Pharm Exam Ii

Front 1

Cardiac myocyte resting potential determined by ?

Back 1

K+ (resting is -90 to -95), which is about what K+ equibrium potential is

Front 2

Where are fast response action potentials normal?

Back 2

atrial and ventricular muscle, and purkinje fibers (resting potential) about -90mV

Front 3

Slow response action potentials normal?

Back 3

SA node and AV node
-Resting membrane potentials about -5 mV

Front 4

Automaticity?

Back 4

slow decrease in K+ efflux
increase in Na+ and Ca++ influx

Front 5

Intrinsic automaticity rates?

Back 5

SA node --> 80-120
AV node --> 40-60
Purkinje (fast response)--> 20-40 bpm

Front 6

Where is Ca++ important or not?

Back 6

Important nodal tissue
Not important purkinje fibers

Front 7

When can Na+ enter cardiac cycle?

Back 7

Only during "OPEN" Na+ channels
-absolute refractory period --> Na+ channels inactivated and Na+ can't enter cell

Front 8

Fast response Vmax is function of ?

Back 8

available "rested" fast Na+ channels
-phase 0 action potential

Front 9

slowresponse Vmax is function of ?

Back 9

available "rested" fast Ca++
channels
-phase 0 action potential
(note: PR interval represents period of slow conduction)

Front 10

Antiarrythmic treatment could cause?

Back 10

EADs --> torsades de pointes

Front 11

Digitalis can cause?

Back 11

DADs

Front 12

Almost all clinically important tachyarrythmias are due to?

Back 12

reentry
-rqs unidirectional block and slowed conduction

Front 13

Class I

Back 13

Block fast Na+ channels

Front 14

Class II

Back 14

Block beta-adrenergic receptors

Front 15

Class III

Back 15

Block K+ chnnels/prolong repolarization

Front 16

Class IV

Back 16

Block Ca++ channels

Front 17

How do Class I drugs act?

Back 17

Block fast Na+ channels that open during PHASE 0 depol.

Front 18

What kind of action potentials act on?

Back 18

Fast response

Front 19

Physiological effect Class I?

Back 19

Slow conduction
-terminate reentrant arrythmias
-protect ventricles in Supraventricular Tachyarrythmias

Front 20

What happes to Phase 0 w/ Class I drugs?

Back 20

Decrease amplitued
Decrease rate of depolarization

Front 21

Problem w/ Class I drugs?

Back 21

May creat REENTRY circuit --> proarrythmic

Front 22

Besides myocardial cells, what else do Class I act on?

Back 22

Pukinje fibers
-->suppress automaticity
-->decrease abnormal automaticity in atrial and ventricular myocytes

Front 23

When does class I bind to Na+ channel/when released?

Back 23

binds --> Open or Inactivated
releases --> rested

Front 24

Besides Na+ block, other physiological effects Class IA drugs?

Back 24

K+ channel block --> increase action potential duration and effective refractory period (similar class III)

Anticholinergic effects --> INCREASE A-V conduction velocity --> speed conduction of impulses through AV node

Front 25

2 class IA drugs? --> what kind of dissociation rate?

Back 25

Quinidine
Procainamide
-intermediate dissociation rate

Front 26

Muscarinic and Alpha Receptor blockade?

Back 26

Quinidine

Front 27

Oral or IV

vs

Oral only?

Back 27

Oral or IV - Procainamide
Oral only--> quinidine

Front 28

Acetylated to NAPA?
*this was a USMLE world question w/ LUPUS syndrome (hint)

Back 28

Procainamide (N-acetyl Procainamide)

Front 29

What does NAPA do?

Back 29

Has class III properties --> blocks K+ channels

Front 30

1/3 patients discontinue due to GI affects?

Back 30

Quinidine
-also "quinidine syncope" --> alpha blockade

Front 31

Lupus-like autoimmune syndrome?

Back 31

Procainamide

Front 32

Pro-arrythmia (Torsades de pointes)

Back 32

Class III --> block K+
-Procainamide (NAPA)

Front 33

Class Ib? what kind of dissociation rates?

Back 33

Lidocaine
-fast dissociation rate, enhanced at Rapid heart rates

Front 34

Big difference of Lidocaine vs Quinidine or Procainamide?

Back 34

Decrease ACTION POTENTIAL DURATION and EFFECTIVE REFRACTORY PERIOD

Front 35

How does Lidocaine (class IB) exhibit use dependence?

Back 35

fast heart rate, depressed fast response action potentials when spend more time in open or active state

Front 36

How must Lidocaine be given for antiarrythmic therapy?

Back 36

IV
**DO NOT GIVE w/ EPI containing solution

Front 37

Toxicity of Lidocaine?

Back 37

local anesthetics (drowsiness, tremors, convulsions)

Front 38

Class IC? what dissociation rate?

Back 38

Flecainide, slow dissociation rate
-act at normal heart rates

Front 39

What feature do all Na+ channel blockers exhibit?

Back 39

use dependence

Front 40

Other action of Flecainamide (besides Na+ channel block)?

