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598 Cards in this Set
- Front
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subclasses of diuretic drugs
|
1. osmotic diuretics 2. carbonic anhydrase inhibitors 3. loop diuretics 4. thiazide diuretics 5. potassium sparing diuretics
|
|
thiazide diuretics drugs
|
chlorothiazide and hydrothiazide
|
|
thiazide diuretic site of action
|
secreted into PCT, inhibit Na and Cl reabsorption in DCT
|
|
use of thiazide diuretics
|
mainstay drug to tx hypertension (HT)
|
|
side effects of thiazide diuretics
|
hypokalemia, hyperuricemia, hypercalcemia, hyperglycemia, hyperlipidemia
|
|
loop diuretic drugs
|
furosemide
|
|
site of action of loop diuretics
|
secreted in PCT, acts on ascending loop
|
|
action of loop diuretics
|
inhibit reabsorption of Cl and Na-K-Cl transporter
|
|
uses of loop diuretics
|
most effective natriuretic and diuretic agents available
|
|
clinical indications for loop diuretics
|
1. CHF 2. edema 3. HT
|
|
side effects of loop diuretics
|
hypokalemia
|
|
K-sparing diuretics drugs
|
spironolactone
|
|
site of action of K-sparing drugs
|
DCT and collecting duct
|
|
action of K-sparing drugs
|
competitive antagonist of aldosterone
|
|
use of K-sparing drugs
|
in combo w/ thiazides or loops to prevent hypokalemia
|
|
side effects of K-sparing drugs
|
hyperkalemia
|
|
ACE inhibitor drugs
|
lisinopril
|
|
mech of action of ACE inhibitors
|
decrease angiotensin II prod by inhibiting the converting enzyme
|
|
use of ACE inhibitors
|
tx HBP in cases that also involve CHF, HA, and chronic kidney failure
|
|
side effects of ACE inhibitors
|
dry cough, angioedema and hyperkalemia
|
|
contraindications of ACE inhibitors
|
2ND AND 3RD TRIMESTERS OF PREGNANCY
|
|
angiotensin II receptor blocker drugs
|
losartan and valsartan
|
|
mech of action of angiotensin II receptor blockers
|
block angiotensin II receptor (AT1)
|
|
use of angiotensin II receptor blockers
|
similar to ACE inhibitors (HT pts w/ left ventricular hypertrophy, diabetic nephropathy)
|
|
side effects of angiotensin II receptor blockers
|
similar to ACE inhibitors but cough and angioedema are less common
|
|
contraindications of angiotensin II receptor blockers
|
2ND AND 3RD TRIMESTERS OF PREGNANCY
|
|
subclasses of anti-lipid drugs
|
1. bile-acid binding resins 2. inhibitors of cholesterol absorption 3. inhibitors of VLDL secretion 4. inhibitors of cholesterol synthesis
|
|
bile acid-binding resin drug
|
cholestyramine
|
|
mech of action of bile acid-binding resin
|
interfere w/ enterohepatic cycline of bile acids which decrease prod. of cholesterol in liver
|
|
use of bile-acid binding resin
|
adjunctive therapy for primary hypercholesterolemia, biliary obstruction, diarrhea
|
|
why does bile-acid binding resin have a weak effect when used alone
|
due to compensatory cholesterol synthesis mechanisms
|
|
bile-acid binding resins used to relieve symptoms of what
|
biliary obstruction
|
|
side effects of bile-acid binding resins
|
GI: constipation, abdom pain/distension, ↓ absorption of fat-soluble drugs (ADEK) and minerals
|
|
inhibitors of cholesterol absorption drugs
|
ezetimibe
|
|
mech of action of inhibitors of cholesterol absorption
|
inhibits intestinal absorption fo dietary/biliary cholesterol
|
|
uses for inhibitors of cholesterol absorption
|
lower LDL, increase HDL
|
|
which has more GI side effects: inhibitors of chol absorp or bile acid-binding resins
|
bile acid-binding resins
|
|
contraindications for inhibitors of cholesterol absorption
|
liver failure (drug ↑ liver enzymes in defected liver)
|
|
inhibitors of VLDL secretion drug
|
niacin
|
|
use for inhibitors of VLDL secretion
|
adjunct therapy to diet modification
|
|
side effects of inhibitors of VLDL secretion
|
flushing, GI upset, hepatoxicity
|
|
inhibitors of cholesterol synthesis drugs
|
simvastatin and atorvastatin
|
|
mech of action of inhibitors of cholesterol synthesis
|
competitively block HMG-CoA reductase: ↓LDL, ↓VLDL, ↓TAGs, ↑HDL
|
|
most effective anti-lipid drug, first line of therapy for primary hyperlipidemia
|
simvastatin/atorvastatin
|
|
uses for inhibitors of cholesterol synthesis
|
1. most effective anti-lipid 2. ↓major coronary events 3. used w/ niacin to ↑HDL and decrease LDL
|
|
side effects for inhibitors of cholesterol synthesis
|
GI, liver enzymes, headache
|
|
precautions/contraindications for inhibitors of cholesterol synthesis
|
liver disease, women in pregnancy and breast feeding, children under 8yrs
|
|
centrally acting sympatholytic drug
|
clonidine
|
|
site of action of clonidine
|
CNS a2-adrenoceptor agonist
|
|
mech of action of clonidine
|
lowers sym outflow, ↑vagal tone thereby ↓CO and TPR
|
|
use of clonidine
|
2nd or 3rd line drug choice for ↓BP and in hypertensive crisis
|
|
side effects of clonidine
|
compensatory H2O and Na retention, sedation, drowsiness, rebound HT of drug w/drawal, dry mouth, constipation, sex dysfunction
|
|
a-adrenoceptor blocker drugs
|
prazosin, terazosin, doxazosin
|
|
mech and site of action of a-adrenoceptor blockers
|
block a1 receptors and cause dilation of As and V's, act in CNS to ↓ sym tone
|
|
a-adrenoceptor blockers more effective when used in comvo w/ what
|
other antihypertensive drugs (b-blockers and hypertension)
|
|
a-adrenoceptor blockers used in pts w/:
|
1. resistant (refractory) HT 2. prostatic hypertrophy 3. CHF
|
|
side effects of a-adrenoceptor blockers
|
CV: orthostatic hypotension, CNS: headache, dizziness, fatigue, GI: nausea, ab pain, sex dysfunction
|
|
b-adrenoceptor blocker drugs
|
cardioselective: atenolol, metoprolol
|
|
mech of action of b-adrenoceptor blockers
|
↓CO by blocking b1, block b1 adrenoceptor-mediated renin release, may have sympatho-inhibitory actions
|
|
uses of b-adrenoceptor blockers
|
tx mild-mod HT, w/ diuretics to further control BP, w/ vasodilator to prevent compensatory response in cardiac and renin release stimulation
|
|
use of sodium nitroprusside
|
drug of choice in hypertensive emergencies management
|
|
compensatory response for b-blockers
|
marked tachycardia, H2O retention and salt retention
|
|
side effects of b-blockers
|
related to metabolism of drug: cyanide → thiocyanate (liver)
|
|
toxicity of accumulation of cyanide
|
excessive hypotension, metabolic acidosis, arrhythmias, death
|
|
toxicity of thiocyanate:
|
weakness, disorientation, psychosis, muscle spasms, convulsions
|
|
Ca channel blockers effects
|
antianginal, antiarrhythmic, dilate peripheral arterioles and ↓BP
|
|
mech of action of Ca channel blockers
|
inhibition of Ca influx into arterial smooth muscle cells
|
|
Ca channel blocker drugs
|
nifedipine, amlodipine, verapamil, diltiazem
|
|
all local anesthetics are...
