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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)
|
-steroids
-thalidomides -clofazimine |
|
What drug do you give to treat cutaneous manifestations of moderate to severe erythema nodosum leprosum (ENL)?
|
Thalidomide
|
|
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?
|
colestipol
|
|
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?
|
Gemfibrozil
|
|
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 |
-steroids
-clofazimine |
|
a side effect of this antimycobacterium is optic neurotis (a decrease in visual activity)
|
Ethambutol
|
|
drugs used for MAC
|
-Clarithromycin
-Azithromycin -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
|
Acetazolamide
|
|
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
|
Acetazolamide
|
|
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
-amiodarone -sotalol |
|
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
|
saralasin
|
|
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?
|
cholestyramine
|
|
antimycobacterium causes severe birth defects
|
thalidomide
|
|
hypolipidemic may impair carbohydrate tolerance
|
niacin
|
|
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?
|
-quinidine
|
|
a broad spectrum - antiarrhythmics
name it which channels does it effect. |
-amiodarone
-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 MOA
|
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?
|
amidarone
|
|
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
|
Tenecteplase
|
|
Less fibrin-specific that t-PA?
|
Reteplase
|
|
Less expensive than t-PA (also a thrombolytic
|
Reteplase
|
|
Ventricular tachycardia after MI, what is it?
|
Reentry near the rim of healed infarction
|
|
What factors stimulate renin release
|
-hypotension
-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
|
Abciximab
|
|
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
|
procainamide
|
|
Acute Rx for AV node reentry? PSVT?
|
-adenosine
-increase vagal tone with carotid sinus pressure -digitalis -edrophonium -phenylephedrine |
|
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
-angina -hypertension |
Verapamil
Diltiazim also - only less good for angina and hypertension |
|
name plasminogen activators
|
t-PA
Reteplase Tenecteplase |
|
To inhibit acid secretion, give ...
|
- histamine H2 antagonists
- prostaglandins -proton pump inhibitors |
|
name: platelet GP IIa/IIIa receptors blockers
|
Abciximab
Eptifibtide Tirofiban |
|
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
|
Isoniazid
|
|
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?
|
Furosemide
|
|
Angiotensin II - vasoconstriction or vasodilate renal
|
renal vasoconstriction
|
|
major side effects of all loop diuretics
|
hypokalemia
|
|
catecholamines - vasodilators or vasoconstricors renal
|
vasoconstrictors
|
|
Which loop diuretics inhibits the Na + 2CL K+ carrier system?
|
torsemide
|
|
which loop diuretic reduces pulmonary congestion and left ventricular filling pressure in heart failure?
|
furosemide
|
|
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
|
triamterene
amiloride spironolactone |
|
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?
|
Thiazides
|
|
drugs used for short term anticoagulent therapy associated with acute primary embolism and disseminated intravascular coagulation
|
heparin
|
|
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
ibutilide |
|
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
|
vasoconstrict
|
|
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?
|
amiodarone
|
|
what drug can : acute sinus conversion to sinus rhythum of PSVT? including when its associated with Wolff-Parkinson White syndrome?
|
Adenosine
|
|
Common treatments for atrial fibrillation(acute rxn) to control ventricular rate
|
verapamil or diltiazem
b bockers digoxin |
|
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
|
NSAIDS
non-steroidal anti-inflammatory drugs |
|
which prostaglandins, increase renal blood flow, promote diuresis, and natriuresis
|
PGE2
PGI2 |
|
for immediate reduction of stomach pain (cheap alternative) use
|
antacids
|
|
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?
|
Thiazides
|
|
Kinins - renal vasoconstrictor or vasodilators
|
renal vasodilators
|
|
This angina occurs during exercise (climbing stairs, etc)
|
External angina
|
|
Name renal vasoconstrictors
|
-Thromboxane A2, TXA2
-Catecholamines -Angiotensin II |
|
Name loop diuretics
|
Furosemide
Ethacrynic acid Torsemide |
|
SE fatal pulmonary fibrosis
|
Amiodarone
|
|
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)
|
-Adenosine
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
|
-hyperaldosterone
-hypokalemia -reduced edema & mortality in patients with CHF |
|
Most renal vasodilators promote ----
|
diuresis
|
|
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?
hypertonic? hypotonic? |
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?
|
Thrombin
|
|
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
|
-nifedipine
-verapamil -diltiazam |
|
which anticoagulent do you never give IV?
|
Thrombin
|
|
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
verapamil diltiazem nifedipine |
|
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
|
minoxidil
|
|
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
|
hemorrage
|
|
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
iorbesartan losartan valsartan |
|
anticoagulent which causes increased neutralization of factors II, IX, X, XI, XII, and Xiii
|
heparin
|
|
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
|
thiazides
|
|
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?
where? name a drug like amiloride |
-amiloride blocks sodium channels in the distal convoluted tubule
triamterene |
|
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 -->
|
-hyperkalemia
-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
|
spironolactone
|
|
Don't use this hypolipidemic in pregnant women
|
statins
|
|
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
|
-dopamine
-pgs, pge2, pgi2 -kinins |
|
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 ACEI |
|
What drugs can you use to treat primary triglyceruridemias?
|
niacin and fibric acid
|
|
heparin MOA
|
-anticoagulent
-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
-hypokalemia -lipid elevation -glucose intolerance -metabolic alkalosis -hyponatremia -hyperuricemia -hypomagnesia |
|
major drug interactions with warfarin
|
increase warfarins effect (inhibit P450 cimetidine and amiodarone)
- decrease warfarin's effect (induce p450) |
|
warfarin is contraindicated in
|
pregnancy
|
|
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 ...
|
B-blockers
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
whereas -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 |
-sibenafil
-vardenafil -tadalofil -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 MOA for CHF
|
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 4. ACEI 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?
|
Dipyridamole
|
|
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)
|
-reserpenine
-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
contraindicated |
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
|
warfarin
|
|
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
|
warfarin
|
|
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) |
DV: DC III
MOA: prolong action potential duration (K channel blockers) |
|
atenolol DC + MOA
|
DC: DC II
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?
|
pyrazinamide
|
|
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?
|
-quinidine
-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
|
-Ace INHIBITORS
-b-blockers -diuretics -vasodilators -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
|
-quinidine
-amiodarone |
|
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
|
pregnancy
|
|
nitroglycerin indications
|
(1) effort-associated (classic) angina
(2) variant angina (3) unstable forms of angina pectoris |
|
causes antihypertensive causes excessive hiresutism (hair growth)
|
minoxidil
|
|
drug sometimes used to treat antihypertensive emergencies (after sodium nitroprusside )
|
diazoxide
|
|
minoxidil MOA
|
dilates arterioles but not veins
-opens potassium channels in smooth muscle membranes --> makes contractions less likely |
|
hydralazine
|
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 |
|
Irbesartan
|
ARB
|
|
This antihypertensives shoUdl not be given to patients with coronary artery disease
|
hydralazine
|
|
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 5. ACEI |
|
This antihypertensive is subject to polymorphic acetylation. Slow acetylaters metabolize this drugs at a different rate than fast acetylators
|
hydralazine
|
|
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
|
hydralazine
|
|
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?
|
diazoxide
|
|
which antihypertensive dilates arterioles but not veins?
|
hydralazine
minoxidil |
|
Side effects of this antihypertensive include a reversible lupus-like syndrome
|
hydralazine
|
|
sildenafil
|
-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
|
-nitrates
-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
|
Acetazolamide
|
|
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?
|
-vasoconstrictors
-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 Treatment 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 |
|
ACEI MOA -->
effect on bradykinin |
ACEI =
-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 ...
|
an ACEI
|
|
Name ACE inhibitors
|
-Benazepril
-Captopril -Enalapril -Fosinopril -Lisinopril -quinapril -ramipril |
|
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
|
Rifampin
|
|
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)
|
Warfarin
|
|
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)
|
kinins
|
|
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
|
diltiazem
|
|
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
|
|
Rifampin
|
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)
|
hydralazine
|
|
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
|
statins
|
|
use of this hypolipidemic increses the risk of gout
|
niacin
|
|
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
|
-hydrochlorothiazide
-chlorothiazide |
|
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
|
ACEI
|
|
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
|
adenosine
|
|
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
-b-blockers -digoxin -warfarin (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
|
acetazolamide
|
|
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
|
-quinidine
-verapamil -amidarone (antiarrhythmics) they inhibit digoxin secretion in urine through p-glycoprotein pump competition |
|
side effects include teratogenicity and eripheral neuropathy
|
-thalomide
|
|
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
|
|
papaverine
|
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
|
ACEI
|
|
which calcium channel antagonists is used mainly for variant angina because of its antispasmotic effects
|
-nifedipine
|
|
therapy for chronic stable angina of effort
|
-long acting nitrates
-b-blockers -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
|
cholestyramine
|
|
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
|
|
indapamide
|
drug interactions include
-additive effects with other antihypertensives -enhanced lithium toxicity -may decrese response to catecholamines |
|
diuretics only indication is antihypertension
|
indapamide
|
|
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
Lidocaine procainamide chronic: ICD4 amiodarone |
|
don't give during pregnancy
|
1. acei - angiotensin converting enxyme inhibitors
2. indapamide 3. ANG II receptors blockers 4. warfarin |
|
acetazolamide
|
diuretics used for centripencephalic epilepsies
petit mal -unlocalized seizures |
|
name and MOA of diuretics that act at the early distal convolution
|
block NaCl cotransporters
chlorothiazide metolazone indapamide |
|
which drugs bin bile acids in the intestines and cause and upregulation of LDL receptors
|
-chloestyramine
-colestipol |
|
cholestyramine
|
-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
|
cholestyrarmine
|
|
4 main uses of diuretics
|
A) nephrotic syndrome
B) CHF C) advanced liver disease D) hypertension |
|
most common important complication of diuretics usage
|
hypokalemia
metabolic disturbances (alkalosis, acidosis glucose intolerance hyperuricemia |
|
name two other drugs act at the same site as indapamide
|
chlorothiazide
metolazone (early distal convoluted tubule) |
|
side effects include acute renal failure, hyperkalemia, and drug cough
|
ACEI
|
|
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
|
-dapsone
-clofazimine -rifampin -thalidomide |
|
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
-CHF -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
|
|
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
|
salmeterol
|
|
asthma & pulmonary disease medications can reduce fluid congestion b/c of alpha effects
|
epinephrine/adrenaline
|
|
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
|
monteleukast
|
|
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
|
rifampin
clofazimine |
|
dapsone indications
|
-mycobacterium leprae
-pneumocystis pneumonia in AIDS |
|
leprosy drugs
|
clofazimine
rifampin dapsone |
|
what is an alternative to dapsone for treating resistant leprosy
|
clofazimine
|
|
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
|
-pyrazinamide
|
|
side effects of isoniazid
|
-hepatotoxicity
-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 |
isoniazid
|
|
which antimycobacterials are bacteriocidal
|
-cidal
-isoniazid in dividing cells -rifampin |
|
antimycobacterials that are bacteriostatic
|
-isoniazid in resting cells
-ethambutol -dapsone |
|
inhibits ETC in mycobacteria
|
pyrazinamide
|
|
different acetylators - fast acetylators and slow acetylators metabolize at different speeds
|
isoniazid
|
|
dopamine MOA
|
-reduce afterload combined with inotropic stimulation
-acts on D, a, b receptors |
|
primary action of this vasodilator for CHF is reduced preload
|
torsemide
|
|
foresemide and torsemide drug interactions
|
NSAIDs interfere with prostaglandin synthesis
|
|
carbohydrate tolerance --> hypolipidemic, vasodilators for CHF?
|
niacin
hydrochlorotriazide |
|
if worried about cyt p450 drug interactions, which statin can you give?
|
pravastatin
|
|
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? |
statins
|
|
hypolipidemic - decreases cholesterol synthesis and upregulates LDl
|
-HMG-CoA reductase inhibitors
-statins |
|
which of the statins is not a prodrug
|
pravastatin
|
|
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
|
|
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
|
gemfibrozil
|
|
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
|
niacin
|
|
used for familal hypercholesterolemia in combination with a resin or reductase inhibitor
|
niacin
|
|
side effects of hypolipidemic - cutaneous vasodilation
|
niacin
|
|
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-blockers -digoxin 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) PSVT 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
|
-digitalis/digoxin
-loop diuretics (thiazides) -ACEI |
|
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
|
phenytoin
|
|
--- receptors mediate long term potentiation when stimulated by glutamate
|
NMDA receptors
|
|
I have acute pain, pulmonary edema, dyspnea, and I need a preanesthetic medication
|
morphine
|
|
of maximal analgesia is 12-15% of morphine - used for moderate pain
|
codeine
|
|
fentanyl
|
80X more potent than morphine, used for general anesthesia
|
|
2 most important excitatory transmitters used for the transmission of pain
|
-glutamate
-substance p |
|
GABA MOA
|
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
|
-haloperidol
-risperidone |
|
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
|
-sedating
-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
|
succinylcholine
|
|
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
|
endomorphins
|
|
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
|
diazepam
|
|
detoxification druring withdrawal from physiological dependence of barbituates, BZs, and ethanol - use -->
|
long acting sedative hypnotics with dose tapering
- chlordiazepoxide -diazepam |
|
idosyncratic blood dyscrasias, aplastic anemia
|
carbamazepine
|
|
anesthetic but not analgesic
|
thiopental sodium
|
|
local amide with higher incidence of cardiac arrhythmias
|
bupivacatine
|
|
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)
|
|
buprenorphine
|
long duration opioids
|
|
don't give with meperdine
|
MAOI probably shoudl avodi TCAS and antipsychotics
|
|
facilitates surgical amnesia
|
diazepam
|
|
name an antidepressant that inhibits cyt p450
|
fluxoetine
|
|
-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
|
buspirone
|
|
1. epilepsy DOC
2. DOC for grand mal 3. status epilepticus |
1. clonazepam
2. diazepam 3. diazepam |
|
DOC for alcohol withdrawal
|
-chlordiazepoxide
-diazepam -oxazepam |
|
SE of THC
SE of LSD |
THC - amotivational syndrome
LSD- alters users sense of time and self may change |
|
Blocks NMDA-type glutamate receptors
Hallucinogens |
-PCP - dangerous hallucinogen
-ketamine - anesthetic agent used for diagnostics & surgical procedures |
|
endogenous compounds with d> uk selectivity
|
enkephalins
|
|
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
|
tramadol
|
|
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
|
bupivacaine
|
|
name amide local anesthetics
|
-remember the i before caine rule
-lidocaine -bupivacaine -ropivacaine |
|
hallucingoen (angel dust, heroin) are DEA shedule
|
one
|
|
antipsychotic contraindicated in pts with long QT
|
haloeridol
|
|
tranylcypromiae pharm
|
fast recovery of MAO due to weak bond to enzyme
|
|
antipsychotic used to treat dementia
|
Risperidone
|
|
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
|
phenytoin
-valproate -carboanzapene also strongly bound |
|
the most common most dangerous hallucinogen is
|
PCP
|
|
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?