Back 40

blocks K+ channel --> (repolarization and prolongs actio potential duration inventricles)

Front 41

As opposed to Lidocaine, how do you take Flecainide?

Back 41

Oral only (recall, Lidocaine is IV only)

Front 42

IB vs IC mnemonic?

Back 42

IB is Best post MI
IC is Contraindicated post-MI

Front 43

Class II drugs act how?

Back 43

Beta adrenergic receptor antagonists

Front 44

Effect of beta blockade? --> what phase?
**magnitude depends on level sympathetic tone

Back 44

Phase 4 depolarization --> autonomic cells (sinus node AND purkinje fibers)

Front 45

Effect of beta blockade? --> general activity?
**magnitude depends on level sympathetic tone

Back 45

Decrease HR and ectopic automaticity (decrease rate phase 4)
-Enhance AV block (slow conduction)
-reduce myocardial contractility and oxygen demand

Front 46

What happens with stimulation of beta-adrenergic receptors?

Back 46

Increased cAMP in myocardial cells-->
phosphorylation of Ca2+ channels and Ca2+ influx

Front 47

2 beta blockers class II?

Back 47

Propanolol and Esmolol

Front 48

potential to block Na+ channels at high concentrations ("Quinidine like action"

Back 48

Propranolol

Front 49

Selective beta-1 blocker?

Back 49

Esmolol

Front 50

Non-selective beta blockers?

Back 50

Propranolol

Front 51

IV only?

Back 51

Esmolol

Front 52

Very short 1/2 life-->about 10 minutes and rapidly degraded by esterases?

Back 52

Esmolol --> this is why give IV

Front 53

Prevent cardiac death in post-MI patients?

Back 53

Propranolol

Front 54

Supraventricular arrythmias treatment?

Back 54

Propranol

Front 55

Why are beta-blockers effective?

Back 55

sympathetic activity of body may contribute to many forms of arrythmias

Front 56

Primary action Phase III drugs?

Back 56

block K+ channels
-Phase 3 depolarization

Front 57

What blocks Phase 0, versus 3

Back 57

Phase 0--> class I (Na+ channel)
Phase 3 --> Class III (K+ channel)

Front 58

Result of Class III drugs

Back 58

prolong action potential duration (prolong refractory period) in atrial and ventricular muscle and Purkinje fibers

Front 59

Class III drugs?

Back 59

Amiodarone (oral and IV)
Bretylium (IV only)

Front 60

Pulmonary fibrosis?

Back 60

Amiodarone

Front 61

Initial adrenergic stimulation, followed by INHIBITION of NE reelase?

Back 61

Bretylium

Front 62

Acts on normal myocardioctyes

Back 62

Bretylium

Front 63

Unique feature Amiodarone

Back 63

Has Class I, II, III properties

Front 64

Why only use Amiodarone short term therapy?

Back 64

long term --> PULMONARY FIBORIS, could also cause Torsades

Front 65

Unique feature of Bretylium

Back 65

Emergency treatment of sustained ventricular fibrillation

Front 66

Primary action Class IV drugs?

Back 66

blockade of L-type Ca2+ channels in myocardial and smooth muscle

Front 67

As w/ Na+ channels, class IV drugs exhibit?

Back 67

Use dependence
--> more effective at faster rates

Front 68

Where do Class IV drugs (like Diltiazem) exert effect?

Back 68

slow response action potentials
-sinus and AV nodes, depolarized or damaged cardiac myocytes

Front 69

What Phases does class IV act? effects?

Back 69

Phase 4--> decrease HR
Phase 0-->slow AV conduction

Front 70

Who contraindictaed for diltizem?

Back 70

CHF

Front 71

How might Diltiazem increase HR?

Back 71

-relaxation of vascular smooth muscle causes decreased arterial pressure, and baroreflex response may INCREASE HR (opp drugs's direct effect on sinus node)

Front 72

Why is Diltizaem effective a treating arrytmias?

Back 72

Slow AV conduction to decrease ventricular rate
-->effect of class IV drugs on AV CONDUCTION is basis for use in treating Supraventricular tachycardias

Front 73

What are the miscellaneous antiarrythmic drugs?

Back 73

Adenosine

Cardiac Glycosides (Digoxin)

Front 74

Blocks Na+/K+ ATPase?

Back 74

Digoxin (cardiac glycosides)

Front 75

Increase in parasympathetic activity

Back 75

Digoxin --> depolarizes baroreceptor nerve endings --> increase parasymp activity

Front 76

Why might First Aid say digoxin provides van gogh effect?

Back 76

cholinergic --> nausea, vomiting, diarrhea, blurry yellow vision (wasn't mentioned in class)

Front 77

Has an ultra-short half life?

Back 77

Adenosine --> must be given by rapid IV bolus

Front 78

How is Adenosine considered "vagomimetic"

Back 78

Acts through G-protein coupled adenosine receptors --> vagomimetic

Front 79

Whch system is most responsive to vasodilation from Nitrate stimulation?