|
vasodilators, except cocaine
|
|
mode of metabolism and incidence of allergy in local anesthetics are determined by
|
chemical comp: ester or amide?
|
|
what happens to local anesthetics as MW and lipid solubility increase?
|
1. become more potent 2. prolonged binding to Na channel 3. more toxic in systemic circ
|
|
ester type locals
|
1. procaine 2. tetracaine
|
|
amide type locals
|
1. lidocaine 2. mepivacaine 3. bupivacaine
|
|
short/long acting ester type locals
|
short: procaine, long: tetracaine
|
|
short/long acting amide type locals
|
short: lidocaine, moderate: mepivacaine, long: bupivacaine
|
|
duration of action of locals determined by
|
retention at site of admin
|
|
termination of locals dependent upon
|
tissue blood flow
|
|
toxicity of locals determined by
|
plasma concentrations
|
|
principal determinant of rate of absorption of local anes into systemic circ is
|
blood flow at site of admin
|
|
how do vasoconstrictors prolong duration of action of LAs
|
reduce rate of systemic absorption
|
|
slower systemic absorption of LAs ↓ plasma drug concentrations which also reduces what toxicity
|
CV and CNS toxicity
|
|
are vasoconstrictors more effective in prolonging action of short acting or long acting LAs?
|
short (procaine and lidocaine)
|
|
metabolism of ester LAs
|
by plasma esterases
|
|
metabolism of amide LAs
|
in liver
|
|
subclasses of diuretic drugs
|
1. osmotic diuretics 2. carbonic anhydrase inhibitors 3. loop diuretics 4. thiazide diuretics 5. potassium sparing diuretics
|
|
subclasses of diuretic drugs
|
1. osmotic diuretics 2. carbonic anhydrase inhibitors 3. loop diuretics 4. thiazide diuretics 5. potassium sparing diuretics
|
|
thiazide diuretics drugs
|
chlorothiazide and hydrothiazide
|
|
thiazide diuretic site of action
|
secreted into PCT, inhibit Na and Cl reabsorption in DCT
|
|
use of thiazide diuretics
|
mainstay drug to tx hypertension (HT)
|
|
side effects of thiazide diuretics
|
hypokalemia, hyperuricemia, hypercalcemia, hyperglycemia, hyperlipidemia
|
|
loop diuretic drugs
|
furosemide
|
|
site of action of loop diuretics
|
secreted in PCT, acts on ascending loop
|
|
action of loop diuretics
|
inhibit reabsorption of Cl and Na-K-Cl transporter
|
|
uses of loop diuretics
|
most effective natriuretic and diuretic agents available
|
|
clinical indications for loop diuretics
|
1. CHF 2. edema 3. HT
|
|
side effects of loop diuretics
|
hypokalemia
|
|
K-sparing diuretics drugs
|
spironolactone
|
|
site of action of K-sparing drugs
|
DCT and collecting duct
|
|
action of K-sparing drugs
|
competitive antagonist of aldosterone
|
|
use of K-sparing drugs
|
in combo w/ thiazides or loops to prevent hypokalemia
|
|
side effects of K-sparing drugs
|
hyperkalemia
|
|
ACE inhibitor drugs
|
lisinopril
|
|
mech of action of ACE inhibitors
|
decrease angiotensin II prod by inhibiting the converting enzyme
|
|
use of ACE inhibitors
|
tx HBP in cases that also involve CHF, HA, and chronic kidney failure
|
|
side effects of ACE inhibitors
|
dry cough, angioedema and hyperkalemia
|
|
contraindications of ACE inhibitors
|
2ND AND 3RD TRIMESTERS OF PREGNANCY
|
|
angiotensin II receptor blocker drugs
|
losartan and valsartan
|
|
mech of action of angiotensin II receptor blockers
|
block angiotensin II receptor (AT1)
|
|
use of angiotensin II receptor blockers
|
similar to ACE inhibitors (HT pts w/ left ventricular hypertrophy, diabetic nephropathy)
|
|
side effects of angiotensin II receptor blockers
|
similar to ACE inhibitors but cough and angioedema are less common
|
|
contraindications of angiotensin II receptor blockers
|
2ND AND 3RD TRIMESTERS OF PREGNANCY
|
|
subclasses of anti-lipid drugs
|
1. bile-acid binding resins 2. inhibitors of cholesterol absorption 3. inhibitors of VLDL secretion 4. inhibitors of cholesterol synthesis
|
|
subclasses of diuretic drugs
|
1. osmotic diuretics 2. carbonic anhydrase inhibitors 3. loop diuretics 4. thiazide diuretics 5. potassium sparing diuretics
|
|
thiazide diuretics drugs
|
chlorothiazide and hydrothiazide
|
|
thiazide diuretic site of action
|
secreted into PCT, inhibit Na and Cl reabsorption in DCT
|
|
use of thiazide diuretics
|
mainstay drug to tx hypertension (HT)
|
|
side effects of thiazide diuretics
|
hypokalemia, hyperuricemia, hypercalcemia, hyperglycemia, hyperlipidemia
|
|
loop diuretic drugs
|
furosemide
|
|
site of action of loop diuretics
|
secreted in PCT, acts on ascending loop
|
|
action of loop diuretics
|
inhibit reabsorption of Cl and Na-K-Cl transporter
|
|
uses of loop diuretics
|
most effective natriuretic and diuretic agents available
|
|
clinical indications for loop diuretics
|
1. CHF 2. edema 3. HT
|
|
side effects of loop diuretics
|
hypokalemia
|
|
K-sparing diuretics drugs
|
spironolactone
|
|
site of action of K-sparing drugs
|
DCT and collecting duct
|
|
action of K-sparing drugs
|
competitive antagonist of aldosterone
|
|
use of K-sparing drugs
|
in combo w/ thiazides or loops to prevent hypokalemia
|
|
side effects of K-sparing drugs
|
hyperkalemia
|
|
ACE inhibitor drugs
|
lisinopril
|
|
mech of action of ACE inhibitors
|
decrease angiotensin II prod by inhibiting the converting enzyme
|
|
use of ACE inhibitors
|
tx HBP in cases that also involve CHF, HA, and chronic kidney failure
|
|
side effects of ACE inhibitors
|
dry cough, angioedema and hyperkalemia
|
|
contraindications of ACE inhibitors
|
2ND AND 3RD TRIMESTERS OF PREGNANCY
|
|
angiotensin II receptor blocker drugs
|
losartan and valsartan
|
|
mech of action of angiotensin II receptor blockers
|
block angiotensin II receptor (AT1)
|
|
use of angiotensin II receptor blockers
|
similar to ACE inhibitors (HT pts w/ left ventricular hypertrophy, diabetic nephropathy)
|
|
side effects of angiotensin II receptor blockers
|
similar to ACE inhibitors but cough and angioedema are less common
|
|
contraindications of angiotensin II receptor blockers
|
2ND AND 3RD TRIMESTERS OF PREGNANCY
|
|
subclasses of anti-lipid drugs
|
1. bile-acid binding resins 2. inhibitors of cholesterol absorption 3. inhibitors of VLDL secretion 4. inhibitors of cholesterol synthesis
|
|
bile acid-binding resin drug
|
cholestyramine
|
|
mech of action of bile acid-binding resin
|
interfere w/ enterohepatic cycline of bile acids which decrease prod. of cholesterol in liver
|
|
use of bile-acid binding resin
|
adjunctive therapy for primary hypercholesterolemia, biliary obstruction, diarrhea
|
|
why does bile-acid binding resin have a weak effect when used alone
|
