Pharmacology - Jingshing Cards

Front 1

-hallucinogenic (partial agonists)@What type of receptor are opiods?$G-protein

Back 1

ultimately act via cAMP modulation@Where are opiod receptors located?$Brain: locus coeruleus

Front 2

Spinal cord: dorsal horn

Back 2

periaqueductral gray matter

Front 3

-act on the NAcc to mediate reward (mu and delta) and aversion (kappa)@natural opiod agonists$endorphins: formed from preprespiomelanocortin

Back 3

have mu affinity

Front 4

dynorphins: formed from cleavage of prodynorphin (may increase or decrease pain

Back 4

increase or decrease addiction

Front 5

enkephalins (met and leu): ???(pain

Back 5

immune function

Front 6

agonist for mu opiod receptors; inhibits release of substance P and other nociceptive neurotransmitters (via decreased Ca2+ entry) and on postsynaptic nociceptive neurons

Back 6

(increase K+ conductance) --> hyperpolarization and inhibition. Weak agonist for kappa and delta opiod receptors@morphine SE$respiratory depression

Front 7

weak anticholinergic activity (tachycardia

Back 7

fever)

Front 8

interact with MAOI@fentanyl$short acting/rapid offset

Back 8

transdermal patches for cancer pain

Front 9

muescle rigidity

Back 9

bradycardia at high doses@sufentanil$more rapid than fentanyl@alfentanil$short acting for general anesthesia@remifentanil$short acting for general anesthesia@tolerance$progressive lack of drug effect with prolonged continuous use@dependence$physiological response to acute withdrawal of narcotic effect@methadone MOA$mu agoinst and NMDA

Front 10

(often used for withdrawal symptoms

Back 10

less severe withdrawal)

Front 11

-rifampin and phenytoin accelerate metabolism@methadone SE$simliar to morphine (respiratory depression

Back 11

nausea and vomiting

Front 12

for moderate pain

Back 12

hiarrhea

Front 13

-seizures w/ SSRI and TCAs@pentazocine MOA$partial mu agoinst

Back 13

kappa agoinst (spinal level analgesia)@pentazocine SE$hallucination

Front 14

CV: bradycardia

Back 14

heart block

Front 15

can cause seizures

Back 15

arrhythmias

Front 16

metabolized by kidney or liver@what is unique about atracurium

Back 16

cisatracurium and mivacurium?$metabolism is independed of hepatic and renal function@fast offset non-depolarizing muscle relaxant$cis

Front 17

warfarin (increase in INR)@atorvastatin$dimer

Back 17

inhibits HMG-CoA reductase

Front 18

metabolized by CYP450 3A4

Back 18

hepatic clearance

Front 19

short half-life@fluvastatin$statin@lovastatin$statin@statin SE$headache

Back 19

myalgia

Front 20

myopathy@gemfribrozil MOA$increases peripheral lipolysis

Back 20

activate peroxisome proliferator-activated receptor-alpha (PPAR-alpha)) and decreases hepatic TG production (via decreasing apoC-III)

Front 21

4) decreased apo-A-I clearance --> decreased HDL catabolism@nicotinic acid SE$--flushing (DP1 receptor interact with PGD2)

Back 21

itching

Front 22

--hepatoxicity

Back 22

GI distress

Front 23

-decreases hepatic production of VLDL and of apolipoprotein B@cholestyramine MOA$nonabsorbable polymer cationic resin that binds bile acids (sandy/gritty)@cholestyramine SE$GI intolerance: constipation

Back 23

bloating

Front 24

(at high doses steatorrhea

Back 24

deficiency of lipid-soluble vitamins)

Front 25

bind other negatively charged drugs@colestipol$cholesterol-lowering resin

Back 25

not used@colesevelam$cholesterol-lowering resin

Front 26

glucouronidated@ezetimibe SE$increased risk of URI@Commonly used DMARD$methotrexate

Back 26

sulfasalazine

Front 27

--drugs used in gout@methotrexate MOA$folic acid analog

Back 27

inhibits dihydrofolate reductase (prevents folate recycling) and decreases synthesis of purine nucleotides

Front 28

intracellular polyglutamation traps drug in cell@methotrexate SE$sensitive tissues: bone marrow

Back 28

buccal and intestinal mucosa

Front 29

--GI: ulcerative stomatitis

Back 29

nausea

Front 30

--leukopenia and liver function alterations@Leucovorin$reduces toxic effect on normal cells by methotrexate (preferentially taken up my normal cells)@cyclophosphamide MOA$alkylating agent (destroys proliferating lymphoid cells

Back 30

B cells >>> T cells)@cyclophosphamide SE$--GI: nausea

Front 31

--amenorrhea

Back 31

male sterility

Front 32

--alopecia@nitrogen mustards$mechlorethamine

Back 32

cyclophosphamide

Front 33

--skin rashes

Back 33

hepatitis

Front 34

--binds to cycophilin

Back 34

complex inhibits calcineurin (protein phosphatase

Front 35

blocks IL-2

Back 35

IL-4

Front 36

variable bioavailability

Back 36

liver insufficiency and dose adjustment according to CSS@Neoral$has slightly increased and less variable bioavailabilty as cyclosporine