Back 79

Veins>Arteries>Arterioles
**veins affected at very low doses

Front 80

Does sublingual or ointment nitroglycerine last longer?

Back 80

Nitroglycerine ointment lass much longer
-but sublingual acts very quickly

Front 81

What are the 2 organic nitrate drugs we need to know?

Back 81

Nitroglycerin
Isosorbide dinatrate

Front 82

What is the difference between Isosorbide dinitrate and Nitroglycerine?

Back 82

Nitro --> short 1/2 life (minutes), sublingual rapid

Isosorbide --> 5 hour half life, better for preventing angina

Front 83

In general, how do Organic Nitrates work?

Back 83

Vasodilate by releasing NO in smooth muscle --> increase cGMP --> smooth muscle relax

Front 84

Organic nitrates act more on preload or afterload?

Back 84

Decrease preload (LVEDP)

Front 85

Problem with Nitrates?

Back 85

Nitrate tolerance --> need 8 hour times when not using

Front 86

Side effects Nitrates?

Back 86

**reflex tachycardia, hypotension, flushing,headache

Front 87

Calcium channel blockers --> how act compared to Nitrates?

Back 87

They decrease AFTERLOAD
-VASODILATE CORONARY ARTERIES
-also reduce Heart Rate --> decreases myocardial O2 consumption

Front 88

"balanced" myocardial, electrophysiologic and vascular effects?

Back 88

Type I
-Verapamil
-Diltiazem

Front 89

Have predominantly vascular effects

Back 89

Type II Ca2+ channel blockers
-Nifidepine

Front 90

Which Ca2+ channel blocker causes most probs?

Back 90

Nifedipine --> 20% patients
-hypotension, headache, peripheral edema

Front 91

Which Ca2+ channel blocker causes least side effects?

Back 91

Diltiazem --> 5%
-hypotension, peripheral edema, AV block, cardiodepression

Front 92

Some side effects of Verapamil

Back 92

moderate --> anywhere from cardiodepression, hypotension, AV blcok, edema, headache, constipation

Front 93

How is Nifidepine different from Diltizem and Verapamil?

Back 93

Nifidipine --> mainly vascular smooth muscle
-Verapamil = ventricle --> balanced myocardial and vascular effects

Front 94

First aid says can also use nifidepine for?

Back 94

Prinzmetal's or Raynaud's

Front 95

How do beta blocker work to treat ischemic heart disease?

Back 95

Decrease myocardial O2 demand
-Decrease Heart rate
-Decrease myocardial contractility

Front 96

Main problem with beta blockers...+ a few side others?

Back 96

**May worsen bronchospasm
-CHF, bradyarrythmias

Front 97

Favorable effect beta blockers

Back 97

Reduce sudden death and infarction

Front 98

beta blocker we learned and why so good?

Back 98

Metoprolol --> proven post-MI effectiveness
-Beta 1>beta2 selectivity

Front 99

What is the basis for combo therapy of beta blockers and diuretics?

Back 99

compensatory response to vasodilators

Front 100

What is the phosphodiesterase inhibitor we learned about?

Back 100

Sildenafil (specifically acts on #5)

Front 101

What is Sildenafil used for?

Back 101

"Fills" the penis to give good erection
-PDE5 inhibitor (Viagra)
-decreased caclium via cGMP = smooth muscle relaxation

Front 102

What is a contraindication for use of Sildenafil?

Back 102

Nitrate use
**also may INHIBIT OR INDUCT CYP3A4

Front 103

First Aid mnemonic Sildenafil?

Back 103

Hot and sweaty --> but then Headache, Heartburn, Hypotension

-Risk life-threatening hypotension if taking nitrates

Front 104

What drug affects myocardial contractility?

Back 104

Digoxin (inotropic)
(Digitalis Glycosides)

Front 105

Where does Digoxin work?

Back 105

Inhibits sodium potassium ATPase -->increases intracellular Na+ --> increases intracellular Ca2+

Front 106

Effects of digitalis on the failing heart?

Back 106

Increased myocardial contractility
Increased sensitivity of baroreceptor nerve endings

Front 107

What is important to remember when administering Digoxin?

Back 107

Loading dose
**Narrow Therapeutic index

Front 108

Drug interactions with Digoxin?

Back 108

Quinidine can double levels
-diruretics as well

Front 109

Digitalis toxicity

Back 109

Cardiac arrytjmia, GI, Neurological

Front 110

Problem with diuretics?

Back 110

Excessive diuresis = volume depletion
-Loss of K+ problematic, esp. if taking digitalis

Front 111

Angiotensin Converting Enzyme Inhibitors? (ACE)

Back 111

Captopril
EnalAPRIL
Lisinopril

Front 112

Mechanism of ACE inhibitor?

Back 112

1. Inhibit conversion angiotensin I to angiotensin II
2. Increase BRADYKININ (vasodiliator) by inhibiting kininase II (may result in cough)

Front 113

Great effects of ACE inhibitors for someone w/ CHF?