due to compensatory cholesterol synthesis mechanisms
|
|
bile-acid binding resins used to relieve symptoms of what
|
biliary obstruction
|
|
side effects of bile-acid binding resins
|
GI: constipation, abdom pain/distension, ↓ absorption of fat-soluble drugs (ADEK) and minerals
|
|
site of action of loop diuretics
|
secreted in PCT, acts on ascending loop
|
|
action of loop diuretics
|
inhibit reabsorption of Cl and Na-K-Cl transporter
|
|
uses of loop diuretics
|
most effective natriuretic and diuretic agents available
|
|
clinical indications for loop diuretics
|
1. CHF 2. edema 3. HT
|
|
side effects of loop diuretics
|
hypokalemia
|
|
K-sparing diuretics drugs
|
spironolactone
|
|
site of action of K-sparing drugs
|
DCT and collecting duct
|
|
action of K-sparing drugs
|
competitive antagonist of aldosterone
|
|
use of K-sparing drugs
|
in combo w/ thiazides or loops to prevent hypokalemia
|
|
side effects of K-sparing drugs
|
hyperkalemia
|
|
ACE inhibitor drugs
|
lisinopril
|
|
mech of action of ACE inhibitors
|
decrease angiotensin II prod by inhibiting the converting enzyme
|
|
use of ACE inhibitors
|
tx HBP in cases that also involve CHF, HA, and chronic kidney failure
|
|
side effects of ACE inhibitors
|
dry cough, angioedema and hyperkalemia
|
|
contraindications of ACE inhibitors
|
2ND AND 3RD TRIMESTERS OF PREGNANCY
|
|
angiotensin II receptor blocker drugs
|
losartan and valsartan
|
|
mech of action of angiotensin II receptor blockers
|
block angiotensin II receptor (AT1)
|
|
use of angiotensin II receptor blockers
|
similar to ACE inhibitors (HT pts w/ left ventricular hypertrophy, diabetic nephropathy)
|
|
side effects of angiotensin II receptor blockers
|
similar to ACE inhibitors but cough and angioedema are less common
|
|
contraindications of angiotensin II receptor blockers
|
2ND AND 3RD TRIMESTERS OF PREGNANCY
|
|
subclasses of anti-lipid drugs
|
1. bile-acid binding resins 2. inhibitors of cholesterol absorption 3. inhibitors of VLDL secretion 4. inhibitors of cholesterol synthesis
|
|
bile acid-binding resin drug
|
cholestyramine
|
|
mech of action of bile acid-binding resin
|
interfere w/ enterohepatic cycline of bile acids which decrease prod. of cholesterol in liver
|
|
use of bile-acid binding resin
|
adjunctive therapy for primary hypercholesterolemia, biliary obstruction, diarrhea
|
|
why does bile-acid binding resin have a weak effect when used alone
|
due to compensatory cholesterol synthesis mechanisms
|
|
bile-acid binding resins used to relieve symptoms of what
|
biliary obstruction
|
|
side effects of bile-acid binding resins
|
GI: constipation, abdom pain/distension, ↓ absorption of fat-soluble drugs (ADEK) and minerals
|
|
inhibitors of cholesterol absorption drugs
|
ezetimibe
|
|
mech of action of inhibitors of cholesterol absorption
|
inhibits intestinal absorption fo dietary/biliary cholesterol
|
|
uses for inhibitors of cholesterol absorption
|
lower LDL, increase HDL
|
|
which has more GI side effects: inhibitors of chol absorp or bile acid-binding resins
|
bile acid-binding resins
|
|
contraindications for inhibitors of cholesterol absorption
|
liver failure (drug ↑ liver enzymes in defected liver)
|
|
inhibitors of VLDL secretion drug
|
niacin
|
|
use for inhibitors of VLDL secretion
|
adjunct therapy to diet modification
|
|
side effects of inhibitors of VLDL secretion
|
flushing, GI upset, hepatoxicity
|
|
inhibitors of cholesterol synthesis drugs
|
simvastatin and atorvastatin
|
|
mech of action of inhibitors of cholesterol synthesis
|
competitively block HMG-CoA reductase: ↓LDL, ↓VLDL, ↓TAGs, ↑HDL
|
|
most effective anti-lipid drug, first line of therapy for primary hyperlipidemia
|
simvastatin/atorvastatin
|
|
uses for inhibitors of cholesterol synthesis
|
1. most effective anti-lipid 2. ↓major coronary events 3. used w/ niacin to ↑HDL and decrease LDL
|
|
side effects for inhibitors of cholesterol synthesis
|
GI, liver enzymes, headache
|
|
precautions/contraindications for inhibitors of cholesterol synthesis
|
liver disease, women in pregnancy and breast feeding, children under 8yrs
|
|
centrally acting sympatholytic drug
|
clonidine
|
|
site of action of clonidine
|
CNS a2-adrenoceptor agonist
|
|
mech of action of clonidine
|
lowers sym outflow, ↑vagal tone thereby ↓CO and TPR
|
|
use of clonidine
|
2nd or 3rd line drug choice for ↓BP and in hypertensive crisis
|
|
side effects of clonidine
|
compensatory H2O and Na retention, sedation, drowsiness, rebound HT of drug w/drawal, dry mouth, constipation, sex dysfunction
|
|
a-adrenoceptor blocker drugs
|
prazosin, terazosin, doxazosin
|
|
mech and site of action of a-adrenoceptor blockers
|
block a1 receptors and cause dilation of As and V's, act in CNS to ↓ sym tone
|
|
a-adrenoceptor blockers more effective when used in comvo w/ what
|
other antihypertensive drugs (b-blockers and hypertension)
|
|
a-adrenoceptor blockers used in pts w/:
|
1. resistant (refractory) HT 2. prostatic hypertrophy 3. CHF
|
|
side effects of a-adrenoceptor blockers
|
CV: orthostatic hypotension, CNS: headache, dizziness, fatigue, GI: nausea, ab pain, sex dysfunction
|
|
b-adrenoceptor blocker drugs
|
cardioselective: atenolol, metoprolol
|
|
mech of action of b-adrenoceptor blockers
|
↓CO by blocking b1, block b1 adrenoceptor-mediated renin release, may have sympatho-inhibitory actions
|
|
uses of b-adrenoceptor blockers
|
tx mild-mod HT, w/ diuretics to further control BP, w/ vasodilator to prevent compensatory response in cardiac and renin release stimulation
|
|
use of sodium nitroprusside
|
drug of choice in hypertensive emergencies management
|
|
compensatory response for b-blockers
|
marked tachycardia, H2O retention and salt retention
|
|
side effects of b-blockers
|
related to metabolism of drug: cyanide → thiocyanate (liver)
|
|
toxicity of accumulation of cyanide
|
excessive hypotension, metabolic acidosis, arrhythmias, death
|
|
toxicity of thiocyanate:
|
weakness, disorientation, psychosis, muscle spasms, convulsions
|
|
Ca channel blockers effects
|
antianginal, antiarrhythmic, dilate peripheral arterioles and ↓BP
|
|
mech of action of Ca channel blockers
|
inhibition of Ca influx into arterial smooth muscle cells
|
|
Ca channel blocker drugs
|
nifedipine, amlodipine, verapamil, diltiazem
|
|
all local anesthetics are...
|
vasodilators, except cocaine
|
|
mode of metabolism and incidence of allergy in local anesthetics are determined by
|
chemical comp: ester or amide?
|
|
what happens to local anesthetics as MW and lipid solubility increase?
