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1427 Cards in this Set

  • Front
  • Back
antiarrhythmic with negative inotropic effects
ca channel blockers
b blockers
class 1a drugs (sodium channel blockers)
what two things increase gastric acid secretion? How?
-increased levels of ca++ ( gastrin + Ach increase levels of Ca++)
-increased levels of camp (histamine increases camp, pgi2 and pge2 decrease camp)
- all act on the protein pump inhibitor
to lower renin release, give
clonidine (centrally acting)
beta blocker or an angiotensin converting enzyme (ACEI)
what type of arrhythmias (ventricular) do you get with reentry?
-extra single systoles
-sustained types of tachycardia
treatment of lepra reactions (erythema nodosum & leprosum reactions)
What drug do you give to treat cutaneous manifestations of moderate to severe erythema nodosum leprosum (ENL)?
Thalidomide MOA
-immunomodulatory agent
-down-regulation of both TNF-alpha and adhesion molecules involved in leukocytes migration
Which bile acid binding drug causes increased hepatic uptake of LDL?
What's the difference between bile acids & niacin?
Bile binding acids = for isolated increases in LDL. Bile acid binding in lumen and prevent reabsorption

Niacin - for familal hypercholestemia, inhibits VLDL secretion
High TG, what drugs to treat?
What's the difference between colestyramine and colestipol?
different indications: CTYRAMINE is used to treat pts with an isolated increase in LDL, COLESTIPOL treats pts with elevated serum total and LDL
treatment of lepra reactions
reversal reactions
a side effect of this antimycobacterium is optic neurotis (a decrease in visual activity)
drugs used for MAC
-Ethambutol, clofazimide, ciprofloxacin, or rifampin
phentolamine for CHF
- predominant effect on arteriorlar vascular bed

- H failure, decrease afterload, increase CO
active tuberculosis (possibly resistnat organisms & HIV patients)
Isoniazid, Rifampin, pyrazinamide, ethambutol or streptomycin
Diuretic used for glaucoma
Name two drug combos used for angina
- nitrates and b-blockers - can prevent a reflex tachycardia, reduce each others undesired SE

- CCB + B blockers + nitrates - all
This diuretic is indicated for treating edema used to CHF, centercephalic epilepsies, glaucoma, acute mountain sickness
When do you use captopril?
-useful in cases where elevated renin release causes
-produces hypotension plus reduced sodium retention
Name long-acting renin-angiotensin inhibitors
Enalapril & lisinopril
To maintain sinus rhythum in chronic atrial fibrillation
-class IC or Ia
Kinins - effect on renal glands
-potent vasodilation
- increase prostaglandin synthesis
-no2 release
-increase cGMP and increased Camp
Dipyridamole MOA
- vasodilator -dilates resistance vessels in coronary beds to increase flow without increasing O2 demand

- thromboembolism - lengthens abnormally shortened platelet survival time
What drug is used for the detection of renin -dependent hypertension
What effects do organic nitrates have on the redistribution of coronary blood flow?
-organic nitrates can selectively increase blood flow to ischemic areas (note: total coronary flow is not reduced)
Bile acid binding resin not effective in pts with homozygous familial hypercholesterolemia?
antimycobacterium causes severe birth defects
hypolipidemic may impair carbohydrate tolerance
diazoxide MOA
- a long acting arteriolar dilator
-prevents smooth muscle contraction by opening potassium channels + stabilizing the membran potential at a more hyperpolarized voltage
- lowers tpr and arterial blood pressure
I have a life threatening ventricular arrhythmia. Give me a drug
Treatment = Procainamide

To prevent the reoccurance of life-threatening ventricular arrhythmias: amiodarone
What regulates GFR
GFR is cappillaries is regulated by the amount of tone contractivity in arterioles
What's the difference between abciximab and Eptifibatide and Tirofiban?
-abciximab - monoclomal antibody that binds IIb/iiia complex on platelets

-Eptifibatide - a fibrinogen sequence analog that binds GP iib/iiia receptors prevents aggregtion
I'm pale (pallor), what might I have?
Iron deficiency (comon presentation)
What's the difference between Thrombopotetin and GM-CSF?
-Thrombopoietin - increases size + number of megakarocytes

GM-CSF (w/ IL3 increases activity of mature granulocytes)
What drug is reserved for pts with no significant/structural heart disease but with atrial fibrillation or atrial flutter?
a broad spectrum - antiarrhythmics
name it which channels does it effect.
-predominantly K channel blockade
-B-blockers, ca channels blocker, and Na channel block
What is the difference between Vit B12 and Folic acid?
FA: essential cofactor for synthesis of aa, purines, & DNA

VB12: a cofactor for several essential biochemical rxns

FA: treat FA deficiency
VB12: treat VB12 deficiency

Notes: VB12 deficiency causes neurological abnormalities
Urokinase and streptokinase MOA
urokinase : human enzyme
streptokinase: bacterial protein (not enzyme)

- combines with plasminogen and increases its conversion to active plasmin. Plasmin formed inside a thrombus allows them to lyse a thrombis from within
t-PA binds fibrin in a thrombus, which convers the entrapped plasminogen --> plasmin. This initiates fibrinolysis and some systemic proteolysis
what's the difference in mechanism between urokinase and t-PA
Urokinase combines with plasminogen to activate conversion to plasmin

t-PA combines with fibrin to activate plasminogen --> plasmin
SE causes hypothroidism or hyperthyroidism?
What is the difference in Rx between atrial fibrillation, atrial flutter, and atrial tachycardia
They are all essentially the same, only use adenosisne top choice for atrial flutter in addition to regular therapy
Thrombolytic that is more fibrin-specific that t-PA
Less fibrin-specific that t-PA?
Less expensive than t-PA (also a thrombolytic
Ventricular tachycardia after MI, what is it?
Reentry near the rim of healed infarction
What factors stimulate renin release
-decreased blood volume
-NA depletion
-increased sympathetic outflow
Pharmacokinetics of Abciximab?
Must be given parenteraly not orally effective
antiplatelet drug used in percutaneous coroncary intervention (e.g. angioplasty, placement of coronary stints) & in acute coronary syndromes
Active tuberculois (susceptible)
-isoniazid and rifampin for 6 months
add pyrazinamide after 2 months
Why do you not give sotalol with class 1a antiarrhythmics? Or Class III aa?
B/c of the potential to prolong refractoriness (QT)
Ventricular tachycardia after MI
acute treatment?
chronic treatment?
acute - lidocaine, procainamide, DC cardioversion

chronic - amiodarone, class III, ICD
What is a partial Thromboplastin time (PTT) for?
PTT monitors the intrinsic coagulation system and is abnormal in deficiencies of factor i, ii, v, ix, x, xi, xii.
What is the difference between a PT test and a PTT test
PT measures deficienceis in factors I, ii, V, Vii, X
(more warfarin like)
PTT measures deficiencies in factors v, viii, ix, x, xi, xii (more heparin like)
NSAIDS on plasma renin activity?
NSAIDS decrease plasma renin activity, decrease renin
SE include weak ganglionic blocking, reduction in vagal tone
Acute Rx for AV node reentry? PSVT?

-increase vagal tone with carotid sinus pressure
Use short term to treat erosive esophagitis, active duodenal ulcers, and GERD
proton pump inhibitors
antacids MOA
They are weak bases that react with gastric acid to form water and a salt and in the process neutralize the acid
nitrogen major effects
decrease preload
decrease venous rtn
decrease SV
decrease cardiac work
decrease O2 demand
How are atrial flutter and atrial tachycardia different from atrial fibrillation
atrial fibrillation: disorganized atrial reentry

atrial flutter: stable reentrant circuit in right atrium

atrial tachycardia: enhanced automaticity, DAD related automaticity or reentry
what drug is used for control of ventricular rate + prophylaxis for repetitive PSVT
Diltiazim also - only less good for angina and hypertension
name plasminogen activators
To inhibit acid secretion, give ...
- histamine H2 antagonists
- prostaglandins
-proton pump inhibitors
name: platelet GP IIa/IIIa receptors blockers
What's the difference between reteplase, t-PA, and tenecteplase?
They are all plasminogen activates (bind to fibrin & activate plasminogen --> plasmin)

Reteplase is a recombinant human t-PA with some aa's deleted (it is less fibrin specific that t-PA and cheaper to make)

Tenecteplase is a mutant form of t-PA with that is more fibrin specific
What's the difference in indications between

(1) histamine H2 antagonists
(2) Proton pump inhibitors
(1) Histamine H2 antagonists for prophylaxis of peptic ulcers, acute stress ulcers, and GERD

(2) proton pump inhibitors = short term treatment of erosive esophagitis, ulcers, and GERD
This antimycobacterium drug may cause peripheral neuropathy
Name three drugs used to accelerate food through through the GI tract. Explain the difference between the three types
(1) bulk laxatives
(2) irritants/stimulants
(3) stool softeners

Bls are hydrophylic collids that form gels and cause water retention and intestinal distention. Whereas, stool softeners become emulsified with stool to make feces soft. Stimulates produce nicinoleic acid
What's the difference between urokinase and fibronolysis?
Both thrombolytics, but urokinase/streptokinase works on old clots

Fibrinolysins only works on young clots (< 3 days)
What is streptokinase used for?
2nd line of defense
used in pts with myocardial infarctions in cases where coronary catherization is not readily available (coronary catherization is better reduces mortality)
name a fibrinolytic
the thrombolytics
Urokinase + streptokinases
Which drugs are used to treat edema caused by CHF?
Loop diuretics - Ethacynic acid + torsemide
What type of diuretic is used to treat pulmonary edema or other edematous conditions?
Angiotensin II - vasoconstriction or vasodilate renal
renal vasoconstriction
major side effects of all loop diuretics
catecholamines - vasodilators or vasoconstricors renal
Which loop diuretics inhibits the Na + 2CL K+ carrier system?
which loop diuretic reduces pulmonary congestion and left ventricular filling pressure in heart failure?
What is a toxicity of folate definiciency?
folate deficiency in pregnant woman can cause congential malformations in newborns

Folate deficiency may also not prevent the development of vascular disease (ischemic heart disease & stroke)
major SE of potassium sparing diuretics
-abnormal elevation of serum potassium levels
-hyperkalemia may be fatal
name K sparing diuretics
alpha agonists on plasma renin activity?
decrease renin activity
what do B-blockers do to plasma renin activity
b-blockers lower plasma renin activity decrease renin activity
Folic acid MOA
essential cofactor for the synthesis of amino acids, purines, and DNA
Which type of diuretics causes NaCl to be excreted and Ca++ to be reabsorbed?
drugs used for short term anticoagulent therapy associated with acute primary embolism and disseminated intravascular coagulation
what are the most efficacious diuretics?
loop diuretics
(furosemide, ethacrynic acid, torsemide)
What diuretics cause impaired carbohydrate intolerance and hyperkalemia?
Thiazides - chlorothiazides and hydrochlorothiazides
What drug can be given to neutralize the action of heparin?
protamine sulfate
this antiplatelet drug increase intracellular camp inhibiting phosphodiesterase activity and by blocking adenosine uptake
Dipyridamote MOA
In the prothrombin time test, you test for deficiencies in factors ----
i, ii, v, vii, and x
To restore sinus rhythum for an acute atrial fibrillation
DC cardioversion
What is a toxicity of vit b12 deficiency?
leads to neurological abnormalities including degeneration of myelin sheaths in axons of the spinal cord and peripheral nerves
what are cardiac toxicities of digoxin
1) 2nd and 3rd degree AVN block
2) various arrhythmias (premature beats, bigeminy)
3) changes in ECG ( increased PR, decreased ST, and decreased QT)
PSVT acute conversion to sinus rhythum use --- which drugs are used for prophylaxis of PSVT (avn reentry)?
1) use adenosine
2) class IV - calcium channel blockers (verapamil & diltiazem)
side effects of iron dextran, how administered too?
hypersensitivty reactions given by deep IM or IV
vasoconstriction or vasodilate TXA2
1st drug for control of ventricular rate in pts with atria flutter or fibrillation?
-verapamil, diltiazim
Which antiarrhythmic is not associated with an increase in mortality in pts with coronary artery disease or heart failure?
what drug can : acute sinus conversion to sinus rhythum of PSVT? including when its associated with Wolff-Parkinson White syndrome?
Common treatments for atrial fibrillation(acute rxn) to control ventricular rate
verapamil or diltiazem
b bockers
what is the difference between atenolol and metoprolol
indications: atenolol has more indications (management of hemodynamically stable pts iwth definite of suspected myocardial infacrction) in addiiton to hypertension + angina?
main use of sotalol
Ventricular arrhythmias?
Which type of drug is used for the healing of duodenal ulcers and peptic ulcers? how?
mucosal protective agents