|
tricyclics
|
|
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
|
phenelzine
|
|
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
|
zolpidem
|
|
has a long half life and a longer duration of action than morphine
|
methadone
|
|
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
|
heroin
|
|
acute opioid poisioning
signs and symptoms treatment |
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
|
baclofen
|
|
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
|
-naltrexone
-naloxone |
|
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?
|
methamphetamine
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?
|
olNZAPINE
USED FOR bipolar disorder |
|
antagonizes action of benzodiazepines - with what result?
|
flumazenil - reverses the sedative effects of benzodiazepines
|
|
phenobarbital MOA
|
antiepileptic
-potentiates GABAergic stimulus -inhibits Ca++ channels -blocks AMPA receptors |
|
used for partial seizures and absence seizures
|
lamotrigine
|
|
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
|
-vasoconstriction
-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
-dextroamphetamine ADD - also methamphetamien & pemoline |
|
drug interactions with MAO inhibitors
|
diuretics
NSAIDS ACEI |
|
pregnant and head injury, what do you not give?
|
morphine
|
|
THC acts on (MOA)
|
cannabinoid receptors CB1 and CB2
|
|
antiepileptic used for all seizure types
|
valproate
|
|
most important side effect that can kill is decreased respiration
|
opioids
|
|
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
|
fentanyl
narcotic analgesic morphine types (mu receptor agonists) |
|
what compound is a benzodiazepine receptor antagonist
|
flumazenil
|
|
used for both partial seizures and tonic clonic, grand mal seizures
|
-phenytoin
-carbamazepine -phenobarbital |
|
antiepileptic given IV or rectally to stop continous seizure activity
|
diazepam
|
|
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
|
paroxetine
|
|
name SSRIs
|
- fluoxetine
- sertraline - citalopram - paroxetine |
|
newer designer antidepressants that target more than one NT
|
multiple mechanism:
- venlafaxime -nefazodone 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 |
halothane
|
|
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
|
-nifazodone
-bupropion |
|
MAOI MOA
|
- 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 )
|
-fluoxetine
-SSRI |
|
I have bipolar disorder (mania -depression)
I need drugs now. |
- lithium
-carbamezepine -valproic acid olanzapine |
|
manic depression drugs
|
0lithium
-carbamazepines -valproic acid |
|
fluoxetine (prozac)
|
#1 drug choice for depression, OCD, panic disorder
|
|
MAOI - contraindication don't give with ---
|
-sympathetic drugs
- SSRIs -tyramine - rich foods |
|
#1 treat the mania of bipolar disorder
|
lithium
|
|
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
|
diazepam
|
|
benzodiazepines used for panic + phobia
|
-alprazolam
-clonazepam buspirone can also be used - the advantages are less likely to get addicted. |
|
increased risk of seizures if nalaxone is used to treat --- overdose
|
tramadol
|
|
only local anesthetic that causes vasoconstriction
|
cocaine
|
|
bulima - 1st line of defense
|
SSRI (Fluoxetine)
|
|
more lipid soluble + crosses the BBB better than morphine
|
Heroin
|
|
drugs that block neuromuscular transmission are either
|
-competitive (non-depolarizing)
-cholinomimetics (depolarizing) |
|
migraine (mild) pharmacological strategy
|
1. NSAIDS
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
|
-phenytoin
-carbamazepine -phenobarbital |
|
antiseizure drug has SE
Nystagmus, gingival hyperplasia, hirsutism |
Phenytoin
|
|
carbamazepine MOA
|
antiseizure
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
|
-Ethosuximide
-Lamotrigine |
|
partial seizures
|
-phenytoin
-carbamazepine -phenobarbital -valproate -GABApentin -Lamotrigine |
|
for status epilepticus
|
-diazepam
-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 ...
|
monoamines
|
|
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
|
ketamine
|
|
benzodiazepines vs. barbituates (clinical uses)
|
benzodiazepines = anxiety, panic attacks, insomnia, muscle spasm
barbituates = anesthesia + seizures |
|
buprenorphine
|
for the relief of moderate to severe pain
|
|
tramadol
|
+ analgesic effects of this drug is only potentially antagonized by naloxone
|
|
meperidine
|
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
|
phenobarbital
|
|
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
|
naltrexone
|
|
most widely used antitussive
|
dextromethorphan
|
|
what is a problem of giving morphine? (not respiratory distress)
|
tolerance
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)
|
naloxone
|
|
a non-narcotic antitussive
|
dextromethorphan
|
|
only for a short term relief of muscle spasms associated with acute, painful, musculoskeletal conditions
|
cyclobenzaprine
|
|
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
|
succinylcholine
|
|
selectively depresses the cough center in the medulla
|
dexomethorphan
|
|
opioid that makes your pupils dilate
|
meperidine
|
|
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
|
morphine
|
|
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
|
methanol
|
|
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
|
naloxone
|
|
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
|
ethanol
|
|
this opioid gets into the CNS fast and then is converted to morphine, why?
|
heroin
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?
|
glutamate
|
|
considerable crossover pharmacology, specific NTs
|
monoamines
|
|
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 ---
|
Two
DEA schedule 2 |
|
chronic pain is a --- disease of the CNS
|
pathological
|
|
competitive antagonist of skeletal muslce nicotinic receptors
|
tubocurarine MOA
|
|
difference between tubocurarine & succinylcholine
|
tubocurarine - non-depolarizing succinylcholine - depolarizing NMJ blocker
MOA 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
|
dantrolene
|
|
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
|
tubocurarine
|
|
for mild to moderate pain. major effects on CNS and bowel
|
codeine
|
|
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
|
hydrocodone
|
|
vd of this drug is similar to body water content
|
ethanol vd
lithium |
|
irreversible MAO Inhibitors
selective for MAO-B |
selegiline
|
|
social anxiety disorder used
|
-zoloft (sertraline)
-paroxetine |
|
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
|
pentazocine
|
|
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
|
oxycodone
|
|
if you have malignant hypothermia - don't use these drugs
|
-succinylcholine
-inhaled general anesthetics |
|
narcotic analgesic used for indication, maintenacne and an analgesic of postoperative care
|
Remifentanil
|
|
--- receptors exhibit molecular heterogeneity
|
GABAa receptors
|
|
most common therapeutic uses of morphine
|
adjuvant to anesthesia
-analgesia |
|
opoid act centrally bind to receptors and inhibit reuptake.
May be used for chronic pain |
Tramadol
|
|
Percodan vs. Vicodin
|
Percodan - oxycodone + aspirin
vicodin - hydrocodone + acetaminophen |
|
a depolarizing NMJ blocking drug
|
succinylcholine
|
|
don't give this skeletal muscle relaxant to clients in whom histamine release is hazardous
|
tubocurarine
|
|
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
|
monoamines
|
|
short acting (24 hours) duration reversible Inhibits MOA-a
|
mocolbemide
|
|
NT excites both inotropic and metabotropic
|
glutamate
|
|
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
|
-Amitryptyline
-imipramine |
|
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
|
baclofen
|
|
sumatriptan/triptans
1. contraindications 2. side effects |
1. contraindications : cardiac ischema, cerebrovascular or peripheral vascular disease
2. side effects: coronary artery spasm |
|
benzodiazepine anxiolytic - sedatives
|
lorazepam
|
|
2nd line antidepressive with incidence of sometimes fatal hypertensive crisis
|
tranylcypromide
|
|
endogenous compound with k > ud
|
dynomorphin
|
|
used for tetanus
|
diazepam
|
|
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
|
strychnine
|
|
what's the difference between hydrocodone and oxycodone
|
strength
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) -Ach -purines -monoamines |
|
NMDA receptors involved in learning & memory
|
glutamate
|
|
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
|
diazepam
|
|
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
|
buprenorphine
|
|
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
|
-dantrolene
-baclofen -diazepam -cyclobenzaprine |
|
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?
|
clonazepam
diazepam lorazepam |
|
benzodiazepine used for anxiety disorder or the treatment of panic disorders
|
-Alprazolam (an anxiolytic)
|
|
Benzodiazepine used for mild anxiety
|
chlordiazepoxide (an anxiolytic)
|
|
ondanseteron MOA
|
-antiemetic
-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
|
hydrocodone
|
|
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 -tachycardia -erectile dysfunction |
|
TCA MOA
|
-blocks 5-HT (serotonin) and NE reuptake
-antimuscarinic -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 |
|
LSD MOA
|
- 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
|
buspirone
|
|
social phobia
|
SSRI
|
|
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
|
-hyperkalemia
-increased ocular pressure -increased intagastric pressure -muscle pain |
|
opioid used to treat alcohol dependence
|
naltrexone
|
|
drug used for severe pain and detoxification + maintenance of narcotic dependence
|
methadone
|
|
one tenth as potent as morphine - used in minor surgeries
|
meperidine
|
|
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
|
metoclopramide
-antiemetic: D2 receptor antagonist in the chemoreceptor trigger zone to reduce diphenydramine -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
|
hydroxyzine
|
|
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
|
pentazocine
|
|
benign, reversible thyroid enlargemetn is a SE
|
lithium b/c decrease tyrosine iodination
|
|
possible life-threatening hepatotoxicity is a side effects
|
MAOI
tranylcypromide |
|
doctor treat my hunnington's disease
|
haloperidol
|
|
used to treat chronic generalized anxiety
|
buspirone
|
|
short term treatment of anxiety
also has hypnotic activity |
zolpidem uses
|
|
#1 seizure med?
alternative meds? |
diazepam
alternatives - lorazepam also clonozepam |
|
contraindicated in pts with porphyria
|
phenobarbital
|
|
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
|
benzotropine
|
|
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
|
carbamazepine
|
|
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
|
procainamide
|
|
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
|
hypotension
|
|
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
|
in pts with severe renal disease (iron chelators are excreted by the kidney)
|
|
SE includes lupus erythromatosus-like syndrome after prolonged use
|
procainamide
|
|
propafenone DC + MOA
|
DC: 1c
MOA: Na channel blocker |
|
CHF with Ef > 45%
|
diastolic type of CHF
weakened cells replaced by fibrous tissue) do not use digoxin |
|
which antiarrhythmic is administred in a stenle solution for rapid bolus injection and has a half life of less than 10 seconds
|
adenosine
|
|
propranolol DC+ MOA
|
DC: class II
MOAL b1 receptors antagonists (non-selective) |
|
prostaglandins PGE2 and PGI2
renal vasodilator or vasoconstritors |
renal vasodilators
|
|
prevents reoccurance life threating ventricular arrhythmias
|
amiodarone
|
|
which test measures extrinsive thromboplastin and
which test measures intrisic thromboplastin? which test is used to monitor coumarin/ warfarin or heparin |
extrinsic thromb = Pt coumarin/ warfarin
intrinsic thromb = PTT heparin |
|
deficiency that cuases macrocytic anemia and peripheral neuropathy
|
vit b12 deficiency
|
|
in addition to being used for CHF what type of arrhythmia is digoxin also used for?
|
atrial fibrillation and atrial flutter
|
|
procainamide DC + MOA
|
DC: 1a
MOA = Na channel blockers |
|
list the major drug categories. Tell me their MOA give me an example
|
1 - sodium channel blockers
II - b blockers III - potassium channel blockers prolonged APD IV - calcium channel blockers IV - multiple MOA |
|
another name for AVN reentry
|
PSVT Paroxysmal supra ventricular tachycardia
|
|
Amiodarone DC + MOA
|
class I - IV - multiple MOA (sometimes listed as class III
|
|
what do diuretics do to digoxins effects ? why ?
|
diuretics cause hypokalemia (a SE) which oeduces the activity of ATPase. which can increase digoxin's effects
|
|
what's the difference between treating a pt with atrial fibrillation or flutter with ca channels blockers or b blockers compared to digoxin?
|
ca channel blockers + B-blockers also have a negative iontropic effects and harmful to pts with systolic CHF )low EF < 45
digoxin has a postiive inotropic and can be used in pts with low EF |
|
I have hypertension
what antianemic drug should not give me |
Epoetin a
|
|
which drugs has SE cinchonism, torsades de pointes , syncope, antimuscarinic effects, diarrhea?
|
quinidine
|
|
why do we not give folic acid alone to treat pernicious anemia
|
b/c you need to determine if the patients also has a vit b12 deficiency. folic acid supplements mask the signs of vitamine B12 deficiency but not prevent the development of irreversible neurological disease due to vitamine b12 deficiency
|
|
fatigue, visual complaints, muscular weakness, nausea, anorexia, psychic complaints, adominal painjs, dizziness, dreams, headache, diarrhea, vomiting
|
signs of digitalis toxicity
|
|
1. name a glycoprotein that stimulates red blood cell production
2. normocytic anemia - erythrocytes are normal, there just aren't enough of them |
how does epoetin alpha help anemia?
what type of anemia does epoetin a cure? |
|
what drug is used mainly to treat
digoxin -induced arrhythmias |
phenytoin
|
|
what type of angina is due to coronary insufficiency due to vessel occlusion
|
exertional (typical angina)
|
|
amiodarone drug interactions
|
many review careful amiodarone is a p450 substrate
am inhibits most cytochrome enzymes can elevate digoxin plasma levels |
|
class III drugs MOA
|
-prolong APD by blocking K channels
-indirectly results in increase ERP b.c of increase APD - increase in ERP abolishes reentry b/c ERP > CT |
|
what does transferrin do?
|
transferrin transports iron around the body
|
|
name 1b drus what are not effective agains?
|
-lidocaine
-phenytoin -tocainide -mexiletine No good for SVTA |
|
which class of antiarrhythmics can have nerologic side effects (stimulation of depression and convulsions
|
class 1b drugs (lidocaine, phenytoin, and mexiletine)
|
|
what do you use to treat methotrexate overdose?
what is the advantage of this drugs over other available drugs? |
-citrovorum factor (leukovorin)
to replinish endogenous folic acid bec methotrxate inhibits DHFR |
|
what's the difference betwene quinidine, procainamide, and disopyramide
|
the side effects
quinidine --> syncope, torsades de pointes, cinchonism (tinnitus, visual disturbances, hearing loss, GI upset) procainamide - much weaker vagal effect than quinidine - SE - systemic lupus erythematosus-like syndrome in 1/5 patients on drug for > 1 year disopyramid - anticholinergic effects |
|
pharmacokinetics of lidocaine
|
DC - 1b
administered iv or im due to extensive 1st pass hepatic metabolism and short half life adminsitered in the ICU generally |
|
these drugs cause irreversible inhibitor of the H+ K+ and ATPase proton pump in the parietal cells
|
proton pump inhibits
|
|
how are subclasses of drug class 1 determined
|
1a, 1b, 1c are distinguished based upon the magnitude of their effect on conduction (decrease upstroke velocity - QRS) and repolarixation (APD in vitro or increased QT
|
|
antimycobacterial that induces p450
|
rifampin
|
|
difference between heparin _ warfin ?
