Drugs Unit 2

Cimetidine

H2 receptor antagonist

Ranitidine

H2 receptor antagonist

Famotidine

H2 receptor antagonist -- Pepcid

Nizatidine

H2 receptor antagonist

Esomeprazole

H+/K+ ATPase Inhibitor -- Nexium

Omeprazole

H+/K+ ATPase Inhibitor -- Prilosec

Maalox

aluminum hydroxide (antacid)

Mylanta

aluminum hydroxide (antacid)

Rolaids

antacid

Tums Ex

calcium carbonate (antacid)

Milk of Magnesia

magnesium hydroxide (antacid)

Amoxicillin

antibiotic gastric ulcer therapy

Clarithromycin

antibiotic gastric ulcer therapy

Tetracycline

antibiotic gastric ulcer therapy

Bismuth compounds

inhibit bacterial growth and prevent H. pylori from adhering to gastric mucosa minor antibiotic effect, protective barrier against acid diffusion and peptic digestion antibiotic and protective lining

bismuth subcitrate

• complex bismuth salt of citric acid - protective agent + antibiotic - mechanism: thought to work by forming a protective coating over GI mucosa

bismuth subsalycylate

• pepto bismol - protective agent + antibiotic - mechanism: thought to work by forming a protective coating over GI mucosa

mannitol

osmotic diuretic - acts on the proximal tubule and descending limb

furosemide

loop diuretic - acts on thick ascending limb - inhibits NA+/K+/Cl- symporter

torsemide

loop diuretic - acts on thick ascending limb - inhibits NA+/K+/Cl- symporter

ethacrynic acid

loop diuretic - acts on thick ascending limb - inhibits NA+/K+/Cl- symporter

bumetanide

loop diuretic - acts on thick ascending limb - inhibits NA+/K+/Cl- symporter

bendroflumethiazide

thiazide diuretic - acts on distal convoluted tubule - inhibits Na/Cl symporter

Triamterene

K+ sparing diuretic - acts at collecting tubule - last place for Na+ retention - inhibits Na+ absorption but doesn't effect K+ -- prevent muscle cramps

Amiloride

K+ sparing diuretic- acts at collecting tubule - last place for Na+ retention - inhibits Na+ absorption but doesn't effect K+ -- prevent muscle cramps

Spironolactone

aldosterone antagonist - acts at collecting tubule - potassium sparing - inhibit effect of RAAS to reduce bp (makes less NA and K channels produced)

Cardiac Glycosides

Digitalis -- digoxin -- drugs used to improve heart output by increasing the muscular contraction -antagonist for Na/K ATPase on CM of cardiomyocite cell

Phosphodiesterase inhibitors

-Block enzyme phosphodiesterase -Increase calcium for myocardial contraction -Cause positive inotropic response -- increased force of constriction and vasodilation -Increase contractility and decrease afterload -Short-term therapy only

diretics (for hypertension)

decrease blood volume - decrease cardiac output - decrease blood pressure

direct vasodilators

relax/open blood vessels --> decreased bp bc less -resistance on blood movement

angiotensin blockers

reduce blood vessel constriction via aldosterone/angiotensin

sympathoplegic agents

sympathetic nervous system -- reduce cardiac output and/or vascular resistance to lover bp

Nitroprusside

direct vasodilator, venous and arterial dilation -- via NO and cGMP to reduce contraction - therapeutic uses: hypertensive crisis, CHF exacerbation

Minoxidil

Direct Vasodilator of arterioles K+ channel opener to hyper polarize smooth muscle

Verapamil

direct vasodilator -- calcium channel blocker - at arteries sm cells

Nifedipine

direct vasodilator -- calcium channel blocker - at arteries sm cells

Diltiazem

direct vasodilator -- calcium channel blocker - at arteries sm cells

ACE inhibitors

"PRIL" Antihypertensive. Blocks ACE from converting angiotensin I to angiotensin II (powerful vasoconstrictor). Decreases BP, Decreased Aldosterone secretions, Sodium and fluid loss.

Benazepril

ACE inhibitor / Angiotensin blocker

Captopril

ACE inhibitor / Angiotensin blocker

Enalapril

ACE inhibitor / Angiotensin blocker

Fosinopril Sodium

ACE inhibitor / Angiotensin blocker

Lisinopril

ACE inhibitor / Angiotensin blocker

Angiotensin receptor antagonists

-sartan -- blocks binding of angiotensis 2 and decreases constriction to get relaxation and lower blood pressure

AT1 -- g protein coupled receptor (varies by cell type)

Losartan

AT1 receptor antagonist / Angiotensin blocker

Valsartan

AT1 receptor antagonist / Angiotensin blocker

Candesartan

AT1 receptor antagonist / Angiotensin blocker

Eprosartan

AT1 receptor antagonist / Angiotensin blocker

Ibesartan

AT1 receptor antagonist / Angiotensin blocker

Telmisartan

AT1 receptor antagonist / Angiotensin blocker

adrenergic receptors

receptor sites for the sympathetic neurotransmitters norepinephrine and epinephrine

Prazosin

alpha 1 antagonist / sympathoplegic agent - outcompete NE and help relax peripheral blood vessels - reduce contraction in heart --> lower cardiac output --> reduce bp