MOA binds + charged groups on proteins and glycoproteins of abnormal and necrotic tissue
acts as a barrier to HCL acid and pepsin
Which drugs complicate the effects of PGs on renal glands
non-steroidal anti-inflammatory drugs
which prostaglandins, increase renal blood flow, promote diuresis, and natriuresis
for immediate reduction of stomach pain (cheap alternative) use
abciximab MOA
a humanizeed monoclonal antibody directly against IIb/IIIa complex. it binds to the receptor complex on platelet and prevents platelet aggregation
difference between 1st generation and 2nd generation sulfonylureas?
-fewer side effects & drug interactions, more commonly prescribed

contraindicated in hepatically impaired pts
What does Erythropoietin do? Where does it act?
stimulates maturation of erythrocyte precursors

It has two sites of action
(1) BFU-E --> CFU-E
(2) CFU-GEMM --> BFU-E (acts synergistically with IL3 and GIN-CSF
4 mechanisms of vasodilation
(1) block L-type calcium channels
(2) increased cAMP
(3) increased cGMP
(4) hyperpolarized cell membrane
Which loop diuretic is effective in patients with renal insufficiency
The loop diuretic Ethacrynic acid
What's the difference between loop diuretics and thiazides?
Place they act: Loop diuretics: loop of Henle
Thiazides - distal convoluted tubule

Transport they block
Thiazides: block NaCl reabsorption, increase Ca++ reabsorption

Loop diuretis - inhibit NaCl reabsorption (some act on the Na2Cl-K+ pump)
What type of diuretics is not used in patients with renal insufficiency?
Kinins - renal vasoconstrictor or vasodilators
renal vasodilators
This angina occurs during exercise (climbing stairs, etc)
External angina
Name renal vasoconstrictors
-Thromboxane A2, TXA2
-Angiotensin II
Name loop diuretics
Ethacrynic acid
SE fatal pulmonary fibrosis
Congenital long QT MOA :
EAD related triggered activity
Class II MOA (antiarrhythmics)
-B-blockers terminate tachyarrhythmias caused by increased sympathetic tone, increase catecholamines, tissue supervision to catecholamines

- reduces pacemaker automaticity (blocks catecholamine stimulation of Ih and Ica)
-reduces delayed after depolarization (DADs) by antagonizing B-adrenergic increase in Ca flux
Drug of first choice for treating pts with AVN reentry (PSVT)
first drug choice for acute treatment
Antidote + treatment for warfarin overdose
-stop giving warfarin
-give fresh plasma
-give Vitamin K
Aspirin MOA
prevents production of thromboxane A2, Irreversible
Indications for spironolactone
-reduced edema & mortality in patients with CHF
Most renal vasodilators promote ----
mild CHF treatment (mild peripheral edema on exertion) normal GFR
thiazides, ACEI
Treatment of Heparin overdose:
(1) stop giving heparin
(2) antidote: protamine sulfate
Deficiency of what compound can make warfarin toxicity worse?
a vitamin K deficiency
Transport that occurs at collecting duct
sodium is exchanged for potassium + hydrogen ions
Where in the nephron is the fluid isotonic?
isotonic - proximal tubule
hypertonic - descending limb loop of henle
hypotonic - ascending limb, loop of henle
Where does ADH act>
on the distal convoluted tubule and collecting duct

ADH increases water reabsorption
Which effects predominate at low doses of nitrates? nitroglycerin
venous effects predominate at low doses, but nitroglycerin does cause dilation of both arterial and venous beds
which coagulation drug should you never give IV?
What % of NaCl is reabsorped in the proximal tubule?
in the loop of Henle?
in the distal convoluted tubule?
-proximal tubule - 60% -70%
-loop of henle --> 15-25%
-distal convoluted tubule --> 8% - 5 %
diuretics are ...
natriuresis is ...
- agents that impair the reabsorption of sodium from tubular contents

-natriuresis is the excretion of sodium in the urine
what is the undesirable side effects of all vasodilator agents especially over administrated by intravenous infusion
-extreme hypotension
What's the difference between typical (exertional angina and variant angina)?
-typical (exertional)
-coronary insufficiency due to vessel occlusion (atherosclerosis)
-attacks usually occur during exercise (climbing stairs, etc.)
-variant prinzmetal's rest angina
-coronary insufficiency due to vasospasm?
-attacks occur during rest unstable
name 3 calcium channel blockers
which anticoagulent do you never give IV?
Thiazide MOA
thiazide increase NaCl excretion in the distal convoluted tubule. Loss of potassium and bicarbonate can result
anticoagulent test used to diagnosis deficiency in factors I,ii, v, vii, and x
prothrombin time test
Name one type of antianginal that can eb used for both vasopastic & effort - associated angina
-ca channel blockers
Where do carbonic anhydrase inhibitors work?
proximal tubule
Treatment for warfarin overdose
(1) stop giving warfarin
(2) give fresh plasma
(3) give Vitamin K
What's the difference between cotting time and bleeding time?
clotting time - the time it takes blood in vitro to clot sufficiently so that the table containg the sample can be inverted

bleeding time- after you cut the ear, the length of time you cna collect blood
what;s the difference between thromus and embolism?
-thrombus -an intravascular blood clot obstructing a blood vessel or cavity of the heart

-embolism - obstruction of a blood vessel by a foreign substance or a blood clot that has been carried by the blood to a site distant from its point of origin
What's the difference between anticoagulents and thrombolytic agents?
-anticoagulents prevent the formation of fibrin clots

-thrombolytic agents remove and break fibrin deposits in blood vessels
hair growth
NO mechanism
No increase gCMP, decrease ca++ (becasue it goes into the SR
overdose of coumarin/ warfarin, what do you give me? why?
Vitamin K2 - cofactor required for the synthesis of factors Viii, IX, and x
major SE of heparin
SE include hemorrhage (especially ovarian hemorrhage can be potentially fatal
Dispersion of refractoriness may occur during ...
(1) an unequal ischemic lesion
(2) an extra conduction pathway
what is the effect of dopamine on glomular filtration rate, renal blood flow, and Na+
-stimulates alpha, beta, and dopamine receptors

-increase renal blood flow
-increase glomerular filtration rate
-increase Na+ excretion
Treat my hypokalemia
1. Kive K+Cl-
2. give a potassium sparing agent
3. combo drug
DC valsartan
ARB, antihypertensive
major SE of heparin
What's the difference between chlorothiazide + hypochlorothiazide?
chlorothiazides can also be used for kidney stones and diabetes insipidus
What ending signifies and ARB?
-sartan as in

anticoagulent which causes increased neutralization of factors II, IX, X, XI, XII, and Xiii
Why do diuretics help CHF
reduce preload and afterload
also counteract sodium retention forces ( at a max CHF) by causing natruersis
diuretics class used for CHF
loop diuretic (thiazides also work)
class of diuretics chiefly associated with hypertension
which type of diuretic blocks the Na+2CL-K+ transporter
loop diuretics
which durgs act on the NaCl cotransporter? Where is this int he nephron?
thiazides in the early distal convoluted tubule
which drugs cause the induction of LDL receptors thereby decreasing LDL in serum?
statins - lovastatin, simvastatin
amiloride acts on?

name a drug like amiloride
-amiloride blocks sodium channels in the distal convoluted tubule

What type of drug acts on mineralocorticoid receptors?
Where? name 2
-aldosterone antagonists bind to mineralocorticoid receptors in the distal convoluted tubule (spironolactone epelerone)
MOA of drugs that work and hte loop of Henle
interferes with Na+2Cl-K+ cotransporter
why are proximal active agents only mildly potent
Na+ ions not absorbed here have multiple opportunities downstream to be absorbed
How do carbonic anhydrase inhibitors work> MOA?
-inhibits reabsorption of sodium bicarbonate

-reduce availability of cellular protons ions for exchange with luminal sodium
Where in the nephron does bulk reabsorption occur?
proximal tubule (60-70%
why are loop diuretics so powerful
-large amounts (15-25%) of NaCl are reabsorbed at this site

-nephron transport sites distal to the loop of henle have limited capabilities to reabsorb NaCl ions rejected in the loop
injudicious results of potassium sparing diuretics -->
-metabolic acidosis

-b/c diuretic inhibits K+ and H+ secretion
which part of the nephron is under control of the mineralcorticoid systems?
How much sodium reabsorption occurs here?
-the late distal convoluted tubule and collected duct
-about 2-3% of the filtered load is absorbed here (sodium)
what types of transport occurs in the late distal convoluted tubule?
Na+ is reabsorbed in exchane for hydrogen and potassium ions
What type of ion transport is found in the loop of henle? ascending limb
an active electroneutral sodium 2 chloride potassium
how is bicarbonate reabsorbed in the proximal tubule
1. an Na/H causes secretion of H ions
2. H ions + bicarbonate = carbonic acid
3. dehydration of carbonic acid - H20 + CO2
4. CO2 diffuses into cell
5. in cell, co2 combines with H20 --> H2CO3
6. net movement. H2CO3 is moved from lumen ot the cells of the proximal tubule
where is most bicarbonate reabsorbed in the nephron?
in the proximal tubule
what can reduce the action of diuretics?
a reduction in GFR (glomerular filtration rate) rduces the supply of ions and water to the tubular system

- it also can decrease renal plasma flow
drug used to treat CHF acts on aldosterone
Don't use this hypolipidemic in pregnant women
this type of angina is unstable - attacks oftern occur during rest
variant angina
DC losartan
ARB, antihypertensive
drugs used for combined dyslipedemias
niacin decreases TG, decreases VLDL and decreases LDL
These HMG-Coa reductase inhibitors have the SE of ...
hepatotoxicity and myopathy
what's the difference in effect between ACEI and ARBS?
(1) ARBS are more specific. They only block Ang II and ATI receptors
(2) ARBS have no effect on Bradykinin, whereas ACEI increase bradykinin
(3) ARBS more completely inhibit ang II action (ACEI only blocks some ang II production becasue there are other ways to make it
What's the difference in mechanism between drugs acting in the early distal convolution and the distal convoluted tubule?
-early distal convolution- sodium chloride cotransporter (thiazides block)

- distal convoluted tubule - exchange Na for K+ and H+ aldosterone antagnonist block)
What is the consequence of adminsitering amiloride or triamtere
mild natriuresis (increase Na+ in urine) inhibit potassium and hydrogen secretion
main use of anticoagulents
pulmonary embolism
coronary thrombosis
with myocardial infarction
peripheral vascular thrombosis
the side effects - hepatotoxicity and myopathy are characteristic of what type of hyperlipidemic?
hmg-coa inhibitors
pharmacokinetics of heparin
should be given by intermittent intravenous injections, intravenous infusion or deep subcutaneous injection
how do all vasodilators affect sodium?
All vasodilators cause sodium retention
why is hydralazine a bad antihypertensive?
-must be used with b-blockers (b/c of reflex tachycardia)
-must be used with diuretics for sodium retnetion
name 2 centrally acting drgus used to treat hypertension
clonidine & methyldopa
What are the best type of diuretics to use for hypertension?
-thiazide diuretics
-potassium sparing diuretics
-loop diuretics (high celeing) -->
can be used for edema reduction decreases volume and decreases bp
drug given to patients undergoing placement of a coronary stint
clopidogrel main indication
protamine sulfate MOA
PS forms a stable salt with acidic heparin. It neutralizes its affect. The anticoagulent activity of both drugs is lost
how should vitamin K be administered?
not by IV

b/c anaphylaxis and fatalitis have occured when it is given iv
what is the advantage of enoxaparin over heparin?
better bioavailabiiltya dn longer half life (SC injection instead of intravenous
what shoudl be monitored when giving heparin?
monitor platelet counts - perform frequently
name renal vasodilators
-pgs, pge2, pgi2
what do b-blockers do to treat angina?
b-blockers block cardiac b1 receptors. thereby decreasing hr, decreasing contractility (negative inotropic effet) and decrease myocardial o2 requirements at rest and during exercise
-reduce silent ischemic
severe CHF, peripheral edema, dyspnea, and pulmonary congestion
combination diuretic therapy
loop diuretics
What drugs can you use to treat primary triglyceruridemias?
niacin and fibric acid
heparin MOA
-straight chained anlonic mucopolysacchards called glycosaminoglycans have anticoagulent properties
-acts at multiple sites in the coagulation system
-heparin interacts with antithrombin (a cofactor) it enhances its ability to inhibit thrombosis
-inactivates clotting factors - iia, ixa, and xa by complexing with them
ca++ antagonists
-selective effects on blood vessels but not on the heart
-reduces vasospasm, reduces preload + afterload
side effects and complications of diuretics
-volume depletion (loop diuretics
-lipid elevation
-glucose intolerance
-metabolic alkalosis
major drug interactions with warfarin
increase warfarins effect (inhibit P450 cimetidine and amiodarone)

