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pharm final Flashcards

1
Q

Acebutolol

A

Class II anti arrhythmia drugs

  • B adrenergic blocker
  • B1 selective blocker, reduces risk of bronchospasm -Partial Agonist (ISA)

diminish phase 4 depolarization, depressing automaticity, especially in nodal tissues

  • treat arrhythms cause by too much symp activity
  • careful in use w/ Ca channel blockers b/c together can too much depress normal cardiac function
  • Membrane stabilizing
  • low lipid solubility ?
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2
Q

Atenolol

A

B1 selective blocker
Not Partial agonist
Not membrane stabilizing
low Lipid soluble

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3
Q

Esmolol

A 
B1 selective blocker
Not partial Agonist
Not Membrane stabilizing
Low Lipid Soluble
rapid action, rapid broken down by plasma esterase's
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4
Q

Metoprolol

A

B1 Selective blocker
Not partial Agonist
Membrane Stabilizing ?
Moderate Lipid Soluble

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5
Q

Nadolol

A 
B1 and B2 blocker
Not partial agonist
no membrane stabilize
Low Lipid solubility
longest activity
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6
Q

Pindolol

A 
B1 and B2 selective blocker
Partial Agonist (ISA), Membrane stabilizer ?
 ISA doesn't affect B2 mediated inhibition, actually enhances the relax adding to anti HTN effect
Moderate Lipid soluble
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7
Q

Propranolol

A

B1 and B2 selective blocker
no partial agonist
Membrane stabilize
High Lipid soluble

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8
Q

Timolol

A 
B1 and B2 selective blocker
no partial agonist
no membrane stabilize
Moderate lipid solubility
used in glaucoma treatment
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9
Q

labetalol

A

a1/B blocker and NO releasing B1 blocker

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10
Q

Clonidine

A

centrally acting adrenergic neuronal inhibitor
not a prodrug
similar action to methyl dopa as a a2 agonist to dampen simp outflow
lower doses than methyldopa, in patch form
no autoimmune SE, rebound HTN
treatment of: adhd, meno hot flash, stress disorder, nicotine and ethos withdrawal

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11
Q

methyl dopa

A

centrally acting adrenergic neuronal inhibitor
converted to alpha-methylNE thats acts as an a2 agonist in central vasomotor centers to dampen simp outflow leading to decreased renin, decreased HR and CO(or not), and most important decreased arterial peripherial pressure
SE:peripheral fluid retention, centrally mediated dry mouth, certain autoimmune disorders, hemolytic anemia, abnormal liver function

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12
Q

Reserpine

A

Peripherally acting Sympathetic neuronal blocker

  • decreases the availability of NE to its receptor by inhibiting NE and DA storage in vesicles, thus less released with each nerve impulse
  • reduces BP via decreased CO and peripheral resistence
  • irreversible effects, thus lower BP may last after drug is stopped
  • SE: sedation and mental depression, may ppt migraines
  • se: nasal congestion, postural hypoTN, bradycardia, fluid retention
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13
Q

Nicotine

A

Ganglionic Stimulant

finish this card

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14
Q

Hydrochlorothiazide

A

Diuretic

distal tubule

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15
Q

Furosemide

A

diuretic

Loop diuretic

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16
Q

Thiazide diuretics

A

inhibitors of apical Na-Cl transport in distal convoluted tubule,
recommended at the initial therapy for chronic primary HTN
hydrochlorothiazide (microzide)
chlorothiazide (Diuril)
chlorthalidone (Thalitone)
indapamide (Lozol)

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17
Q

indapamide

A

Thiazide diuretics

  • thiazides ^ LDL, total cholesterol and triglycerides
  • indapamide does not so used in pts with ^ LDL( may also have direct affect on vascular smooth muscle via Ca channel blockade
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18
Q

K sparing diuretics

A 
Inhibitors of renal Na channels
-triamterene
-amiloride 
aldosterone receptor blockers
-spironolactone
-eplerenone
-drospirenone
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19
Q

triamterene

A

k sparing diuretic

  • secreted in prox tubule by organic base secretory system
  • t1/2= 4 hours, metabolized in liver to active metabolite 4-hydroxyttriamterene
  • block apical Na channels and spare K by decreasing basal Na/K ATPase and by reduced electrochemical gradient
  • not powerful so used in combination w/other diuretics and counterbalance K wasting of loop and thiazides
  • Liddle syndrome(pseudohyperaldosteronism)
  • TOX- hyperK-> arrhythmia, not administered with spironolactone, caution with RAAS blockers, cause kidney stones
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20
Q

spironolactone

A

aldosterone receptor blocker
used in combination with loop diuretics and thiazides to prevent K wasting
treat hyperaldosteronism
-TOX- hyperK-> arrhythmia, antiandrogeneffects,

