Final Review MOA Flashcards

(47 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

triamterene

A

non-aldosterone antagonist

MOA- block sodium potassium pumps

USES- electrolyte benefits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

amiloride

A

non-aldosterone antagonist

MOA- block sodium potassium pumps

USES- electrolyte benefits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Mannitol

A

Osmotic Diuretic,

Theraputics: prophalaxis of renal failure,
intracranial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

HCTZ

A

Thiazide diuretic-

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Loop diuretics

A

work by preventing the reabsorption of 20% of solute.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ace inhibitors

A

MOA- decreases levels of angiotension 2 thus dilating the vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

(sartans)
telmisartan
losartan

A

Angiotension 2 receptor blocker

no accumulation of bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

(prils)
Lisinopril
Caropril

A

ACE Inhibitor

MOA- decreases levels of angiotension 2 thus dilating the vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

metolazone

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

sodium polystyrene sulfate

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tubocurarine and atracurium

A

Block nic m receptors

Does not effect cns

Antidote is physostigmine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Albuterol

A

Beta 2 agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Nateglinide (STARLIX) Repaglinide (Prandin)
MOA-stimulates beta islet cells to release insulin Dosing: prior to each meal Adverse effects: hypoglycemia, wt gain
26
Metformin (Glucophage) MOA
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
MOA of Glitazones TROGLITAZONE (removed from market), PIOGLITAZONE (ACTOS), ROSIGLITAZONE (AVANDIA)
–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
Alpha Glucosidase Inhibitors- ** ACARBOSE (PRECOSE) and miglitol (Glyset)
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
PRAMLINITIDE (SYMLIN) MOA
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
Incretin mimetic agents- | EXENATIDE (BYETTA) AND SITAGLIPTAN (Januvia)
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
(topical) Epinephrine: Prototype for sympathomimetics
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
Isoproterenol
Adrenergic Agonist Agent 1st selective beta agonist Receptors: Stimulates Beta 1-2 ( <3 , lung, uterus) Uses: CHF, AV Block, COPD, Asthma, Preterm Labor
33
Dopamine
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
Dobutamine
Adrenergic Agonist Agent Receptors: Beta 1 Only Uses: Coding, heart failure, bradycardia ADE: HTN, Tachycardia, arrhythmia, MI, Angina
35
Terbutaline
Adrenergic Agonist Agent Noncatacholamine Receptors: Beta 2 Selective only Uses: Asthma- Pre mature labor ADE: Tremors, Increased Blood Glucose
36
``` Adrenergic Agonist Agents Isoproterenol Epinepherine Dopamine Dobutamine Ephedrine Terbutaline ```
``` Cholinergic Agonists Bethanechol Pilocarpine Acetylcholine Muscarine ```
37
Acetylcholinesterase Inhibitor
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
Neuromuscular Blocker
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
Non sulfa loop diuretic
Ethacrynic Acid
40
What is the MOA of acetaminophen
Moa unlike other NSAIDS, limited to CNS- good for pain and fever.---not for inflammation
41
Propylthiouracil (PTU)
MOA: Blocks thyroid hormone synthesis by preventing oxidation of iodide by peroxidase
42
Levothyroxine-
(T4) (Synthroid)-
43
MOA for radioactive Iodine
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
MOA of NSAIDS
inhibit cyclooxygenase (COX) an enzyme that converts arachidonic acid into prostaglandins and related compounds like prostacyclin, thromboxane A2, etc.
45
CELECOXIB (Celebrex) Moa
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
CLONIDINE -
Central Acting Alpha 2 Agonists works by stimulation of alpha 2 in CNS, whoas NE Stimulation w/o depleting Receptor Remember rebound HTN
47
Beta 2 stimulation ,
causes bronchodilation, Relaxation of Smooth Muscle (preterm labor), skeletal muscle contraction, increase blood glucose Drugs: Terbutaline Isoproterenol Epinepherine