- decrease warfarin's effect (induce p450)
warfarin is contraindicated in
heparin blocks which factors

warfarin blocks which factors
heparin II, IX, X, XI, XII, XiII

warfarin II, Vii, IX, X
NSAID effects on ACEI effects?
-NSAIDS block PG synthesis
-NSAIDS also block bradykinin mediated vasodilation, therefore they impair the hypotensive effects of ACEI
how do diuretics treat hypertension?
1. decrease blood volume (decrease Bp and pressure )

2. with continued use, diuretics decrease TPR even when blood volume returns to normal
What does the PT test mean?
Test the extrinsic thromboplastin system, tests for deficiencies in factor I,II, V, VII, and X
When treating hyperlipedemia in diabetes, which drug should you be careful about giving and why?
niacin b/c one of the side effects is glucose intolerance
which factors does enoxaparin block?
inhibits clotting factors IIa (prothrombin) and Xa
With atorvastatin, you must monitor levels of ...
alanine and aspartate
dipyridamole drug class
DC: vasodilatior
platelet adhesion inhibitor
Name the major groups of drugs acting at the proximal tubule

give an example
carbonic anhydrase inhibitors (acetazolamide)
treat dyastolic dysfunction with ...
calcium channel blockers
therapeutic uses of coumadin/warfarin
-prophyalaxysis + treatment of venous thromboses + pulmonary embolism
-treatment of thromboembolic complication sto reduce the risk of death, recurrent myocardial infarction + thromboembolic events
heparin effects
-has little or no effect except on blood coagulation + blood lipid metabolism

- increases activity of antithrombin III (antithrombin III) neutralizes activated clotting factors II,IX, X, XI, XII, and XIII
What are the three main types of drugs used to treat angina>
(1) organic nitrates compounds
(2) propranolol and other B-blockers
(3) calcium antagonists
What's the difference between thrombolytic agents and antiplatelet agents
-thromboembolytic agents = remove and break fibrin deposits which occur in bood vessels

-antiplatelet agents are used to reduce atherosclerosis
used for pulmonary embolism, coronary thrombosis associated with myocardial infarction, peripheral vascular thrombosis, severe injury to the extremities and rheumatic heart disease
anticoagulent agents
aldosterone MOA
works in the distal parts
-genomic mechanism (increased expression of ENOC channels

old antagonists increases Na+ and decreases K+ (wasting)
which drugs blocks PDE5?
original purpose of drugs

-pulmonary hypertension
What's the difference between heparin indications and warfarin indications
heparin is for short term anticoagulent therapy, while warfarin is more long term

both for prophylaxis treatment of venous thrombosis and thromboembolics associated with atrial fibrilation

pharm: warfarin: 100% bioavailability
Heparin: intermitt intravenous injections
ACEI reduce angiotensin II and aldosterone levels, decrease Left ventricular filling pressure, decrease TPR, increase CO
What is a side effect of guanethidine, reserpine, MAOI, and ganglionic blockers
postural hypertension
which antihypertensive can be used as monotherapy?
calcium entry blocking agents + ACEI
prostaglandin effects on renal excretion?
-increase renal blood flow
- promote diuresis
-promote natriuresis
What's the difference in renal effect between prostaglandin PGE2 and prostaglandin PGI2?
PGE2 - causes vasodilation blocks H20 reabsorption and increases diuresis

PGI2 - increases renin secretion, increases cAMP levels
What is the difference between Verapamil and Diltiazim?
- Verapamil is better for angina & hypertension.
-has a longer half life (7.4 hours max)
-different side effects - constipation + asystole in addition to bradycardia + AV node conduction block
stepwise approach versus monotherapy
- mild hypertension
1. weight reduction
2. sodium intake reduction
3. thiazide diuretics or B-adrenergic blockers
5. Calcium channel blocker
6. angiotensin receptor blocker
clinical indications for B-blockers (antiarrhythmics
-prevent re-infarction & sudden death following an MI
-treat exercised induced arrhythmias
-prevent reoccurance of AVN reentry (pts with PSVT)
-control ventricular rate, increase AVN ERP
What type of drug class do you give to treat deep vein thrombosis, leading to pulmonary embolism - and in pts undergoing surgery?
think anticoagulents
(warfarin, heparin, enoxaparin)
2 indications for warfarin
1) prophylaxis and treatment of venous thrombosis
2) for the treatment of thromboembolic complications associated with atrial fibrilation and cardiac value replacement
which antianginal not only dilates resistance vessels in the coronary beds but also inhibits platelet aggregation?
pharmacokinetics of warfarin
-100% bioavailability
99% becomes bound to plasma albumin

- there is an 8-12 hour delay in warfarin action

-small Vd
what's the difference in indications between ACEI and ARBS?
-both work for hypertension, ACEI can also be used for CHF and to prevent glomerular daage in diabetes
difference between heparin's indication and warfarin's indication?
-heparin - for short term with acute pulmonary embolim

vs. warfarin is for pulmonary embolism + thromboembolic complications
what can you combine vasodilators with to improve treatment of CHF?
-vasodilators + inotropic agents
What tests should be monitored when going an anticoagulent?
-check prothrombin time and bleeding time measurements
Moderate hypertension therapy
1. thiazide diuretics
2. b-blockers + centrally-acting agent
3. ACE inhibitors
4. calcium entry blockers
5. angiotension receptor blocker
sodium nitroprusside MOA
short acting vasodilators
-decreases arterial impedence
-decreased venous pooling
which cofactor must be activated in both the intrinsinic and extrinsic coagulation pathways what is the role of this factor?
factor x -
(in intrinsic pathways - factors IX and XI are also activated)
Factor X cleaves two peptide bonds in prothrombin to form thrombin
name 2 antiplatelet drugs ---
1) aspirin
2) clopidogrel
what are the indications for nifedipine?
prophylactic treatment
1) typical (effort associated) stable (angina)
2) Prinzmetal's (variant) angina pectoris
3) hypertension
what drugs should you avoid while taking propranolol (b/c of drug interactions)
-calcium channel blockers
-combination with haloperidol causes hypotension & cardiac arrest
-phenytoin& & rifampin increases propanolol's clearance
what's the effect of warfarin on vitamin K?
-warfarin prevents the reductive metabolism of the inactive form of vitamin K back to its active form by Vitamin K epoxide reductase
which antiplatelet drug irreversibly blocks the ADP receptor on platelets, thereby reducing platelet aggregation
clopidogrel MOA
drugs used to treat familal dyslipidemia
use niacin and or atorvastatin
what d b-blockers do to angina vs. arrhythmias
angina - decrease myocardial oxygen requirements by decreaseing heart rate, contractility, and bp

arrhythmia - reduce mortality and sudden death after MI
which type of angina is b-blockers not used for
b-blockers are not used for variant angina
what antianginal is used for acute attacks?
nitroglycerin (nitric oxide) sublingual
this anticoagulent is used for prophylaxis and treatment of thromboembolic complications associated with atrial fibrillation and cardiac valve replacement
verapamil can be used for angina, but if the pt has --- don't use it!
don't use in patients with systolic CHF
b-blockers are often combined with --- to treat angina
organic nitrates
what's the difference between sublingual nitroglycerin tablets and nitroglycerin tablets?
nitroglycerin tablets (sublingual) are used for acute attacks

nitroglycerin patches - are used for prophylaxis against typical angina
tell me about digoxins TI
relatively low TI ( approx. 2 )
do organic nitrates have a bigger effect on the reduction of preload or the reduction of afterload?
have a greater effect on the reduction of preload
what's the difference between hydralazine and sodium nitroprusside
MOA: hydralazine - dilates arterioles not veins
sodium nitroprusside --> dilates arterioles +/- vessels

Indications -
hydralazine - essential hypertension
sodium nitroprusside - hypertensive emergencies and severe heart failure
blocks the carboxylation of several glutamate residues in prothrombin & factors VII, IX, X
fatigue, anorexia, nausea, vomiting, diarrhea, dreams, muscle weakness, 2nd or 3rd degree AV conduction block, and various arrhythmias
digoxins famous side effects
what is the primary indication for digoxin?
What drugs do you use to treat A fib (pts have stretched atria Afib) (atrial fibrilation) and systolic CHF)
What deficiencies are seen in pregnant women?

How do you treat these conditions
(1) megalopblastic anemia due to a deficiency of folic acid --> use folic acid to treat

(2) iron deficiency due to blood loss during pregnancy --> use ferrous sulfate
AA classification

sotalol (DC & MOA)
MOA: prolong action potential duration (K channel blockers)
atenolol DC + MOA
MOA: B1 adrenergic receptor antagonist
quinidine MOA
Mixed Na + K channel blocker
lidocaine DC + MOA
DC: 1b
MOA: Na channel blocker
what drugs are used to treat pernicious anemia ?
what type of anemia is PA?
-folic acid and vitamin B12 are used to treat pernicious anemia (megaloblastic anemias due to folic acid deficieny)
-PA is a type of megaloblastic anemia
when would you use iron dextran instead of ferrous sulfate?
-pts with iron deficiency in whom oral administration is unsatisfactory or impossible (malabsorptions syndrome, dialysis pt)
warfarin MOA
-block carboxylation of many glutamate residues in prothrombin factors VII, IX, and X
-since these factors are not carboxylated, they are inactive coagulation
how does sodium nitroprusside reduces severe heart failure?
-in patients with heart failure & low CO, the CO often increases due to a reduction in afterload
What antimycobacterium do you give for resistant organisms?
antimycobacteria used as a preventive therapy (true chemoprophylaxis
isoniazid for 3 months if skin test + or subclinical infection isoniazid for 12 months
what is a potentially life threatening siutation resulting from treatment of atrial flutter
-if you treat w a class ia drug you can get a potentially life-threatening acceleration of ventricular rate b/c drug knock out AVN filtration ability
angina caused by coronary insufficiency due to vasospasm is called ...
variant rest angina
pulmonary fibrosis
major side effect of amiodarone
which drug interactions with digoxin? What is the effect?
-decrease cl and increases vd of digoxin, resulting in a doubling of p digoxin

- amiodarone
short half life 1-4 minutes
tolerance can develop
nitroglycerin pharmacokinetics
give folic acid (pts with Will's disease have a deficiency of folic acid)
i have wil's disease. Give me a drug. Tell me about my disease.
common treatments for CHF? the improtant one
-digoxin(only for systolic effects)
ventricular cardiac arrhythmias man (especially post MI) b/c class 1b, not effective against STVA
what do you use lidocaine for?
What's the difference between hydralazing vs. minoxidil
-both dilate only arteries but
hydralazine is used for essential hypertension and minoxidil is used only for treating hypertension that is sympatomatic or associated with target organ damage
what is the difference between ferrous sulfate and iron dextran
1) name an oral (absorable) iron preparation

2) name a parental iron preparation
antiarrhythmics that interact with digoxin
atrial/ventricular tachycardia MOA
-DAD related
atrial enhanced automaticity
ventricular --> DADs triggered by sympathetic tone
difference betewen adenosine & amiodarone
amiodarone -broad spectrum antiarrhythmic

adenosine - endogenous nucleotide antiarrhythmic
where is ih most commonly found, If you block ih, what happens?
In plays a critical role in regulating automaticity in purkinje fibers, but play only a minor role in the SA node. Blocking Ih reduces automaticity in ectopic pacemaker
ACEI are contraindication
nitroglycerin indications
(1) effort-associated (classic) angina
(2) variant angina
(3) unstable forms of angina pectoris
causes antihypertensive causes excessive hiresutism (hair growth)
drug sometimes used to treat antihypertensive emergencies (after sodium nitroprusside )
minoxidil MOA
dilates arterioles but not veins
-opens potassium channels in smooth muscle membranes --> makes contractions less likely
which drug is used to treat essential hypertension
what are the primary effects of orgnaic nitrates on angina?
- dilation of arterial (resistance) and venous (capitance) vessels