|
herparin is a direct acting drug
warfarin is an indirect acting drug? heparin is given iv, warfarin is oral |
|
ang II effects on vasculature
|
causes vasoconstriciton, increase rise in BP
|
|
renins effect on bp, why?
|
end results increases bp and increase blood volume
|
|
b-agonists on plasma renin activity
|
increased renin activity
|
|
symptoms include paresthesias, and eweakness in peripheral nerves, progressing to spasticity, ataxia and CNS dysfunction
What drug to treat? |
neurological abnormalities from vit b12 deficiency
treat with vitamin B12 |
|
adenosine drug class
|
endogenous nucleotide antiarrhythmics
|
|
i have normocytic anemia, what type of patient am I likely to be?
what drug would you give me? |
-give me epoetin a b/c it stimulates red blood cell production
I am a 1. cancer pt - chemotherapy pts 2. AZTs treatment AIDS pt (HIV pts) 3. chronic renal failure 4. anemia b/c I didn't get a bood transfusion following surgery for whatever reason |
|
drugs (antiarrhythmics contraindicated in asthma
|
sotalol and propranolol
|
|
when are b1 selective blockers contraindicated?
|
-sinus bradycardia
-heart block -cardiogenic shock -overt cardiac failure |
|
3 antidiarrheals types
|
1. antimotility agents - inhibits parasympathetics activation. block ach release
2. adsorbents - absorbs intestinal toxins + microorganisms 3. agents modifying fluid + e transports decreases fluid secretion |
|
name trmbolytics
|
urokinase
streptokinase t-pa reteplase |
|
name an angiotensin II
antagonist |
losartan - oral competitive ang II antagonist
|
|
difference between v. tachycardia after MI, v. tacycardia without structural heart dx ventricular fibrillation
|
v. tachycardia after MI - reentry near rim of healed infarction
v. tachycardia without structural heart dx. DAD triggered by increase sympathetic tone ventricular fibrillation disorganized reentry |
|
dopamine renal vasodilator or constrictor
|
renal vasodilator
|
|
aspirin indications
|
what drug is used for
1. antiplatelet effects 2. antiinflammatory effects 3. MI prophylaxis 4. transients ischemic attacks |
|
class I antiarrhythymics MOA used for?
|
4. selective block of early extrasystoles effects
1. increse ERP 2. class 1a prolongs APD by blockign K+ channels 3. selective depression of conduction in depolarized tissure - bidirectional block used for multifocal premature beats -sustained tachycardia -sustained flutter and fibrillation |
|
side effects include hyperkalemia
|
ACEI
potassium sparing diuretics |
|
indapamide
|
this diuretic is contraindicated in pregnancy
|
|
ventricular tachycardia without structural heart dc
|
acute - b-blocker
verapamil adenosine chronic verapamil and b-blockers |
|
why are calcium antagonists used to treat angina?
|
-mechanism blockage of calcium influx via l-type channels into cardiac and vascular smooth muscle --->
produces decreased contractility, vasodilation, etc ... |
|
chronic Rx
AV nodal reentry treatment (PSVT) |
-verapamil or diltiazem
-b-blockers -digoxin -ablation |
|
renal excretion of digoxin is proportional to glomerular filtration rate
|
pharmacokinetcs of digoxin
|
|
digoxins famous drug interactions
|
-potassium depleting diuretics
-calcium -quinidine -verapamil -amiodarone -erythromycin, clarithromycin -tetracycline |
|
how does nifedipine effect chronic (effort associated) stable angina differently than prinzmetal's variant on vasospastic angina (think MOA)
|
effort associated - nifedipine decreases arterial pressure at rest by dilating peripheral arterioles and decreasing afterload (TPR). THis reduces myocardial O2 consumption.
variant associated - dilates the main coronary arteries + inhibits coronary artery spasm |
|
name prodrugs
|
-mercaptopurine
-fluorouracil -thioguanine -cytarabine cycloplos methotrexate |
|
interactions with cyt p450
|
-metabolized by cyt p450
imatinib p450 biactivation -dacarbazine -tamoxifen |
|
actinomycin D indications
|
-Wilm's tumor, choriocarcinoma
|
|
Topotecan indications
|
advanced ovariaran
cancer + small cell lung cancer |
|
burkitts lymphoma
|
cyclophosphamide
vincristine methotrexate |
|
treat my acute lymphocytic leukemia (ALL)
|
induction: Vincristine
Prednisone doxorubicin maintenance: methotrexate mercaptopurine |
|
which drug is M phase specific?
|
paceitaxel (the spiderman poision, spiderman like Mary Jane)
Vinblastine is also m-phase specific |
|
which drug is s phase specific
|
cytarabine
|
|
which drug blocks cell dividion in the late s-G2 phase of the cell cycles
|
etoposide
|
|
treatment for small cell lung cancer?
|
1. etoposide + PEB
2. Topotecan 3. Paclitaxel |
|
what drugs are used to treat choriocarcinoma?
|
1. methotrexate
2. Dactinomycin or Actinomycin D |
|
What does procarbazine interact with? (2 drug) (drug interaction)?
|
interacts with ethanol for anautabuse rxn
procarbazine is a MAO inhibitors and potentiates drug effects that are MAO substrates |
|
drugs used for osteogenic sarcoma?
|
1. doxorubicin
2. cisplatin 3. high doses of methotrexate (use leucovorin to balance against high doses of methotrexate |
|
primary indications of mercaptopurine?
|
acute lymphocytic leukimia (ALL)
+ acue myelocytic leukemia (AML) |
|
when is mercaptopurine contraindicated?
|
-contraindicated in renal failure
|
|
what compound can be found in high concentrations in smokers urine?
|
radioactive polonium-210
|
|
what compounds are present in second hand smoke?
|
dimethylnitrosamide (DMNA) and nornitrosinicotine carcinogen
|
|
which two drugs need to be activated by cyt p450 to be active (alkylating agents)
|
1. cyclophosphamide
2. dacarbazine |
|
what do thiolated purine analogs do? name two? what type are they?
|
-inhibit glutamine dependent synthesis
-inhibit xanthine oxidase agents - mercaptopurine thioguanine --> guanine analogs |
|
lethal synthesis type I mechanisms?
|
1. type 1: (purine) mercaptopurine + thioguanine
|
|
lethal synthesis type II mechanism?
|
type 2: pyrimidine
5-fluorouracil hydroxyurea |
|
which drugs used in testicular cancer are cell cycle specific
|
-bleomycin - G2
-Vincristine -Etoposide |
|
what is high dose-intermittent therapy called?
what diseases is it especially good for? |
1. pulse therapy - for acute leukemia testicular cancer + Wilm's tumor
2. recruitment therapy |
|
1. burkitts?
|
1. methotrexate + cyclophosphamide
|
|
2. ALL?
|
cyclophosphamide
|
|
3. AML?
|
danuorubicin
|
|
4. Breast cancer?
|
tramoxifen doxorubicin
|
|
5. ovarian?
|
paclitaxel + cisplatin
|
|
6. lung?
|
cisplatin + paclitaxel + docltaxel
|
|
which drug helps shorter neutropenia?
|
1. growth factor G-CSF
|
|
2. which drug(s) affect platelets more than white blood cells for toxicity
|
2. nitrosoureas (cisplatin affects red blood cells more)
most drugs decreased white BC > decreases platelets > decreases RB |
|
treatment options for advanced ovarian cancer
|
1. cisplatin
2. topotecan |
|
dacarbazine side effects
|
hepatic necrosis
|
|
methotrexate indications
1. mercaptopurine indications |
methotrexate ALL, chlorocarcinoma, burkitts, lymphoma, breast cancer
2. ALL + AML |
|
trastuzumab side effects
tamoxifen is metabolized by? |
1. cardiomyopathy
2. tamoxifen is met by cyt p450 |
|
side effects st. cisplatin
|
-nephrotoxicity + ototoxicity
|
|
side effects of imatinib
|
imatinib = hepatotoxicity + edema
|
|
which drugs causes cardiomyopathy as a side effects?
|
trastuzumab (a monoclonal antibody to EGF receptors)
doxorubicin --> causes cardiotoxicity leading to CSF |
|
name 4 plant alkaloids
|
1. Irinotecan
2. topotecan 3. paclitaxel 4. etoposide |
|
which antitumor agents have broad spectrum aplications of solid tumors
|
1. doxorubicin --> solid tumors
2. paclitaxel --> breast, ovarian, bladder, head, neck, small + non-small cell lung cancer |
|
indications for methotrexate?
|
ALL (acute lymphoeytic leukemia
-chlorocarcinoma -burkitt's lymphoma -breast cancer |
|
what's the difference between complete response to chemotherapy, partial respons and muinor response?
|
1. complete --> disappearance of tumor by physiological examination + radiography studies
2. partial --> greater than 50% decrease 3. minor --> greater than 25% but less than 50% decrease |
|
what scales are used to measure performance status in cancer pts?
what do the numbers mean? for what numbers are chemotherapy likely to work? |
ECOG and karnofsky
0 = normal 1= symptomatic 2 = out of bed 3 = in bed > 50% of the time 4 = bedridden Pts with ECOG > 2 have very little chance of responding to therapy |
|
name alkylating agents
|
1. busulfan
2. cyclophosphamide 3. dacarbazine 4. mechlorethamine 5. melphalan 6. nitrosoureas |
|
1. thioguanine MOA?
2. thioguanine can be combined with this drug to give a synergistic effect against /// ? |
1. MOA = inhibits several enzymes in the purine nucleotide pathway, decrease guanine nucleotides interfere with DNA & RNA synthesis
2. combine with cytarabine to treat adult acute leukemia |
|
what is the primary indications for 5-fluorouracil
|
-colorectal cancer
-solid tumor |
|
what is the mechanism of 5-fluorouracil
|
Mechanism of Action: a prodrug that undergoes a complex series of biotransformations to ribosyl and dexoxyribosyl nucleotide metabolites. One of these (FdUMP) forms a covalently bound ternary complex with thymidylate synthase and the reduced folate N5-N10-methylenetetrahydrofolate, a reaction critical for the synthesis of thymidylate. This results in an inhibition of DNA synthesis through a "thymineless death". 5-FU is also converted to FUTP, which is incorporated into RNA, where it interferes with RNA processing & mRNA translation. In addition, 5-FU is converted FdUTP, which can be incorporated into DNA, resulting in inhibition of DNA synthesis & function. Its cytotoxicity is therefore due to effects on both DNA- and RNA-mediated events.
|
|
what is methotrexat activated to
|
Must be bioactivated intracellularly to polyglutamate derivatives, which are selectively retained within cancer cells & have increased inhibitory effects on enzymes involved in folate metabolism, making them important determinants of the duration of action of methotrexate.
|
|
what is the mechanism of drug resistance to methotrexate
|
Drug Resistance: tumor cell resistance has been attributed to: 1) decreased cellular uptake (which may be related to incresed activity of P-glycoprotein), 2) decreased polyglutamate formation, 3) synthesis of increased levels of DHFR through gene amplification, and 4) altered DHFR with reduced affinity for methotrexate.
|
|
what is the similarity and the difference between thioguanine and mercaptopurine MOA
|
thioguanine and mercaptopurine both inhibit DNA and RNA synthesis by inhibiting DNA and RNA synthesis by inhibiting enzymes in the purine pathway
thioguanine - purine nucleotide pathway, decrease GMP mercaptopurine - purien nucleotide interconversion, decrease AMP |
|
the most likely mechanism of drug resistance to cytarabine?
|
increased levels of non-specific phosphatases
|
|
name 2 anthracycline antibiotics
|
1. daunorubicin
2. doxorubicin |
|
3 MO drug resistance to alkylating agents
|
Drug Resistance: Cancer cells can acquire a resistance to alkylating agents by at least 3 mechanisms including: 1) increased ability to repair DNA lesions; 2) decreased permeability to the alkylating drug; 3) increased production of glutathione or increased glutathione S-transferase which catalyzes the conjugation of the drug to gluathione.
|
|
name 2 natrual products used as antitumor drugs
|
1. bleomycin
2. actinomycin D or dactinomycin |
|
what is the difference between leukemia and lymphoma?
|
leukemia: progressive disease of blood forming organs, characterized by distorted proliferation of leukocytes in blood and bone marrow
lymphoma: any neoplastic dissorder of lymphoid tissues |
|
What is the difference between daunorubicin and doxorubicin?
|
danuorubicin: Indications: acute myelocytic leukemia (AML) "only"
Drug: Doxorubicin (Indications: broad spectrum of clinical indications including solid tumors (e.g. breast cancer) and hematoligic malignancies. side effects daunorubicin: Side Effects: dose-limiting myelosuppression & cardiotoxicity doxorubicin: Side Effects: myelosupression and cardiotoxicity including acute transient ECG changes (reversible) and chronic cardiomyopathy leading to the development of congestive heart failure. The development of CHF is related to the cumulative dose taken over time: ~1% at 450-500 mg/m2; ~11% at 500-600 mg/mm2; ~33% at >600 mg/mm2. |
|
name 5 antimetabolites (cancer drugs)
|
1. cytarabine
2. 5-FU 3. Methotrexate 4. Thioguanine 5. Mercaptopurine |
|
what is the difference between vinblastin and vincristine?
|
diff side effects: vincristine : allopecia and peripheral neuropathy
vincristine has a wider spectrum of clinical activity than vinblastine vincristine is used for acute lymphoblastic leukemia (ALL) vincristine is also used to treat hematological malignancies (hodgkin, non-hodkin lymphoma, multiple lymphoma) |
|
what are the two break down products of cyclophosphamide?
|
1. acrolein - break down of aldophosphamide
2. an inactive metabolite (carboxyphosphamide) |
|
what enzyme is responsible for bioactivation
|
--> the enzyme responsible for bioactivation is cyt p450
|
|
what drug is used against kaposis sarcoma?
|
(tumor in connective tissue)
vinblastine |
|
what is a pitfall of using actinomycin D or Dactinomycin to treat wilms tumor choriocarcinoma
what is it's MOA |
/1. a highly toxic drug
2. inhibits transcription resulting in cell death by intercolating into DNA |
|
what alkylating agent is used to treat brian tumors and metastatses?