|
1. become more potent 2. prolonged binding to Na channel 3. more toxic in systemic circ
|
|
ester type locals
|
1. procaine 2. tetracaine
|
|
amide type locals
|
1. lidocaine 2. mepivacaine 3. bupivacaine
|
|
short/long acting ester type locals
|
short: procaine, long: tetracaine
|
|
short/long acting amide type locals
|
short: lidocaine, moderate: mepivacaine, long: bupivacaine
|
|
duration of action of locals determined by
|
retention at site of admin
|
|
termination of locals dependent upon
|
tissue blood flow
|
|
toxicity of locals determined by
|
plasma concentrations
|
|
principal determinant of rate of absorption of local anes into systemic circ is
|
blood flow at site of admin
|
|
side effects of b-blockers
|
related to metabolism of drug: cyanide → thiocyanate (liver)
|
|
toxicity of accumulation of cyanide
|
excessive hypotension, metabolic acidosis, arrhythmias, death
|
|
toxicity of thiocyanate:
|
weakness, disorientation, psychosis, muscle spasms, convulsions
|
|
Ca channel blockers effects
|
antianginal, antiarrhythmic, dilate peripheral arterioles and ↓BP
|
|
mech of action of Ca channel blockers
|
inhibition of Ca influx into arterial smooth muscle cells
|
|
Ca channel blocker drugs
|
nifedipine, amlodipine, verapamil, diltiazem
|
|
all local anesthetics are...
|
vasodilators, except cocaine
|
|
mode of metabolism and incidence of allergy in local anesthetics are determined by
|
chemical comp: ester or amide?
|
|
what happens to local anesthetics as MW and lipid solubility increase?
|
1. become more potent 2. prolonged binding to Na channel 3. more toxic in systemic circ
|
|
ester type locals
|
1. procaine 2. tetracaine
|
|
amide type locals
|
1. lidocaine 2. mepivacaine 3. bupivacaine
|
|
short/long acting ester type locals
|
short: procaine, long: tetracaine
|
|
short/long acting amide type locals
|
short: lidocaine, moderate: mepivacaine, long: bupivacaine
|
|
duration of action of locals determined by
|
retention at site of admin
|
|
termination of locals dependent upon
|
tissue blood flow
|
|
toxicity of locals determined by
|
plasma concentrations
|
|
principal determinant of rate of absorption of local anes into systemic circ is
|
blood flow at site of admin
|
|
how do vasoconstrictors prolong duration of action of LAs
|
reduce rate of systemic absorption
|
|
slower systemic absorption of LAs ↓ plasma drug concentrations which also reduces what toxicity
|
CV and CNS toxicity
|
|
are vasoconstrictors more effective in prolonging action of short acting or long acting LAs?
|
short (procaine and lidocaine)
|
|
metabolism of ester LAs
|
by plasma esterases
|
|
metabolism of amide LAs
|
in liver
|
|
clearance of amide LAs is dependent upon
|
hepatic blood flow and normal liver function
|
|
side effects of metabolites of amide LAs
|
can produce grand mal seizures and depress respiration
|
|
which type of nerve fiber is more sensitive to LAs
|
small unmyelinated nerve fibers
|
|
functions in order of sensitivity to blockade to LA
|
1. pain 2. touch 3. adrenergic vasocon 4. temp 5. proprioception 6. motor function
|
|
toxicity of LA determined by:
|
1. properties of LA 2. rate of absorption
|
|
allergy to LAs most common w/ what type of LA
|
ester containing p-aminobenzoate
|
|
most common cause of morbidity and mortality when using LA
|
failure to support respiration
|
|
systemic toxicity of LA primarily affects what 2 organ systems
|
CNS and CV system
|
|
drug of choice for anticonvulsive needs for tonic-clonic seizures assoc w/ LAs
|
intravenous lorazepam or diazepam
|
|
short-acting ester rapidly metabolized by plasma cholinesterase
|
procaine
|
|
what is the hapten in procaine that mediates anaphylaxis for sulfonamides, diuretics, and ester type LAs
|
p-aminobenzoic moiety
|
|
procaine should not be used w/o what?
|
vasoconstrictor
|
|
long-acting ester-type LA that is more potent and produces more prolonged anesthesia than procaine
|
tetracaine
|
|
disadv of tetracaine over procaine
|
increased systemic toxicity
|
|
ester-type LA that is potent vasoconstrictor
|
cocaine
|
|
side effects of cocaine when used in eye or to mucous membranes
|
ischemic necrosis and can destroy cornea or nasal septum
|
|
systemic administration of cocaine is assoc w/ what
|
1. hyperpyrexia 2. HT, stroke, sudden cardiac death
|
|
legitimate use for cocaine
|
surgery requiring incisions or manipulation of mucous membranes
|
|
most commonly used LA and antiarrhythmia drug
|
lidocaine
|
|
metabolites of lidocaine have what activity
|
CNS stimulatory, but lack antiarrhythmic activity
|
|
amide-type LA w/ moderate duration of action
|
mepivacaine
|
|
uses for mepivacaine
|
1. infiltrations 2. blocks 3. spinal and epidural
|
|
disadv of mepivacaine
|
high systemic toxicity (less than bupivacaine)
|
|
amide-type LA that is long acting
|
bupivacaine
|
|
side effect of bupivacaine
|
cardiovascular toxicity (short term depression of myocardial contractility)
|
|
action of cocaine
|
inhibits NE uptake into sym neurons
|
|
direct electrical charge forcing drug into cutaneous tissues
|
iontophoresis (lidocaine can be admin this way)
|
|
general anesthesia must exhibit what physiologic components
|
1. analgesia 2. amnesia 3. inhibition of sensory and autonomic reflexes 4. decreased skeletal muscle tone
|
|
altered or diminished state of consciousness
|
conscious sedation
|
|
conscious sedation must have what physiologic components
|
1. analgesia 2. amnesia 3. retained responsiveness to verbal commands
|
|
conscious sedation is useful for what procedures
|
cardiovascular, GI, dental
|
|
T/F: reduction in skeletal muscle tone is required in conscious sedation
|
F
|
|
danger of what is reduced in conscious sedation
|
hypoxia
|
|
conscious sedation is what stage of anesthesia
|
deep plane of stage 1
|
|
stages of anesthesia
|
1. analgesia w/o loss of consciousness 2. excitation 3. surgical 4. medullary depression
|
|
characteristics of pt in stage 2 anesthesia
|
unconscious and amnestic but may show agitation and excitation, pupils dilated, irregular BP and resp, retching vomiting breath holding
|
|
characteristics of pt in stage 3 anesthesia
|
regular resp, stable BP, autonomic and sensory reflexes suppressed
|
|
characteristics of stage 4 anes
|
BP and resp may be depressed
|
|
volatile anesthetics
|
desflurane, isoflurane, sevoflurane
|
|
high amts of inspired NO can produce what
|
hypoxia
|
|
NO is good agent for what/ bad for what
|
good for analgesia and amnesia, bad for muscle relaxation
|
|
why does NO have rapid onset/offset
|
low blood solubility
|
|
T/F: NO produces malignant hyperthermia
|
F
|
|
long term exposure to trace amts of NO produces
|
blood dyscrasias, bone marrow supp, peripheral neuropathies, increased spontaneous abortions
|
|
vitamin b12-dependent enzyme imp for RBC formation in marrow and lipid metab in peripheral nerves
|
methionine synthase
|
|
IV anesthetics
|
barbiturates, benzodiazepines, propofol
|
|
barbiturate drugs
|
thiopental, thiamylal, methohexital
|
|
benzodiazepine drugs
|
diazepam, medazolam, lorazepam
|
|
barbiturates useful for
|
induction of surgical anes, causing anes in 10-30 sec
|
|
what terminates general anesthesia for barbiturates
|
redistribution, not metab or renal excretion
|
|
T/F: barbiturates produce balanced anesthesia
|