-increased exercise tolerance
which antianginals are used as prophylaxis
for both typcial + variant angina :
--> nitroglycerin patches (not sublingual)
--> isosorbide dinitrate

For typical angina only
-b-blockers (propranolol)
what are b-blockers used for? in angina
B-blockers are only used for prophylaxis of typical angina
what;s the difference between nitroglycerin and isosorbide dinitrate
The 1/2 life + route of administration

nitroglycerin - sublingual half life 1-4 minutes

isosorbide dinitrate - oral dosing half life 1 hour
This antihypertensives shoUdl not be given to patients with coronary artery disease
hydralazine MOA
-dilates arterioles, not veins
-results in decreased arterial blood pressure
-decreased peripheral vascular resistance
-causes a reflex increase in HR, SV and CO
name antihypertensives
1. minoxidil
2. sodium nitroprusside
3. diazoxide
4. hydralazine
This antihypertensive is subject to polymorphic acetylation. Slow acetylaters metabolize this drugs at a different rate than fast acetylators
diuretics for edema associated with CHF
-all loop diuretics (Furosemide less than ethacrynic acid + Torsemide)

- Triamterene (K sparing diuretics)
-acetazolamide (carbonic anhydra. inhibitors
which antihypertensive causes a reflex increase in heart rate
which antihypertensive agent is given for hypertensive emergencies & severe heart failure
sodium nitroprusside
which antihypertensive agent dilates both arterial vessels and venous vessels
sodium nitroprusside
which antihypertensive is a long acting arteriolar dilatior?
which antihypertensive dilates arterioles but not veins?
Side effects of this antihypertensive include a reversible lupus-like syndrome
-for erectile dysfunction
-a selective inhibitor of phosphodiesterase type 5 (PDE5) results in increased cGMP, blood flow into penis
digoxin immune fab MOA + DC
DC: digoxin antidote

MOA: antibodies that bind to digoxin. The complex is then excreted through the kidneys

indications: used for life-threatening digoxin toxicity
Therapy for vasoplastic angina
-calcium channels blockers
what's the difference between papaverine + sildenafil
Papaverine: vasodilarot
sildenafil: erectile dysfunction drug

Papaverine: inhibitors phosphodiesterases
sildenafil: inhibitors phosphodiesterase type 5
name that carbonic anhydrase inhibitors
aspirin MOA
-aspirin irreversibly inhibits both isoforms of COX
-reduces formation of TXA2

-also interferes with chemical modulators of the kallikren system inhibits granulocyte adherence to damage vascular
why is niacid useful for treating familal dyslipidemia
it is useful b/c it reduces VLDL levels
What are saralasin and losartan?

Which is better?
They are both angiotensin II inhibitors
only Losartan has few side effects - therefore its better
(sarlasin may cause hypertension )
What do vasoconstrictors do to GFR?
-decrease hydrostatic pressure
-decreases GFR decreases glomerular filtration rate
what do vasodilators do to GFR in capillaries
-vasodilators decrease pressure in the afferent arterioles

-increases raise GFR
-increases raises hydrostatic pressure in capalliaries
3 major factors in peptic ulcer disease and treatment
1. infection with H. Pylori
2. Increased HCL acid secretion
3. Inadequate mucosal defenses against acid

1. antimycobacterials
2. 2 week course of triple therapy, with a proton pump inhibitors and antibiotics
name an antidote used to reverse digoxin toxicity
digoxin immune Fab
major drug interactions of quinidine
hepatic eliminartion is increased by drygs that induce P450 (phenobarbital, phenytoin & rifampin)
What's the international normalized ratio?
INR = a more sensitive test of prothrombin time using human thromboplastia measures relative PTT

INR = (PT test/ PT normal)
Pharmacokinetics of sodium nitroprusside
given IV drugs
Effects of ACE on bradykin and on ang II
ACE --] inhibits bradykinin
ACE increases Ang II levels
effect on bradykinin
-inhibits peptidyl dipeptidase (ACE)
-prevents conversion of ang I --> ang II
-elevates levels of bradykinin
-lowers ang II levels
if it ends in pril it's a ...
Name ACE inhibitors
sodium nitroprusside MOA
-dialates both venous & arterial vessels
- results in reduced TPR & venous return
-releases NO = incresed intracellular cGMP, decrease Ca++ and relaxes vasulars smooth muscles
what is the advantage of the international normalized ration over the PT test?
INR is more sensitive
- it also is relative (between labs)
Why are other vasodilators agents (other than nitroglycerin and dipyridamole, etc is not sed to treat angina?
because they increase blood flow, but also increses O2 demand on heart
antimycobacterial used for both tuberculosis and leprosy
Tuberculosis - MDR
use combination of 3 drugs to which the organisms is susceptible
this anticoagulent is used to treat venous thrombosis (it is also used for prophylaxis purposes)
name the 2 types of angina and tell me the difference
-exertional angina - attacks occur during exercise

-variant rest angina --> attacks occur during rest
what drug metabolism sidenafil?
metabolized by cyt p450
which part of the nephron has NaCl Cotransporters (major transport mechanism here
NaCl cotransporters @ early distal convoluted tubule
how does nitroglycerin effects myocardial o2 consumption and delivery
myocardial O2 consumption demand is decreased bc of the arterial + venous effect of nitroglycerin
nitrals may increase mo2 delivery in variant angina
What is the only current use of verapamil
-not used for antihypertensive events
-used only for PSVT
-blocks Ca++ entry into the AV node
How do thiazide diuretics help hypertension
appear to alter arteriolar tone
2 drugs used to treat familal dyslipidemia
niacin + atorvastatin
What;s the difference between traimterene and amiloride?
place of action

triamtere - collecting tubule
amiloride - distal convoluted tubule & collecting duct

action - same action but amiloride also reduces H+ secretion

indications - triamtere is used mainly for edema associated with heart failure
which diuretics block na entry through na selective ion channels
k sparing diuretics - triamtere + amiloride
what's different about ethacrynic acid compared to other loop diuretics
-acts on the ascending loop of henle + the proximal and distal tubules
torsemide + Furosemide only work on the ascending limb of the loop of henle
What compound promotes prostaglandin synthesis ( a potent vasodilator)
how do organic nitrates (nitroglycerin) help angina
-these drugs release nitic oxide
-these drugs result in decreased O2 demand by
-reducing preload and afterload
1. how do organic nitrates reduce preload

2. How do they reduce afterload
1. They reduce preload by causing venous dilation (big effect)

2. They reduce afterload by dilating the arteries (small effect
which calcium antagonists is used for both typical + variant angina
name to obsolete antianginal drugs illicitly used to prolong erections
sodium nitrate + amyl nitrites
inhibits RNA synthesis by inhibiting DNA dependient RNA polymerase
Rifampin MOA
Isoniazid MOA
antimycobacterium that inhibits biosynthesis of mycolic acids which are important for mycobacterial cell wall synthesis
antimycobacterium that makes you piss red orange
warfarin/coumadin, coumarins
anticoagulent that blocks synthesis of factors II, VII, IX, X
The effects of prostaglandins on renin excretion
prostaglandins increses renin, thereofre COX2 inhibitors decrese renin
severe hypertension therapy
1. thiazide diuretics
2. direct vasodilators
3. B-blocker to block reflex tachy
4. guanethidine or clonidine
5. calicum entry blocker
6. calcium channel blocker
7. alpha receptor blocker
8. angiotensin receptor blocker
SE = lupus erythematosus syndrome (antihypertensive)
if i have chronic renal failure, what drug is safe to give me (antianemic drug) and which is not safe?
-you can give me Epoetin alpha

-do not give me deferoxamine (an iron chelator)
don't take --- with sildenafil
nitrates - b/c can cause profound hypotension if injected together
coumarin activity MOA
-antagonizes vit Ks role
-blocks synthesis of factors II, VII, IX, X
hypolipidemic should be avoided in pregnancy
use of this hypolipidemic increses the risk of gout
through what factors does heparin influence factors II, IX< X, XI, XII, XIII
Antithromin III
Competitive inhibitors of HMG-CoA reductase are called ....
statins (lovastatin & simvastatin)
what type of transport occurs at the distal convoluted tubule?
sodium reabsorption is active, cl- follows passively
Name 2 thiazides
class 1b antiarrhythmics are effective against ...

class 1b antiarrhythmics are not effective against
-think, b only works on the bottom half the heart effective only against ventricular arrhythmias, not effective against supraventricular arrhythmias
acetazolamide MOA
-carbonic anhydrase inhibitors
-acts at the proximal tubule
-inhibits proton source (Na/H exchanger) necessary for absorption of sodium bicarbonate can K+ indicrectly
which drug used in the treatment of CHF must be given by continuous infusion intravenous infusion
sodium nitroprusside
niacin MOA
decrease TG
decrease VLD esp LDL
what are the two important things about digitoxin
-hepatic metabolism
-half life is approx 1 week
is used for the treatment of normal & high renin hypertension, CHF, and may prevent glomerular damage in diabetes
what transport processes maintain the volume and composition of body fluid in the kidney?
-glomerular filtration
-tubular transport (anionic + cationic transport systems
-passive transports
This drug is competitively antagonized by caffine, theophylline, and dipyridamol
how do you block 2nd and 3rd degree AVN block caused as a SE of digoxin , Why?
atropine - a muscarinic antagonists, blocks parasympathetic b/c AVN block is due to excessive increase in vagal tone
to control ventricular rate in chronic atrial fibrillation
-verapamil or diltiazem
(don't use in pts with evidence of myocardial damage
what is the difference between nifedipine + verapamil
does the opposite to the heart?
nifedipine reduces afterload and preload via peripheral vasodilation
diuretics used for symptoms of a cute mountain sickness
how do digoxin effects the heart
- increase vagal tone (through barorreceptors mediated - central vagal stimulation

-positive inotropic effect (due to inhibition of the Na/K pump - enhance ica, increse SR release
digoxin MOA
-binds to Na/K ATPases
-increases vagal tone, therefore increase AVN ERP and decrease automaticity

esp in SAN + atria (vagal inervation is big here)
what drugs should you not give with digoxin? Why
-amidarone (antiarrhythmics)
they inhibit digoxin secretion in urine through p-glycoprotein pump competition
side effects include teratogenicity and eripheral neuropathy
when do you use a PT
drug tests used:

-useful in measuring Vit K
-useful in liver disease
-monitor oral anticoagulation therapy to ensure a decrease in factors II, VII, X
therapy for unstable angina
-aspirin, herparin
-anticoagulents and antiplatelet drgus
clofazimine MOA
builds to DNA and inhibits template function
competitively inhibits the enzyme dihydropteroate synthase - thus blocking folic acid synthesis
dapsone MOA
vasodilator inhibits phosphodiesterase increases cAMP
used for cerebal + peripheral ischemia with arterial spasm
side effect in acute renal failure in pts with bilateral renal artery stenosis
which calcium channel antagonists is used mainly for variant angina because of its antispasmotic effects
therapy for chronic stable angina of effort
-long acting nitrates
-calcium channel blocerks
reflex tachycardia results from hypotension caused by which drug used to treat CHF
sodium nitroprusside
what two drugs shoudl digoxin be given with if possible
-use with a diuretic and an ACEI
bile acid binding resin useful in treating pts with isolated increases in LDL
name binding acid binding resins (hypolipidemics)
cholestyramine + colestipol
prodrug hypolipedimics
the statins - lovastatins and simvastatins
these drugs decrease TP and increase HDL
fibric acid derivates gemfibrixil and fenofibrate
used to treat conditions with hypertriglyceridemias _ dysbetalipoprotenima
fibric acid derivatives
drug interactions include
-additive effects with other antihypertensives
-enhanced lithium toxicity
-may decrese response to catecholamines
diuretics only indication is antihypertension
congenital long QT acute Rx and chronic Rx
acute - pacing, magnesium, isoproteronol

chronic - b-blockers, pacers
ventricular fibrillation acute treatment chronic treatment
acute: DC caridoversion

don't give during pregnancy
1. acei - angiotensin converting enxyme inhibitors

2. indapamide
3. ANG II receptors blockers
4. warfarin
diuretics used for centripencephalic epilepsies
petit mal
-unlocalized seizures
name and MOA of diuretics that act at the early distal convolution
block NaCl cotransporters

which drugs bin bile acids in the intestines and cause and upregulation of LDL receptors
-hypolipedimic increases TG and increase VLDL most
diuretic class primarily associated with edema from CHF
-potssium sparing diuretics
-loop diuretics also work
this bild acid binding resin may delay or reduce absorption of concoitant oral medication
4 main uses of diuretics
A) nephrotic syndrome
C) advanced liver disease
D) hypertension
most common important complication of diuretics usage
metabolic disturbances (alkalosis, acidosis
glucose intolerance
name two other drugs act at the same site as indapamide
metolazone (early distal convoluted tubule)
side effects include acute renal failure, hyperkalemia, and drug cough
what is one of the most potent vasoconstrictors
one of the most potent vasoconstrictors in ang II
pyrazinamide MOA
inhibits ETC in mycobacterial (Not sure
name drugs used for leprosy
drugs used for prophylaxis for prophylaxis of peptic ulcers acute stress ulcers and GERD
cimetidine, rantidine, famotidine, and nizatidine
how do you control gastric acid secretion in patients with peptic ulcer
histamine is the major factors controlling gastric acid release

can give a histamine H2 antagonist to block gastric acid secretion
what drug is ineffective in treating familal dyslipideMia
binding resins don't work
what diseases cause a reduction in GFR
-organic diseases
-congestive heart failure
- antihypertensive
drug interactions with ACEI
-potassium sparing diuretics - b/c may cause hyperkalemia

-NSAIDs b.c they block the hypotensive effects of ACEI by blocking bradykinin - mediated vasodilation
nephrotic syndrome
excrete greater than 3-3.5 g of protein/ 24 hrs

--> hypoalbuminemia, hyperlipidemia
ACEI indications
-normal L high resin hypertension
-may prevent glomerular damage in diabetes
cholestyramine MOA
-binds bile acids in the intestinal lumen & prevents reabsorption

-upregulation of LDL receptors
best for chronic asthma
-corticosteroids - beclamethasone, bidesonide, fluticasone
i am a patient who requires more than occasional inhalations of b2 agonists for symptoms relief
use corticosteroids aersol
cromolyn sodium MOA nedocromil sodium
- inhibiory effect on mast cell + eosinophils

-prevents release of cell mediators
Respiratory drug

-can be affected by liver disease, cigarette smoking _ diet changes

-narrow therapeutic index
theophylline side effects
high dose
(1) convulsions
(2) cardiac arrhythmias
(3) death

lots of drug interactions
hansen's disease
use WHO short course antibacterial regiments
who treatment of for leprosy
rifampin, dapsone, clofazimine (X2 year minimum
drugs used in reversing the lepra reaction and erythema nodossum leprossum
lepra rxn - steroids, clofazimine

ENL- steroids, thalidomide, clofazimine
antimycobacterial used for H. pylori infections
bismuths + metronidazole , tetracycline, amox, clarithromycin
theophylline MOA
-inhibit cell surface receptors for adenosine
-causes direct bronchodilator and has anti-inflammatory acts
-adenosine receptor modulate - adenylate cyclase activity
belcamethasone MOA -->
which drugs share the same MOA
-budesonide + fluticasone
-inhibits phosphotipase A2, thereby inhibiting production of inflammatory cytokinesis
-inhibit lymphocytic + eosinophilic mediated airway inflammation in asthmatics not curative
prophylaxis of chronic asthmas
- 1 degranulating inhibitors cromolyn sodium _ nedocromil sodium

-leukotrienes (monteleukast _ zileuton)
ipratroprium bromide MOA
-degree of muscarinic involvemtn in bronchomotor responses varies among patients
pharmacokinetcs of ipratropium bromide
can be given in high doses b/c is poorly absorbed
a bronchodilators used for maintaines treatment of bronchospasm associated with chronic obstructive pulmonary disease
ipratropium bromide antimuscarinic bronchodilator
long term treatment - along actign B2 selective sympathetic
asthma & pulmonary disease medications can reduce fluid congestion b/c of alpha effects
acute asthma
-use short acting b2 agonists
-epinephrine (unwanted side effects)

-albuterol (B2 selective)
what's the difference between monteleukast and zileuton
-different pats of the pathway -
monteleukast and leukotriene inhibitor

- zileuton - leukotriene pathway inhibitor

different mechanism - monte - LTD4 receptor antagonists
zileuton - 5-lipoxygenasese inhibitor
an LTD4 receptor antagonists
name a

1. leukotriene inhibitors
2. leukotriene pathway inhibitors
1. monteleukast
2. zileuton
what is the advantage of azithromycin over clarithromycin
-less likely to efffect the QT interval than clarithromycin

-only taken once a day
which antimycobacterial cannot be administered pimozide
clarithromycin b/c prolongs the QT interval
What's the difference between dapsone + clofazimine?
-dapsone --> first line of defense
clofazimine --> 2nd defense

different MOA

Dapsone - competitively inhibits enzyme dihydropteroate synthetase block folic acid synthesas

clofazimine --> binds to DNA + inhibits template function
red colored urine
dapsone indications
-mycobacterium leprae
-pneumocystis pneumonia in AIDS
leprosy drugs
what is an alternative to dapsone for treating resistant leprosy
This type of hypolipidemic drug activates lipoprotein lipase
fibric acid derivatives
gemfibrozil and fenotibrate
-antimycobacterial used as a sterilizing agent against residual intercellular organisms for tuberculosis bacilli
side effects of isoniazid
-peripheral neuropathy
-may indice hemolytic anemia in pts iwth G6P dehydrogenase deficiency
ethambutol MOA
-inhibits the synthesis of arabinogalactan (a component of mycobacterial cell walls) bacteirostatic
side effects of this antimycobacterial include
hepatoxicity, peripheral neuropathy, can ay indice hemolytic anemia in pts iwth G6P dehydrogenase deficiency
which antimycobacterials are bacteriocidal

-isoniazid in dividing cells
antimycobacterials that are bacteriostatic
-isoniazid in resting cells
inhibits ETC in mycobacteria
different acetylators - fast acetylators and slow acetylators metabolize at different speeds
dopamine MOA
-reduce afterload combined with inotropic stimulation
-acts on D, a, b receptors
primary action of this vasodilator for CHF is reduced preload
foresemide and torsemide drug interactions
NSAIDs interfere with prostaglandin synthesis
carbohydrate tolerance --> hypolipidemic, vasodilators for CHF?
if worried about cyt p450 drug interactions, which statin can you give?
side effects of this hypolipidemic is elevations of serum aminotransferase
statins- HMG-Coa reductase inhibitors
lovastatin MOA
-specific inhibitors of HMG-Coa reductase which catalyzes conversion - HMG-CoA --> mevalonate
-mevalonates is a precursor of cholesterol
-decreases cholesterol synthesis + upregulation of LDl
-decreased oxidative stress + vascular influentia
which hypolipidemic do you use after MI?
irrespective of lipid levels?
hypolipidemic - decreases cholesterol synthesis and upregulates LDl
-HMG-CoA reductase inhibitors
which of the statins is not a prodrug
for high ldl to treat use
isolated: cholestyramine
what's the difference bteween niacin and gemfibrozil
both decrease triglycerides, decrease LDl, and decrease VLDL
but ...

niacin - familial hyperlipidemia
gemfibrozil - hypertriglyceridemas and dyslipoproteienma
used for hypertriglyceridemia snad dysbetalipoproteinemia
gemfibrozil 0 ligand for nuclear Tx receptor PPAR alpha
PPAR - alpha is asociated with which hypolipidemic?
gemfibroxil MOA
-functions as a ligand for nuclear transcription receptors - peroxisome proliferator- activated receptor alpha (PPAR-alpha)
name fibric acid derivatives
niacin MOA
-inhibit VLDL secretions in hepatocytes
-inhibits intracellular lipase of adipose tissue via receptor mediated signaling
-decrease catabolic rate for HDL
-reduce VLDL by decreaseing influx of free fatty acids into the liver
what is the most effective hypolipidemic for increasing HDL levels
used for familal hypercholesterolemia in combination with a resin or reductase inhibitor
side effects of hypolipidemic - cutaneous vasodilation
ethambutol MOA
not well understood - but inhibits syntehsis of arabinogalacan, an essential component of mycobacterial cell walls. Enhance activity of lipophilic drugs such as rifampin
tuberculosis resistant isoniazid
rifampin and ethambutol
atrial fibrillaiton and atrial flutter can be treated by ...
ca channel blockers

b/c these drugs increase AV node ERP
Ca channel blockers MOA
slow AVN conduction
increas AVN ERP

this prevents reoccurances of AVN reentry (increase AVN ERP)

control ventricular rate in pts with atrial tachyarrhythmias (increase AVN ERP)
vitamin K
drug used to treat hypoprothrombinemia secondary to factors limiting absorption of synthesis of vitamin K
moderate CHF treatment, decrease GFR, moderate peripheral edema vascular congestion
-loop diuretics (thiazides)
which antihypertensives have SE - interferes with glucose metabolism & risk of diabetes and uricoic acid, increase plasma lipid levels
thiazide diuretics
antiseizure med nystagmus, gingival hyperplasia and hirustrism
--- receptors mediate long term potentiation when stimulated by glutamate
NMDA receptors
I have acute pain, pulmonary edema, dyspnea, and I need a preanesthetic medication
of maximal analgesia is 12-15% of morphine - used for moderate pain
80X more potent than morphine, used for general anesthesia
2 most important excitatory transmitters used for the transmission of pain
-substance p
1. GABAa -= binding opens CL ion channesl caused hyperpolarization and inhibiton of neuronal firing
2. GABAb - metabotropic receptors decrease spasticity
3. GABA c -inotropic
testosterone DEA schedule
Schedule III
Antipsychotic drugs for which extrapyramidal symptoms are a side effect
name 3 atypical antipsychotics and the main receptor they inhibit
1. rieperidone - blocks D2 and 5HT2 - schizo and dementia

2. clozapine - blocks D4 and a1 -used for resistant schizo

3. olanzapine - block 5-HT2 > DI - D4 - used for bipolar disorder
lithium MOA
-antimanic drugs
-prevents mood swings - mood stability in pts with manic depressive orders

-resembles sodium, enters the cell using Na + channels --> accumulates intracellulary b/c not pumped out by Na/K atpase
-causes partial depolarization of cells
-reduces hormone ADH induced cAMP production
-inhibis depolarization evolved NT release
-inhibits several enzymes involved in normal recycling of membrane phosophoinositol decreas PIP2, decrease IP3, decrease DAG
Benzodiazepine is used for insomina
flurazepam (a hypnotic)
drugs used to treat heroin withdrawal
methadone (agonist)
naltrexone (antagonist)
buprenophine - more potent long acting
what are the three opioid receptor types
what's the difference between them>?
u, k,s

u - most important responsible for analgesic effects + major side effects
k = responsible for some analgesic effects
which type of pain do opioids work for? WHich type of pain are they ineffective against?
opiods are for acute pain, not chronic pain
used for insomnia
-benzodiazepine like drugs (zolpidem & zaleplon
1st line of defence for OCD
SSDRI (fluoxetine (Prozac))
if you have a family history of hypothermai, don't give this skeletal muscle relaxant
diazepam (valium) is a DEA schedule --- what is it>?
scheudle IV
diazepam is an anxiolytic and an antiepileptic
primary NTS at the dorsal horn fo the spinal cord
glutamate + substance p
endogenous compounds with u >> dk selectivity
teat seizures associated with alcohol withdrawal with ...
short acting lorazepam
for anxiety (long term)

for anxiety (short term)
- diazepam (long term)

- alprazolam (short term)
DOC muscular disorders especially cerebral palsy and MS
detoxification druring withdrawal from physiological dependence of barbituates, BZs, and ethanol - use -->
long acting sedative hypnotics with dose tapering