Front 37

NOT bioequivalent and cannot be used interchangeably@cyclosporine SE$--nephrotoxicity (afferent arteriolar constriction

Back 37

tubular toxicity

Front 38

--tremor

Back 38

seizures

Front 39

--gum hyperplasia

Back 39

hirsutism

Front 40

--anemia

Back 40

leukopenia

Front 41

--nephrotoxicity (afferent arteriolar constriction

Back 41

tubular toxicity

Front 42

--tremor

Back 42

seizures

Front 43

--gum hyperplasia

Back 43

hirsutism

Front 44

--anemia

Back 44

leukopenia

Front 45

--cytokine release syndrome (fever

Back 45

chills

Front 46

--low incidence of adverse effects@abatacept$fusion protein of human IgG to CTLA4 (which binds to CD80 and 86 on APC)

Back 46

blocks T cell activation

Front 47

--treats moderate to severe RA (refractory to DMARDS)

Back 47

high TNF-alpha levels

Front 48

--skin rash

Back 48

GI

Front 49

--severe skin rahs

Back 49

hepatitis

Front 50

--inhibits metabolism and inactivation of mercatopurine

Back 50

azathioprine

Front 51

--used for prophylaxis against gout attacks@cholchicine SE$--GI: nausea

Back 51

vomiting

Front 52

--Bone marrow: temporary leukopenia followed by leukocytosis

Back 52

aplastic anemia and agranulocytosis with long-term use

Front 53

--long term use can lead to myopathy@probenecid MOA$competes with uric acid for weak acid carrier transporter (inhibits uric acid reabsorption)@probenecid SE$--GI

Back 53

skin rash

Front 54

--inhibits renal excretion of penicillins

Back 54

indomethacin

Front 55

--treats IBD and RA@sulfasalazine SE$sulfa allergy (rash

Back 55

fever

Front 56

--direct receptor-based effects inhibit excitatory neurotransmission and enhance inhibitory neurotransmitter action@solubilities order of inhaled anesthetics$Nitrous Oxide

Back 56

Desflurane

Front 57

--nighttime@Halothane SE$arrhythmic

Back 57

hepatitis

Front 58

--depresses ventilation

Back 58

venous tone

Front 59

--depresses ventilation

Back 59

venous tone

Front 60

--depresses ventilation

Back 60

venous tone

Front 61

--more potent in hemorrhagic shock@propofol$--acts on GABAa receptor

Back 61

also acetylcholine and glycine

Front 62

--does not decrease BP

Back 62

RR

Front 63

--minimal eff@ketamine$--produce analgesia and dissociated anesthetic state

Back 63

hypnosis

Front 64

--releases endogenous catecholamines (increases BP

Back 64

HR

Front 65

1) and 2) required; need either 3) or 4)@benzodiazepine and narcotic$synergistic sedative and hypotensive responses

Back 65

respiratory depression@substance abuse$--a maladaptive patter of substance use

Front 66

5) great deal of time spent trying to obtain

Back 66

using

Front 67

(heroin

Back 67

LSD

Front 68

(amphetamine

Back 68

cocaine

Front 69

(anabolic steroids

Back 69

acetaminophen with codeine

Front 70

(alprazolam

Back 70

butorphanol

Front 71

(acetaminophen or actifed with codein

Back 71

robitussin AC with codeine

Front 72

--more drug needed to achieve same effect

Back 72

or

Front 73

--a common

Back 73

but not defining characteristic of abused drugs@cocaine MOA$blocks reupdate of DA

Front 74

--metabolized by the liver CYP2D6@how to treat alcohol withdrawal$acute: treat symptoms@how to treat stimulant overdose$benzodiazepine to manage anxiety@how to treat sedative withdrawal$long-acting barbituate (phenobarbital

Back 74

gradual dose reduction)@how to treat hallucinogent intoxication$talking down

Front 75

activation of mu receptor

Back 75

-supraspinal and spinal analgesia

-respiratory depression

-sedation/euphoria

-ileus

-nausea/vomiting

-pruritis

uninary retention

miosis

Front 76

activation of delta receptor

Back 76

-modulates mu receptor activity

Front 77

activation of kappa receptor

Back 77

-dysphoria

-diuresis

-hallucinogenic (partial agonists)

Front 78

What type of receptor are opiods?

Back 78

G-protein, ultimately act via cAMP modulation

Front 79

Where are opiod receptors located?

Back 79

Brain: locus coeruleus, midbrain, medulla, NAcc

Spinal cord: dorsal horn, periaqueductral gray matter, substantia gelatinosa

Front 80

How to opiod receptors act?