F: only produce loss of consciousness and amnesia
|
|
benzodiazepines useful for
|
induction of surgical anes or conscious sedation
|
|
drug of choice of benzodiazepines
|
midazolam
|
|
T/F: benzodiazepines produce sedation and amnesia
|
T: but lack analgesic quality
|
|
benzodiazepine action can be terminated by benzodiazepine receptor antagonist called
|
flumazenil
|
|
IV anes w/ rapid onset/offset and imp to induce general anes and conscious sedation
|
propofol
|
|
termination of propofol general anesthesia
|
rapid redistribution
|
|
anaphylactoid rxns from propofol can occur as a result of
|
emulsifying agent
|
|
side effects of propofol
|
inhibit platelet function and increase bleeding times
|
|
where does Ca and PO4 intake take place
|
small intestine
|
|
where does Ca undergo absorption/secretion
|
absorption in duodenum and upper jejunum, and secretion in ileum
|
|
phosphorus absorption occurs where
|
jejunum
|
|
what results can the effects of small bowel disease and kidney disease have on disrupting Ca and PO4 metab
|
resulting in bone reabsorption and osteoporosis
|
|
2 hormones that are primary regulators of Ca and PO4
|
1. parathyroid hormone 2. vit D
|
|
UV light can activate vit D in skin from its precursor which is
|
7-dehydrocholesterol
|
|
principal physiologic actions of parathormone
|
1. increase serum Ca 2. reduce serum PO4
|
|
effects of parathormone upon bone reabsorption are
|
1. low doses ↓ bone reabsorption 2. high doses stimulate bone reabsorption
|
|
|
|
|
renal actions of parathormone
|
1. ↑ Ca and Mg reabsorption 2. ↓PO4 reabsorption 3. ↑ renal formation of 1,25 (OH) vit D3
|
|
what parathormone antag is used to tx osteoporosis and admin subcutaneously
|
teriparatide
|
|
principal pharmacologic actions of vit D
|
1. ↑ serum Ca and PO4 concen 2. ↑ intestinal absorption of Ca and PO4 3. ↓ Ca and PO4 excretion
|
|
net effect of vit D upon bone
|
↑ bone reabsorption under influence of parathormone
|
|
what form of vit D stimulates Ca absorption in jejunum
|
1,25 OH vit D
|
|
what form of vit D stimulates osteoblastic activity
|
24, 25 OH vit D
|
|
what form of vit D stimulates osteoClastic activity
|
1, 25 OH vit D
|
|
polypeptide prod by parafollicular cells of thyroid
|
calcitonin
|
|
mech of action of calcitonin
|
opposite of parathormone: ↓ serum Ca and PO4 by ↓ Ca and PO4 reabsorption in kidney
|
|
calcitonin effect on osteoclastic activity
|
↓
|
|
pharmacologic agents used to tx disorders in bone-mineral metab
|
1. calcium 2. estrogen/raloxifene 3. thiazide diuretics 4. fluroide 5. bisphosphonates 6. vit D
|
|
when are calcium supplements ineffective
|
when deficiency of vit D
|
|
selective estrogen receptor modulator
|
raloxifene
|
|
problems w/ chronic estrogen admin
|
1. ↑ risk for endometrial carcinoma 2. helps in growth of breast cancer
|
|
potential risk for cancer when using estrogen/raloxifene is offset by decreased risk of
|
cardiovascular disease
|
|
actions of raloxifene
|
partial agonist at estrogen receptor-a and antag at estrogen receptor-b
|
|
mech of action of thiazide diuretics
|
↓Ca concen in urine by ↑Ca ion reabsorption, also reduce formation of kidney stones
|
|
which diuretics ↑calciuria and ↑excretion of Ca, causing kidney stones
|
high-ceiling diuretics i.e. furosemide
|
|
oral fluoride given in large doses to osteoporosis pts can cause what side effects
|
N and V, GI blood loss, arthralgia
|
|
mech of action of bisphosphonates
|
↓ rate of osteoclastic dissolution of HA in bone and may be toxic to osteoclast, causing premature death of osteoclast
|
|
effect of bisphosphonates on bone formation and bone resorption
|
bone resorption dramatically slowed w/ no change in osteoblastic formation
|
|
bisphosphonate drugs
|
alendronate (oral) and zolendronate (IV)
|
|
how much of bisphosphonate drugs are absorbed w/ oral admin
|
10%
|
|
bisphosphonates cannot be used in the presence of what
|
peptic ulcer and reduced renal function
|
|
how is vit D administered
|
inactive prodrug (vit D2)
|
|
|
|
|
which mediators of acute inflam are mediators of pain
|
bradykinin and prostaglandins
|
|
which mediators of acute inflam are mediators of chemotaxis
|
PGs and leukotrienes
|
|
which mediators of chronic inflam effect prostaglandin prod
|
interleukins and TNF-a
|
|
which mediators of chronic inflam effect macrophages and granulocyte activation
|
GM-CSF and interferons
|
|
which mediator of chronic inflam effects fibroblast chemotaxis and proliferation
|
PDGF
|
|
general properties of NSAIDS
|
1. anti-inflammatory 2. analgesic 3. antipyretic
|
|
why would inhibition of COX-2 have a therapeutic advantage
|
b/c it's involved in PG prod at site of inflammation but not at other sites i.e. GI and kidney
|
|
protypical drug for peripherally acting analgesic
|
aspirin
|
|
protypical drug for anti-inflammatory and antipyretic
|
aspirin
|
|
how is aspirin eliminated
|
in urine as salicylic acid or glucuronic acid conjugate
|
|
mech of action of aspirin
|
non-selective COX-1 and COX-2 inhibitor but does NOT inhibit lipoxygenase
|
|
antipyretic effects of aspirin can only be demonstrated in
|
febrile pt
|
|
why are platelets sensitive to aspirin
|
b/c do not have capability to synthesize new cyclo-oxygenase
|
|
major disadvantage of salicylates
|
effects on gut
|
|
how does aspirin effect GI
|
interferes w/ gastric mucosal cells to resist acid penetration --> irritation and distress
|
|
general uses for aspirin (4)
|
1. inflammation 2. anti-inflammatory (combine w/ opiods to enhance relief) 3. fever 4. pain
|
|
specific uses for aspirin (5)
|
1. transient ischemia 2. alters effect of PGI and TXA on platelet agg and vasc s.m. 3. unstable angina 4. MI 5. prevent re-infarct
|
|
some symptoms of side effects of aspirin
|
GI upset and gastric ulcer, ↓hearing, vertigo, ↑uric acid levels, etc
|
|
Overdose toxicity of aspirin commonly occurs in children as what disease
|
Reye's syndrome
|
|
symptoms of aspirin overdose
|
depresses resp center, metabolic acidosis, uncoupline of oxidative respiration
|
|
contraindications of aspirin
|
pregnant women (effects on PGs) and kids w/ history of recent viral infection
|
|
how are selective COX-2 inhibitors diff from non-specific NSAIDS
|
fewer GI side effects, no impact on platelet agg
|
|
selective COX-2 inhibitor drugs
|
1. celecoxib 2. valdecoxib 3. meloxicam
|
|
which COX-2 inhibitor is most/least selective
|
most: celecoxib, least: meloxicam
|
|
use of selective COX-2 inhibitors
|
anti-inflammation and pain relief
|
|
pharmacokinetics of selective COX-2 inhibitors (metab and elim)
|
metabolized by liver cytochrome P450 enzymes, eliminated by kidneys
|
|
T/F: selective COX-2 inhibs have overall less side effects
|
F: less w/in 6 mo, same overall
|
|
who is celecoxib contraindicated in
|
those w/ sulfa allergies
|
|
other contraindication for selective COX-2 inhib
|
renal failure
|
|
what is the significance that acetaminophen acts more in CNS (inhibiting COX-3) and less in periphery
|
accounts for lack of anti-inflammatory and anti-platelet activity
|
|
use for acetaminophen
|
headache, myalgia, postpartum pain, fever
|
|
pharmacokinetics of acetaminophen
|
metab by liver microsomes and excreted in urine
|
|
T/F: acetaminophen is unaffected by renal function
|
T
|
|
acetaminophen used in pts w/ what type of disorders/problems?