- chlordiazepoxide
idosyncratic blood dyscrasias, aplastic anemia
anesthetic but not analgesic
thiopental sodium
local amide with higher incidence of cardiac arrhythmias
DOC - tonic clonic & grand mal
phenytoin and carbamezipine
DOC partial seizure
phenytoin and carbamezipine
DOC status epilepticus q
phenytoin and diazepam
DOC myoclonic seizures
clonazepam + valproic acid
DOC absence seizures
Ethosuzimide (alternative clonazepam and valproic acid)
long duration opioids
don't give with meperdine
MAOI probably shoudl avodi TCAS and antipsychotics
facilitates surgical amnesia
name an antidepressant that inhibits cyt p450
-slower onset of action than BZ
-no muscle relaxation or anticonvulsant activity
busprione --> for chronic anxiety with symptoms of irritabilitya dn hostility especially in ex-drug abusers
treatment of generalized anxiety disorders --> acts on the 5-h-t receptors
1. epilepsy DOC
2. DOC for grand mal
3. status epilepticus
1. clonazepam
2. diazepam
3. diazepam
DOC for alcohol withdrawal

THC - amotivational syndrome

LSD- alters users sense of time and self may change
Blocks NMDA-type glutamate receptors

-PCP - dangerous hallucinogen
-ketamine - anesthetic agent used for diagnostics & surgical procedures
endogenous compounds with d> uk selectivity
major side effects of morphien
decreased respiration

also: miosis, block of cough reflex, emesis, GI distress, cardiovascular effects, constipation, nausea, depressed renal function, pruitis and tolerance
a centrally acting analgesic (not chemically related to opiates
difference between hydrocodone and tramadol?
hydrocodone is an antitussive and a narcotic analgesic, while tramadol is a centraly acting analgesic

hydrocodone shoudl eb used with caution in pts iwth head injuries

tramadol should not be used with naloxone
inhalation GA MOA
may activate GABA-A receptors _ depress spontaneous evoked activity of neurons in the brain
amide local anesthetics associated with high incidences of cardiac arrhythmias
name amide local anesthetics
-remember the i before caine rule

hallucingoen (angel dust, heroin) are DEA shedule
antipsychotic contraindicated in pts with long QT
tranylcypromiae pharm
fast recovery of MAO due to weak bond to enzyme
antipsychotic used to treat dementia
name 2 drugs under DEA schdule 1
PCP & heroin
contraindicated with SSRI fluoxetine
-drugs metabolized by cyt p450
-MAOI presumably also
antiepileptic drug - highly bound to plasma protein
-carboanzapene also strongly bound
the most common most dangerous hallucinogen is
antiepileptic used only for partial seizures
GABA pentin
opioid administration
-oral administration of opioids
-huge first pass effect but the amount that can get into the blood is still sufficient
what should not be administered with meperidine?
lithium MOA
-alters sodium transport in nerve and muscle cells
-inhibits the recycling of neuronal membrane phosphoinositides involved in the generation of secondary messengers
antidepressants that shoudl not be given to the elderly
TCAs becasue of the severe side effects
DOC for atypical depression
amide local anesthetic s
-medium duration of action
-long duration of action
medium - mepivacaine
long- ropivacaine
Which inhaled GA is an incomplete anesthetic
nitrous oxide
MAC > 100%
what type of patients can thiopental sodium and methohexital not be used for ?
-contraindicated in pts with porphyria
hypnotic used for short term treatment of insomnia
has a long half life and a longer duration of action than morphine
what's the difference between glycine and gaba>
they are both inhibitory NTS but glycine increases Cl permeability, while GABA works on GABA A and GABA B
DEA schedule I
acute opioid poisioning
signs and symptoms
1. comatose, miosis, cyanosis
2. treatment - artificial respiration and give naloxone
what's the difference between inotropic receptrs and metabotropic receptors
inotropic: ligand gated ion channels, fast

metabotropic: g protein coupled receptors, slow
name 2 areas of the brain, regions, where opioids work
PAG and RVM - regions of the brain with lots of opioid receptors
skeletal muscle relaxant used for allievation of severe spasticity resulting from multiple sclerosis & in patients with spinal cord injuries
durham - humphrey admendment
define what drugs are prescripiton and which are over the counter
kefauver-Harris amendment
establishes stronger drug-saftey regulation establishes clinical testing phase i-IV
1. DEA schedule III drug
2. DEA schedule IV drug
3. DEA schedule V drug
1. testosterone
2. diazepam
3. codeine
name a narcotic antagonist
opioid MOA - where does it block?
1. presynaptic SP receptors
2. opioids can also effect calcium release in the presynaptic terminal, so that the SP NTS are not released
used for ADD in children greater than 6 years old? Other uses of this drug?

other uses - short term treatment of obesity
can be used for post-traumatic stress & premenstrual dysphoric disorder + social anxiety disorder
sertraline (zoloft)
blocks 5-HT2 > D1- D4 etc. Uses?
USED FOR bipolar disorder
antagonizes action of benzodiazepines - with what result?
flumazenil - reverses the sedative effects of benzodiazepines
phenobarbital MOA
-potentiates GABAergic stimulus
-inhibits Ca++ channels
-blocks AMPA receptors
used for partial seizures and absence seizures
pharmacological action of morphine
1. analgesia
2. euphoria
4 uses of diazepam
1. anxiolytic
2. alcohol withdrawl
3. muscle spasm
4. seizure
what are tricyclic antidepressants used for now?
-as an alternative for enuresis and chronic pain
epinephrines effect on LA
-decrease systemic toxicity
-decrease bleeding (local)
-increase duration of action of LA
cocaine MOA
Mechanism of Action: blocks monoamine reuptake transport into nerve terminals; Na channel blocker
cocaine indications
Indications: topical anesthesia of the upper respiratory tract (due to its combined vasoconstrictor & local anesthetic properties); use in EM as an ingredient in TAC (tetracaine, adrenaline & cocaine) prior to wound cleaning & suturing.
tell me about cocaine mixed with alcohol
Major drug Interactions: MAOI inhibitors would be expected to increase cocaine's effects & toxicity. Ethanol consumption will convert cocaine to cocaethylene, a derivative that has a half life of 3-4 hours and shares a similar pharmacology as cocaine. Most cocaine abusers consume ethanol to prolong their high. This may also increase cocaine's cardiotoxicity.
for ADD or narcolepsy
-ritalin methylphenidate

ADD - also methamphetamien & pemoline
drug interactions with MAO inhibitors
pregnant and head injury, what do you not give?
THC acts on (MOA)
cannabinoid receptors CB1 and CB2
antiepileptic used for all seizure types
most important side effect that can kill is decreased respiration
NSAID used for short term management of acute pain requiring analgesia at the opiate level
ketorolac (can be used in place of opioids in patients whom nausea and vomiting is a problem
used in hospital for severe and chronic pain
narcotic analgesic morphine types (mu receptor agonists)
what compound is a benzodiazepine receptor antagonist
used for both partial seizures and tonic clonic, grand mal seizures
antiepileptic given IV or rectally to stop continous seizure activity
valproate MOA
antiepileptic enhanves GABA mediate inhibitors
-blocks Na channels
-blocks K currents
-blocks T types Ca++ channels
partial agonist @ alpha adrenergic receptors in blood vessels resulting in vasoconstriction

SE = Saint Anthony;s fire
Ergotamine MOA
possibly live threatenting hepatic failure - why its used as a 2nd line of defense for ADD
pemoline major toxicity
chemical structures unrelated to benzodiazepines and barbituates
tell me about the chemical structure of zolopidem
for which antidepressant is it especially important to avoid an abrupt withdrawal
name SSRIs
- fluoxetine
- sertraline
- citalopram
- paroxetine
newer designer antidepressants that target more than one NT
multiple mechanism:

- venlafaxime

i.e. inhibit neuronal uptake or serotoin & norepinephrine + antagonizes central 5-Ht 2 receptors + alpha 1 adrenergic receptors
local anesthetic effects
1. what increses duration of action
2. what decreases LA effects
1. increase duration of action - hydrophobicity
2. decrease LA effects
inflammation (extracellular acidosis)
fluoxetines (norfluoxetine) metabolite is active and has an 8 day half life
pharmacokinetics of fluoxetines - length of action
This inhaled anesthetic sensitizes the heart to epi-induced arrhythmias
-rare but can induce hepatitis
which drugs cause an increase in CO2
what does it mean>
what drug can you give to treat
opioids can cause an increase in Co2
give Dantrolene to treat
may eb headed for malignant hypothermia
cause less sexual dysfunction than selective serotonin reuptake inhibitors
- increased amine levels by interfereing wtih metabolism
- increased vesicle stores of NE+ serotonin
-irreversible + non-selective
Antidepressant used for bulima nervosa (list drug type/classification )
I have bipolar disorder (mania -depression)
I need drugs now.
- lithium
-valproic acid
manic depression drugs
-valproic acid
fluoxetine (prozac)
#1 drug choice for depression, OCD, panic disorder
MAOI - contraindication don't give with ---
-sympathetic drugs
-tyramine - rich foods
#1 treat the mania of bipolar disorder
typical antipsychotic drugs
-blocks D2> D1
-typical drus include chlorpromazine & Haloperidol
Bupropion (contraindicated in patients suffering from seizure disorders)
used in pts trying to break their addiction to smoking cigarettes
this drugs has direct depressants effects on monosynaptic reflex pathways in the spinal cord - thus it can produce skeletal relaxation without sedation
benzodiazepines used for panic + phobia

buspirone can also be used - the advantages are less likely to get addicted.
increased risk of seizures if nalaxone is used to treat --- overdose
only local anesthetic that causes vasoconstriction
bulima - 1st line of defense
SSRI (Fluoxetine)
more lipid soluble + crosses the BBB better than morphine
drugs that block neuromuscular transmission are either
-competitive (non-depolarizing)
-cholinomimetics (depolarizing)
migraine (mild) pharmacological strategy
2. Acetaminophen
3. Caffeine
4. sumatriptan
Two series of alkaloids in opium?
Phenanthrenes + Benzylisoquinolines
which opioid receptor is responsible for most of the opioids analgesic effects?
u receptors (also responsible for side effects)
Lamotrigine MOA
(Carbamazepine too)
antiepileptic blocks Na channels
Phenytoin MOA
-blocks Na channels
-increases GABA-mediated
-decreases Ca++ influx
for generalized tonic-clonic (grand-mal) seizures
antiseizure drug has SE

Nystagmus, gingival hyperplasia, hirsutism
carbamazepine MOA
blocks sodium channels
antiseizure drug has SE idiosyncratic blood descrasis, aplastic anemia
carbamazepine SE
antiseizure drug blocks t-type ca++ channels
Ethosuximide MOA
for absence (petit mal) seizures
partial seizures
for status epilepticus
-lorazepam both benzodiazepam/ antiepileptic
name 2 benzodiazepines that are antiepileptic
diazepam + lorazepam
which inhaled antiesthetic may cause megaloblastic anemia?
nitrous oxide

-from prolonged exposure due to a decrease in methionine synthase activity
what's the difference between methanol and ethanol?
methanol and its metabolites are much more potent toxins than ethanol
inhibitory NTs
glycine + GABA
difference between glutamate and GABA?
glutamate is a primary excitatory NT, while GABA is the primary inhibitory NTs.
serotonin and catecholamines are ...
SE of propofol
-marked hypotensions (greater than that causes by barbs
this drug is used primarily in patients with limited cardiac or respiratory reserves
Etomidate: short duration of action little effect on CV or respiration
a dissociative anesthetic used for shock states (hypotensive, pts at risk for bronchospasm) and children + young adults for short procedures
benzodiazepines vs. barbituates (clinical uses)
benzodiazepines = anxiety, panic attacks, insomnia, muscle spasm

barbituates = anesthesia + seizures
for the relief of moderate to severe pain
+ analgesic effects of this drug is only potentially antagonized by naloxone
this opioids has no antitussive effects
anti-histamine and anti-serotonergic agent

SE= sedative & weight gain
prophylaxis of severe migraine (cyproheptadine MOA)
side effects
treatment of alcohol withdrawal
1. without hepatic dx
2. with hepatic dx
w/o hepatic dx
1. diazepam + chlorodiazepoxide

w/ hepatic dx

1. oxazepam + lorazepam
name a sedative -- hypnotic & antiepileptic
have selective anticonvulsant effect without marked sedation
phenobarbital & clonazepam
methylphenidate MOA
compared to Dextroamphetamine MOA
Methylphenidate: blocks reuptake of dopaminergic neurons (mild effects)