Back 80

inhibit ascending transmission of pain information from the spinal cord and activating descending pain control circuits

-act on the NAcc to mediate reward (mu and delta) and aversion (kappa)

Front 81

natural opiod agonists

Back 81

endorphins: formed from preprespiomelanocortin, have mu affinity, analgesic, well-being, addiction

dynorphins: formed from cleavage of prodynorphin (may increase or decrease pain, increase or decrease addiction, play a role in weight regulation

enkephalins (met and leu): ???(pain, immune function, gut function, weight, memory)

Front 82

opiod effects on CNS

Back 82

analgesia, sedation, euphoria, dysphoria, miosis, itching

Front 83

opiod effects on respiratory

Back 83

increase PCO2, decrease RR, increase obstructed breathing

Front 84

opiod effects on CV

Back 84

histamine relea --> hypotension, bradycardia

Front 85

opiod effects on GI

Back 85

constipation, nausea, sphincter of oddi spasm

Front 86

opiod effects on GU

Back 86

increase ureteral tone

Front 87

morphine MOA

Back 87

morphine 6-glucoronide --> enhance

agonist for mu opiod receptors; inhibits release of substance P and other nociceptive neurotransmitters (via decreased Ca2+ entry) and on postsynaptic nociceptive neurons, (increase K+ conductance) --> hyperpolarization and inhibition. Weak agonist for kappa and delta opiod receptors

Front 88

morphine SE

Back 88

respiratory depression, nausea and vomiting, pruritis, constipation and miosis, dependence, overdose, increased sphincter of oddi tone

Front 89

morphine withdrawal symptoms

Back 89

lacrimation, rhinorrhea, diaphoresis, piloerection, nausea, tachypnea

Front 90

morphine overdose symptoms

Back 90

coma, pinpoint pupils, respiratory depression

Front 91

dilauded

Back 91

for patients with excessive morphine side effects; 5X as potent as morphine

Front 92

meperidine

Back 92

aka demerol

stimulant (euphoria)

weak anticholinergic activity (tachycardia, fever)

avoid the basal rate; buildup of metabolite normeperidine can lead to seizures

interact with MAOI

Front 93

fentanyl

Back 93

short acting/rapid offset, transdermal patches for cancer pain

100X as potent as morphine

muescle rigidity, bradycardia at high doses

Front 94

sufentanil

Back 94

more rapid than fentanyl

Front 95

alfentanil

Back 95

short acting for general anesthesia

Front 96

remifentanil

Back 96

short acting for general anesthesia

Front 97

tolerance

Back 97

progressive lack of drug effect with prolonged continuous use

Front 98

dependence

Back 98

physiological response to acute withdrawal of narcotic effect

Front 99

methadone MOA

Back 99

mu agoinst and NMDA

(often used for withdrawal symptoms, less severe withdrawal)

-similar potency as morphine

-extremely long onset and half-life

-rifampin and phenytoin accelerate metabolism

Front 100

methadone SE

Back 100

simliar to morphine (respiratory depression, nausea and vomiting, pruritis, constipation and miosis, dependence, overdose, increased sphincter of oddi tone)

Front 101

codeine MOA

Back 101

methylated form of morphine


binds to mu receptor (weak agoinst because must be demethylated)

for moderate pain, hiarrhea, cough suppression

Front 102

codeine SE

Back 102

NAUSEA, constipation, vomiting

Front 103

butorphanol MOA

Back 103

mu partial agonist and kappa agoinst (spinal-level analgesia)

migraines

Front 104

tramadol

Back 104

-mu agonist

-seizures w/ SSRI and TCAs

Front 105

pentazocine MOA

Back 105

partial mu agoinst, kappa agoinst (spinal level analgesia)

Front 106

pentazocine SE

Back 106

hallucination, dependence, respiratory depression (at relatively low ceiling, can overdose)

Front 107

naloxone MOA

Back 107

mu antagoinst

Front 108

naloxone SE

Back 108

pulmonary edema

Front 109

methyltrexone

Back 109

reverses peripheral morphine SE w/o reversing central effect, cannot enter CNS

Front 110

butophanol SE

Back 110

dysphoria, hallucinations, withdrawal, respiratory depression

Front 111

nalbuphine MOA

Back 111

kappa agoinst, complete mu antagonist

Front 112

procaine MOA

Back 112

blocks Na+ ion channels preferential effect on rapidly firing>slowly firing, myelinated>unmyelinated, and smaller > larger nerve fibers

Front 113

procaine SE

Back 113

CNS (occurs at lower drug level): restlessness, paresthesias, tinnitus, tremors, convulsions, nystagmus, shivering, confulsions, death

CV: bradycardia, heart block, hypotension

Front 114

short duration anesthetics

Back 114

chloroprocaine

Front 115

medium duration anesthetics

Back 115

mepivacaine, lidocaine

Front 116

long-duration anesthetics

Back 116

bupivacaine, etidocaine

Front 117

topical anesthetics

Back 117

benzocaine, tetracaine, cocaine, lidocaine

Front 118

ways to use local anesthetics

Back 118

topical, field blocks, intravenous blocks, nerve blocks, central axis blocks (epidural, spinal)

Front 119

order of sensory modalities for local anesthetics

Back 119

temperature, pain, proprioception, motor blockade (least to greatest)

Front 120

lidocaine

Back 120

amide, short-intermediate duration

Front 121

bupivicaine

Back 121

long duration of action

2-4 fold greater CV toxicity

reverse by intralipid

amide

Front 122

benzocaine

Back 122

ester

used topically for mucesitis

can cause metremoglobinemia

Front 123

cocaine

Back 123

ester

blocks catecholamine reuptake

can cause seizures, arrhythmias, MI, stroke, etc.