|
blood disorders, GI disease, lung problems (bronchospasm from NSAIDS), kids w/ recent viral diseases
|
|
adverse effects/toxicity of acetaminophen
|
liver toxicity (esp w/ alcohol)
|
|
what is the most serious effect of acetaminophen overdose
|
hepatotoxicity (accumulation of toxic metabolite)
|
|
all other NSAIDS, generally, cause what problems
|
gastric irritation and renal toxicity
|
|
other NSAIDS are contraindicated in whom
|
ppl w/ severe asthma, nasal polyps, urticaria, salicylate hypersensitivity
|
|
what is the largest group of aspirin alternative
|
phenylproprionic acid derivatives
|
|
how do phenylproprionic acid derivatives produce anti-inflam and analgesic actions
|
inhibit cyclo-oxygenase and PG synthesis
|
|
ibuprofen has less GI effects than _____, less fluid retention than _____
|
less GI effects than aspirin, less fluid retention than indomethacin
|
|
small/large doses of ibuprofen have what effect
|
small: analgesic, larger: anti--inflam
|
|
half life of ibuprofen vs naproxen
|
ibuprofen: 2hr, naproxen: 12-15hr
|
|
GI effects of naproxen vs aspirin and ibuprofen
|
less than aspirin but double that of ibuprofen
|
|
naproxen has drug interactions w/ what type of drug
|
anti-coags
|
|
indole and indene derivatives are only selective for what
|
COX-1
|
|
uses for indomethacin
|
patent ductus arteriosus, gout and general pain/inflam
|
|
disadv of using indomethacin
|
more toxic than most NSAIDS, at high doses, 1/3 pop must quit using
|
|
adverse effects of indomethacin
|
severe GI, headache w/ dizziness, confusion depression, thrombocytopenia, aplastic anemia
|
|
pyrrole derivative drug
|
ketorolac
|
|
use for ketorolac
|
analgesic for postop pain requiring analgesia at opioid level
|
|
effects of ketorolac vs morphine
|
comparable effects, but less drowsiness, nausea, vomiting
|
|
adverse effects of ketorolac
|
GI (more serious and faster onset), bleeding (inhibition of platelet function)
|
|
do combination analgesics work in CNS or periphery?
|
periphery
|
|
contraindications to NSAIDS
|
kids, pts risk from bleeding abnormality or anticoag therapy, ulcer, asthma, kidney failure, liver disease
|
|
drug interactions with NSAIDS
|
anti-hypertensives (b-blockers, ACE inhibs, diuretics) and reduces effects of these
|
|
acetaminophen enhances effect of what drug
|
warfarin
|
|
what would you avoid by using NSAIDS over opioids
|
block source of pain (inflam-except acetaminophen) and avoid side effects of drowsiness, dizziness, N and V
|
|
which NSAIDS would you perscribe for mild pain
|
1. acetaminophen 2. aspirin 3. ibuprofen 4. naproxen
|
|
which NSAIDS ould you perscribe for mod/severe pain
|
1. aspirin+codeine 2. aspirin+caffeine 3. hodrocodone+acetaminophen 4. hydrocodone+ibuprofen
|
|
which categories of drugs would you give for RA
|
immunosuppressive, anti-malarial, anti-TNF-a
|
|
immunosuppressive drug
|
methotrexate
|
|
mech of action of methotrexate
|
inhibits and kills inflammatory immune cells by inhibiting DNA syn
|
|
what enzyme does methotrexate inhibit
|
dihydrofolate reductase
|
|
drug of choice for mild-moderate RA
|
methotrexate
|
|
anti-malarial drugs
|
chloroquine and hydroxychloroquine
|
|
why is hydroxychloroquine preferred
|
lower incidence of ocular toxicity
|
|
other adverse effects of hydroxychloroquine besides ocular toxicity
|
GI and dermatologic disturbances
|
|
use of hydroxychloroquine
|
pts just starting therapy (mild RA), can be used in more severe cases when NSAIDS no longer effective
|
|
penicillamine has what properties
|
both immunosuppressive and immunostimulant, but no antibacterial activity
|
|
indications for penicillamine
|
RA that is refractory to salicylates or related cpds
|
|
adverse effects of penicillamine
|
skin rash, GI disturbance, nephropathy
|
|
sulfasalazine is used to treat what 2 disorders
|
ulcerative colitis and RA in pts not responding adequately to NSAIDS
|
|
sulfasalazine is converted into the gut into what 2 cpds, and what are their functions
|
sulfonamide - antibacterial, salicylate - anti-inflammatory
|
|
advantage of sulfasalazine
|
lower toxicity than most DMARDS
|
|
adverse effects of sulfasalazine
|
N&V, bloody diarrhea and anorexia
|
|
drugs used to tx RA pts just starting therapy (mild RA)
|
hydroxychloroquine and sulfasalazine
|
|
TNF-a is produced by what/activated by what
|
produced by macrophages, activated by T cells
|
|
anti-TNF-a drug
|
infliximab
|
|
mech of action of infliximab
|
antibody against TNF-a
|
|
infliximab is more effective in combo w/ what
|
methotrexate (immuno-supressive)
|
|
general concepts of tx for RA
|
1. start w/ NSAID 2. add DMARD 3. scale up to methotrexate 4. add TNFa if methotrexate fails
|
|
major contributor to gout
|
decreased secretion
|
|
drugs used to tx gout
|
uricosurics-prebenecid and sulfinpyrazone, allopurinol, indomethacin
|
|
mech of action of probenecid and sulfinpyrazone
|
block tubular reabsorption of uric acid so ↑ urinary excretion of uric acid and ↓ serum urate concen
|
|
use for probenecid and sulfinpyrazone
|
tx chronic gout to prevent uric acid deposits and mobilize uric acid deposition
|
|
adverse effects of prebenecid and sulfinpyrazine
|
GI irritation and allergic dermatitis
|
|
allopurinol inhibits what enzyme
|
xanthine oxidase
|
|
rate limiting enzyme in uric acid formation
|
xanthine oxidase
|
|
mech of action of allopurinol
|
↓ syn of uric acid and ↓blood and urine concen
|
|
use for allopurinol
|
chronic gout
|
|
adverse effects of allopurinol
|
acute attack of gouty arthritis, skin rash and GI intolerance
|
|
drug interactions of allopurinol
|
↑ effects of anti-cancer drugs and enhances effects of warfarin
|
|
drug of choice to tx symptoms of acute gouty arthritis
|
indomethacin
|
|
CNS neurotransmitters
|
1. AAs 2. Ach 3. monoamines 4. others
|
|
examples of monoamines
|
NE, Epi, serotonin (5-HT), dopamine
|
|
anti-seizure drugs to tx general seizures
|
1. phenytoin 2. carbamazepine 3. valproic acid
|
|
prototype drug to tx general seizures
|
phenytoin
|
|
phenytoin affects what channels
|
Na
|
|
GABA mech of action
|
either causes Cl to rush in or K to rush out - causing more negative mem potential
|
|
carbamazepine mimics what
|
GABA
|
|
why would you not give valproic acid to pregant person
|
causes spina bifida
|
|
drugs used to tx absence seizures
|
ethosuximide and valproic acid
|
|
mech of action of ethosuximide
|
ca channel blocker
|
|
adv of using ethosuximide over valproic acid
|
less hepatotoxicity, doesn't cause birth defects
|
|
what would you give a woman of child bearing age for seizures
|
ethosuximide (instead of valproic acid)
|
|
general diff in mechs of action b/w benzos and barbs
|
benzos cause Cl channel to be open more frequently, barbs cause channel to be open longer duration
|
|
prototypical benzo
|
diazepam
|
|
drug to tx dementia-alzheimer's
|
donepezil
|
|
adv of using donepezil over other dementia drugs
|
less liver damage
|
|
antidepressant agents
|
amitriptyline (tricyclic anti) and fluoxetine (SSRI)
|
|
CNS stimulants
|
1. cocaine 2. amphetamine 3. methylphenidate
|
|
3 mechanisms to tx parkinson's
|
1. stim dopamine receptor 2. inhibit dopamine breakdown 3. replace dopamine
|
|
dopamine receptor stimulation agent
|
bromocriptine
|
|
drugs that inhibit dopamine breakdown
|
Selegiline (MAO inhibition) and entacapone (COMT inhibition)
|
|
dopamine replacement drugs
|
levodopa, carbidopa/levodopa
|
|
drugs to tx schizophrenia
|
1. haloperidol 2. risperidone
|
|
mech of action of haloperidol
|
dopamine blocker
|
|
adverse effects of haloperidol
|
can cause tardive dyskinesia i.e. parkinson's symptoms
|
|
which would you rather give to tx schizo?