Dextroamphetamines: causes releases of monoamine and competes for reuptake with monoamine (stronger CNS effects)
What are the advantages of codeine over morphine?
-causes less respiratory depression
-less addiction
-less euphoria
-slower developement of tolerance
a longer duration of action compared to naloxone & therefore more appropriate drugs for long-term treament of addiction to heroin r other opioids
most widely used antitussive
what is a problem of giving morphine? (not respiratory distress)
psychological + physical dependence
give an example of a full agonist + partial agonists + weak agonists antagonists
full - morphine
partial - oxycodone
weak - codeine
antagonist - naloxone
antagonist that blocks all receptors (u, k, d)
a non-narcotic antitussive
only for a short term relief of muscle spasms associated with acute, painful, musculoskeletal conditions
dantrolene MOA
-produces skeletal muscle relaxation by interfering with relaxation by interfereing with release of calcium from the sarcoplasmic reticulum through SR calcium channel complex
succinylcholine MOA
what type of skeletal muscle relaxant
- a depolarizing NMJ blocker

MOA - 1. phase I : excites skeletal muscle by binding nicotinic receptors

2. phase II = then prevents connection by prolonging the time that receptors at the NMJ cannot respond to Ach
Skeletal muscle relaxant that's contraindicated if you have a genetic disorder of plasma pseudocholinisterases
selectively depresses the cough center in the medulla
opioid that makes your pupils dilate
a narcotic antagonist used as an antidote against resporatory depression resulting from overdosage or sensitivity to narcotics
naloxone hydrochloride
side effects include constipation, nausea, vomiting (emesis), dizziness, sedation, respiratory distress, sedation, respiratory distress , miosis, circulatory depression, shock apnea
used for morphine or fentanyl dose
naloxone: short duration of action
chronic ethanol consumption can ---
induce cyt p450. This can increase hepatoxicity of acetaminophen
side effects include blurred vision, retinal damage, and metabolic acidosis with an evaluated anion gap
what are endomorphins, b-endomorphines, enkephalins,and dynomorphins, and what's the difference?
they are all endogenous opioids

endomorphins = u> dk
b-endomorphins - u> dk
enkephalins = d> uk
dynomorphins = k> ud
in acute pain, which pain are opioids effective at blocking? Which fibers mediate this pain?
opoids block dull second pain mediated by c-fibers
it is less effective at blocking sharp, first pain mediated by alpha delta fibers
opioid antagonists used to treat respiratory depression induced by natural + synthetic narcotics like butorphanol, methadone, nalbuphine, pentazocine + propoxyphene. DOC when nature of depressant drug is unknown
what drugs are used with oxycodone for a synergistic effects
synergistic effects
oxycodone + acetaminophen = percoset

oxycodone + aspirin = percodan
arrange codeine, morphine, oxycodone in order of potency
morphine> oxycodone > codeine
a CNS depressants
this opioid gets into the CNS fast and then is converted to morphine, why?
b/c its more lipid solubule and crosses the BBB better
what is the one type of chronic pain that opioids have some action agonists?
-opioids are sometimes useful against cancer pain
dangerous pharmacodynamic interactions between MAO inhibitors and
SSRIs (selective serotonin reuptake inhibitors)
what's the difference between

1. neurotransmitters
2. neuromodulators
3. neurohormones
1. NTs exert effects within a single synapse (fast)

2. neuromodulators act on multiple synapses (slower onset)

3. neurohormones - released into blood, act globaly (slowest onset)
what is the primary excitatory NT in the CNS?
considerable crossover pharmacology, specific NTs
difference between morphine + codeine?
morphine : full agonists PAIN RELIEF?

codeine : partial agonists mild to moderate pain relief

tolerance can also develops with morphine use, much less likely with codeine
cocaine is a DEA schedule ---
DEA schedule 2
chronic pain is a --- disease of the CNS
competitive antagonist of skeletal muslce nicotinic receptors
tubocurarine MOA
difference between tubocurarine & succinylcholine
tubocurarine - non-depolarizing succinylcholine - depolarizing NMJ blocker

T -competitive antagonist of nicotinic antagonists of nicotonic receptors in skeletal muscle

S - D excites skeletal muscle prevents contraction by prolonging NMJ responses time to Ach
skeletal muscle relaxant used to treat malignant hypothermia
MOA of analgesia?
basically the spinal cord mediates transmission of pain signals to the brain --> if you block anywhere in this pathway you get an analgesic effet
Name a DEA schedule II drug its drug class + utility
cocaine = CNS stimulant

uses: topical anesthetic for the upper respiratory tract
and int he TAC prior to wound cleaning and suturing
1. short acting opoid antagonist
2. long acting opoid antagonist
1. naloxone
2. naltrexene
succinylcholine contraindications
-genetic disorders of plasmacholinesterases

-family hisotry of malignant hypothermia
at high blood contraceptives, the rale of oxidation (of ethanol) follows ---
zero order kinetics for ethanol
Name a depolarizing neuromuscular blocking drug
for mild to moderate pain. major effects on CNS and bowel
give an example of a DEA schedule III drug + its uses
testosterone (Androgen)
-abuses use this drug to increase muscle mass & strength
produces opioid only mild euphoria
methadone that's why they're used to treat heroin withdrawal
weak acting opioid agonist with actions like codeine shoudl be used with caution in patient wtih head injuries
vd of this drug is similar to body water content
ethanol vd
irreversible MAO Inhibitors
selective for MAO-B
social anxiety disorder used
-zoloft (sertraline)
pharm of lithium
-narrow therapeutic window
-distribution space of lithium approximates that of total body water
phenobarbital indications
1. sedation
2. hypnosis
what do you use for
-surgical relaxation
-control of ventillation
-treatment of convulsion
NMJ blocking drugs
controlled substances act
legal foundation of gov't fight against drug abuse
establishes DEA schedules
controlled substances act
prophylaxis of severe migraine
1. b-blockers (propranolol, timolol)
2. calcium channel blockers (verapamil)
3. TCA 5-HT2 receptor antagonists
4. H1 antagonists
5. anticonvulsants (valproate)
1. skeletal muscle relaxant used during surgery to set fractures + dislocations

2. skeletal muscle relaxants used as an adjunct to facilitates ET tubation
1. d-tubocurarine
2. succinylcholine
a partial agonist of morphine, it will precipitates an abstinence syndrome in morphine abusers
2 mechanisms by which opioids work
1. presynaptically - decrease opioids decrease calcium influx, decrease NT release

2. postsynaptic - opioids block receptors in spinal cord, by increasing k+ conductance --> IPSP
indicated only for opiate tolerant clients
if you have malignant hypothermia - don't use these drugs
-inhaled general anesthetics
narcotic analgesic used for indication, maintenacne and an analgesic of postoperative care
--- receptors exhibit molecular heterogeneity
GABAa receptors
most common therapeutic uses of morphine
adjuvant to anesthesia
opoid act centrally bind to receptors and inhibit reuptake.

May be used for chronic pain
Percodan vs. Vicodin
Percodan - oxycodone + aspirin
vicodin - hydrocodone + acetaminophen
a depolarizing NMJ blocking drug
don't give this skeletal muscle relaxant to clients in whom histamine release is hazardous
acute pain is what type of a signal?
a physiological signal
pure food and drug act
prohibits mislabeling and adulteration of food, establishes official agencies that monitor food and drug manufacturing
harrison-narcotic act
identifies what a narcotic is and establishes classes of abusable drugs
NT only acts on metabotropic receptors
short acting (24 hours) duration reversible Inhibits MOA-a
NT excites both inotropic and metabotropic
ingestion is potentially fatal, call poision control immediately, treat with activated charcol, gastric lavage, breathing difficulties
isopropyl alcohol (rubbing alcohol)
morphine contraindications
1. head injury or craniotomy
2. pregnancy
3. hepatic failure
inotropic receptors
are ligand gated ion channels when open allow movement of specific ions down their electrochemical gradient
what's the difference between cyclobenzaprine + diazepram + baclofen?
cyclobenzaprine : for short term relief of muscle spasm

diazepram: for relief of skeletal muscle spasm caused by local pathology (inflammation, trauma, or cerebral palsy)
baclofen: for severe spaticity from MS or spinal cord injury
+ baclofen?
panic disoorder - 1st line of defense
MAOI & SSRIs (benzodiazepines might also work)
Name monoamines
histamine, norepinephrine, dopamine, and serotonin
name TCAs
monoamines type of receptors
all receptors are metabotropic
nicotonic, 5-ht3, glycine, + GABA-A receptors are ...
ionotropic receptors
baclofen MOA
- a GABA- B receptor agonist. Activation of receptors increases K conductance (hyperpolarization) that produces a presynaptic inhibitory effect to reduce the release of excitatory NTs by decreasing Ca influx
Phenobarbital MOA
-potentiates GABAergic stimulates by incresing duration of GAB-gated Cl channel opening
-compared to benzodiazepines, barbs are less selective
-also suppresses exulatory NTs (glutamate) + exert non-synaptic membrane effects

-lowers margin of safety compared to BZs
morphine metabolism
hepatic conjugation to glucuronides
1. short opoid duration of action

2. long duration of action compared to morphine (full agonists)
fentanyl - short acting
methadone - long acting
A GABA-B receptors antagonists ( a skeletal muscle relexant

1. contraindications
2. side effects
1. contraindications : cardiac ischema, cerebrovascular or peripheral vascular disease

2. side effects: coronary artery spasm
benzodiazepine anxiolytic - sedatives
2nd line antidepressive with incidence of sometimes fatal hypertensive crisis
endogenous compound with k > ud
used for tetanus
name MAOI
phenlzine, selegiline, tranylcyromine, mocolbemide
caffine MOA and indications
MOA: adenosine receptor antagonists (increase intracellular camp)

indications: sleep retardant, migraine, apnea of prematurity
antidepressants - SE is prolong QRS
TCA amitryptyline can lead to potentially fatal cardiac arrhythmias
name hypnotics with chemical structures unrelated to BZ and barbituates
zolpidem & hydroxyzine
what's the difference between selegiline and mocolbemide?
selegiline: irreversibel MAO inhibitor selective for MAO-B (less likely to cause cheese reaction)
mocolbemide - short acting reversible inhibitors of MAO-A
Name a glycine antagonist
what's the difference between hydrocodone and oxycodone
hydocodone - weak aagonist
oxycodone - full agonist

MOA - hydrocodone = narcotic analgesic + antitussive

oxycodone - narcotic analgesic only
what's the difference between the two intravenous anesthetics
thiopental sodium - repeated intravenous doses lead to prolonged anesthetics becasue fatty tissues act as a reservoir

methohexital - duration of action 1/2 as long as thiopental
doesn't concentrate in fatty tissue
what's the difference between the two intravenous anesthetics
thiopental sodium - repeated intravenous doses lead to prolonged anesthetics becasue fatty tissues act as a reservoir

methohexital - duration of action 1/2 as long as thiopental. doesn't concentrate in fatty tissues
a potent, long acting partial agonist. can be used for heroin addiction
buprenorphine - naltrexone can also be used for heroin addiction (long acting) but its an antagonist
name classes of NTs
-peptides (neuromodulators, neuropeptide y)
-Excitatory amino acids (glutamate)
-inhibitory amino acids (GABA, glycine)
NMDA receptors involved in learning & memory
glutamate interacts with ...
AMPA, Kainate, + NMDA
NT involved in regulation of pain, asthma, psoriasis, inflammatory bowel disease into CNS, emesis, migraine, schizophrenia, depression & anxiety
substance p
where is substance p found?
in the periphery and in the CNS
treatment for methanol poisioning
1. suppress metabolism by alcohol dehydrogenase to toxic products by giving ethanol