Front 124

succinylcholine MOA

Back 124

nicotinic agoinst (Nm subtype) --> depolarizing (not inactivated by acetylcholinesteratse)

rapid degradation

Front 125

pancuronium MOA

Back 125

competitive antagonist for Nm; non-depolarizing (can be overcum by neostigmine)

metabolized by kidney or liver

Front 126

what is unique about atracurium, cisatracurium and mivacurium?

Back 126

metabolism is independed of hepatic and renal function

Front 127

fast offset non-depolarizing muscle relaxant

Back 127

cis, vec, roc

Front 128

slow offset non-depolarizing muscle relaxant

Back 128

curare, pancuronium

Front 129

order of sensitivity to NMBs

Back 129

pharyngeal muscles, limb muscles, face muscles, diaphragm (most to least sensitive)

Front 130

succinylcholine SE

Back 130

hyperkalemia, increased IOP, IGP, bradychardia in children, MH trigger

Front 131

pancuronium SE

Back 131

tolerance, tachycardia, prolonged use --> prolonged paralysis

Front 132

curare SE

Back 132

hypotension (via histamine release)

Front 133

edrophonium

Back 133

noncarbamate AchE inhibitor (short half-life, cannot be used therapeutically, diagnoses myasthenia gravis)

Front 134

Baclofen MOA

Back 134

activates GABAb (produce inhibitory GABA signals via second messengers) --> decreased stimulation of musces

Front 135

dantrolene

Back 135

decreases Ca2+ release from SR

Front 136

oxycodone

Back 136

oral opioid agonist, given in combination with aspirin (= percodan), acetaminophen ( = percocet)

Front 137

hydrocodone

Back 137

oral opiod agonist, given in combination with acetaminophen (= vicodin) and ibuprofen (=combunox)

Front 138

propoxyphene

Back 138

less potent opiod

Front 139

rosuvastatin

Back 139

HMG-CoA reductase inhibitor, metabolized by CYP450 2C9 (metabolite has 1/6 to 1/2 inhibitory activity)

renal and hepatic clearance

Long half life

2 fold increase in AUC in Japanese/Chinese populations

Front 140

drugs rosuvastatin interacts with

Back 140

cyclosporine (11-7 fold increase in ros.)

gemfibrozil (increase in ros. level)

antacid (take 2 hours after ros.)

warfarin (increase in INR)

Front 141

atorvastatin

Back 141

dimer, inhibits HMG-CoA reductase

metabolized by CYP450 3A4, hepatic clearance

long half-life

Front 142

simvastatin

Back 142

CYP450 3A4 metabolism

renal and hepatic clearance

short half-life

Front 143

pravastatin

Back 143

CYP450 2C9 metabolism

renal and hepatic clearance

short half-life

Front 144

fluvastatin

Back 144

statin

Front 145

lovastatin

Back 145

statin

Front 146

statin SE

Back 146

headache, myalgia, fatigue, GI intolerance, flu-like syptoms

increase in liver enzymes (get baseline ALT)

myopathy

Front 147

gemfribrozil MOA

Back 147

increases peripheral lipolysis, activate peroxisome proliferator-activated receptor-alpha (PPAR-alpha)) and decreases hepatic TG production (via decreasing apoC-III), increase HDL via increasing apoA-I and apoA-II expression

Front 148

gemfribrozil SE

Back 148

GI distress, rash, myopathy, gallstones, potentiates effects of warfarin and sulfonylureas

Front 149

clofibrate

Back 149

less-well tolerated, gall bladder toxicity

Front 150

fenofibrate

Back 150

causes greater HDL increases

Front 151

steps to minimize the risk of muscle toxicity with fibrate-statin combination therapy

Back 151

--use statin alone for non-HDL-C goals

--use fish oils or niacin rather than fibrates

--keep the doses of the statin and fibrate low

--dose the fibrate in the AM and the statin in the PM

--avoid (cautiously use) combo in renal impairment

--assure no interactions

--teach the patient to recognize muscle symptoms

--discontinue therapy if muscle symptoms are present and CK is >10 times the upper limit of normal

Front 152

Niacin MOA

Back 152

1) inhibits hormone-sensitive lipase in adipose tissue

2) reduction of triglyceride synthesis reduces VLDL synthesis

3) increase peripheral lipoprotein lipase activity

4) decreased apo-A-I clearance --> decreased HDL catabolism

Front 153

nicotinic acid SE

Back 153

--flushing (DP1 receptor interact with PGD2), itching, headache

--hepatoxicity, GI distress

--hyperglycemia and reduced insulin sensitivity

Front 154

nicotinic acid MOA

Back 154

don't really know how work

-decreases hepatic production of VLDL and of apolipoprotein B

Front 155

cholestyramine MOA

Back 155

nonabsorbable polymer cationic resin that binds bile acids (sandy/gritty)

Front 156

cholestyramine SE

Back 156

GI intolerance: constipation, bloating, abdominal pain, flatulence

(at high doses steatorrhea, deficiency of lipid-soluble vitamins)

no systemic toxicity

bind other negatively charged drugs

Front 157

colestipol

Back 157

cholesterol-lowering resin, not used

Front 158

colesevelam

Back 158

cholesterol-lowering resin, used frequently

--bind other negatively charged drugs

--impede the absorption of drugs and/or fat-soluble vitamins

Front 159

ezetimibe MOA

Back 159

inhibits intestinal cholesteral absorption by jejunal enterocytes (no effect on absorption of lipid-soluble vitamins)

glucouronidated

Front 160

ezetimibe SE

Back 160

increased risk of URI

Front 161

Commonly used DMARD

Back 161

methotrexate, sulfasalazine, leflunomide, biologics (anti-TNF-alpha, IL-1 receptor antagonist, abatacept, rituximab)