what other alkylating agent crosses the BBB? |
1. nitrosoureas - penetrate BBB
Busulfan also penetrates the BBB can lead to seizures as a side effect. |
|
5-fluorouracil MOA
what enzyme does 5-fluorouracil inhibit majro SE? |
Mechanism of Action: a prodrug that undergoes a complex series of biotransformations to ribosyl and dexoxyribosyl nucleotide metabolites. One of these (FdUMP) forms a covalently bound ternary complex with thymidylate synthase and the reduced folate N5-N10-methylenetetrahydrofolate, a reaction critical for the synthesis of thymidylate. This results in an inhibition of DNA synthesis through a "thymineless death". 5-FU is also converted to FUTP, which is incorporated into RNA, where it interferes with RNA processing & mRNA translation. In addition, 5-FU is converted FdUTP, which can be incorporated into DNA, resulting in inhibition of DNA synthesis & function. Its cytotoxicity is therefore due to effects on both DNA- and RNA-mediated events.
inhibits target enzyme thymidylate synthetase major SE : myelosuppression |
|
Describe the chenucak structural requirements for carcinogenicity of polycyclic aromatic hydrocarbons (PA)
|
1. compound must be coplanar
2. methyl substitution can enhance or detract from cardiogenicity 3. a plenanthrene nucleus must be present is a tricyclic aromatic hydrocarbon occuring in coal tar 4. Requires bioactivation by cyt p450 to the epoxide form |
|
which one of the following agents can produce hearing loss and removal impairment
a. cisplatin b. nitrogen mustard c. melphalan d. mercaptopurine e. vinblastine |
a. cisplatin
|
|
which of the following cancer chemotherapeutic agents is least likely to exhibit cross resistance to other agents listed?
a. actinomycin D b. doxorubicin c. 6-mercaptopurine d. vincristine e. bleomycin |
c. mercaptopurine is a small molecule. All the others listed are bulky natural products transported out of the cells, adn multidrug resistance phenyotype can confer cross resistance
|
|
which of the following anitcancer drugs inhibit DNA dependate RNA synthesis marks as a result of intercalculation between adjacent guanine cytosine base pain in double standardred DNA?
a. dactinomycin b. flutamide c. methotrexate d. paclitaxel e. vinblastine |
a. dactinomycin binds tightly to double stranded DNA interferes with RNA synthesis
|
|
Which of the following classes of anticancer drugs is used in the treatmetn of this pateint is cell cycle specific and is used in MOPP + ABVD
|
Bleomycin and V+O (plant alkaloids) are cell cycle specific
|
|
What are the side effects of most alkylating agents
|
1. myleosuppression (Busulfan has the most myleosuppresion)
2. GI side effects 3. Nausea and Vomiting |
|
Which cells are susceptibles to alkylating agents
|
1. alkylating agents are not cell cycle specific
2. rapidly dividing cells are most susceptible to alkylating agents |
|
name (2) vinca alkaloids
|
1. Vinblastine
2. Vincristine |
|
EWhat is the only indication of daunorubicin
|
AML only acute myelocytic leukemia
|
|
what type of anti tumor agent is it?
MOA? |
2. anthacycline antibiotic
3. MOA inhibit Topo II intercalcates into DNA, thereby blocking DNA and RNA synthesis |
|
What drugs inhibit the proliferation of human tumor cells that overeexpress HER2
|
Trastuzumab
|
|
which drug(s) inhibit Topoisomerase II?
Which drugs inhibit topo I? |
1. topo II = 1. daunorubicin, 2. doxorubicin 3. etoposide
2. Top I : 1. irinotecan, 2. topotecan |
|
Which alkylating agent is frequently given orally (most are given IV
|
cyclophosphamide
|
|
which drug can be used to treat ALL and AML?
|
mercaptopurine
|
|
what is the difference in MOA between the antimetabolite 5-Fluorouracil, methotrexate, and thioguanine
|
1. Mechanism of Action: a prodrug that undergoes a complex series of biotransformations to ribosyl and dexoxyribosyl nucleotide metabolites. One of these (FdUMP) forms a covalently bound ternary complex with thymidylate synthase and the reduced folate N5-N10-methylenetetrahydrofolate, a reaction critical for the synthesis of thymidylate. This results in an inhibition of DNA synthesis through a "thymineless death". 5-FU is also converted to FUTP, which is incorporated into RNA, where it interferes with RNA processing & mRNA translation. In addition, 5-FU is converted FdUTP, which can be incorporated into DNA, resulting in inhibition of DNA synthesis & function. Its cytotoxicity is therefore due to effects on both DNA- and RNA-mediated events.
2. methotrexate: Mechanism of Action: a folic acid antagonist that inhibits dihydrofolate reductase (DHFR), interfering with the synthesis of thymidylate, purine nucleotides & the amino acids serine & methionine, thereby interfering with the formation of DNA, RNA and proteins. Must be bioactivated intracellularly to polyglutamate derivatives, which are selectively retained within cancer cells & have increased inhibitory effects on enzymes involved in folate metabolism, making them important determinants of the duration of action of methotrexate. 3. Thioguanine: Mechanism of Action: inhibits several enzymes in the the purine nucleotide pathway (denovo purine biosynthesis), resulting in inhibition of nucleotide interconversion (e.g. IMP --> GMP), resulting in a decrease of intracellular guanine nucleotides, interference in DNA & RNA synthesis. |
|
Which cells are susceptible to alkylating agents?
|
1. alkylating agents are not cell cycle specific
2. rapidly dividing cells are most susceptible to alkylating agents |
|
name 2 vinca alkaloids
|
1. vinblastine
2. vincristine |
|
what is the only indication of daunorubicin
|
AML only
|
|
what type of antitumor agent is it
MOA? |
anthacycline antibiotic
3. MOA inhibit TOPO II intercalates into DNA, thereby blocking DNA and RNA synthesis |
|
What drug inhibits the proliferation of human tumor cells that overexpress HER2
|
Trastuzumab
|
|
which drugs inhibit ToPO II
|
etoposide
daunorubicin doxorubicin |
|
What drugs inhibit TOPO I
|
irinotecan
topotecan |
|
which alkylating agetn is frequently given orally (most are given IV)
|
cyclophosphamide
|
|
which drug can be used to treat AML and ALL?
|
Mercaptopurine
|
|
What is the difference in MOA betwene the antimetabolites 5-FU, methohexate, and thioguanine
|
1. 5-FU - thymine less death DNA and RNA effects + Proteins
2. Methotrexate - folic acid antagonists inhibit dihydrofolate reductase DNA, RNA and proteins 3. Thioguanine inhibit enzyme in purine nucleotide pathway , decrease guanine nucleotide |
|
which drug has side effects leading to congestive heart failure?
What are the other side effects of these drugs? |
doxorubicin
other side effecs: myelosuppression cardiotoxicity chronic cardiomyopathy and CHF releated to cumulative dose over tome |
|
Alkylating agent MOA
|
Mechanism of Action: Aklylating agents have a chemical structure that contain a bifunctional nitrogen mustard moiety which includes two reactive alkyl groups (hence the term aklylation). These groups can cyclize in an aqueous environment to form a highly electrophilic "immonium ion" that can covalently bind to any nucleophilic compound, including the N-7 nitrogen position on guanine, which therapeutically is a major site of action. Consequently they can produce a cross-linking of DNA when both akyl groups react with pairs of guanine residues in DNA (intrastrand or interstrand). Crosslinking of DNA ultimately results in breaks of the DNA sequence, and cell death. FWIW: these agents can also react chemically with other cellular components containing nucleophilic groups (sulfhydryl, amino, hydroxyl, carboxyl & phosphate groups). Although aklylating agents are not cell cycle specific, rapidly dividing cells are most susceptible to their effects.
|
|
What is diferent about the MOA of 5-FU compared to methotrexate?
|
5-fu : Mechanism of Action: a prodrug that undergoes a complex series of biotransformations to ribosyl and dexoxyribosyl nucleotide metabolites. One of these (FdUMP) forms a covalently bound ternary complex with thymidylate synthase and the reduced folate N5-N10-methylenetetrahydrofolate, a reaction critical for the synthesis of thymidylate. This results in an inhibition of DNA synthesis through a "thymineless death". 5-FU is also converted to FUTP, which is incorporated into RNA, where it interferes with RNA processing & mRNA translation. In addition, 5-FU is converted FdUTP, which can be incorporated into DNA, resulting in inhibition of DNA synthesis & function. Its cytotoxicity is therefore due to effects on both DNA- and RNA-mediated events.
Methotrexate: Mechanism of Action: a folic acid antagonist that inhibits dihydrofolate reductase (DHFR), interfering with the synthesis of thymidylate, purine nucleotides & the amino acids serine & methionine, thereby interfering with the formation of DNA, RNA and proteins. Must be bioactivated intracellularly to polyglutamate derivatives, which are selectively retained within cancer cells & have increased inhibitory effects on enzymes involved in folate metabolism, making them important determinants of the duration of action of methotrexate. |
|
What two drugs cause mitotic arrest? What is the difference in their mechanism ?
|
1. vinblastin and paclitaxel
2. diffference in mechanism paclitaxel enhances tubulin polymerization vinblastine promotes depolymerization its blastin away all MTs this interferes with chromosome segregation |
|
what drugs can kill cells in all stages of the cell cycle?
|
cisplatin
|
|
what drug can eb given to protect the body from the side effects of cyclophosphamide
|
mensa - the Na+ salts of methylethyl sulfonate can be given to protect the bladder from the toxic effects of cyclophospamide
|
|
allopurinol
|
uricosic agent (adjuvant in Rx of blood dyscrasias
MOA: reduces uric acid syntehsis from purines by inhibiting xanthine oxidase -treatment of pts with blood dyscrasias (leukemia, lymphoma) and other maligancies with cancer chemotherapy resulting from elevated levels of serum purines |
|
G-CSF or Filgrastin
|
-recombinant GCSF
- regulates the production of neutrophils indicatoins: decreases the incidence of infection especially in patients with nonmyeloid malidancies on myelosuppressive drugs -reduce the time to neutrophil recovery |
|
trastuzumab
|
-HER2 is observed in 25-30% of primary breast cancer
-monoclonal antibody to EGF receptor -inhibits the proliferation of human tumor cells that overexpress HER2 -indications for pts with metastatic breast cancer whose tumors overexpress the HER2 protein SE cardiomyopathy |
|
procarbazine
|
-inhibits the syntehsis of DNA, RNA + protein, produces chromosomal breaks
-used in MOPP for Hodgekin's |
|
Tamoxifen
|
Drug Class: Antiestrogen
Mechanism of Action: a competitive partial agonist-inhibitor of estrogen and binds to the estrogen receptor of estrogen-sensitive tumors. It has a 10 fold lower affinity for ER than does estradiol, indicating the importance of ablation of endogenous estrogen for optimal antiestrogen effect. Indications: Exteremly effective useful for: 1) treament of both early-stage and metastatic breast cancer, 2) as a chemopreventative agent in women at high risk for breast cancer; 3) treatment of endometrial cancer. |
|
cyclophospamide
|
Drug Class: Antineoplastic (Alkylating Agent)
Indications: One of the most widely used alkylating agents. A broad spectrum anticancer drug that can be given alone, but is more commonly given in combination with other drugs (e.g. CHOP, CAF or CMF). Major indications include non-Hodgkin's lymphoma, leukemias, multiple myeloma, breast & ovarian cancer. Side Effects: Hemorrhagic cystitis occurs occasionally (& common side effects listed above). Mensa (Na salt of methylethylsulfonate) can be given to protect the bladder from the toxic effects of cyclophosp |
|
rituximab
|
Drug Class: Monoclonal Antibody
Mechanism of Action: a genetically engineered chimeric murine/human monoclonal IgG1 (human Fc) antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The CD20 antigen is expressed on > 90% of B-cell non-Hodgkin's lymphomas. The mechanism of action includes complement-mediated lysis, antibody-dependent cellular cytotoxicity, and induction of apoptosis in the malignant lymphoma cells. This drug appears to be synergistic with chemotherapy for lymphoma. Indications: therapy of patients with relapsed or refractory B cell non-Hodgkin's lymphoma. |
|
cisplatin
|
Mechanism of Action: an inorganic metal complex that kills cells in all stages of the cell cycle, inhibits DNA synthesis, and binds DNA through the formation of interstrand cross-links similar to other alkylating agents. The primary binding site is N7 of guanine, but may form covalent interactions with other nucleotides. Platinum complexes appear to synergize with certain other anticancer drugs (cisplatin is the P in PEB drug combinations).
Indications: testicular carcinoma, breast, ovarian & bladder cancer. SE: Nephrotoxicity and Ototoxicity |
|
Imatinib
|
Drug Class: Antineoplastic "designer drug"
Mechanism of Action: an inhibitor of the tyrosine kinase domain of the Bcr-Abl oncoprotein. Imatinib prevents the phosphorylation of the kinase substrate by ATP. (see Notes below). Indications: treatment of chronic myelogenous leukemia (CML). Side Effects: hepatotoxicity, edema, fluid retention. tyrosine kinases associated with the platelet-derived growth factor receptor, stem cell factor and c-kit are also inhibited by Imatinib. |
|
Bleomycin
|
Drug Class: Antitumor Peptide
Mechanism of Action: bleomycin is a small peptide that contains a DNA binding region & an iron-binding domain at opposite ends of the molecule. It acts by intercollating into DNA & reacts with ferous ions (Fe2+) to produce free radicals that cause DNA fragmentation, resulting in single & double strand breaks, and inhibition of DNA biosynthesis. Bleomycin is a cell-cycle specific drug that causes accumulation of cells in the G2 phase of the cell cycle. Indications: Hodgkin's disease , Non-Hodgkin's lymphoma, testicular carcinoma Side Effects: little myelosuppression (unusual for antineoplastics), and as a result it can be combined with other drugs that do produce myelosuppression (e.g. BACOP, ABVD, PEB). Lung toxicity drug interactions - metabolized by cyt p450 |
|
compare drug mechanism of antimetabolites vs. anticancer antibiotics
Name them |
antimetabolites: compete for utilization of normal metabolites
1. mercaptopurine - exhibits feedback inhibition of all purine biosynthesi and incroporated into DNA 2. thioguanine - inhibits enzyme sin purine synsthesis pathways 3. 5- Fu - inhibits thymidylate synthase anticancer antibiotics --> inhibit nucleic acid synthesis by blocking DNA replication of transcriptions |
|
what is the advantages of ifosfamide over cyclophosphamide?