Back 113

1. vasodilation
2. decrease aldosterone
3. decrease sympathetic activity
4. Decreased cardiac remodeling

Front 114

First ACE inihibtor?

Back 114

Captopril

Front 115

Major difference between Captopril and Enalapril?

Back 115

EnalAPRIL /-APRIL drugs are prodrugs
-->substantially longer 1/2 life (11 hours vs 2 hours for Captopril)

Front 116

Enalapril more or less side effects than Captopril?

Back 116

Similar, but fewer GI effects

Front 117

CAPTOPRIL mnemonic to remember adverse effects?

Back 117

Cough
Angioedema
Proteinuria
Taste Changes
hypOtension
Pregnancy probs (2nd and 3rd trimesters)
Rash
Increased renin
Lower angiotensin II + HYPOkalemia

Front 118

How is Losartan different from Captopril/others?

Back 118

Does NOT cause cough b/c it is an Angiotensis Receptor Blocker
-->does not cause Bradykin byproduct!

Front 119

Is Lisinopril as active as Captopril -->

Back 119

yes

Front 120

What are the Antiotensin Receptor Blockers (2)

Back 120

Valsartan
Losartan

Front 121

How do Angiotensin II receptor blockers work?

Back 121

bind receptors and displace angiotensin II from receptor
**KEY-->DO NOT INHIBIT BREAKDOWN OF BRADYKININ!!! --> don't cause cough

Front 122

Which works longer, Losartan or Valsartan?

Back 122

LOsartan works LOnger (6-9 hours) vs 6 hours

Front 123

Do ACE inhibitors and blockers reduce preload or afterload?

Back 123

Tricky --> BOTH :)!

Front 124

FYI, what to note about Spironolactone and Eplerenone?

Back 124

block aldosterone binding mineralcorticoid receptr
-->May cause HYPERkalemia
-may have significant impact on myocardial remodeling

Front 125

First beta blocker labeled for treatment of mild to moderate heart failure?

Back 125

Carvedilol

Front 126

Mechanism of Carvedilol

Back 126

Nonselective beta and alpha-adrenergic receptor antagonist

Front 127

First line therapy for structural heart dz w/ no symptoms?

Back 127

ACE inhibitors or ARBs in all patients, beta blockers in selected patients

Front 128

What might you try after than

Back 128

Diuretics and Digoxin --> once symptomatic

Front 129

When should you use Inotrpes

Back 129

Refractory symptoms requiring special intervention

Front 130

Which drugs affect primarily preload?

Back 130

Nitrates

Front 131

Which drugs primarily affect afterload?

Back 131

Hydralazine

Front 132

tranpsorts cholesterol to the liver, where it is broken down to become part of bile that is excreted in feces?

Back 132

HDL

Front 133

transports cholesterol from liver to other organs --> build plasma membranes/make sterols --> plaque deposits and coronary artery dz --> "bad cholesterol"

Back 133

LDL

Front 134

FYI, what to note about Spironolactone and Eplerenone?

Back 134

block aldosterone binding mineralcorticoid receptr
-->May cause HYPERkalemia
-may have significant impact on myocardial remodeling

Front 135

First beta blocker labeled for treatment of mild to moderate heart failure?

Back 135

Carvedilol

Front 136

Mechanism of Carvedilol

Back 136

Nonselective beta and alpha-adrenergic receptor antagonist

Front 137

First line therapy for structural heart dz w/ no symptoms?

Back 137

ACE inhibitors or ARBs in all patients, beta blockers in selected patients

Front 138

What might you try after than

Back 138

Diuretics and Digoxin --> once symptomatic

Front 139

When should you use Inotrpes

Back 139

Refractory symptoms requiring special intervention

Front 140

Which drugs affect primarily preload?

Back 140

Nitrates

Front 141

Which drugs primarily affect afterload?

Back 141

Hydralazine

Front 142

tranpsorts cholesterol to the liver, where it is broken down to become part of bile that is excreted in feces?

Back 142

HDL

Front 143

transports cholesterol from liver to other organs --> build plasma membranes/make sterols --> plaque deposits and coronary artery dz --> "bad cholesterol"

Back 143

LDL

Front 144

Lipid lowering drugs can cause myopathy/renal failure?

Back 144

Statins

Front 145

How do statins act?

Back 145

Competitively inhibit HMG-CoA Reductase --> RLS cholesterol synthesis

Front 146

When is it best to give statins?

Back 146

At night (during night cholesterol synthesis increases)

Front 147

What are the Statins we need to know?

Back 147

Simvastatin
Pravastatin
Atorvastatin

Front 148

Simvastatin
Pravastatin
Atorvastatin
-prodrug (simple diffusion)

Back 148

Simvastatin

Front 149

Simvastatin
Pravastatin
Atorvastatin
-uptake by OATP2

Back 149

Pravastatin

Front 150

Which is not high first hepatic metabolism b/c of P450 3A4, 2C9

Back 150

Pravastatin

Front 151

Which takes about 20 hours to reach peak plasma concentration?