2. hemodialysis
3. treat acidosis with bicarbonate
used for the relief of skeletal muscle spasm due to reflex spasm caused by local pathology (inflammation or trauma or upper motor neuron disorders - (cerebral palsy) tetanus
ester local anesthetic
- esters
-tetracaine (long duration)
-2-chloroprocaine (short onset, short dur)
-procaine (short duration)
naloxone may not be effective in reversing respiratory depression by this drug
cyclobenzaprine vs. baclofen
baclofen can be used in patients with spinal cord injuries, cyclobenzaprine is ineffective in patients with spinal cord injuries
more potent + addicting than codeine
oxycodone (Percodan)
food, drug, and cosmetic act
no drugs can be marketed until proven safe
name spasmolytics
nausea management
1. metoclopromide (dopamine antagonists)
2. diphenydramine + dimenhydrinate (H1 antagonists)
3. Ketoralac
Lithium toxicity
-narrow therapeutic windows
-SE includes polydypsia, polyuria, + diabetes insipidus
-highly toxic levels include seizure, circulartory collapse and coma
-don't be dehydrated or you can get severe toxicity
benzodiazepine used as an antiseizure med?
benzodiazepine used for anxiety disorder or the treatment of panic disorders
-Alprazolam (an anxiolytic)
Benzodiazepine used for mild anxiety
chlordiazepoxide (an anxiolytic)
ondanseteron MOA
-serotonin receptor 5-HT3 antagonists serotonin binding to 5-HT3 receptors stimulates vagal effererent nerves, stimulating vomiting
barbiutates MOA
-increase duration of GABA mediated chloride channel opening
-block glutamate (excitatory)
-block sodium channels
-exert GABA-mimetic effects
triptans (e.g. sumatriptans) MOA
-activation of the serotonin receptors 5HT1 B-D inhibits activation of the trigeminal nerve & mennigal vasodilation
-produce vasoconstriction
treat acute attack of moderate or severe migraine headache
1. ergotamines (alpha-receptor blockers)
2. MAOI (phenylzine)
3. anticonvulsants (valproate)
4. 5HT antagonists (methylsergide)
5. opioids (reserved)
6. Triptans
ethanol MOA
-CNS depressants
-ethanol effects a # of membrane proteins involved involved in neurotransmissions, includes enhancement of GABA + GABA-A receptors + inhibiton of glutamate in opening NMDA receptor channels
narcotic analgesic + an antitussive agent
TCA side effects
-antimuscarinic effects = dry mouth, constipation, urinary retention, aggravation of glaucoma
-antihistamine: sedation
-NA channel blockers increase QRS arrhythmics
-alpha blockade : orthostatic hypertension
-erectile dysfunction
-blocks 5-HT (serotonin) and NE reuptake
-antihistamine effects
-NA channel block
- SE orthostatic hypertension + weight gain
benzodiazepines for anxiety
-chlordiazepoxide (mild anxiety)
- alprazolam (management of anxiety disorder)
buspirone MOA
a partial agonist of the 5-HT a serotonin receptor
diazepam MOA
skeletal muscle relaxant
-acts on the limbic system, the thalamus and the hypothalamus
-induces a calming effect
- agonism & antagonism (partial agonist) at 5-HT receptor subtypes
short acting benzodiazepine sedative; used as an adjunct to general anesthesia
what are it's 3 clinical indications>
1. preoperative sedation
2. amnesia
3. anxiolysis

midazolam (BZ)
anxiolytic drug + 5-HT1a partial agonist
social phobia
angel dust side effects
phenyclidine - most dangerous hallucinogen

1. psychosis
2. dissociation
3. disorientation
4. loss of pronociception
5. catatonic posturing
6. aggressive behavior
adverse effects of depolarizing blockade
-increased ocular pressure
-increased intagastric pressure
-muscle pain
opioid used to treat alcohol dependence
drug used for severe pain and detoxification + maintenance of narcotic dependence
one tenth as potent as morphine - used in minor surgeries
what are NMJ blocking drugs used for?
-surgical relaxation
-control of ventilation
-treatment of convulsion
monoamine MOA
-receptors are metabotropic
-receptors are G-protein coupled (when stimulated, they effect CA or K channels)
-considerable cross over pharmacology
1. what tye of receptors does morphine act on
2. where does morphine act?
1. morphine acts on all receptors subtypes
2. morphine acts
a. in the spinal cord to inhibit NT release and neuron activity
b. at opioid receptors in the brain (PAG + RVM)
c. at site of injury to inhibit nociceptors
glutamate MOA
excites inotropic receptors (ligand gated ion channels - NMDA, AMPA, & kainate) + metabotropic (G protein coupled) receptors - basically does both
SSRI side effects
-sexual dysfunction
-weight gain
Metabotropic receptors
- g protein coupled
-leads to ion channel activation
transduction of phospholipases, guanyl cyclase, and protein kinase activation
-slow response
MDMA (exstasy) MOA
CNS stimulant and hallucinogen
MOA: release of serotonin, dopamine, and NE
-distorts perception of time, facilitates intrapersonal communication
-acts as a sexual enhancer
metoclopramide MOA vs. diphenhydramine MOA
-antiemetic: D2 receptor antagonist in the chemoreceptor trigger zone to reduce

-antihistamine + antiserotonergic agent
-H1 receptor inhibitor, muscarinic, alpha adrenoceptor
-decrease GI hyperactivity
acute alcohol use may ...
metabolism of drugs due to decreased metabolism & decreased liver blood flow (tricyclic antidepressants, phenothiazines, sed-hypnotic drugs)
cyclobenzaprine MOA
-not clear but
-acts within the CNS and the brain stem to reduce tonic somatic motor activity
-metabotropic receptor subfamily
muscarinic Ach receptors monoamine receptors histamine
anesthesia (MOA)
1. enhance GABA effects
2. block nicotinic receptors (analgesia)
3. activate K+ channels hyperpolarize
4. block NMDA glutamate)
5. inhibit synaptic proteins
6. enhance glycine effects
drug interactions with morphine
-sedative hypnotics
-antipsychotic drugs
-MAO inhibitors
benzodiazepine hypnotics
-tenezepam (short term managemetn of insomnia)
-flurazepam (insomnia)
name an anticonvulsant used for prophylaxis of severe migraines
-valproic acid
-blocks neuronal Na channels and reduces the repetive firing of neurons
hypnotics - actions are due to suppression of activity in certain key regions of the subcortical area of the CNS
pharmacokinetics naloxone vs. naltrexone
naloxone: t1/2 1-4 hours
iv use only

naltrexone : t1/2 = 10 hours
oral use only
used for moderate pain - acts on k receptorsa and u receptors
benign, reversible thyroid enlargemetn is a SE
lithium b/c decrease tyrosine iodination
possible life-threatening hepatotoxicity is a side effects
doctor treat my hunnington's disease
used to treat chronic generalized anxiety
short term treatment of anxiety
also has hypnotic activity
zolpidem uses
#1 seizure med?
alternative meds?
alternatives - lorazepam
also clonozepam
contraindicated in pts with porphyria
levodopa MOA
MOA - symptoms of parkinsons related to depletion of scriatal dopamine
-dopamine is a metabolic precursor of dopamine but crosses the BBB
- carbidopa
- a dopa decarboxylase inhibitor in the periphery
-an aromatic amino acid decarbozylation inhibitor
carbidopa reduces peripheral dopamine formation
what is sinement?
-levodopa + carbidopa
- don't give to pts with history of melanoma
drug of first choice for parkinsons disease
bromocriptine (sinemet also works)
bromocriptine MOA
- D2 agonist
ergot derivative activates D2 receptors
-does not require enzymatic conversion ot an active metabolite have no potential toxic metabolites
atropine MOA
1. improves rigidity and tremor in parkinsons by decreasing Ach activation
2. preanesthetic med , decrease respiration and secretion
3. restor cardiac rate when vagal stimulation is produced by intra-abdominal surgical traction
4. decrease AV block produced by digitalis
5. overcome severe bradycardia
6. antidote for CV collapse
drug like atropine may improve tremor and rigidity of parkinsonism, no effect on bradykinesia
effects of selegiline on dopamine? why?
effect on amatadine of dopamine
selegilline : retards breakdown of dopamine prolongs antiparkinson effect, allows reduction of dose of L-dopa needed
MAO-B inhibitor

amantidine - potentiates dopaminergic function by influencing synthesis/ release of reuptake of dopamine
major side effect of levodopa limitating factor in therapy
dyskinesias (repetive involuntary gross movemetn of face + limbs , treat by decreaseing levodopa dose
don't use levodopa with ....
non selective MAOI like tranylcypromine b/c it can cause a severe hypertensive crisis
half life of carbamazepine is ---
12-18 hours
antiepileptic used to treat trigeminal neuralgia _ other pain syndromes
the lower the MAC the ---

the higher the partition oil-gas coefficient the ----
more potent the anesthetic agent
how can you increase the rate of anesthetic induction?
- increase anesthetic concentration
-increase rate and depth of ventillation
-change pulmonary blood flow
which inhaled anesthetics can cause cardiovascular system depression?
halothane isoflurane too
what is neuroleptic malignant syndromes - treat me
results from too rapid block of dopamine in pts with highly sensitive to extrapyramidal effects

treat with dantrolene or diazepam
1. prostatic hypertropy also avoid in pts with angle-closure glaucoma
benztropine shoudl eb used in caution with patient swith ....
verapamil DC and MOA
class IV
MOA: calcium channel blockers
iron poisoning due to multiple transformations
deferoxamine is the answer
CHF with EF < 40 %
what type?
what drug?
systolic type of CHF
(weakened force of ejection)
can used digoxin
which drugs should not be given as monotherapy becasue they can increase ventricular rate?
class Ia agents including procainamide and quinidine
what is the difference between the class 1a antiarrhythmics quinidine and procainamide
quinidine : for atrial flutter and fibrillation

procainamide: for life threatening ventricular arrhythmias (is also effective against atrial arrhythmias
metroprolol DC and MOA
dc: DC II
MOA: B1 selective adrenergic receptor antagonists
what is Ih
ih is a nonselective Na/K pacemaker current
what is ferritin?
ferritin is the stored form of iron - stores iron in the liver and the heart
if a pregnant woan has a folic acid deficiency, the baby might have a ...
what drug would you use to treat this?
ans: a neural tube defect
in megaloblastic anemia
treat with IL-11
i overdosed in ferrous sulfate. what's my antidote?

what's its drug class and MOA
1. deferoxamine - what's it used for?

2. drug class - iron chelator
MOA> binds iron avidly (loosely bound iron)
it can't compete with already bound iron (biologically chelated iron
drug used for life threating ventricular arrhythmias
i have microcytic anemia - what drug should you give me and why
give me ferrous sulfate
iron deficiency causes microcytic anemia due to the formation of small erythrocytes with insufficient hemoglobin, By giving ferrous sulfate, you give a iron source so that erythrocytes will be normal sized (with porphyrin ring)
what is the only class II and class III antiarrhythmic we've studied?
-sotalol - blocks K channels and b-adrenergic receptors
ventricular fibrillation MOA
disorganized reentry
what is the difference between

epotein a
ferrous sulfate and iron dextran
vitamin B12 and folic acid
epotein a - stimulates RBC production in normocytic anemia pts

2. ferrous sulfate - iron source in pts with microcytic anemia
3. drugs used to treat megalopblastic anemia (vitamin B12 treats pernicious anemia, folic acid should only be given to pts with pernicious anemia
what is atrial fibrillation? the MOA
disorganized atrial reentry
verapamila dn diltizim DC and MOA
DC: calcium channel blockers
mOA: blocks L-type calcium channels
permature atrial nodal or ventricular beat
don't treat don't do anything
how do you promote GI motility
wich receptors, which action
-antidopanergic (D2)
-activates serotonin receptors (5 HT3
i have a left main coronoary artery leion, what should I do ?
get bypass surgery
if you don't have serious lesions in the left main coronary artery you shoudl use drug treatments
can we use NO to treat calcified flow limiting lesions of the coronary artery?
no - cannot dilate a plaque or plaque area
which side does nitroglycerin act on
effects arterial side
major SE of nitroglycerin
variant angina treatment
-give nitroglycerin first
-give ca++ blockers to maintain

don't give B-blockers
ventricular tachycardia without structural heart dx what is it?
DAD's triggered by increase in sympathetic tone
quinidine DC and MOA
class ia , na + channel blocker
which clas sof antiarrhythmias has anticholinergic SE b/c they block m2 receptors and block autonomic ganglia
major side effect of class 1a drugs?
what is unusual about the pharmacokinets of amiodarone?

the pharmacokinetics of adenosine?
-amiodarone has a very long half-life (10-50 days)

adenosine has a t1/2 of ten seconds
which drugs reduce mortality and sudden death after MI
b-blockers propranolol
atrial/ ventricular fibrillation
disorganized reentry
in what type of patients can deferozamine not be used to treat iron poisioning