Who contains a phenylalanine? |
ifosfamide --> hemorrhagic cystitis --> cyclosphosphamide analog
--> melphalan |
|
The m is MOPP is for ...
toxicities you forget - secondry 1. bleomycin 2. cisplatin 3. cyclophosphamide 4. Etoposide 5. Mercaptopurine 6. Paclitaxel |
m is for mechlorethamine
1. alopecia 2. ototxicity, BMS 3. Alopecia 4. alopecia 5. GI disturbances 6. peripheral neuropathy + alopecia |
|
which alkylating agent causes profound myelosuppression in all patient ?
|
busulfan
|
|
differences in mechanism between irinotecan and imatinib?
|
irnotecan - topo I inhibitor
used for colonorectal cancer imatinib - inhibits tyrosinekinase domain of Bcr-Abl oncoprotein -used for CML |
|
when do you use intermittent, high dosing?
|
1. drugs acting on all phases fo the cell cycle
b. tumors in which a majority of cells are actively proliferating c. toxicity effects schedule |
|
Two reason to give a drug contious infusion or with frequent dose administration?
|
1. drug is rapidly metabolized or excreted
2. drugs are phase specific + act only on one potion of the cell cycle |
|
what chemical mediator is responsible for nausea + vomiting? why? which drugs produce this effects?
|
serotonin interacts with there receptors in the chemoreceptors trigger zone to produce vomiting
dacarbazine, doxorubicin, high dose cyclophosphamide nitrogen mustard, dactinomycin |
|
what are three major toxicities of bleomycin
|
1. acute pneumonitis
2. pulmonary fibrosis 3. oxygen toxicity |
|
1. drugs causing nephrotoxicity
2. drugs that cause neurotoxicity |
1. cisplatin - acute renal failure
2. methotrexate - acute tubular necrosis neurotoxicity - vinca alkaloids = peripheral neuropathy |
|
most important side effects of
1. adriamycin 2. methotrexate 3. cyclophosphamide |
1. adriamycin - cardiotoxicity
2. methotrexate - cirrhosis of the liver 3. cyclophosphamide - hemorrhagic cystitis |
|
what side toxicities (i.e. what other cells) does chemotherapy effect?
|
chemotherapy effects rapidly proliferating cells, therefore chemo effects gastrointestinal mucosa hair follicles and bone marrow
|
|
what type of anticancer drug most commonly causes alopecia
|
rapid turn over of hair follicles
alkylating agents etoposides authracyclines (doxorubicin), dactinomycin, and the vinca alkaloids |
|
what is another name for adriamycin
|
doxorubicin
|
|
define doubling time
define growth fraction tumors most susceptible to a chemotherpay curve have a high or low growth fraction |
1. doubling time - time required for a neoplasm to double its cell numbers
2. growth fraction - the fraction of cells actively proliferating 3. high |
|
explain log kill & log kill hypothesis
|
chemotherapeutic agents: work by first-order kinetics - the drugs kill a constant fraction of tumor cells rather than a fixed # of cells
log kill --> the killing of a fraction f cells rather than an absolute number. in adjuvant chemotherapy --> concept remove detectable tumor (109) the body removed eradicates remaining cells |
|
why is combination chemotherapy used?
Examples |
- use drugs with different mechanisms of action and or which act on different phases of the cell cycle to delay the development of resistanct cells and to maximize cell kill
-MOPP + PEB -choose drugs with differing non-overlapping toxicities. |
|
1. adjvant chemotherapy
2. neoadjuvant chemotherapy |
1. chemotherapy used in addition to another treatmment modality, such as surgery or radiotherapy witht he goal of eridacting micrometastasis prevent relapse
2. neoadjuvant - use chemotherapy prior to surgery or radiation - organize reduce load |
|
Why do we use bone marrow transplant in chemotherapy patients
|
we can't give high enough doses of chemo therapy drugs b/c of myleosuppresion
by getting a bone marrow transplant resure allows us to give a higher previously lethal doses of chemotherapy by allowing means to repopulate the bone marrow |
|
3 type of bone marrow transplant
|
allogenic - bone marrow from an HLA matching donor transfer to another pts
autologous: graft individual marrow to himself collect before remission --> give after peripheral stem cell transplants = harvest progenitor cells by plasma-pharesis |
|
what immunotherapy can be used to help cancer pts with infections
|
1. BCG
2. Interferons 3. Interleukin-2 4. Differentiating agent retinoids 5. monoclonal antibodies 6. amgiogenesis inhibitors |
|
Describe the three steps in the progession from DNA damage to cancer
|
initation: DNA damage
promotion: cell with DNA damage encounters (often chemical) incourage cell multiplication + cell division) progession = developing tumor becomes malignant |
|
list regiments
1. hodgekins 2. non-hodgekins 3. testicular carcinoma 4. AML 5. ALL 6. CML |
list regiments
1. hodgekins = ABVD or MOPP 2. non-hodgekins = CHOP and BACOP 3. testicular carcinoma = PVB 4. AML = Cytarabine 5. ALL = MOPP 6. CML |
|
A cancer cells that is resistant to the effects of both vincristine + methotrexate probably has developed that resistance
a) changes in the properties of the target enzymes b) decreased activity of an activing enzyme c) increase in expression of p-glycoprotein transporter d) Increase in proteins that are involved in DNA repair e) increase in production of drug trapping molecules |
c) p-glycoprotein transporters more foreign cells (increased expression)
|
|
what drug cause significant peripheral neuropathy
|
vincristine
|
|
what is a complete carcinogen
|
drug containing both a initiator and a prometer
|
|
which drugs are safe to be given intrathecally to treat meningial + brain cancer
|
1. cytarabine
2. methotrexate |
|
what are the three classes of chemotheraoy? and give examples
|
class 1: non-cell cycle dependent
e.g. radiation, mechlorethamine, carmustine class 2: phase specific e.g. cytarabine (s phase), bleomycin (G2/M) class 3: Kill proliferating cells prefrentially to resting cells (non0cell cycle specific ) e.g. cyclophosphamide, dactinomycin, 5- FU |
|
What do you ave to do if you are giving an s-phase specific or G2/M phase specific drugs? Why? which ones?
|
cytarabine + bleomycin
b/c they affect only a small proportion of the cells population at a given time they are often given at very frequent intevals or by continous infusion |
|
treat my breast carcinoma
|
cyclophosphamide , methortrexate, cyclophosphamide + doxorubicin = fluorouracil or paclitaxel . doxorubicin + paclitaxel, Tamoxifen
|
|
wHAT TWO ALKYLATING AGENTS ARE used to treat multiple myeloma ?
What is the benefit of one over the other? |
multiple myeloma = mechlorethamine
melphalan The advantage of melphalan over, mechlorethamine is that it is less carcinogen |
|
Treat my non-Hodgkins Lymphoma
|
BACOP (Bleomycin, Doxorubicin, cyclophosphamide, vincristine, prednisone)
CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone) |
|
What drug is used to treat Wilm's tumor?
|
Actinomycin D or Dactinomycin + Vincristine
|
|
What compounds are good for cancer prevention
|
1. BHA + BHT in cereal promote glutathione, which destroys dangerous electrophiles
2. Antioxidants are good - destroys free radicals that might damage DNA 3. Differentiating agents promote differeentiation |
|
what is common of many carcinogen?
|
1. Many needs to be bioactivated by cyp-450 to be carcinogen in the body
most are prodrugs externally most carcinogens are activated to reactive, electrophilic compounds |
|
Which alkylating agent is used primarily to treat Hodgkin's disease?
What are the side effects? |
1. Dacarbazine in combination with other drugs (bleomycin can also be used)
2. side effectss - hepatic necrosis (MOPP + ABVD) (Bleomycin SE = lung toxicity and some myelosuppression) |
|
treat my hodgekins
|
MOPP (Mechlorethamine, vincristine, procarbazine, predisone)
ABVD (Doxorubicin, bleomycin, vinblastine, dacarbazine |
|
DOC and secondary drugs for testicular cancer
|
1. Etoposide + PEB (Cisplatin + etoposide + bleomycin)
2. Bleomycin |
|
What is the primary drugs used to treat colorectal cancer? other choices
|
1. irinotecan with 5-FU & leucovorin
2. Irinotecan by itself if 5-FU is ineffective |
|
Compare drug used for
1. acute myelogenous leukemia? 2. chronic myelogenous leukemia ? |
1. AML --> cytarabine + daunorubicin + mercaptopurine
2. CML --> Imatinib (treatment) Busulfan + cyclophosphamide --> a conditoning regement used before cell transplantation |
|
What is the DOC for AML?
a secondary drug choice used? |
daunorubicin + cytarabine
1. cytarabine is the DOC. It inhibits DNA polymerase, & blocks DNA synthesi. Cytarabine can be incorporated into DNA and RNA and leads to chain elongation interference 2. 2nd drug: mercaptopurine |
|
what drugs do you give to treat chronic myelogenous leukemia (CML)
What drugs do you give as a condition regimen prior to cell transplant |
1. give busulfan (conditioning regiment)with cyclophosphamide
2. imatinib = treatment |
|
a chemopreventative agent for women at high risk for breast cancer?
|
tamoxifen
|
|
1. paclitaxel MOA
2. what semisynthetic analog of paclitxael is approved for a second-line therapy therapy of various cancer |
MOA: a mitotic spindle poision that binds microtubules & enhances tubulin polymerization. M-phase specific
uses: breast, ocarian, bladder, head and neck , small cell lung cancer. 2. docetaxel |
|
a competitive partial agonist - inhibitor of estrogen used for early-stage and metastatic breast cancer?
|
tamoxifen
|
|
what is another name for F-CSF?
|
What is another name for filgrastin?
|
|
Antibody that binds to the CD20 antigen formal on B lymphocytes
|
Rituximab
|
|
What phase is cytarabine most active against?
2. What is the mayor indications for cytarabine? 3. cytarabine MOA? 4. What's special about its pharmacokinetics? |
1. cytarabine is s phase specific
2. acute myelogenous leukemia (AML) 3. competitively inhibits DNA polymerase incorporate into DNA strands leading to chain termination 4. metabolized rapidly, must be given by continous infusion |
|
regulates the production of neutrophils
|
G-CSF or Filgrastin
|
|
CMF -->
COP --> |
COP - cyclophosphamide, vincristine, prednisone
CMF - cyclophosphamide, methotrexate, fluorouracil |
|
name the disease?
abnormal chromosomal translocation that results in the formation |
--> CML
non-hodgkins --> rituximab |
|
i have renal problems are macrolides, safe for me?
|
yes. b/c biliary excretion
|
|
name 4th generation cephalosporin + list incations
|
cefepime - better for gram negative bacteria (lower MIC values) active against enterobacter
|
|
can erythromycin be used systemically?
for meningitis? |
1. non, not absorbed
2. no, doesn't cross the BBB |
|
macrolides should not be used in ----
|
HIV or cancer patients, no immunocompromised pts - need better drugs
|
|
macroide MOA
|
inhibits translocation step
|
|
how are macrolides excreted?
|
biliary + fecal
|
|
name 3rd generation cephalosporins
|
-cefotaxime
-ceftriaxone -ceftazidime |
|
what is special about 3rd generations cephalosporins
|
-penetrate the CSF (useful for meningitis)
-also active against gram negative bacilli |
|
carbapenem MOA
|
imipenem is structurally related to b-lactam antibiotics
|
|
can macrolides be used for bilary infections?
|
yes b/c high [] in bile
|
|
what are extended & broad spectrum penicills more effective against _ why?
|
-gram negative bugs b/c of an enhanced ability to penetrate the gram negative outer membrane
|
|
side effects of cephalosporins
|
hypersensitivity
|
|
hypersensitivity to penicillin
what don't use? what do you use? |
Don't use cephalosporins
use vancomycin |
|
meningitis
|
penetrates CSF
3rd gen ceph and ceftriaxone |
|
penicillins MOA
|
-bind and inactivating PBPs inhibits transpeptidation reaction and block cross-linking of the cell walls cell wall tysis results b/c of high internal osmotic pressure inactivation of the inhibitor of autolysins
|
|
penicillinase resistant penicillins MOA
|
same as pen G + resistant to B-lactamase
|
|
repository penicillins
|
penicillins G procaine -
IM + adequate serum levels for 12 hours penicillin G benzathine -IM adequate serum levels for 1 month |
|
anaerobic infections in boxes + joints (B. fragilis)
|
clindamycin penetrates into bones and joints
|
|
what are the two major advantages of extended & broad specrum penicillins?
|
1. inactivated by B-lactamase
2. greater activity against gram negative bugs |
|
benefits of fourth gen ceph
|
-greater activity against organisms (lower MIC)
- active against enterobacter -more resistant to b-lactamase |
|
clindamycin MOA
|
binds 50 s ribosomal subunits inhibits peptidyl transferase no more peptide
|
|
MRSA - vancomycin resistant I have staph or strep
|
streptogramins (combo drugs)
|
|
multi drug resistant gram + cocci
|
streptogramins
|
|
steptogramins MOA? USes?
|
-proteins synthesis inhibitor
-used for staph + strep when vancomycin resistant _ MRSA multidrug resistant gram + cocci |
|
are they oral? macrolides
|
yes
|
|
which drug side effects cardiac arrhythmias
|
erythromycin
|
|
what is a toxicity of erythromycin and clarithromycin but not azithromycin
|
interaction with cyp-p450
|
|
legionnaires
|
macrolide erythromcyin
|
|
streptomcyin
|
old, mainly used for tuberculosis
|
|
what type for meningitis?
bacteriostatic? or bacteriocidal? |
-cidal
|
|
list aminoglycosides
|
-gentamycin
-netilmycin -amikacin -tobramycin -streptomycin |
|
-vancomycin
toxicities |
-nephrotoxicity
-phleboscelerotic (vein enlargement) -ototoxicity (hearing loss) |
|
two reasons to use vancomycin
|
-pts allergic to penicillin (especially for endocarditis)
- indications --> b-lactamases producing MRSA |
|
why shoudl you be carful about administering vancomycin (CWI) with an aminoglycoside
|
hard on renal b/c renal excretion + similar toxicity
nephrotoxicity and ototoxicity |
|
how is vancomycin excreted?
|
renal
|
|
side effect of fast administration of vancomycin
|
hypotension, red man syndrome from histamine release
|
|
2nd line of defense from staph infection + strep ?