21
Q

eplerenone

A

aldosterone receptor blockers

k sparing diuretic

22
Q

PrazoSin

A

Prototype selective a1 blocker- competitive
-long term treatment of mild to moderate HTN, decreased BP by decreasing TPR
-Relax smooth muscle of bladder neck, relieve urinary obstruction
-MUST BE TAKEN AT LEAST 3X DAY,slowly increase dose
raynauds treatment
SE:First dose phenomenon orthostatic HypoTN, Na H20 retention, reflex tachycardia, not as much as non selective

23
Q

DoxazoSin

A

newer selective a1 blocker than prazosin
use and side effect just life Prasozin, but with longer half lives(dose 1x/day) so better long term control of HTN and BPH, slowly increase dose
Relax smooth muscle of bladder neck, relieve urinary obstruction
raynauds treatment
SE:First dose phenomenon orthostatic HypoTN, Na H20 retention, reflex tachycardia, not as much as non selective

24
Q

nebivolol

A

selective B1 blocker and NO releaser from vascular endothelium

  • decreased NO degradation
  • BP is dropped due to decreased TPR
  • use-HTN pts with decreased endothelial cell function, mild to mod primary HTN
  • SE: similar to B blockers with less rebound HTN with cessation
25
Selective arteriolar vasodialators
hydralazine minoxidil decrease BP by decreasing TPR thru direct dilating arterioles( not arteries or veins)
26
hydralazine
-Selective arteriolar vasodialators-decrease BP by decreasing TPR thru direct dilating arterioles( not arteries or veins) -works by releasing NO from endothelium -high first pass effect with rapid acetylators -alone- increase hydrostatic pressure in capillaries leading to edema and retention of H2O and Na in the Kidney, also Symp and renal compensation-> massive catecholamine and renin release SE: tachycardia, edema, and loss of affect, lupus like reaction -use - effective as "third drug" to diuretics and B blockers
27
minoxidil
-Selective arteriolar vasodialators-decrease BP by decreasing TPR thru direct dilating arterioles( not arteries or veins) -via an active metabolite to open ATP SENSATIVE K CHANNELS in smooth muscle -alone- increase hydrostatic pressure in capillaries leading to edema and retention of H2O and Na in the Kidney, also Symp and renal compensation-> massive catecholamine and renin release SE: tachycardia, edema, and loss of affect, hair growth -use - effective as "third drug" to diuretics and B blockers
28
Ca channel blockers
Verampamil- heart specific DIltiazem- heart specfic Nifedipine "..DIPINE"- act in arterial tissue Felodipine
29
Ace inhibitors
Captopril enalapril- prodrug activated to enalaprilat lisinipril fosinipril- prodrug, good when used in renal insufficiency pt quinapril-prodrug ramipril-prodrug
30
ARBs | Angiotensin II receptor blockers
Losartan Valsartan Candesartan-prodrug converted in GI tract
31
Renin Inhibitors
Aliskiren | inhibits conversion of angiotensinogen to angiotensin 1
32
Nitroglycerin
antianginal agent - decreases peripheral resistance and thus preload( low doses and Afterload(higher doses) - decreases O2 demand of cardiac cells by decreasing cell tension
33
Isosorbide dinitrate
antianginal agent - decreases peripheral resistance and thus preload( low doses and Afterload(higher doses) - decreases O2 demand of cardiac cells by decreasing cell tension
34
ranolazine
anti anginal drug -proposed MOA - shifting of energy production in heart from fatty acids to sugars to reduce O2 demand - or inhibits late Na channel to reduce calcium overload and reduce O2 demand -usually used in combo to treat chronic stable angina SE: dizzy, headache, nausea,constipation, can prolong cardiac QT interval, verapamil can increase affact by increasing abs, diltiazem interferes with its metabolism
35
Bile acid binding resins drugs
cholestyramine colestipol colesevelam
36
cholestyramine
Bile acid binding resin -in intestine exchange Cl- for Bile acids and sequester them from reabs -overall effect is decreased LDL by Liver taking up more to have cholesterol to synthesize bile acids -initially increases VLDL( don't use in high VLDL pts) and may increase HDL -USE: high LDL hyperlipidemia , SE: no systemic toxiciticy, resins can sequester other drugs and nutrients in GI tract and should be taken at separate times, interfere w/ fat soluble vitamins/iron abs
37
colestipol
Bile acid binding resin -in intestine exchange Cl- for Bile acids and sequester them from reabs -overall effect is decreased LDL by Liver taking up more to have cholesterol to synthesize bile acids -initially increases VLDL( don't use in high VLDL pts) and may increase HDL -USE: high LDL hyperlipidemia , SE: no systemic toxiciticy, resins can sequester other drugs and nutrients in GI tract and should be taken at separate times, interfere w/ fat soluble vitamins/iron abs
38
Statins