Metoprolol

beta 1 antagonist / beta blocker / sympathoplegic agent - block receptor in heart muscle and decrease contractile force - cause structural change at juxtaglomerular cells to avoid NE binding and reduce baroreceptor response --> reduce renin secretion and RAS response (decreased bp)

Propranolol

beta 1 antagonist / beta blocker / sympathoplegic agent - block receptor in hear muscle and decrease contractile force - cause structural change at juxtaglomerular cells to avoid NE binding and reduce baroreceptor response --> reduce renin secretion and RAS response (decreased bp)

statins

lower cholesterol in the blood and reduce its production in the liver by blocking HMG-CoA reductase enzyme that produces it at rate limiting step--helps prevent atherosclerosis -competitively inhibit HMG-CoA reductase

- deplete intracellular pools of sterols -increase transcription of LDL receptors (in liver) --> removal of LDL and LDL precursors from plasma

mevastatin

HMG-CoA reductase inhibitor/antagonist

lovastatin

HMG-CoA reductase inhibitor/antagonist

atorvastatin

HMG-CoA reductase inhibitor/antagonist -- lipitor

simvastatin

HMG-CoA reductase inhibitor/antagonist

pravastatin

HMG-CoA reductase inhibitor/antagonist

rosuvastatin

HMG-CoA reductase inhibitor/antagonist

simvastatin + ezetimibe

combintation - HMG-CoA reductase inhibitor/antagonist - cholesterol absorption inhibitor -- prevents fat absorption -- hella bad side effects when released tho

Gemfribrozil

Fibric acid derivative -- PPARa agonist - increase LPL activity - increase HDL synthesis- alter VLDL composition to inhibit LDL - inhib fatty acid synthesis and promote fatty acid oxidation

Oral hypoglycemic agents

medication taken by mouth to decrease blood sugar levels in persons with type 2 diabetes; not used for persons with type 1 diabetes

Sulfonylureas

increase insulin secretion by blocking potassium channel to depolarize cell to influx calcium and trigger insulin secretion

tolbutamine

Sulphonylurea -- increase insulin secretion

glyburide

Sulphonylureas -- increase insulin secretion

Meglitinides

glinides

increase insulin secretion by blocking potassium channel to depolarize cell to influx calcium and trigger insulin secretion

repaglinide

Meglitinide -- increase insulin secretion

nateglinide

meglitinide -- increase insulin secretion

DPP-4 inhibitors

indirectly stimulate insulin secretion -- inhibit DPP4 enzyme from cleaving GLP peptides

sitagliptin

DPP-4 inhibitor

GLP1 Analog

more GLPs for patient which promotes insulin secretion and glucagon decrease

Liraglutide

GLP-1 analog

Semaglutide

GLP-1 analog

Antihyperglycemic agents

Medications taken by type 2 diabetics to lower blood glucose levels by a variety of mechanisms -- without producing hypoglycemia -- Biguanides _+ metformin

metformin

via AMPK liver glucose output is inhibited, glucose absorption in the gut is inhibited, and glucose uptake by muscle and adipose is increased

Alpha-glucosidase inhibitors

Acarbose + Miglitol

acarbose

alpha-glucosidase inhibitor -- no sugar breakdown -- less sugar can be absorbed -- reduced glucose in blood

miglitol

alpha-glucosidase inhibitor -- no sugar breakdown -- less sugar can be absorbed -- reduced glucose in blood

SGLT inhibitors

Sodium glucose co-transporter inhibitor -- drugs that increase glucose excretion -- prevent glucose reabsorbtion at nephron -- proximal convoluted tubule

dapagliflozin

SGLT2 inhibitor

canagliflozin

SGLT-2 inhibitors

thiazolindinediones

lowers blood glucosse by increasing insulin sensitivity

agonist for PPAR gamma-- Increases insulin sensitivity at peripheral receptor site

rosiglitazone

Thiazolidinedione -- increase insulin sensitivity

pioglitazone

Thiazolidinedione -- increase insulin sensitivity

Anti-hyperthyroid drugs

inhibit —> I- uptake, organification, and coupling

Perchlorate (ClO4-)

An anti-hyperthyroid drug that inhibits iodide uptake by inhibiting Na/I transporter — single dose

Iodide (high doses)

anti-hyperthyroid that inhibits own transporter — mechanism not understood — 2 days

Propylthiouracil (PTU)

Anti-hyperthyroid — inhibits peroxidase enzyme that oxidizes I- —> inhibits coupling reaction —> inhibits peripheral deiodination

Radioactive iodine (131 I)

emits b radiation which causes follicular cell necrosis, colloid disappearance, could destroy thyroid gland

B1- adrenergic receptor antagonists (for hyperthyroid)

regulate hear rate and bp symptoms

glucocorticoids (for hyperthyroid)

inhibit deiodinase conversion of t4—>t3

antipyretic effects (reduce body temp)

levothyroxine

synthetic T4

for hypothyroidism

liothyronine

synthetic T3

for hypothyroidism

porcine desiccated thyroid

for hypothyroidism

thyroid gland material from pig is crushed and dried and taken as a supplement