3rd? last? |
1. penicillinase resistant penicillins
2. clindamycin 3. streptogramins 4. linozolid |
|
lifethreatening bacterium
|
3rd generation ceph and aminoglycoside
|
|
klebsiella UTI
|
1st generation ceph, cephalexin and cefaclor
|
|
typhoid fever, samonella, and typhoid
|
ceftriaxone is DOC
ampicillin is used in the 3rd world (cheap) |
|
main use of ceftriaxone
|
meningitis
|
|
meningicocal meningitis
|
ceftriaxone
|
|
meningicocal bacteriamia use ...
|
use 3rd generation ceph ceftriaxone
|
|
difference between 1st and 2nd generation cephalosporins
|
increased activity against gram negative bascillae, greater stability against b-lactamase inactivation
|
|
used for surgical prophylaxis
|
cefazolin
|
|
in general --> UTIs are resporatory infections -->
|
Use 1st generation cephalosoporins, cephalexin or cefazolin
|
|
UTI Klebsiella pneumoniae
|
cephalexin
|
|
To treat pneumonia Klebsiella pneumoniae respiratory infections
|
Ans. use piperacillin (mega penicillins) or better yet or better yet use a 1st generation cephalosporins - cephalexin or cefazolin
|
|
which penicillin are susceptibles to B-lactamases and which aren't
|
ans. all susceptibles
|
|
ceftriaxone
|
-drug choice for gonorrhea
-parentarlly long half-life |
|
Why is the use of CWSI with aminoglycosides synergistics
|
CWSI breaks down cell walls, making it easier for amino glycosides to penetrate even gram + cocci with staph infections
|
|
i have a serious infection life threatening
|
synergistics combination CWSI + aminoglycosides
|
|
what are cephalosporins ineffective against
|
enterococci --> use penicillins
|
|
can you use 3rd generation cephs to treat staph or strep
|
no, use penicillinase resistant penicillins
|
|
cefaclor
|
-oral
-h. influenza |
|
aminoglycoside MOA
|
bind 30s ribosome inhibit protein synthesis
frozen @ elongation step miscoding results if made |
|
resistance to aminoglycosides MOA
|
acylation
adenylation decreased drug uptake |
|
why are aminoglycosides ineffective against anerobes? Which ones?
|
bacteroides fragilis closterium
need oxygen for oxygen dependant active transport process |
|
which aminoglycoside is least resistant
|
amikacin
(b/c less ways to activate) |
|
aminoglycoside toxicity
|
nephrotoxicity + irreversible + ototoxicity
|
|
what can aminoglycosides not be used for?
|
gram positive anaerobes strep pneumonia
|
|
aminoglycosides cross BBB?
|
no don't cross BBB
not useful for meningitis |
|
where do aminoglycosides distribute
|
small vd
vd = 1/4 of body weight b/c vd is all extracellular fluid - doesn't distribute into tissues |
|
pseudomonas aeruginosa
|
ceftazidime (can't use carbenicillin b/c of b-lactamase)
|
|
if B-lactamase is present use --
|
-use carbapenems (imipenem/ cilastatin)
- or cephalosporin |
|
treat my staph aureus infection
|
use penicillinase resistant penicillins - oxacillin, cloxacillin, dicloxacillin
|
|
treat my strep infection
|
use a macrolide like erythromycin
|
|
cephalexin
|
-oral
-esp klebsiella pneumonia -relatively stable against b-lactamase -for gram + except enterotococci |
|
UTI with pseudomonas with B-lactamases
|
cephedrine (3rd)
|
|
what is penicillin G active against?
inactive against? |
active against gram negative cocci (gonococci + meningococcus and al gram + bacteria)
inactive against : gram negative bascilla (gram negative rods) |
|
name gram + rods
|
staph aureus + streptococcus
|
|
what are cephalosporins not generally used for?
|
enterobacter (except cefepime) and staph aureus and strep
|
|
GI infection from bacteroides fragilis
|
ticarcillin
|
|
staph aureus is a ...
|
gram + cocci
|
|
I am a streptococcus, I am a ---- bacterian
|
gram + cocci
|
|
oral cephs
|
-cephalexin
-cefprozil -cefaclor whad do they have in common? |
|
do aminoglycosides work in pelvic infections
|
no, use cefoxitin
|
|
pelvic infection likely bacteria?
antibiotic treatment? |
b. fragilis anaerobic
use cefoxitin for abdominal + pelvic infections |
|
1 have gonorrehea, give me an antibiotic
|
or cefoxitin possibly or amoxicillin + clauvanic acid possible
ceftriaxone |
|
antibiotic used to treat anaerobic infections
|
use cefoxitin
|
|
tonsilitis
|
use amoxicillin if B-lactamase use clauvalinic acid
|
|
BAD side effect of clindamycin
|
can lead to superinfection overgrowth
|
|
excretion - clindamycin - okay in renally compromised
|
renal and biliary
yes, can be used in renally compromised |
|
These drugs ending in -udine are this type of drug
one drug ends with -iridine, what type of drug is it? What about uridine? |
-uridine - NRTI = lamvudine, stavudine, zidovudine
-iridine - delavirdine - NNRTI (non-nucleoside reverse transcriptatse inhibitor) -uridine - thymidine analogs |
|
what does probenecid do?
|
probenicid blocks the secretory pump which for instance can inhibit the rapid ecretion of Pen G by the renal acid secretory mechanism
|
|
MOA of nucleoside reverse transcriptase inhibitors NRTI
|
-competitively inhibits HIV-1 reverse transcriptase & can be incrorporated into the growing viral DNA chain to cause DNA chain termination. Each requires intracytoplasmic activation as a result of phosphorylation by cellular enzymes to the triphosphate form
|
|
differences between NRTIS and NNRTIS
|
NRTI - compete with nucleoside triphosphates require intracellular activation to be active
NNRTI - do not compete with nucleoside triphosphates, do not require phosph to be active resistance to NNRTIs is generally rapid |
|
non-nucleoside reverse transcriptase inhibitors (NNRTIS)
|
MOA: NNRTIs bind directly to a side on the HIV-1 RT, resulting in blockade of the RNA and DNA dependent DNA polymerase activities. The bidning side is near to but distinct from that of the NRTI
|
|
common side effects of NNRTI
|
- drug hypersensitivity
-seriou possibly life-threatening skin rashes. (Steven-Johnson syndrome can occur) |
|
pyrophosphate analog MOA
name that pyrophosphate |
MOA : an inorganic phosphate compound that inhibits
1. viral DNA polymerase 2. RNA polymerase 3. HIV reverse transcriptase (competes for the pyrophosphate binding = "Fos"carnet is a pyrophosphate |
|
which drugs inhibit Peptidyl transferase?
|
Clindamycin and chloramphenicol
|
|
herpes simplex (Acyclovir resistant)
|
Foscarnet
|
|
CMV DOC + alternative
|
ganciclovir + valganciclovir
alternatives: Foscarnet + vidarabine |
|
Herpes simplex (encephalitis) DOC + alternative
|
acyclovir and vidarabine
|
|
which antifungals penetrate the CSF?
|
fluconazole
flucytosine "flu" gets to your head man all the other antifungals such |
|
dermatophyte infection DOC and second line of defense
|
griseofulvin then ketoconazole
|
|
antifungals that interact with cyt p450
|
griseofulvin - induces Cyt p450
ketoconazole - inhibits mammalian cyt p450 |
|
which drugs are fungicidal
which drugs are fungiostatic? |
fungicidal - polyene antifungals - amphotericin B and nystatin (azoles can reach fungicidal effect at high concentrations)
fungistatic - azoles - ketoconazole , itraconazole, fluconazole, fluycytosine, griseofulvin, caspofungin |
|
systemic candida treatment
|
-amphotericin B + flucytosine
2nd line of defense - Fluconazole |
|
what are the pharmacokinetics advantages of fluconazole?
|
1. oral bioavailability
2. good CSF penetration - cna be used for meningitis 3. has fewer hepatic interacting a wide therapeutic index and permitting aggressive dosing |
|
which antifungal has antiandrogenic side effects? what are other side effects?
|
ketoconazole
1. hepatoxicity 2. hypersensitivity - anaphylaxis 3. antiandrogenic effect (lower testerone effect) |
|
name 3 NNRTIS
|
1. nevirapine
2. delavirdine 3. efavirenz |
|
name nucleoside reverse transcriptase inhibitors (NRTIS)
|
1. Lamivudine
2. Didanosine 3. AZT 4. Stavudine 5. Abacavir |
|
AZT zidovudine
|
-antiretroviral , NRTI
-deoxythymidine analog for HIV 1 infections -avoid giving with other myelosuppressive drugs |
|
what drugs cause myelosuppresion> or bone marrow suppression?
|
1. myleo - common SE for NRTIs - zidovudine, didanosine, lamivudine, stavudine (ganciclovir, ribavirin)
2. BMS - vidarabine (purine analog) antiviral |
|
imipenem
|
-used as a last resort not used for common infections
-rapidly metabolism in the kidneys -highly resistant against B-lactamase -a carbapenem used against staph aureus, streptococcus, gram - cocci + anaerobes |
|
flucytosine
|
-converted to F-dUMP + FUTP, which inhibit DNA and RNA synthesis
-narrow spectrum -for serious infections caused by candid and cryptococcus -not good in patients without renal function oral only |
|
DOC for clostridium perfringens - type of bug?
|
peniciillin G
gram positive bacilli |
|
DOC for penicilin resistant infections
|
vancomycin + ceftriacxone + rifampion + levofloxocin
|
|
DOC for streptococcus pneumonia (pneumococcus
|
penicillin G or Penicillin V
|
|
DOC for escherichia coli? type of bug?
|
ceftriaxime, ceftizoxime, ceftriaxone, ceftazidime, or cefepine
enteric gram negative baascilla |
|
DOC for proteus mirabilis? type of bug?
|
ampicillin
enteric gram negative bascillae |
|
DOC for proteus, indole positive (includes proteus vulgaris) type of bug?
|
cefotaxime, ceftizoxime, ceftriaxone, ceftazidime, or cefepine
enteric gram negative bascili |
|
DOC for salmonella typhi
type of bug? |
ceftriaxone or a fluoroquinolone
|
|
DOC for Haemophilus influenzae?
1. meningitis, epiglotitis, arthritis, and other infections 2. upper respiratory infections and bronchitis |
1. cefotaximine or ceftriaxone
2. Trimethoprim -sulfamethoxazole |
|
DOC for pseudomonas aeruginosas? UTI
Type of bug? |
ciprofloxacin
enteric gram negative bascillae |
|
DOC for pseudomonas pseucloniallel?
Type of bug? |
ceftazidime
gram negative bascillae |
|
ketoconazole
|
SE : causes torsades de pointes
MOA: impairs the synthesis of ergosterol (a component of cell membranes) -poor penetration into the CSF -causes fatalities -contraindicated when terfenadine and astemizole are administered together. -inhibits mammalian cytp450 |
|
pseudomonas aeruginosa
|
piperacillin or carbenicillin, ceftazidime
Taz like pseudo mona |
|
common SE fo NRTIS
|
1. myelosuppresion, including neutropenia and severe anemia
2. lactic acidosis and severe hepatomegaly |
|
give me a drug to treat herpes simplex keratitis
|
idoxuridine or trifluridine given in eye drops
vidarabine will also work |
|
pseudomonas aeruginosa
|
carbenicillin (if no B-lact)
ceftazidime if B-lactamase |
|
H. influenzae - no B-lactamase
yes B-lactamase |
1. no B-lact = ampicillin
2. yes B-lact - Ceftriaxone or cefaclor |
|
b. fragilis
|
ticarcillin
cefoxitin |
|
what spectrum does ampicillin have not covered by pen g?
|
-covers e coli, proteus mirabilis, H. influenza
|
|
antacids + H2 antihistamines interferes wtih ___ 's bioavailability
|
ketoconazole
|
|
antifungals contraindicated in pregnancy
|
griseofulvin - because of teratogenicity
|
|
varicella-zoster (DOC + alternate)
|
acyclovir
alternate - foscarnet |
|
differentiate between ganciclovir + valgancicloir in terms of therapeutic indications
|
ganciclovir : DOC for CMV (cytolomegalovirus)
valganciclovir: prodrug used primarily for CMV retinitis in immunocompromised pts and transplant pts (retinitis - inflammation of the retina) |
|
Interferons alpha MOA
|
- a polypeptide cytokine
MOA: activates ribonucleases, which degrade viral mRNA - blocks protein synthesis by inhibiting the translation initiation complex, resulting in suppression of the new viral particle generation |
|
Ribavirin MOA -
|
- a synthetic triazine riboside analog, has a two prong effect
- converted intracellularly to 5' triphosphate derivative which inhibits viral RNA polymerase -also inhibits capping of viral mRNA at the 5' position |
|
cryptococcal (fungal) meningitis DOC treatment and prophylaxis
|
-fluconazole - secondary prophylaxis
-flucytosine - used with amphotericin B for cryptococcal meningitis why good? b/c both F's penetrate the BBB |
|
DOC for oropharyngeal candida
|
fluconazole
2nd line of defense : nystatin or ketoconazole |
|
hypokalemia and hypomagnesemai are side effects of which antifungal drugs?
|
amphotericin B
|
|
8 drug sthat work on anaerobes
|
1. clindamycin
2. piperacillin & mezlocillin (extended spectrum) 3. ticarcillin 4. metronidazole 5. penicillin G 6. cefoxitin 7. chlroamphenicol 8. imipenem |
|
SE of flucytosine administration
|
-dose dependent bone marrow suppression
neutropenia, thrombocytopenia, and anemia |
|
I have complete renal failure and I'm allergic to penicillin, give me a drug
|
macrolides
clofaximine |
|
which antiviral does not require activation to block DNA polymerase actiivty?
|
foscarnet is a trisodium salt of phosphonoformate
It completes for pyrophosphate binding side on DNA polymerase and blocks cleavage of the pyrophosphate group rom nucleotides during DNA synthesis |
|
I need a drug for respiratory syncytial virus
|
RSV - use ribavirin
|
|
Antivirals with CNS toxicity side effects
|
amantadine
some rimantadine, ganciclovir |
|
antivirals with drug interactions with zidovudine (AZT)
|
-Acyclovir
-Valganciclovir -Interferon alpha |
|
avoid drug interactions with nephrotoxic drugs (Antivirals)
|
Foscarnet - avoid aminoglycosides amphotericin B)
Valganciclovir |
|
Drug interactions with probenecid (antiviral)
|
-acyclovir, valacyclovir
-valganciclovir |
|
Drug interactions with coricosteroids (antiviral)
|
vidarabine
|
|
oral second generation cephalosporin active against B-lactamase producing H. influenza, primarliy used for sinusitis otitis and lower respiratory tract infections
|
cefprozil
|
|
gram + penicillinase producing staphylococci infections
|
1. use cloxacillin or dioxacillin (oral)
2. if severe use parental admin of oxacillin or nafcillin |
|
drugs to treat B fragilis
|
-ticarcillin
-cefoxitin |
|
Drug used to treat pseudomembranous colitis?