Back 151

Atrovastatin

Front 152

Are statins highly bound?

Back 152

yes --> >95% protein binding in plasma

Front 153

Biggest side effects of stains?

Back 153

Myopathy and Renal Failure
-Neuropathy
-Contra moms
-Liver problems

Front 154

Drug Drug interactions statins?

Back 154

-P450 3A4 --> increased Coumarin levles
-OAT2 inhibitors - gemfibrozil --> increased circulating statin levels

Front 155

Good news about statins?

Back 155

first choice for treatment of most patients w/ hypercholesterolemia

Front 156

Which statin can you take w/ or w/o food and anytime of day?

Back 156

Atorvastatin

Front 157

How do Bile Acid-binding Resins (sequestrants) work?

Back 157

Bind anionic bile acids in intestinl lumen
-->resin-bile acid complex cannot be absorbed --> excreted in stool

Front 158

How does lowering concentration of bile acids help?

Back 158

causes hepatocytes to increase conversion of cholesterol to bile acids --> decreases intracell cholesterol
-->increase number hepatic LDL receptors
-->increased uptake LDL particles

Front 159

What are the Bile acid binding resins we learned about (3)

Back 159

Cholestipol, Cholestyramine, Colesevelam

Front 160

Why is Colsevelam especially good, but why bad?

Back 160

take a little bit less, but first aid says patients hate b/c tastes bad

Front 161

When are bile-acid binding resins not useful?

Back 161

Patient w/ hypertriglyceridemia (high TG w/o elevated LDL)
-useful only where LDL is elevated, can also increase HDL cholest. some

Front 162

Side effects Bile acid binding residues?

Back 162

May increase TG
-Gi distress/Constipation, bloating
-decreased absorption of other drugs; take 1 hr or 3 hrs before taking the resin

Front 163

How does Ezetimibe act?

Back 163

inhibits cholesterol absorption
-brush boder jejunem enterocytes (Niemann-Pick C2-like protein)

Front 164

major impact on cholesterol ezetimibe?

Back 164

inihibts cholesterol absorption by ~55%
-reduces LDL 18%

Front 165

Two big actions of fibric acids?

Back 165

1. Decreased synthesis of VLDL (decrease in VLDL, increase HDL, ecrease in trigylcerides, +/- LDL)
2. Complex MoA involving PPAR-alpha agonism and altered gene expression

Front 166

What are the 2 fibric acid derivatives we need to know?

Back 166

Fenofibrate
Gemfibrozil

Front 167

How are Fenofibrate
Gemfibrozil different?

Back 167

Fenofibrate - 20 hr t1/2
Gemfibrozil - 1.1 hr t1/2

Front 168

Why is Fibric acid activation of PPAR-alpha so useful?

Back 168

Decrease plasma triglyceride levels
Increase plasma HDl
-increases activity of lipoprotein lipase, esp. in skeletal muscle

Front 169

Fibrates are most effective at?

Back 169

Reducing VLDL (TG), smaller decrease in LDL but useful increase in HDL

Front 170

Major HDL lipoproteins vs VLDL?

Back 170

PPAR-alpha
-increase ApoAI and AII (HDL)
-decrease ApoCIII (VLDL)

Front 171

Main side effects fibrates?

Back 171

myalgias, rhadomyolysis, gallstones, etc.

Front 172

Important interaction of fibrates?

Back 172

Increased Rhabdomyolysis with STATIN!!!

Front 173

Drug interactions of Fibrates (Gemfibrozil and Fenofibrate)?

Back 173

Warfarin --> increase of free warfarin concentration--> bleeding

Cyclosporine --> increased clearance of this immunosupressant --> acute organ transplant rejection

Front 174

Most effective agent for raising HDL?

Back 174

Nicotinic acid (Niacin, Vitamin B3)

Front 175

What does Nicotinic acid act on/not?

Back 175

Reduces VLDL and LDL
-No effect on synthesis of cholesterol or excretion of bile acids

Front 176

user problem with niacin?

Back 176

frequent dosing

Front 177

What does niacin (B3) act on?

Back 177

decreases activity of hormone sensitive lipase

Front 178

Biggest problem with niacin

Back 178

Ulcers

Front 179

First aid mentions a few problems with niacin

Back 179

Red, flused face (decreased w/ aspirin), hyperglycemia (acanthosis nigricans), Hyperuricemia --> exacerbates gout
Itching

Front 180

Contraindications

Back 180

-->liver d, severe gout, peptic ulcer

Front 181

Safe combos?

Back 181

Niacin + resin
(first choice against heterozygous famililal hypercholesterolemia)

Front 182

Safer combos

Back 182

Statin + bile acid sequestrant --> LDL-lowering

Front 183

Riskier combos

Back 183

Statins + fibric acid or Niacin
-->greater incidence myopathy

Front 184

Which type of OR (opoid receptor) produces some Dysphoria

Back 184

Kappa (think of the kappas being high)

Front 185

How do opoids act presynaptically?