Front 162

Less commonly used DMARD

Back 162

azathioprine, gold, minocycline, cyclosporine, scylophosphamide, penicillamine

Front 163

Immunosuppressive drugs

Back 163

--NSAID,

--corticosteroids,

--calcineurin inhbitors,

--mTOR inhibitors,

--anti-metabolites,

--biologics,

--drugs used in gout

Front 164

methotrexate MOA

Back 164

folic acid analog, inhibits dihydrofolate reductase (prevents folate recycling) and decreases synthesis of purine nucleotides, thymidylate and serine and methionine

affects S phase

intracellular polyglutamation traps drug in cell

Front 165

methotrexate SE

Back 165

sensitive tissues: bone marrow, buccal and intestinal mucosa, malignant cells

--GI: ulcerative stomatitis, nausea, abdominal distress

--leukopenia and liver function alterations

Front 166

Leucovorin

Back 166

reduces toxic effect on normal cells by methotrexate (preferentially taken up my normal cells)

Front 167

cyclophosphamide MOA

Back 167

alkylating agent (destroys proliferating lymphoid cells, B cells >>> T cells)

Front 168

cyclophosphamide SE

Back 168

--GI: nausea, vomiting

--Bone marrow

--hemorragic cystitis (at higher doses)

--electrolyte disturbanes

--cardiotoxicity

--amenorrhea, male sterility

--alopecia

Front 169

nitrogen mustards

Back 169

mechlorethamine, cyclophosphamide, ifosfamide, chlorambucil, pelphalan

Front 170

azathioprine MOA

Back 170

resembles adenine, converted into 6-MP ->->-> incorporated into DNA -> cell death

toxic to B and T lymphocytes after antigenic stimulation (cellular and humora immunity)

Front 171

azathioprine SE

Back 171

--GI irritation at high doses

--bone marrow depression (more likely with polymorphic TPMT deficiency)

--requires xanthine oxidase for inactivation

--skin rashes, hepatitis, intersitial pneumonitis

Front 172

mycophenolate mofetil

Back 172

--inhibitor of IMP dehydrogenase (required for de novo synthesis of GMP)

--S phase specific

--inhibits T and B cell responses

--meabolized to mycophenolic acid by tissue and plasma esterases

--MPA gets glucoronidated for renal excretion

Front 173

leflunomide

Back 173

inhibitor of pyrimidine synthesis (treament for rheumatoid arthritis)

Front 174

cyclosporine

Back 174

--acts on T cells

--binds to cycophilin, complex inhibits calcineurin (protein phosphatase, required for IL-2 production via NFAT)

--metabolized by CYP3A4

blocks IL-2, IL-4, IFN gamma, TNF alpha, CD 40 L



variable bioavailability, liver insufficiency and dose adjustment according to CSS

Front 175

Neoral

Back 175

has slightly increased and less variable bioavailabilty as cyclosporine

NOT bioequivalent and cannot be used interchangeably

Front 176

cyclosporine SE

Back 176

--nephrotoxicity (afferent arteriolar constriction, tubular toxicity, thrombotic microanglopathy, chronic vascular and tubular toxicity, magnesium wasting, hyperkalemia)

--hypertension

--tremor, seizures

--gum hyperplasia, hirsutism

--hepatotoxicity

--anemia, leukopenia, thrombocytopenia

Front 177

tacrolimus MOA

Back 177

binds FKBP, complex inhibits calcineurin

10-100 more potent than cyclosporine

metabolized by CYP3A4

less nephrotoxic

dose according to Css

Front 178

tacrolimus SE

Back 178

--glucose intolerance

--nephrotoxicity (afferent arteriolar constriction, tubular toxicity, thrombotic microanglopathy, chronic vascular and tubular toxicity, magnesium wasting, hyperkalemia)

--hypertension

--tremor, seizures

--gum hyperplasia, hirsutism

--hepatotoxicity

--anemia, leukopenia, thrombocytopenia

Front 179

sirolimus MOA

Back 179

binds FKBP and inhibits mTOR (blocks T and B cell proliferation)

metabolized by CYP3A4

Front 180

sirolimus SE

Back 180

--less nephrotoxic than tacrolimus

--hyperlipidemia and thrombocytopenia (not seen in tacrolimus)

--additive or synergic nephrotoxicity with CSA

--antiproliferative (impaired wound healing)

Front 181

everolimus

Back 181

similar to sirolimus

Front 182

antithymocyte globulin MOA

Back 182

deplete T cells by inducing complement-mediated lysis and antibody-depended cell-mediated cytotoxicity

Front 183

antithymocyte globulin SE

Back 183

--'flu-like' symptoms

--cytokine release syndrome (fever, chills, dyspnea, nausea, vomiting, pulmonary edema and cardiovascular collapse)

