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598 Cards in this Set

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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