Back 185

decreases Ca2+ influx and synaptic vesicle release in response to APs

Front 186

How do opoids act postsynaptically

Back 186

activate Mu-OR --> increases K+ conductance --> decreases the postsynaptic response to excitatory neurotransmission

Front 187

Opoids also inhibit adenyl cyclase --> what does this do?

Back 187

decrease of cAMP and inhibition of Na+ channels

Front 188

Strong Mu OR agonists include (5)

Back 188

Morphine
Heroin
Methadone
Meperidine
Fentanyl

Front 189

What is the gold standard Mu OR agonist?

Back 189

Morphine

Front 190

Main pharacological effects morphine?

Back 190

Analgesia
Suppression of cough (ORs in CTZ)
Respiratory depression
Reduce GI motility --> constipation
Bronchoconstriction and hypotension --> don't use in asthma

Front 191

How is morphine given?

Back 191

High first pass
-->given injection (IV or IM) or slow-release tablets

Front 192

How is morphine metabolized

Back 192

Liver --> problem with neonates

Front 193

What happens if morphine used with MAO-I?

Back 193

Hypertensive crissis possible --> blocks reputake serotonin

Front 194

classic feature of someone with morphine ooverdose?

Back 194

Pinpoint pupils, respiratory depression

Front 195

Hypertensive crisis?

Back 195

Opoids hyperstimulate postsynaptic serotonin receptors by blocking serotonin re-uptake

Front 196

How does Heroin compare to Morphine?

Back 196

Not stronger but faster
-->very lipid solube, readily crosses BBB, short half life

Front 197

Why is Methadone a handy drug?

Back 197

USed for treatment of Opoid abuse --> in presence of methadone, morphine does not cause the normal EUPHORIA or physical abstinence syndrome

Front 198

What features about Methadone make it an appropriate treatment of Opoid abuse?

Back 198

longer duration of action >24 hours --> less w/drawal effects

Front 199

Problems with Methadone

Back 199

Respiratory depression
-Rifampin (TB tx) lwoers levels of methadone

Front 200

Unique feature of Meperidine?

Back 200

Does NOT produce pnpoint pupil

Front 201

Who do you never give Meperidine to?

Back 201

MAO-I --> resp. depression, hyperpyrexia, convulsions

Front 202

Meperidine drug interactions?

Back 202

pentobarbital and thiopental, heparin, methicillin, sodium bicarb
*MAO-I

Front 203

Meperidine life-threatening side effects?

Back 203

Significant anitmuscarinic effects (contra if tachycardia)
Negative ionotropic action
Resp depression
Cardiac arrest

Front 204

How does Fentanyl compare with morphine?

Back 204

similar but more POTENT and FAST-ACTING

Front 205

Fentanyl drug interactions?

Back 205

incompatible with pentobarbital and thiopental
-if taken w/ MAO-I may precipitate hypertensive crisis

Front 206

Fentanyl, like many other drugs, can cause?

Back 206

Respirtory depression

Front 207

WHat are some Mild agonists of Opoid receptors?

Back 207

Codeine
Hydrocodone
Oxycodone
Propoxyphene

Front 208

How is codeine used?

Back 208

in combination with aspirin or acetaminophen

Front 209

Other use of codeine besides pain management?

Back 209

Antitussive and antidiarrheal treatment

Front 210

Bad drug combo codeine?

Back 210

Coma is possilbe when combined w/ CHLORDIAZEPOXIDE
-note: alcohol will make sleepy

Front 211

Why is Hydrocodone not as good as Codeine?

Back 211

more addiciting and slightly more antitussive action
-also respiratory depression

Front 212

Oxycodone, like codeine, is given in cobo with Acetaminophen and asprin --> how is its potency?

Back 212

10-12 X more potent than codeine
-also alters perception of pain
-no antitussive action

Front 213

Life threatening unique side effect Oxycodone?

Back 213

HepatOtOxicity --> OxycOdOne

Front 214

Really bad side effect of Propoxyphene

Back 214

Fatalities reported with alcohol, less effective than codeine (also resp. depression, like most)

Front 215

What are 3 Opoids with mixed receptor actions?

Back 215

Buprenophine
Pentazocine
Tramadol

Front 216

How does Buprenorphine compare with morphine?

Back 216

Partial Mu agonist--> 25-50X that of morphine

Kappa antagonist >3 times than Naloxone

Front 217

How long does Buprenorphine act?

Back 217

slow dissociation from Mu receptors

Front 218

What particular use does Buprenorphine have?

Back 218

Reduce Opiate addiction

Front 219

Drug interactions of Buprenorphine

Back 219

possible resp or CV collapse w/ diazepam

Front 220

Life threatening side effects

Back 220

Resp depression (like most)

Front 221

Primary action of Pentacozine?

Back 221

KAPPA receptors (analgesia) agonist

Front 222

Where else is Pentacozine an antagonist?

Back 222

Mu and Delta receptors

Front 223

What may happen if use Pentaxozine in Mu dependent people?

Back 223

Precipitate withdrwal syndrome

Front 224

How is Pentacozine different from morphine?