|
risperidone - less side effects, decreased chance of causing tardive dyskinesia
|
|
drugs to tx manic-depressive syndrome
|
lithium and valproic acid (seizures)
|
|
both lithium and valproic acid depress what phase of manic-depressive syndrome
|
manic phase
|
|
3 mechanisms to tx emesis
|
1. block dopamine at CTZ 2. block CNS 5-HT receptors 3. block CNS histamine receptors
|
|
drug that blocks dopamine at CTZ
|
haloperidol (also used for schizophrenia
|
|
drug that blocks CNS 5-HT receptors
|
ondansetron
|
|
haloperidol given to tx what disorders
|
schizo and emesis
|
|
drug that blocks CNS histamine receptors
|
promethazine (phenergan)
|
|
mech to tx migraine
|
stimulate 5-HT receptor
|
|
drug to tx migraine
|
sumatriptan
|
|
sumatriptan effects oppose what drug
|
ondansetron
|
|
which opioid receptor functions by sedation, inhibition of resp, slowed GI, modulation of hormone and NT release
|
m
|
|
which opioid receptor functions by modulation of hormone and NT release
|
d
|
|
which opioid receptor functions by psychotomimetic effects, slowed GI transit
|
k
|
|
2 opioid G-prot coupled actions on neurons
|
1. close Ca channels (inhibit NT release) 2. open K channels (hyperpolarize)
|
|
endogenous opioids that mediate psych response to pain, involved in memory mood states, reg of appetite drives
|
endorphins
|
|
endorphins have high affinity for which receptor
|
m
|
|
endogenous opioids located in brain and S.C. and function as NTs
|
enkephalins
|
|
enkephalins have high affinity for which receptors
|
d
|
|
dynorphins have high affinity for which receptors
|
k
|
|
great amt of med is needed to maintina therapeutic effect, or effect is lost over time
|
tolerance
|
|
w/drawal syndromes would occur if stopped abruptly, dose reduced rapidly, or antag is given
|
physical dependence
|
|
neurological disorder, charac by continued compulsive use despite harm...is pathological state
|
addiction
|
|
strong opioid agonist drugs
|
morphine (prototype), meperidine, methadone
|
|
moderate opioid agonist drugs
|
codeine and oxycodone
|
|
weak opioid agonist drug
|
propoxyphene
|
|
opioid antag
|
naloxone
|
|
k agonist and weak m antag
|
pentazocine
|
|
pentazocine is opioid w/ mixed receptor actions and produces major effects on
|
CNS and GI tract, has morphine-like effects=euphoria
|
|
what is a better anti-tussive than codeine and why
|
dextromethorphan b/c selectively blocks cough mechs w/o producing other actions seen w/ opioids
|
|
good antidiarrheals that don't produce as many S.E.'s as other general opioids
|
diphenoxylate and loperamide
|
|
opioid w/ mixed receptor actions that is high phys and psych dependence
|
pentazocine (strong k agonist)
|
|
opioids are most effective against what type of pain
|
visceral
|
|
tolerance to opioids does not affect what action
|
miosis
|
|
drug of choice for pulmonary edema
|
morphine
|
|
opioids effect on CV system
|
minimal, but w/ parenteral admin can cause local histamine release, vasodil and bronchospasm
|
|
opioid effect on GI tract
|
↓ secretions, ↓propulsive activity, ↑ resting tone
|
|
what can occur do to increased sphincter tone from opioids
|
biliary colic and postop urinary retention
|
|
why is heroin more potent than morphine
|
can cross BBB, convert to morphine and act
|
|
opioid deveoped for its atropine-like anticholinergic effects, had rapid onset and short duration
|
meperidine
|
|
how are the effects of methadone diff from morphine
|
similar potency, but doesn't prod peaks and valleys of response due to long duration of action
|
|
use of methadone
|
replacement therapy in pts addicted to heroin
|
|
drug similar to meperidine but 50-80x more potent than morphine, used for anesthesia and analgesia
|
fentanyl
|
|
drug that is intermediate b/w strong and mod opioids, modest m stim effects, inhibits some serotonin and NE uptake into CNS neurons
|
tramadol
|
|
use of tramadol
|
in hospitals for pain relief, less addiction liability
|
|
drug for mild-mod pain, less potent than morphine, rarely produces addiction, combined w/ NSAID
|
codeine
|
|
use for oxycodone and hydrocodone
|
analgesia
|
|
propoxyphene has potency for pain relief similar to what
|
aspirin (weak opioid agonist)
|
|
if high enough doses, propoxyphene acts like what
|
morphine
|
|
naloxone blocks which opioid receptors
|
all 3, but preference for m
|
|
T/F: naloxone is effective orally
|
F
|
|
does naloxone have long/short duration when given i.v.---repeated injections given for?
|
short duration - repeated injections for opioid overdose
|
|
opioid antidiarrheals
|
diphenoxylate and loperamide
|
|
mech of action of diphenoxylate and loperamide
|
alter GI motility and anti-secretory activity
|
|
are opioids more effective for sharp, intermittent pain or severe, constant pain
|
severe,constant
|
|
drug used for cancer pain control
|
morphine
|
|
what happens if you repeat dosing of methadone
|
accummulation of drug b/c long half life
|
|
T/F: opioid analgesics can be used for obstetric labor
|
T
|
|
what would you give pt w/ dyspnea from pulmonary edema assoc w/ L vent failure
|
morphine I.V
|
|
how are opioids used in anesthesia
|
premeds before anes and surgery b/c of their sedative, anxiolygic, analgesic props
|
|
contraindications for opioids
|
1. impaired pul function 2. head injury and trauma 3. pregnancy
|
|
specialized uses for barbiturates
|
thiopental for anesthesia induction and phenobarbital for epilepsy
|
|
primary reason for some benzos used for short duration invasive procedures
|
amnesic action
|
|
what are the only 3 benzos that can be given IV
|
1. diazepam 2. midazolam 3. lorazepam
|
|
what types of sedative-hypnotics are preferred for anxiety states
|
drugs w/ intermedate or long durations of action
|
|
what types of sedative-hypnotics are preferred for sleep disorders
|
drugs w/ short durations of action
|
|
benzos (drugs)
|
1. midazolam 2. lorazepam 3. alprazolam 4. diazepam 5. chlordiazepoxide
|
|
short acting benzo used to induce anesthesia (w/ pain reliever), not to relieve pain
|
midazolam
|
|
why can lorazepam, alprazolam, diazepam and chlordiazepoxide not be used for sleep?