What is pc? |
Vancomycin
(pseudomembranous colitis associated with the use of clindamycin, due to an overgrowth of clostridium difficile |
|
treat staphylococcal enterocolitis , streptococcal or enterococcal endocarditis
|
-use vancomycin
|
|
what enzyme converst valganciclovir to ganciclovir?
|
stomach esterases
|
|
antivirals
-iv administration only? -subcutaneously only? -topical only? |
IV - foscarnet + vidarabine + ganciclovir
subcutaneously - interfereon alpha topical - Idoxuridine + trifluridine (thymidine analogs) |
|
I have Hep C , what durg combination would you give me?
|
ribavirin with interferons alpha-2beta
|
|
interferon alpha-2 b
|
-antiviral, antihepatitis virus B and C
-MOA - a recombinant cytokine with a host of antiviral properties = inhibits RNA and DNA viral replication =activates ribonucleases that degrade mRNA =inhibits translation initiation complex -DOC for Hep B and Hep C SE flu like symptoms |
|
acyclovir
|
-not effective against CMV
-antiviral, anti-herpes and varicella zoster virus - an acyclic guanosine derivative that causes DNA chain termination, inhibits the viral DNA polymerases by preventing chain elongation -CI DOC for herpes zoster (shingles) and recurrent genital herpes (HSV-2). HSV-encephalitis and varicella zoster |
|
what's the difference between acyclovir and valacyclovir?
|
valacyclovir is a prodrug activated by stomach acid, acyclovir is just eh drug
acyclovir can be used for herpes encephalities and varicella zoster, they both work for herpes zoster and genital herpes |
|
what si the difference between ganciclovir and valganciclovir
|
1. valganciclovir - can be used in transplant pts in addiiton to immunocompromised pts
-valganciclovir to produg of ganciclovir, oral administration results in higher plasma levels 2. different side effects (ganciclovir causes bone marrow toxicity, myelosuppresion, and CNS toxcitiy) Valganciclovir hematologic dysfunction + renal function impariment |
|
zidovudine
|
-AZT
-Antiretroviral, NRTI -a deoxythymidine analog -HIV infections (give with HAART) -avoid concurrent myelosuppresion |
|
drug of choice for enterobacter?
type of bug |
imipenem
enteric gram negative bugs |
|
Drug: Chloramphenicol
|
Drug Class: Antibiotic (wide spectrum & bacteriostatic)
Mechanism of Action: Binds to 50S ribosomal subunit and inhibits peptidyl transferase and blocks protein synthesis Indications: Used outside of the United States. Side Effects: Bone marrow suppression and idiosyncratic aplastic anemia. Gray baby syndrome. Superinfection. |
|
sulfonamides MOA
|
Mechanism of Action: Competitively inhibit incorporation of para-aminobenzoic acid (PABA) into dihydropteroic acid, a precursor of folic acid. Bacteriostatic. Resistance can occur due to decreased drug uptake, altered target enzyme and escape mechanism by alteration in cell permeability.
|
|
Which drugs bind ot eh 50s ribosomal subunit
|
chloramphenicol
macrolides azithromycin clindamycin |
|
which drugs bind to the 30 s subunit
|
aminoglycosides
tetracyclines |
|
ciprofloxacin
|
Mechanism of Action: Interference with the activity of DNA gyrase Bactericidal. Chromosomally mediated acquired resistance.
Indications: Methicillin susceptible and methicillin resistant strains of Staph. aureaus, Streptococcus. Side Effects: GI (nausea & vomiting), CNS (mainly at high concentrations), skin reactions, cartilage toxicity and joint swelling in children, tendonitis (not recommended in pregnant woman and infants < 8 yr old). |
|
amantadine
|
Drug Class: Antiviral, anti-influenza-A virus
Mechanism of Action: Interferes with uncoating of the viral RNA of influenza A within infected host cells, thus preventing viral replication. Clinical Indications: A Prophylactic DOC for influenza-A virus. Is not as effective if taken after viral infection. Contraindications: Contraindicated in pregnancy due to teratogenic effects in animals. |
|
name two non-specific anti-influenza A and B
|
zanamivir and oseltamivir
|
|
sulfonamides are contraindicated, when?
|
newborns
during the last two months of pregnancy |
|
foscarnet
|
Clinical Indications:A DOC for acyclovir resistant HSV or VZV infections. Alternative drug against CMV infections.
Major drug Interactions: Nephrotoxic drugs (e.g. aminoglycoside, amphotericin B, pentamidine). |
|
What is the HAART and why do we use it?
|
Highly Active Antiretroviral Therapy. A cocktail of 3 or 4 drugs used to produce a more effective reduction in plasma HIV as well as an increase in CD4 cell counts. Typical drug combinations include 2 "acceptable" NRTI's plus either an NNRTI or a PI.
Note: Not all NRTI's can be combined to produce adequate antiviral efficacy, e.g. don't combine stavudine with zidovudine (see below). |
|
DOC for neisseia meningitis (meningococcus) type of bug?
|
penicillin G
gram negative cocci |
|
DOC for neisseria gonorrhoeae (gonococcus)
what type of bug? |
ceftriaxone
ciproflozacin gram negative cocci |
|
DOC for clostridium difficle
type of bug? |
metronidazole
gram positive bacilli |
|
DOC for klebsiella pneumoniae?
Type of bug? |
cefotaximine, ceftizoxime, ceftriaxone, ceftazidime, or cefapime
enteric gram negative bascila |
|
zanamivir
|
Drug Class: Antiviral, anti-influenza virus (A and B)
Mechanism of Action: Inhibits influenza neuraminidase which blocks the cellular release of the virus particle Clinical Indications: Treatment of acute uncomplicated influenza A and B (oral inhalation). |
|
which enzyme activates ganciclovir, valganciclovir, valacyclovir, and acyclovir (guanosine analogs)
|
viral thymidine kinase (TK)
|
|
what does the ending -dine indiccate? Name two drugs with this ending and indicate their MOA
|
-dine indicates a thymidine analog
-antiviral thymidine analgos are idoxuridine and trifluridine Mechanism of Action: Tri-fluoro thymidine analog, activated intracellularly to tri-phosphates which then inhibit DNA polymerases. |
|
Name two thymidine analogs (2)
|
idoxuridine and trifluridine
|
|
name a purine analog
|
vidarabine
|
|
name guanosine analogs
|
acyclovir, valacylovir, ganciclovir, valganciclovir
|
|
what is the difference between oseltamivir and zanamivir?
and what aer they classified as? |
zanamivir is orally inhaled with no systemic absorption
Oseltamivir is administrered orally and is readily absorbed 2. they are both non-specific anti-influenza anti-virals that block neuroamidaze |
|
rimantadine
|
Mechanism of Action: Interferes with uncoating of virus
Indications: Prophylactic for influenza-A virus. Preferred over amantadine due to lower CNS toxicity & increased metabolism. Contraindications: Contraindicated in pregnancy due to teratogenic effects in animals. -prefered over amantatdine because of less CNS toxicity |
|
why is rimantadine prefered over amantadine as a prophylactic
and what is it a prophylactic for? |
less CNS toxicity than amantadine
prophylactic for influenzae-A |
|
which drugs can treat CMV? cytolomegalovirus
which drugs cannot be used against CMV? MOA for drugs (2)? |
1. CAN - ganciclovir and valganciclovir -alternative is foscarnet
2. CANNOT - acyclovir cannot be used 3. MOA - DNA chain termination also inhibtis viral DNA polymerase |
|
name two anti-influenza A antivirals (specific)
|
amantadine and rimantadine
|
|
ribavirin
|
Drug Class: Antiviral, anti Respiratory Syncytial Virus (RSV).
Mechanism of Action: A triazine riboside analog. Converted intracellularly to a 5'-triphosphate derivative that inhibits viral RNA polymerase and capping of viral mRNA at the 5' position. Clinical Indications: Used as an aerosol DOC for treating infections by the respiratory syncytial virus (RSV) and as a DOC in combination with Interferon-alpha-2b for hepatitis-C virus infection. |
|
what is the difference between idoxuridine and trifluridine?
|
Idoxuridine can eb incorporated into viral DNA, resulting in faulty DNA and the inability of the virus to infect tissue and reproduce
Both are topically applied but trifluridine is the DOC for the topical treatment of HSV keratitis and is used to treat cutaneous infections by acyclovir resistant HSV strains |
|
trifluridine
|
-antiviral, antiherpes, HSV 1 and 2
-phosphyorylated to trifluoro thymidine analog which then inhibit DNA polymerase -DOC for topical treatment of HSV Keratitis and cutaneous infections by acyclovir resistant strains of HSV - topically applied in eye drops ophthalmic preps |
|
MOA for non selective (A+B) antiinfluenza virus
|
zanamivir and oseltamivir are anti-influenza virus antivirals
MOA - blocks virus particle release and aggregation -inhibits influenza neuraminidase |
|
vidarabine
|
-purine analog, antiviral, antiherpes simplex virus (HSV 1 and 2
-purine analog is phosphorylated and activated intracellularly which inhibits DNA polymerase activity SE toxicity = bone marrow toxicity |
|
name two guanosine prodrug analogs
name two guanosine analogs |
prodrugs : valacyclovir + valganciclovir
regular drug: acyclovir and ganciclovir |
|
name two non-specific influenza anti-virals
|
zanamivir and oseltmavir
|
|
which antifungals can be used to treat candida fungi
|
nystatin & flucytosine
difference: flucytosine has diff mechanism and also inhibits cryptococcus |
|
amphotericin B
|
-selective fungal effect - binds to ergosterol in the cell membrane with a resultant change in permeability allowing leakage of intracellular components
infusion related toxicity and slower onset of toxicity IV admin |
|
What is a pharmacokinetic advantage of administratering fluconazole compared to itraconazole or ketoconazole
|
it has fewer hepatic enzyme interactions and the widest therapeutic index, therefore you can aggressively dose
|
|
SE of amphotericin B
|
Infusion - related toxicity: fever chills, muscle spasm, vomiting, headache & hypotension
slower onset of toxicity: some degree fo renal damage If above > 4 g cucmulative |
|
which antifungal agent has a large impact on mammalian cells? What is the drug interactions
|
ketoconazole
(some mammalian cell toxicity if high concentration of amphotericin B -inhibit mammalian cyt p450 |
|
what is special about fluconazole that is not true of itraconazole or ketoconazole
|
-fluconazole crosses the BBB, and is therefore the azole of choice int eh treatment and secondary prophylaxis of cryptococcal meningitis
itraconazole + ketoconazole have poor CSF penetration |
|
what are the three mechanisms of action for antifungal agents?
name examples from each type |
1. binds ergosterols or sterols in the cell membrane results in a change in membrane permeability and leakage of intracellular components e.g. amphotericin B and nystaitin
2. prodrug gets converted to FUTP& FdUMP which inhibits RNA and DNA synthesis e.g. flucytosine 3. inhibit cyt-p450 dependant synthesis of ergosterol, a vital coponent of cell membranes e.g. ketoconazole, itraconazole and fluconazole |
|
what is the difference between nystatin and amphotericin B?
|
roughly the same mechanism but
amphotericin B has selective fungal effects, amphotercin B binds to ergosterol, resulting in a change in membrane permeability (leaky intracellular contents). Nystatin binds to sterols in also not effective against bacteria, protozoa, viruses, wheras amphotericin B has a broad spectrum |
|
which drugs inhibit cyt p450?
which drugs inhibits induces cyt p450 |
inhibit - erythromycin, clarithromycin & ketoconazole
-induce rifampin |
|
name 2 synergistic drug combinations and explain why they are synergistic
|
-CWSI + aminoglycosides --> CWSI weakens cell wall allowing easier penetratition penetration by aminoglycosides
-trimethoprim + sulfa drugs (block two steps in the synthesis of folic acid, which bacterial cells need |
|
alterative drugs in patients with a history of severe (anaphylatic) penicillin allergry
|
-aztreonam
-macrolides -vancomycin -clindamycin |
|
drugs contraindicated in pregnancy + children
|
-tetracycline (bone growth retardation, teeth stain)
-fluoroquinoles (cartilage toxicity) -thalidomide (teratogenic birth defects) -metronidazole (mutagenic & carcinogenic potential) -chloramphenicol (gray baby syndrome) -sulfonamides (contraindication in new borns + late) - amantadine -rimantadine |
|
what drug is associated with gray baby syndrome
|
chlorampheniol (infant doesn't make enough glucoronyl transferase )
|
|
mupirocin
|
topical antibacterial
MOA: inhibit isolucyl tRNA synthetase Indication : topical treatment of minor skins infections, such as impetigo, also indicated for intranasal application for elimination of methicillin-resistant s. aureus |
|
1. whcih produgs and drug guanosine analog are used to treat HSV (herpes simplex virus) and VZV (varicella zoster virus)
2. prodrugs and drug used to treat HSV and CMV cytomegalo virus |
1. acyclovir and valacyclovir
2. ganciclovir and valganciclovir |
|
1. route of administration for ZORA
2. which has a different administration |
1. ORAL MAN!
2. zanamivir has oral inhalation |
|
nitrofurantoin
|
urinary antiseptic
lower urinary tract infection --> exerts antibacterial activity in urine but little systemic antibacterial action |
|
what is the one drug that ends in -avir but is not an antiretroviral protease inhibitor?
what type of drug is it? |
abacavir
it is an NRTI antiretroviral nucleoside reverse transcriptase inhibitor |
|
antiviral that cause bone marrow toxicity?
that cause serious nephrotoxicity |
-idoxuridine + trifluridine
high doses of interferon alpha -vidarabine -ganciclovir foscarnet: serious nephrotoxicity |
|
antiviral with severe teratogenic effects?
|
-Amantadine + rimantadine
-ganciclovir -ribavirin |
|
the side effects of this antiviral are flu-lke symptoms
|
interferon alpha used for hepatitis B and C infections
|
|
side effects if fatal dysfunction such as pancreatitis, sepsis, and multiple organ failure
|
valganciclovir
|
|
difference between (doxcyclin + minocyclin) and tetracycline
|
-doxycyclin and minoccline are more lipophilic therefore they have alonger serum 1/2 life
-they are give 1X day -eliminated biliary route --> treat biliary infection contrast : tetracyclin = 2X day + renal elimination |
|
what are doxycyclin and minocyclin NOT useful for?
|
UTIs
|
|
what interferes with tetracyclin absorption and why?
|
calcium or magnesiu, salts in antacids chelate tetracylins forming an insoluble complex metal
|
|
can tetracyclins be used to treat meningitis
|
no, tetracyclins do not cross the BBB
|
|
can chloramphenicol be used to treat meningitis caused by H. influenzae
|
yes, bacteriocidal effects against H. influenzae
b/c highly sensitive at low concentration |
|
how is chloramphenicol metabolized?
|
metabolized by hepatic metabolism via the enzyme glucuronyl transferase
--> puts glucuronic acid olecule @ hydroxyl group of chloramphenicol --> more polar --> more elimination |
|
which organisms are sensitive to chloramphenicol
|
-clostridium perferingens
-bacteroides -h influenzae |
|
are fluoroquinolenes bacteriostatic or bacteriocidal
|
bacteriocidal inhibits DNA gyrase
|
|
what should not be taken concurrently with fluoroquinoles? why?
|
don't take antacids
they reduce bioavailability of fluoroquinoles |
|
can fluoroquinoolones be used for prostatitis?