HMB CoA reductase inhibitors mainly in the liver-> overall reduction in circulation endogenous cholesterol -increased LDL receptors in liver and peripheral tissue to decrease LDL in blood -Most powerful LDL lowering agent(IDL and VLDL also reduced) - no reduced HDL, slightly increase SE-increased serum aminotransferase, myopathy can lead to rhabdo ( must monitor creatine kinase levels) -contraindicate- liver disease and pregnancy and lactation
39
Gemfibrozil | fenofibrate
fibric acid analogues increased clearance of VLDL via increased lipoprotein lipase activity, via increased PPAR-a activity fenofibrate-increases hepatic LDL R->decreases LDL both-better at decreasing VLDL and thus triglycerides -USE- primary high VLDL, secondary hyper lipid due to apolipoprotein E deficit feno is a prodrug SE- B: gallstone, GI upset, gemfibrozil- myopathy with statin
40
Niacin
inhibits intracellular lypolysis in fat cells by inhibiting Hormone sensitive lipase - reduced VLDLs by depleting the liver of Fatty acids needed to make triglycerides - lower VLDL -> lower IDL and LDL in plasma - increases extract lipoprotein lipase to further reduce VLDL - decreases lipoprotien(a)(major component of LDL) and INCREASES HDL VIA DECREASE CLEARANCE OF HDL APOLIPOPROTEIN A-1 - use- all primary type hyperlipidemias, HDL deficiency - short duration, metabolized to inactive vitamin nicotimamide
41
niacin SE
flushing itching or burning feeling of skin PG mediated and relieved by taking aspirin 30 min before taking drug some hypoTN in those on antiHTN drugs - increase liver enzyme -mild hyper glycemia and glucose intolerance in diabetics -GI disturbance and peptic ulcers -nonspecific renal affects- elevated uric acid
42
Omega 3 Acid ethyl esters
inhibit synthesis of triglycerides in liver ->decreased VLDL MOA-1. increased B oxidation of eFFA 2. deceased delivery of EFFA to liver 3. decreased synthesis of eFFA 4. decreased synthesis triglyceride synthesizing enzyme slightly increased HDL, NO AFFECT ON LDL USE: combination with statins to treat high LDL and VLDL w/o increased risk of myopathy as with vibrate combination
43
Ezetimibe
Cholesterol abs inhibitor - inhibits cholesterol Abs in brush border of small intestine by inhibiting specific protein mediated transport system - effect is to decrease LDL in circulation - used alone or in combo with statins to treat High LDL type hyperlipidemias - enterohepatic recirculation of active metabolite - fibrates enhance and BA binding resins decrease availability - may raise HDL, unsure effect on VLDL - SE: diarrhea, higher risk of increased liver enzymes when used with statins
44
thiazolidinediones
increase insulin sensitivity in target tissues -PPARgamma agonists - increased sensitivity to insulin stimulate uptake of glossy and fatty acids, alters adipokine production - increased sensitivity in liver and muscle too -long term lower Triglyceride and slight increase HDL and LDL -highly bound, long t1/2 and met in liver -SE-weight gain and edema(most important) osteoporosis and fracture in women, increased risk of CHF, contra- preg, hepatic inpairment( freq LFT needed), heart failure
45
Class IV anti arrhythmia drugs
Verapamil Diltiazem block Votage sensative L type Ca channels decrease inward current carried by calcium
46
repaglinide
Meglitinides, insulin secretagogues, REPAGLINIDE, nateglinide MOA-require functioning Beta cells--> only intreating early Type 2 diabetes, -Bind to K ATP channel on B cells and inhibit their activity causing depolarization-> influx of calcium-> insulin release - quickly absorbed, highly bound, met in liver -Hypoglycemia( less frequent w/ nateglinide) -contra- hepatic impairment, renal insufficiency USE- DM type 2, quicker acting so more preprandial dosing, can be used in sulfer allergies, mono therapy or w/ metformin
47
Flecainide
Class 1C anti arrhythmic drugs - interacts more slowly w/ phase 0 Na channels more than other class 1 drugs - marked depression of phase 0 slope in Na dependent myocardial fibers - inhibits some K channels and also blocks late opening Na channel-> no net effect on action potential duration or ERP - increases threshold for phase 0 - USE- reserved for severe arrthymia resistant to other drugs -well absorbed, minimal biotransformation - SE-negative intrepid effects aggravate CHF,, dizzy nausea, headache, blurry vision, aggravate arrhythmias/ induce Vtach aggravated by hyper K
48
Acarbose
alpha glucosidase inhibitor -competitive inhibitor of enteric a-glucosidase( enzyme that breaks down complex carbs and oligosaccharides) -delay post prandial abs of gluscose -attenuates plasma glucose increases post prandial-> insulin sparing effect -SE- GI disturbance(fart, drhea, ab pain) -contra- IBS, any condition worsened by gas - USE- type 2 DM, prior to each meal, mono therapy or with other meddler insulin -in mild to mod hypoglycemia pts should be given dextrose not sucrose

Pharmacology drew (9 decks)

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