--vascular leak syndrome

--local pain and erythema

--hypersensitivity/anaphylactic reactions

--rescue of acute rejection

Front 184

muromonab

Back 184

--murine monoclonal

--CD3 on surface of T cells (thymocytes and mature T cells)

--cytokine release syndrome is less with second generation of CD3 antibodies

Front 185

alemtuzumab

Back 185

--first approved fully humanized monoclonal

--bind to CD52 on mature (normal and malignant) B and T lymphocytes

--SE: myelosuppression and opportunistic infections

Front 186

basiliximab

Back 186

--bind to CD25 (alpha subunit of IL-2 receptor) on activated lymphocites

--no significant T cell depletion

--low incidence of adverse effects

Front 187

daclizumab

Back 187

--bind to CD25 (alpha subunit of IL-2 receptor) on activated lymphocites

--no significant T cell depletion

--low incidence of adverse effects

Front 188

abatacept

Back 188

fusion protein of human IgG to CTLA4 (which binds to CD80 and 86 on APC), blocks T cell activation

--used for refractory rheumatoid arthritis

Front 189

entanercept MOA

Back 189

--soluble receptor dimer

--TNFR linked to Fc portion of human IgG

--treats moderate to severe RA (refractory to DMARDS), high TNF-alpha levels, long half-life

Front 190

entanercept SE

Back 190

URI/TB, diarrhea, headache, sinusitis/rhinits

Front 191

infliximab MOA

Back 191

monoclonal antibody that binds to soluble and transmembrane forms of TNF alpha (treats severe Crohn's disease and RA)

Front 192

adalimumab

Back 192

anti-TNF alpha monoclonal antibody used to treat RA

Front 193

infliximab SE

Back 193

nausea, fatigue, vomiting, URI

Front 194

allopurinol MOA

Back 194

--hypoxanthine analog (inhibits xanthine oxidase, which converts xanthine to uric acid)

--metabolized by XO to alloxanthine (also XO inhibitor) and excreted renally

Front 195

allopurinol SE

Back 195

--nephrolithiasis

--skin rash, GI, headache, leukopenia

--severe skin rahs, hepatitis, eosinophilia

--can precipated acute gouty arthritis (used with colchicine)

--inhibits metabolism and inactivation of mercatopurine, azathioprine, theophylline and warfarin

Front 196

cholchicine MOA

Back 196

--binds tubulin (impairs neutorphil motibility)

-- inhibits oxidation of glucose nad subsequent lactic acid production in neutrophils

--used for prophylaxis against gout attacks

Front 197

cholchicine SE

Back 197

--GI: nausea, vomiting, diarrhea, abdominal pain, hemorrhagic gastroenteritis

--Bone marrow: temporary leukopenia followed by leukocytosis, aplastic anemia and agranulocytosis with long-term use

--alopecia

--long term use can lead to myopathy

Front 198

probenecid MOA

Back 198

competes with uric acid for weak acid carrier transporter (inhibits uric acid reabsorption)

Front 199

probenecid SE

Back 199

--GI, skin rash, stone formation

--inhibits renal excretion of penicillins, indomethacin, and sulfonylureas

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sulfinpyrazone

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similar to probenecid, has antiplatelet effects (inhibits platelet granule release, adherence to subendothelial cells, and prostaglandin syntheisis)

Front 201

sulfasalazine MOA

Back 201

minimal absorption of the drug in the upper GI tract, bacteria break azo bond and free salicylate derivative (local anti-inflammatory molecule)

--treats IBD and RA

Front 202

sulfasalazine SE

Back 202

sulfa allergy (rash, fever, Stevens-Johnson syndrome, hepatitis, nephritis, bone marrow suppression)

Front 203

hypnosis

Back 203

loss of awareness/perception of the environment

Front 204

sedation

Back 204

decreased responsiveness but can arouse to full awareness

Front 205

amnesia

Back 205

loss of remembrance of events (retrograde, anterograde)

Front 206

analgesia

Back 206

conscious insensibility to pain

Front 207

what do inhaled anesthetics do?

Back 207

--muscle relaxation (i.e. uterus, bronchial smooth muscle)

--depress ventilation and response to CO2/O2

--trigger malignant hyperthermia

--analgesia

--hypnosis

--amnesia

--abolition of autonomous reflexes

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meyer-overton

Back 208

--lipid solubility best correlates with inhaled anesthetic potency

--inhaled anesthetics insert themselves into lipid bilayers and disrupt ion channel function

Front 209

direct receptor effects of inhaled anesthetics

Back 209

--anesthetics bind to GABAa (and other) receptor complexes in the brain

--direct receptor-based effects inhibit excitatory neurotransmission and enhance inhibitory neurotransmitter action

Front 210

solubilities order of inhaled anesthetics

Back 210

Nitrous Oxide, Desflurane, Sevoflurane, Isoflurane, Halothane (most to least soluble)

Front 211

stages of anesthesia

Back 211

1) alert to loss of consciousness

2) Hyperexcitability

3) surgical anesthesia

4) Coma

Front 212

MAC

Back 212

minimum alveolar concentration (alveolar concentration of anesthetic at which 50% of patients cease to move when exposed to noxious stimulus)