Back 224

MUCH less Euphoria than morphine
-still can cause resp depression though

Front 225

unique side effect pentacozine?

Back 225

Increases BP and thus myocardial workload --> should NOT be administered in MI

Front 226

How is tramadol a unique analgesic?

Back 226

Inhibits Norepinephrine and serotonin re-uptake in CNS --> central acting

Front 227

what receptor does tramadol act?

Back 227

weak Mu receptor agonist

Front 228

Drug interactions tramadol?

Back 228

MAO-I

Front 229

Side effects unique to tramadol?

Back 229

Urine retention, constipation, anxiety, anorexia, rash

Front 230

2 Opoid antagonists?

Back 230

Naloxone and Naltrexone

Front 231

What is the action of opoid antagonists in normal people?

Back 231

Not really much action

Front 232

Are there any side effects to Naloxone or Naltrexone

Back 232

NONE! :)

Front 233

First Pure Opoid ANTAGONIST
-affinity for all 3 types of opoid receptors

Back 233

Naloxone

Front 234

Naloxone vs Naltrexone half life

Back 234

Naloxone --> first and slowest 1/2 life

Naltrexone has longer duration of action/1/2 life

Front 235

When use Naloxone?

Back 235

Life threatening situations for narcotic overdose (heroin)

Front 236

When Use Naltrexone?

Back 236

Detoxification

Front 237

Baby side effects Naloxone

Back 237

=too rapid reversal may cause sweating, arrhythmias/tachycardia, nausea, vomiting

Front 238

Naltrexone side effect

Back 238

Hepatotoxicity

Front 239

Why is the lcinical use of opoids limited?

Back 239

tolerance and dependance

Front 240

How does one become tolerant to morphine?

Back 240

desens. of mu and delta receptors by PKC, PKA, and beta-adrenergic receptor kinase

etorphine and enkephaline, but not morphine cause rapid internalization of mu receptor

Front 241

Opoid abstinance syndrome?

Back 241

Early --> piloerection (cold turkey), anxiety, drug requests, dilated pupils
Late-->nausea and vomiting, diarrhea, fever, ab pain, tachycardia, insomnia

Front 242

proposed mechanism of general anesthetics?

Back 242

increase the activity of GABA receptors and potassium channels and decrease the activity of acetylcholine receptors and glutamate receptors

Front 243

What do Barbiturates do well?

Back 243

Rapid onset Anesthesia

Front 244

What do Barbiturates do poorly?

Back 244

Poor Analgesia, little muscle relaxation

Front 245

Good features about Barbiturates?

Back 245

Rapid onset, terminated by redistribution

Front 246

How can you make terminal 1/2 lives of barbiturates longer?

Back 246

continued infusion

Front 247

What barbiturate still has relatively rapid clearance, even with continued injusion?

Back 247

Methohexital

Front 248

Who are barbiturates contraindicated in

Back 248

Porphyria

Front 249

Are barbiturates potentially helpful for seizures?

Back 249

yes

Front 250

Who requires higher induction dose of barbiturates?

Back 250

Neonates and infants

Front 251

Barbiturate toxicity?

Back 251

decreased cerebral metabolism, blood flow, blood pressure, respiration, muscle tremors, hiccups

Front 252

What does Methohexital have especially bad sideeffects?

Back 252

Paradoxical excitation (muscle tremors)

Hiccups

Front 253

What is the most commonly used barbiturate?

Back 253

Thiopental

Front 254

What are the 3 barbiturates we learned?

Back 254

Thiopental
Thiamylal (not recommended for use)
Methohexital

Front 255

Mechanism of action of barbiturates?

Back 255

Facilitate GABAa action by increase duration of Cl- opening, thus DECREASE neuron firing

Front 256

How is Propofol similar to barbiturates?

Back 256

Onset and duration (redistribution important)
**similar toxicities
**Potentiates GABAa

Front 257

How is Propofol different from Barbiturates?

Back 257

High degree of clearance (hepatic) --> less "hangover" than thiopental
**good for short procedures

Front 258

Why might sensitive people not like propofol?

Back 258

Pain on injection (FYI MJ supposedly died from propofol)

Front 259

What drug is cardiostable, so used in patients with risk for hypOtension?

Back 259

Etomidate --> used for induction

Front 260

Why is Etomidate only used for induction?

Back 260

Poor analgesia

Front 261

Toxicity we need to know about Etomidate?

Back 261

Nausea and Vomiting
Suppression of adrenocortical stress response
**note: fentanyl prolongs elimination 1/2 life

Front 262

How does Ketamine act, compared to barbiturates, etomidate, and Propofol?

Back 262

Blocks GLUTAMATE receptors, not GABAergic

Front 263

Who is Ketamine used in?

Back 263

patients w/ risk for Hypotension or brochospasm since it increases blood pressure and is a bronchodilator
-->useful in children undergoing short painful procedures

Front 264

What kindof state does Ketamine put patient in?