|
too long lasting/powerful
|
|
use for lorazepam, alprazolam, diazepam and chlordiazepoxide
|
anti-anxiety
|
|
drugs that can tx status epilepticus via IV
|
diazepam and chlordiazepoxide
|
|
benzo antag
|
flumazenil
|
|
serotonin drug, not benzo, acts on serotonin for anxiety, is prone to addiction
|
buspirone
|
|
disadv for buspirone
|
takes a few weeks to kick in
|
|
benzo-like compounds used for sleep
|
zolpidem, zaleplon, eszopiclone
|
|
why are zolpidem, zaleplon, eszopiclone not as potent/addictive as benzos
|
b/c these drugs only work at 1 benzo site on Cl channel whereas benzos work on 2
|
|
zolpidem, zaleplon, eszopiclone and benzos can be reversed w/ what
|
flumazenil
|
|
drug that acts on melatonin receptors, affects sleep/wake cycles
|
used to tx sleep
|
|
T/F: flumazenil can reverse effects of buspirone
|
F
|
|
drug that increases DA prod w/in basal ganglia
|
levodopa
|
|
drug that is MAO-B inhibitor and blocks pthwy in DA metabolism and increases duration of action of DA
|
selegiline
|
|
DA receptor agonists by directly stimulating CNS post-syn DA receptors
|
bromocriptine and pramipexole
|
|
anticholinergic drug that blocks Ach release b/c there is no DA production to inhibit Ach release
|
benztropine
|
|
COMT inhibitors that block alternate pathwya in DA metab
|
tolcapone
|
|
primary therapy for parkinson's disease
|
DA replacement (L-DOPA)
|
|
why do you combine L-DOPA w/ carbidopa
|
so you can reduce dose of levodopa and reduce peripheral side effects
|
|
taking a "drug holiday" from levodopa will help w/ what adverse effects and not help w/ others?
|
helps w/ neurologic (dyskinesias) and behavioral but DOE NOT help w/ on/off phenomenon
|
|
dopamine agonists
|
bromocriptine and pramipexole
|
|
advantage of using DA agonists over levodopa
|
1. longer duration of action, 2. less likely to produce response fluctuations and dyskinesias 3. don't need to be enzymatically converted
|
|
disadv of using DA agonists
|
less effective
|
|
function of DA agonists in more advanced stages of parkinson's
|
1. help w/ on-off problems 2. tx pts refractory to levodopa due to progressive loss of CNS dopaminergic neurons
|
|
non-selective DA receptor agonist that stimulates D1 and D2-like Da receptors
|
bromocriptine
|
|
selective DA receptor agonist that stimulates D1 only and produces fewer side effects
|
pramipexole
|
|
drug that increases striatal CNS DA levels by reducing its metabolic inactivation
|
selegiline
|
|
selegiline use in early parkinsons stages
|
monotherapy w/ modest effects
|
|
selegiline use in later stages
|
combined w/ levodopa to allow reduction of L-DOPA doses and attempt to delay dyskinesias and motor dluctuations
|
|
COMT inhibitors to tx parkinson's
|
entacapone and tolcapone
|
|
muscarinic receptor antag to tx parkinson's
|
benztropine
|
|
side effect of tolcapone
|
potentially fatal hepatotoxicity
|
|
clinical effects of benztropine
|
improves tremor and rigidity but has little effect on bradykinesia
|
|
only class of drugs that is effective in tx of anti-psychotic drug-induced parkinsonism
|
musc receptor antags - benztropine
|
|
contraindications for using muscarinic receptor antagonist
|
prostatic hyperplasia and angle-closure glaucoma
|
|
|
|
|
historically, reserpine was found to cause
|
depression
|
|
mech of action of reserpine
|
inhibit storage of amine NTs
|
|
prototypical TCA
|
amitriptyline
|
|
chemistry of TCAs resemble what (classic schizo/anti-psychotics)
|
phenothiazines
|
|
metab of TCAs
|
rapidly cleared by first-pass
|
|
elim half life of TCAs
|
range from 12-76 hrs
|
|
T/F: TCAs have high plasma protein (PP) binding and are very lipid soluble (like warfarin)
|
T
|
|
MOA or TCAs
|
1. nonspecifically target 5-HT and NE receptors 2. bind to a-adrenergic, histaminergic and cholinergic receptors
|
|
why do TCAs have such broad side effects
|
b/c they also bind to a-adrenergic, histaminergic and cholinergic receptors
|
|
TCAs should be reserved for use on these types of pts:
|
1. previous responder to another TCA 2. healthy 3. non-suicidals 4. refractory to newer agents (SSRIs)
|
|
anticholinergic adverse effects of TCAs
|
anti-slud: blurred vision, dry mouth, urinary retention, constipation
|
|
a-adrenergic block adverse effects of TCAs
|
orthostatic hypotension, male impotence, dizziness
|
|
antihistamine adverse effects of TCAs
|
sedation
|
|
T/F: SSRIs are more effective than TCAs
|
F: they have MUCH LESS INCIDENCE OF ADRs BUT NO MORE EFFECTIVE
|
|
prototypical SSRI
|
fluoxetine
|
|
SSRI agents
|
1. fluoxetine 2. paroxetine 3. citalopram 4. sertraline
|
|
SSRI agent that can be stimulating
|
sertraline
|
|
SSRIs metabolized by
|
cytochrome P450s
|
|
MOA of SSRIs
|
SPECIFICALLY increase serotonin levels in brain by inhibiting reuptake
|
|
uses of SSRIs
|
drug of choice for initial tx of depression
|
|
ADRs of SSRIs
|
1. N&V and dry mouth 2. insomnia and drowsiness 3. sexual dysfunction 4. weight gain
|
|
which SSRI may have less incidence of sexual dysfunction
|
escitalopram
|
|
drug of choice for bipolar disorder
|
lithium
|
|
MOA of lithium
|
competes w/ K, Mg, Ca, and Na in body
|
|
MOA of lithium in CNS
|
1. ↑ catecholamine destruction 2. ↓ NT release 3. ↓sensitivity of postsyn receps to NTs
|
|
ADRs of lithium
|
CNS, GI, muscular, heme
|
|
lithium drug interactions
|
NSAIDS and tetracycline decrease clearance of lithium
|
|
prototypical traditional antipsychotic
|
chlorpromazine
|
|
MOA of traditional antipsychotics
|
non-specifically inhibit dopamine
|
|
uses of traditional antipsychotics
|
used in pts not responding to other agents
|
|
ADRs of traditional antipsychotics
|
1. EPS 2. parkinsonism 3. tardive dyskinesia 4. NMS (neuroleptic malignant syndrome)
|
|
early-onset EPS
|
psudoparkinsonism, acute dystonia, akathisia
|
|
late-onset EPS
|
tardive dyskinesia, tardive dystonia, tardive akathisia
|
|
NMS occurs due to what
|
dopamine blockade
|
|
NMS characterized by:
|
1. hyperthermia 2. muscular rigidity 3. autonomic instability 4. altered consciousness
|
|
examples of non-traditional antipsychotic agents
|
haloperidol and risperidone
|
|
disadvantages of haloperidol
|
1. greatest chance of EPS 2. drug most assoc w/ NMS
|
|
advantage of haloperidol over phenotiazines
|
less likely to cause sedation and hypotension
|
|
MOA of risperdone
|
specifically inhibit serotonin
|
|
use for risperdone
|
first line agent for tx of psychosis
|
|
adverse effects of risperdone
|
similar to typical antipsychs but much less severe and w/ much less incidence
|
|
important for dentistry about antidep/antipsych
|
1. neuroleptic facial mvmts 2. ↑ sedation when given w/ opioids 3. ↑oral candidiasis 4. ↓salivation 5. NSAIDS interaction w/ lithium
|