Front 213

MAC awake

Back 213

the MAC at which consciousness is lost

Front 214

MAC classic

Back 214

MAC at which movement no longer occurs

Front 215

MAC BAR

Back 215

MAC at which BP and HR no longer change with stimulation

Front 216

Factors that increase MAC

Back 216

--hyperthermia

--chronic ETOH use

--increased catechol level

--daytime

Front 217

Factors that decrease MAC

Back 217

--hypothermia

--pregnancy

--hypotension

--hypoxemia

--acute ETOH use

--nighttime

Front 218

Halothane SE

Back 218

arrhythmic, hepatitis, metabolized by liver

Front 219

isoflurane SE

Back 219

tachycardia, pungent, most common

Front 220

desflurane SE

Back 220

most pungent, auonomic hyperactivity

Front 221

sevoflurane

Back 221

least pungent, nephrotoxic metabolite

Front 222

nitrous oxide

Back 222

teratogenic, not metabolized

Front 223

diazepam

Back 223

--GABAa to enhance Cl-flux

--produces hypnosis and amnesia (non-analgesic)

--tolerance and withdrawal

--minimal cardiovascular effects when used alone (significant effect when given with narcotics)

--CAN DEPRESS RESPIRATION

--Known sleep inducer

--reversible with flumazenil

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lorazepam

Back 224

--GABAa to enhance Cl-flux

--produces hypnosis and amnesia (non-analgesic)

--tolerance and withdrawal

--minimal cardiovascular effects when used alone (significant effect when given with narcotics)

--CAN DEPRESS RESPIRATION

--Known sleep inducer

--reversible with flumazenil

Front 225

midazolam

Back 225

--GABAa to enhance Cl-flux

--produces hypnosis and amnesia (non-analgesic)

--tolerance and withdrawal

--minimal cardiovascular effects when used alone (significant effect when given with narcotics)

--CAN DEPRESS RESPIRATION

--Known sleep inducer

--reversible with flumazenil

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thiopental

Back 226

--GABAa to enhance Cl- flux,

--barbiturate,

--produces hypnosis and amnesia

--produces tolerance and withdrawal

--acidic structure (high pH to stay water soluble)

--depresses ventilation, venous tone, and contractility

--acute intermittent porphyria

--reduce brain O2 consumption

--more potent in hemorrhagic shock

Front 227

methohexital

Back 227

--GABAa to enhance Cl- flux,

--barbiturate,

--produces hypnosis and amnesia

--produces tolerance and withdrawal

--acidic structure (high pH to stay water soluble)

--depresses ventilation, venous tone, and contractility

--acute intermittent porphyria

--reduce brain O2 consumption

--more potent in hemorrhagic shock

Front 228

pentobarbital

Back 228

--GABAa to enhance Cl- flux,

--barbiturate,

--produces hypnosis and amnesia

--produces tolerance and withdrawal

--acidic structure (high pH to stay water soluble)

--depresses ventilation, venous tone, and contractility

--acute intermittent porphyria

--reduce brain O2 consumption

--more potent in hemorrhagic shock

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propofol

Back 229

--acts on GABAa receptor, also acetylcholine and glycine

--produces hypnosis and amnesia

--depresses ventilation and circulation

--most hypotensive of all IV agents

--no tolerance effect

--most reliable offset

intraliid emulsion (eggs)

--contraindicated in children

Front 230

etomidate

Back 230

--Acts on GABAa receptor

--does not decrease BP, RR, respiratory drive

--myoclonus

--suppresses adrenal synthesis

--produces hypnosis and amnesia

--minimal eff

Front 231

ketamine

Back 231

--produce analgesia and dissociated anesthetic state, hypnosis

--releases endogenous catecholamines (increases BP, HR, bronchodilator)

--raises ICP

--minimal effects on respiratory drive

--causes nightmares

--inhibit excitatory glutamate signalling NMDA

(PCP derivative)

Front 232

dexmedetomidine

Back 232

--shuts down catecholamine synthesis

--alpha2 agonist

--produces hypnosis and amnesia also analgesia

--minimal respiratory depression

--bradycardia and hypotension

--relatively slow onset

Front 233

delirum

Back 233

1) acute onset or fluctuating course

2) inattention

3) disorganized thinking

4) altered level of consciousness

1) and 2) required; need either 3) or 4)

Front 234

benzodiazepine and narcotic

Back 234

synergistic sedative and hypotensive responses, respiratory depression

Front 235

substance abuse

Back 235

--a maladaptive patter of substance use

--clinically significant impairment or distress

--one or more of the following (recurrent use resulting in failure to fulfill major role obligations; recurrent use in situations where it is physically hazardous; recurrent substance-related legal problems; continued use despite persistent or recurrent social or interpersonal problems caused or exacerbated by the drug; not meeting criteria for substance dependence

Front 236

substance dependence

Back 236

1) tolerance

2) withdrawal

3) substance is often taken in larger amounts or a longer period of time than was intended

4) persistent desire or unsuccessful efforts to cut down or control use

5) great deal of time spent trying to obtain, using, or recovering from substance

6) important activities are given u or reduced because of use

7) use continued despite knowledge of problems related to the drug

need at least 3

Front 237

classes of abused drugs

Back 237

--stimulants/anorectics

--sedatives/tranquilizers

--hallucinogens

--cannabinoids

--opiods

--inhalants (most dangerous)