for meningitis |
yes - concentrates in prostate
no-does not cross the BBB |
|
enterobacter
|
-imipenem
-2nd line, 3rd gen cephs and carbenicillin |
|
DOC for staph
|
1. pen G
2. penicillinase producing if MRSA 3. vancomyin or cephalosporins (1st gneration) if allergic rxn --> vancomycin or fluoroquinolones (oral, better) |
|
can fluoroquinolones be used on anaerobes ? which ones?
|
no ineffective against clostridium and bacteroides
|
|
indications for fluoroquinolones?
|
UTI with gram-organisms
STDs gonorrhea - gonococcal organisms are b-lactamase prodrugs |
|
fluoroquinolone side effects
|
-GI discomfort
-CNS toxicity -cartilage toxicity -long QT elongation (like erythromycin) |
|
c. difficle
|
metronidazole
|
|
therapeutic indications of metronidazole
|
anaerobes
closterium difficle closterium perfringes bacteoides h. pylori |
|
do sulfonamides cross the BBB?
|
yes crosses the BBB
|
|
how are antifungial drugs delivered
|
lysomes are used to carry antifungal drugs directly to the infections site which reduces cellular toxicity
|
|
what fungal species are typically seen in HIV patients?
|
-candidiasis, cyptococcosis + histoplamosis
-opportunisitc fuckers |
|
toxicity of protease inhibitors
|
1. dyspepsia, nausea, vomitting, diarrhea
2. insulin resistance, glucose intolerance, diabetes mellitus 3. hyperlipidemia: hypertriglyceridemia, hyperchlolesterolemica 4. liver toxicity |
|
antiretroviral drug interactions
|
1. PI+ NNRTI - liver metabolized
ritonavir = PI-booster 2. NNRTI induces + nevirapine induce + inhibits efavirenz (e.g. ritonavir + saquinavir) |
|
feever + confusion : pts has dental disease with history of heart murmur no penicillin allergy, echocardiogram shows vegitatins on the calcified aortic arch
|
ampicillin and gentamicin
|
|
symptoms: urinary frequency, dysurea, low grade fever, pyuria and bacilli
|
sulfamethoxazole + trimethoprim
|
|
fever , pumlent wound drainage with gram + cocci 5 days post-colostomy for diverticular abscess
|
ampicillin and gentamicin
|
|
symptoms and severe headache rigid neck, sensitivity to bright lights
|
symptoms of meningitis
use 3rd gen ceph ceftrioxone |
|
most suitable for a pts with renal insufficiency
1. chlortetracycline b. demedocycline c. doxycycline d. methacycline e. oxytetracycline |
doxycyline
|
|
dentist is going to remove toooth in patient with abnormal heart valve
|
ampicillin
|
|
prostatic infection
|
trimethoprim
|
|
which two bacteria cannot be treated by aminoglycosides and why?
|
B. fragilis and clostridium their anaerobic
|
|
didanosine
|
-deoxyadenosine analog
antiretroviral, NRTI -fatal & non-fatal pancreatitis -myelosuppression, neutropenia, severe anemia, lactic acidosis + severe hepatomegaly |
|
which antivirals when activated inhibit DNA polymerases?
inhibit RNA polymerase? inhibit both |
DNA polymerase:
idoxuridine (thymidine analog) vidarabine (purine analog) RNA polymerase ribavirin - riboside analog foscarnet (HIV reverse transcriptast) |
|
ganciclovir and valganciclovir
MOA: indications, major drug interactions |
MOA: activated by tK, inhibits viral DNA polymerases. Produces DNA chain termination
CI: DOC for CMV retinitis in immuno-compromised patients SE: can results in organfailure, sepsis, etc. fatal dysfunction |
|
which antiviral inhibits RNA polymerase instead of DNA polymerase?
|
ribavirin acts on RNA polymerase insterads of DNA polymerase
|
|
which antivriral acts on DNA polymerases, RNA polymerase and HIV reverse transcriptase
|
foscarnet
|
|
metronidazole
|
-ANTIPROTOZOAL and antibacterial against anaerobes
-selective for bacteria and protozoa -forms nitro anion radical and hydroxylazine which binds with DNA causing single strand breaks. Bacteriocidal -contraindicated in pregnacy -SE: GI discomfort, metallic taste, disulfiram like reactions |
|
pharmacokinetics of sulfonamides
|
metabolism of hepatic acetylation
|
|
side effects of sulfonamides ]
name sulfonamides and the drug they are administered with |
SE: stevens johnson syndrome, hemolytic anemia, kernicterus (a toxic encephalopathy in infants)), contraindicated in new borns and last two months
2. sulisoxazole, sulfamethoxazole, and pregnancy, trimethoprim, administered with |
|
sulfonamides MOA
|
use of sulfamethoxazole clinically is in combination with trimethoprim in a 5:1 ratio, known as cotrimoxazole, trimethoprim is an inhibitor of dihydrofolate reductase and provides a sequneital blockade of synthesis of tetrahydrofolate
|
|
aminoglycosides-how excreted?
|
renal
|
|
salmonella typh in bile duct
|
ans. ampicillin, why? ampicillin achieves high [] in bile ducts
|
|
enterobacter UTI
|
carbenicillin (not covered by ampicillin + amoxicilllin)
|
|
when would you use carbenicillin instead of amoxicillin & ampicillin
|
pseudomona & enterbacter UTI
|
|
therapeutic indications for aminoglycosides
|
-UTI pseudomonas
-prophylaxis for endocarditis -primarily for gram negative bugs -when combined with CWI - uses --> staph, strep, viridans, MRSA, enterococcal |
|
i'm going in for surgery - need surgery prophylaxysis but allergic to penicillin
|
vancomycin
|
|
gram + bascilla (rods)
|
-anthrax
-castilium perfringens -castilium difficle |
|
pharmacokinetics of aminoglycosides (3 things)
|
1. administered only in a hospital with therapeutic monitoring must monitor co
2. minimal metabolism 3. extracellular distribution |
|
vancomycin MOA
|
vancomycin inhibits peptidoglycan synthase thereby inhibiting cell wall cross linking
peptidoglycan synthase - brings peptidoglycans outside membrane cross-linking |
|
pharmacokinetics of vancomycin
|
-parental
-can be given orally to treat for local GI tract infection because not absorbed |
|
when is oral vancomycin used?
|
i have a growth of c difficule in my GI tract
|
|
not useful against gram negative
|
what is vancomycin not useful for
|
|
MRSA
|
-use penicilllin resistant penicillins
cephalosporins don't work |
|
macrolide toxicity
|
GI upset esolate salt of erythromycin causes cholestatic jaundice
-cyp450 inhibit (not azithromycin) |
|
advantage of clarithromycin over erythromycin
|
-respiratory infections more effective against gram negative
-h. influenza -MAC mycobacterium avium complex in HIV patients |
|
erythromycin macrolide indications
|
1. upper respiratory with staph and strep
2. legionnaires 3. alternative to penicillin hypersensitive pts |
|
pen V
|
first oral penicillin
|
|
which penicillin is often combined with clavulanate acid and why?
|
ticarcillin - we combine for inhibition of b-lactamases
|
|
plasma mediated alteration of binding site
|
macrolide mech of resistance
|
|
erythromycin
|
drug used in colonrectal surgery b/c no absorption
|
|
clindamycin crossess BBB?
|
no, no, meningitis
|
|
alternative prophylaxis for endocarditis
|
clindamycin
|
|
bacterial endocarditisi use
|
1st generation ceph like cephalexin or cefazolin
or penicillin G benzatnin |
|
i have siphilus, give me an antibiotic
|
ceftriaxone
|
|
antibiotic for abdominal surgical operations
|
use cefoxitan
|
|
gram positive rod
|
anthrax is a ...
|
|
gram + rod
|
clostilum difficile is a ...
|
|
gram negative cocci
|
gonococcus & meningococcus
|
|
castilium perfringens is a ...
|
gram + rod
|
|
what type of bacteria is meningococcus?
|
gam negative cocci?
|
|
gram negative cocci
|
what type of bacteria gonococci
|
|
list extended and broad spectrum penicillins
|
-ampicillin
-amoxicillin -carbenicillin -ticarcillin -piperacillin |
|
PEN G is adminstered
|
IV or IM (parental)
|
|
what are three isoxazole penicillins?
|
oxacillin, cloxacillin, dicloxacillin
|
|
penicillinase resistant penicillins name them
|
methicillin (not used clinically)
isoxazole penicillins naficillin |
|
h. influenzae respiratory infections
|
ampicillin or amoxicillin
|
|
2 carbapenems
|
imipenem
cilastatin |
|
name a monobactam and what is it used for?
|
aztreonam active against gram negative rods
|
|
first generation cephalosporins
|
cephalexin
cefazolin |
|
second generation cephalosporins
|
cefoxitin
cefaclor cefprozil cefuroxime axetil |
|
infection with castilium perfringens
|
pen G
|
|
UTI with pseudomonas
|
carbenicillin or cephedrine (3rd genration), can't use amoxicillin or ampicillin
|
|
infections with pseudomonas no b-lactamases
|
carbenicillin
|
|
pneumonococcal pneumonia use
|
cephalexin
|
|
difference between penicilins and cephalosporins
|
penicilins are effective against enterococci, cephalosporins don't work on enterococci
|
|
h. influenza with b-lactamaze resistnat what is no longer useful and what do you use?
|
cefaclor
|
|
proteus mirabilis UTI
|
ampicillin and amoxicillin
|
|
e coli UTi
|
ampicillin or amoxicillin (extended spectrum)
|
|
reflex tachycardia
|
non selective alpha 1 and alpha 2 blockers
b2 agonists |
|
phenylephrine
|
a1 agonist
|
|
hypertension treatment
|
ace inhibitors
b blockers diuretics |
|
clonidine
|
a2 agonist (antihypertensive)
|
|
albuterol
|
B2 agonist
|
|
Terbutyline
|
B2 agonist
|
|
dobutamine
|
b1 agonist
|
|
doxazosin
|
long activng a1 selective blocker
|
|
ends in sin
|
alpha 1 selective blocker
|
|
treatment of pheochromocytoma
|
phentolamine or pehnoxybenzamine (nonselective irreversible alpha 1 and alpha2 blocker)
|
|
methoxamine
|
alpha one agonist
|
|
Reserpine
|
antihypertensive
SE+ suicidal tendencies inhibitor of catecholamines vesicular uptake transporter resulting in depletion of neuronal catecholamine stores, decreased CO, decreased PVR |
|
imipramine
|
antidepressant
-tricyclic amine blocks repuptake of norepinephrine serotonin |
|
edrophonium
|
-anticholinesterase
-short and rapid-acting diagnosis of myasthemia gravis & whenever need curare antagonist for cholinergic reactions |
|
methyldopa
|
-antihypertensive
-alpha 2 agonist prodrug -lowers arterial pressure decrease false neurotransmission |
|
phenoxybenzamine
|
alpha non-selective antagonist
irreversible binder, binder, binds convalently vasodilator for pheochromocytoma for hypertension |
|
propranolol
|
nonselective beta blocker
block b1 & B2 competitive for hypertension arrhytmias angina prevents sudden death + reinfarction & migraine |
|
guanethidine
|
antihypertensive, adrenergic neuron-blocking agents
4 - mech -> tyramine-like, reserpine-like cocaine-like, betrylium-like |
|
alpha blockers
|
terazosin
tamsulosin doxazosin prazosin |
|
yohimibine
|
alpha 2 blockers
increased sympathetic outflow increased bp, no clinical role |
|
antihypertensive
|
reserpine, bretylium, guanethidine, methyldopa, prazosin, clonidine
|
|
prazosin
|
alpha 1 bocker antihypertensive
not accompanied by reflextachy cardia |
|
phenylephrine
|
synthetic alpha, agonist, vasal constriction, nasal decongestion, pressor agent, maintain bp
|
|
bretylium
|
-antihypertensive & antiarrhythmics
-interferes with release of catecholamines for attempted resentation from vfib |
|
Terbutaline
|
b2 adrenergic agonist prevent bronchospasm in pts with asthma
SC administration |
|
doxazosin
|
alpha selective blocker
once a day dosing |
|
succinylcholine
|
-nicotinic cholinomimetic and NMJ blocker (depolarizing type)
uses: adjunct to general anesthesia contraind: genetic disorders of pseudocholinesterase from history of malignant hyperthermia |
|
dopamine
|
low dose d, intermed b, increases HR, high d1 = vasoconstriction including renal
for: shock due to ML, septic, surgery, with MAOI lasts longer |
|
phentolamine
|
non-selective alpha antagonist blocks alpha 1 &2 - leads to tachycardia IM or IV
|
|
physostgmine
|
-reversible cholisterase inhibitor
-to reverse effects upon CNS caused by toxic doses of drugs -crosses BBB |
|
tubocurarine
|
-nondepolarizing neuromuscular blocking agent
- muscle relaxant during surgery for setting fractures & dislocations -most likely to cause histamine release |
|
ipratropium
|
-antimuscarinic (like atropine)
-treatment of bronchospasm associated with asthma, COPD -inhalation, aerosol, - a local site specific effect |
|
origin of preganglionic parasympathetic
|
craniosacral
|
|
sympathetic
|
thoracolumbar
|
|
trimethaphan
|
-nondepolarizing ganglionic blockers, + doesn't cross BBB
-blocks nicotinic receptor for hypertnsive emergencies & discesting aortic aneurysim SE= cyclopegia, decrease BP and increase HR decrease GI |
|
zerostygmia
|
dry mouth - symptoms of atropine salivary glands are blocked
|
|
side effects of nicotinic antagonists
|
orthostatic hypertension postural hypertension, urinary retension, sexual dysfunction
|
|
metoprolol
|
b1 selective blocking agent
for hypertension + angina ectoris following abrupt cessation of therapy |
|
cocaine
|
-CNS stimulant blocks monamines reuptake channels
-blocks Na channels + cardiac K |
|
tyramine
|
indirect acting sympathomimetic
-MAO I prolongs affects -cocaine blocks reuptake dopamine in fermented food cheese and beer |
|
ephedrine
|
direct + indrectly act sympath
-dierect a + B indirect tyramine like -diet supression, bronchodilator |
|
what's in a dense core vesicle
|
NE, DOP, dop B-hydroxylase,
chromaranin ATP loop b-hydronon converts DOP --> NE |
|
isoproterenol
|
nonselective Beta agonist B1, B2
for heart blocker or cardiac arrests SE: tachycardia |
|
CNS effects
|
sedation, confusion, ataxia, (decreased pathway), loss of reflex, slurred speech, convulsion
|
|
angiotensin II
|
vasoactive peptide a potent pressor agent
|
|
atropine
|
-preanesthetic medication
- to restore cardiac rate and arterial pressure during anesthesia -muscarinic blockers |