Q

Metformin (Glucophage) MOA

A

is a BIguanides- approved in 1994

MOA Decreases production of glucose in the liver and enhances utilization by the muscle

DOES NOT CAUSE HYPOGLYCEMIA

A1C reduction- 1-2%

Place in therapy- now considered drug of choice for initial use. Also has a role in pre-diabetes

***Diabetes Prevention Program: all pre-diabetics received either intensive lifestyle changes or metformin therapy or placebo

27
Q

MOA of Glitazones

TROGLITAZONE (removed from market),

PIOGLITAZONE (ACTOS),

ROSIGLITAZONE (AVANDIA)

A

–activating the peroxisome proliferator-activated receptor gamma (PPAR-gamma)

PPAR-gamma improves insulin resistance

So Glitazones decrease insulin resistance

ADE
Fluid retention
Raises plasma lipid levels
Liver toxicity

28
Q

Alpha Glucosidase Inhibitors-

** ACARBOSE (PRECOSE) and miglitol (Glyset)

A

MOA complex carbs have to be reduced to monosaccharides ay alpha-glucosidase (enzyme located in the brush border of sm. Intestine). These drugs inhibit this enzyme.

A1C reduction ½ %

PK: minimally absorbed- stays in GI tract- if not absorbed, it goes to bowel and bacteria breaks it down

ADE: substancial GI flatulence, cramps, abd distention, borborygmi, diarrhea, rare liver toxicity.

Hypoglycemia- you need glu tablets, sandwich wont work fast and will delay the absorbtion

GI tract issues minimized after time

29
Q

PRAMLINITIDE (SYMLIN) MOA

A

New class of drugs (amylin mimetics) used to complement the effects of insulin

Amylin- hormone produced by pancreas, used in conjunction w/ insulin, released in conjunction w/ insulin- slows digestive tract

MOA decreases post plandial glucose- delays gastric emptying

Therapeutic usage- injected along with prandial insulin (type 1 and 2)- cant be mixed

A1C reduction- 50%

If you get 3 novalog injections youll need 3 symlin injections= 6 injections daily

Side effects decrease

hypoglycemia

nausea

30
Q

Incretin mimetic agents-

EXENATIDE (BYETTA) AND SITAGLIPTAN (Januvia)

A

GLP-1is a peptide hormone that’s released from the cells of the GI tract in response to carb containing meal. GLP-1 slows gastric emptying, stimulates beta islet cells to release insulin, inhibits glucogon release, and increases satiety.

Exenatide is a synthetic GLP-1 and sitgliptan blocks the enzyme responsible for breaking down endogenous GLP-1

A1C reduction 0.8%

Adverse effects GI (nausea, vomiting) especially with exenatide- weight neutral

31
Q

(topical) Epinephrine: Prototype for sympathomimetics

A

Adrenergic Agonist Agent

Receptors: alpha 1-2 and beta 1-2

Uses: delays absorption of local anesthetics through alpha 1, control superficial bleeding, elevates BP, decreases nasal congestion, dilates eyes, AV Block, Cardiac Arrest, Anaphalactic shock.

Kinetics: IV , Topical

ADE- 
HTN
Necrosis
Tachycardia
Dysrhythmias
angina
MI
increase in Blood sugar
32
Q

Isoproterenol

A

Adrenergic Agonist Agent

1st selective beta agonist

Receptors: Stimulates Beta 1-2 ( <3 , lung, uterus)

Uses: CHF, AV Block, COPD, Asthma, Preterm Labor

33
Q

Dopamine

A

Adrenergic Agonist Agent

Catacholamine, Concentration Dependent on receptors

Receptors: Alpha 1 (high dose)
                 Beta 1 (Moderate Dose)
                 Dopamine (Low Dose)

Uses:
dilates kidney vasculature at low dose
Code for MI

34
Q

Dobutamine

A

Adrenergic Agonist Agent

Receptors: Beta 1 Only

Uses: Coding, heart failure, bradycardia

ADE: HTN, Tachycardia, arrhythmia, MI, Angina

35
Q

Terbutaline

A

Adrenergic Agonist Agent

Noncatacholamine

Receptors: Beta 2 Selective only

Uses: Asthma- Pre mature labor

ADE: Tremors, Increased Blood Glucose

36
Q 
Adrenergic Agonist Agents
Isoproterenol
Epinepherine
Dopamine
Dobutamine
Ephedrine
Terbutaline
A 
Cholinergic Agonists
Bethanechol
Pilocarpine
Acetylcholine
Muscarine
37
Q

Acetylcholinesterase Inhibitor

A

Physostigmine
Neostigmine
Edophonium

MOA: Increases contraction of skeletal muscle by stimulation of Nic M Receptors

Primary Use: Myasthenia gravis

ADR: Muscarinic Man

If Toxic Give Atropine

Reverses anticholinergic toxicity

38
Q

Neuromuscular Blocker

A

Non-Depolarizing sticks around- use in ICU
Tubocurarine- Long Acting
Atracurarine- Intermediate Acting

NO EFFECT ON CNS

Uses: Muscle relaxation, diagnose Myasthenia Gravis

ADE- Respiratory arrest

Depolarizing Gets Out Quick
Succitalcholine 4-10 min

39
Q

Non sulfa loop diuretic

A

Ethacrynic Acid

40
Q

What is the MOA of acetaminophen

A

Moa unlike other NSAIDS, limited to CNS- good for pain and fever.—not for inflammation

41
Q

Propylthiouracil (PTU)

A

MOA: Blocks thyroid hormone synthesis by preventing oxidation of iodide by peroxidase

42
Q

Levothyroxine-

A

(T4) (Synthroid)-

43
Q

MOA for radioactive Iodine

A

MOA concentrated in the thyroid. Emmission of beta particles destroys thyroid tissue. Beta particles have a very limited ability to penetrate tissues, thus it doesn’t usually go outside the thyroid. Very specific to the thyroid

adioactive iodine- can destroy thyroid

For graves disease, or thyroid cancer- lights up thyroid

44
Q

MOA of NSAIDS

A

inhibit cyclooxygenase (COX) an enzyme that converts arachidonic acid into prostaglandins and related compounds like prostacyclin, thromboxane A2, etc.

45
Q

CELECOXIB (Celebrex) Moa

A

selectively inhibits COX2

Uses- analgesia, inflammation

Adverse drug effects- GI ulcers, CV events, renal impairment, sulfa allergy…increased risk of stroke and heart attack

46
Q

CLONIDINE -

A

Central Acting Alpha 2 Agonists

works by stimulation of alpha 2 in CNS, whoas NE Stimulation w/o depleting Receptor

Remember rebound HTN

47
Q

Beta 2 stimulation ,

A

causes bronchodilation, Relaxation of Smooth Muscle (preterm labor), skeletal muscle contraction, increase blood glucose

Drugs:
Terbutaline
Isoproterenol
Epinepherine

Pharmacology 1 (6 decks)

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