--ethanol

--nicotine

--methylxanthines

--dissociatives (ketamines)

--steroids

Front 238

schedule 1

Back 238

potential for abuse; no currently accepted medical use

(heroin, LSD, mescaline, peyote, cannabis, MDMA)

Front 239

schedule 2

Back 239

high potential for abuse; accepted medical use

(amphetamine, cocaine, fentanyl, hydromorphone, merperidine, methylphenidate, morphine, oxycontin, methamphetamine, pentobarbital, secobarbital)

Front 240

schedule 3

Back 240

intermediate potential for abuse; medical use

(anabolic steroids, acetaminophen with codeine, aprobarbital, butalbital, ketamine, paregoric, pentobarbital rectal suppository, thiopental

Front 241

schedule 4

Back 241

low potential for abuse, medical use

(alprazolam, butorphanol, chloral hydrate, chlordiazepoxide, diazepam, flurazepam, phenobarbital, propoxyphene, zolpidem)

Front 242

schedule 5

Back 242

very low potential for abuse

(acetaminophen or actifed with codein, robitussin AC with codeine, ephedrine and pseudoephedrine)

Front 243

tolerance

Back 243

--rightward shift in dose-response curve

--more drug needed to achieve same effect, or, diministed effect from same dose

--tolerance depends on the drug and on the outcome measure

Front 244

physical dependence

Back 244

--adverse symptoms experienced upon abrupt cessation of chronic use of a drug

--does not occur with all abused drugs

--does occur with some drugs that are not abused (e.g. anticholinergics)

--a common, but not defining characteristic of abused drugs

Front 245

cocaine MOA

Back 245

blocks reupdate of DA, NE, and 5HT (serotonin)

Front 246

amphetamine MOA

Back 246

facilitates release of DA, NE, and 5HT

Front 247

heroin

Back 247

mu opiod receptor agonist, indirect actions on DA

Front 248

nicotine

Back 248

nicotinic acetylcholine receptor agonist, indirect actions on DA

Front 249

marijuana

Back 249

endogenous cannabinoid receptor agonist CB1; indirect actions on DA

Front 250

alcohol

Back 250

actions on many receptor types (GABAa, serotonin, opiod, DA, glutamate)

Front 251

hallucinogens

Back 251

serotonin 2A and 2C receptors, indirect actions on DA

Front 252

MDMA MOA

Back 252

--stimulates serotonin release from presynapitc vesicles

--blocks reuptake through occupation of SERT

--MAOI

--also dopamine and noradrenaline release

--metabolized by the liver CYP2D6

Front 253

how to treat alcohol withdrawal

Back 253

acute: treat symptoms

Front 254

how to treat stimulant overdose

Back 254

benzodiazepine to manage anxiety

Front 255

how to treat sedative withdrawal

Back 255

long-acting barbituate (phenobarbital, gradual dose reduction)

Front 256

how to treat hallucinogent intoxication

Back 256

talking down, reassurance, benzodiazepines or neuroleptics without anticholinergic effects

Front 257

howt to treat opiate intoxication

Back 257

nalorphine or naloxone

Front 258

how to treat opiate withdrawal

Back 258

methadone in gradually decreasing doses; clonidine to reduce symptoms

Front 259

how to treat phencyclidine intoxication

Back 259

haloperidol or theothixene, diazepam relieves some symptoms

Front 260

symptoms of alcohol withdrawal

Back 260

alcohol craving, tremor/instability, nausea, sleep disturbance, tachycardia, hypertension, sweating, perceptual distortion, seizures, delirium tremens (severe agitation, confusion, visual hallucinations, fever/sweating, tachycardia/diarrhea, dilated pupils)

Front 261

alcohol withdrawal delirium:

Back 261

assess for malnutrition, anemia, gastritis, cirrhosis, electrolyte imbalance, dehydration

Front 262

stimulant overdose symptoms

Back 262

delusions, paranoia, dilated pupils, increased heart rate, blood pressure, temperature

Front 263

barbiturate withdrawal symptoms

Back 263

anxiety, insomnia, paranoia, visual hallucinations, nausea and vomiting, delirium, seizures

Front 264

hallucinogen intoxication symptoms

Back 264

perceptual distortions, paranoia, intense anxiety, visual hallucinations, feeling of invulnerability, religious experience

Front 265

opiate intoxication symptoms

Back 265

nausea, euphoria, drowsiness, apathy, constipation, analgesia, decreased heart rate and body temperature, slurred speech, pupil constriction

Front 266

opiate withdrawal symptoms

Back 266

anxiety, nausea, hot and cold flashes, yawning, persping, tearing, pupils dilated and unresponsive to light, gooseflesh, runny nose, diarrhea, vomiting, insomnia

Front 267

phencyclidine intoxication

Back 267

hostile, agitated, suspicious, paranoid, ataxic, dissociation of somatic sensation, sensorium clouded, position sense is impaired, muscle rigidity, spasticity

Front 268

types of substance abuse therapies

Back 268

agonist therapies, antagonist therapies, aversive therapies, targeting other disorders that exacerbate the drug problem