Back 264

It is an IV anesthetic by itself (analgesic) and provides amnesia despite the patient being awake (Dissociative state)

Front 265

Describe someone in dissociative anesthesia/cataleptic state

Back 265

Profound Analgesia, are amnesiac, and are unresponsive to commands

Eyes open, move limbs involuntarily, breathe spontaneously

Front 266

Ketamine drug interactions?

Back 266

potentiates non-depolarizing muscle relaxants --> (ketamine+theophylline --> seizures), toxicity includes delirium and cataleptic state

Front 267

What drugs provide pain at injection site?

Back 267

Propofol, Etomidate (methohexital)

Front 268

Who use for patients at risk for hypotension?

Back 268

Etomidate or Ketamine

Front 269

Who use for patients at risk for bronchospasm

Back 269

Ketamine

Front 270

Decreases blood pressure and depresses respiration?

Back 270

Propofol

Front 271

Can produce nausea and vomiting, suppresses stress response

Back 271

Etomidate

Front 272

Can cause cataletpic state?

Back 272

Ketamine

Front 273

Emergence delirium

Back 273

Ketamine

Front 274

Slow clearance after continous infusion?

Back 274

Thiopental

Front 275

More rapid recovery?

Back 275

Propofol

Front 276

The above questions are very high yield, at least make srue you know them very well!!!

Back 276

Do it

Front 277

Musculalar rigidity?

Back 277

Opoids and Ketamine

Front 278

Hallucinations and emergence delirium?

Back 278

Katamine

Front 279

Steroidogenesis inhibition?

Back 279

Etomidate

Front 280

Reduces pain threshold (???)

Back 280

Thiopental

Front 281

Increases cerebral blood flow, while other decrease?

Back 281

Ketamine

Front 282

How does blood gas coefficient relate to induction of anethesia and duration of action?

Back 282

Higher blood/gas partition coefficient, longer it takes to induce anestheia and the longer duration of action

Front 283

Lower cardiac output causes slower or faster induction?

Back 283

Faster

Front 284

One thing to know about Halothane?

Back 284

Liver toxcity --> drug induced hepatits and hepatic necrosis

Front 285

Other big side effect Halothane?

Back 285

Malignant Hypothermia --> genetic predispostion
-->use dantolene as treatment

Front 286

Ptoency, induction? Halothane

Back 286

Very potent
Slow induction (high blood gas coefficient)
note: also decreases cerebral blod flow

Front 287

One thing to know about Enflurane?

Back 287

Increased seizure activity (pro-convulasant)

Front 288

One thing to know about Isoflurane?

Back 288

Dilates coronary arteries (potential for "coronary steal", use avoided in patients w/ coronary heart dz)

Front 289

What is coronary steal

Back 289

if coronary heart dz, may perfuse dead tissue with oxygen as result of mass vasoidilation, taking it from where it is needed

Front 290

One thing to know about Desflurane?

Back 290

Coughing, salivation, bronchospasm in awake patients (strong airway irritant and therefore not used for induction)

Front 291

Sevoflurane fact to know?

Back 291

toxicity concern rapidly developing nervous system
**RAPID USE, TURN OFF/ON quickly

Front 292

Methoxyflurane fact to know?

Back 292

withdrawn because Fluoride ions cause kindey damage

Front 293

What drug could cause impotent?

Back 293

Nitrous oxide
MAC = 105!!!!

Front 294

What concentration can you not used N2O (nitrous oxide) above?

Back 294

80% --> result in hypoxia --> adjunct to other anesthetics at 50-70%

Front 295

Where might Nitrous Oxide accumulate?

Back 295

Gas-filled spaces and can cause bowel distension, pneumothorax, pain with obstructed inner ear

Front 296

What do you need to give at the end of anesthesia invovling N2O?

Back 296

100% oxygen to avoid diluting O2 in lung, causing "diffusional hyoxia"

Front 297

Who is N2O contraindicated in?

Back 297

Patients with Pulmonary Hypertension due to increased vascular resistance!!!

Front 298

Metabolite toxicity of inhalation anesthetics?

Back 298

Trifluoracetylchloride --> halothane
Kidney damage w/ methoxflurane

Front 299

What inhalation anesthetics migh cause malignant hyperthermia?

Back 299

Halogenated agents (all but N2O), especially worse w/ Halothane

Front 300

Do neuromuscular blockers have Analgesic properties?

Back 300

No

Front 301

What are Non-depolarizing neuromuscular blockers? vs the one depolarizing NMB we learned about?

Back 301

-onium/-urium drugs and d-Tubocuraine are non-depolarzing

Depolarzing --> succinylcholine

Front 302

Shared action of Non-depolariing NMJ blockers?

Back 302

COMPETITIVE ANTAGONISTS at NICOTINIC RECEPTORS of the NMJ
-->compete w/ acetycholine

Front 303

Prototype Non-depolarizing Neuromuscular blocker?

Back 303

d-Tubocurarine

Front 304

Are non-depolarzing NMJ blockers orally active?

Back 304

no

Front 305

Sequence of paralysis NMJ non-depol blockers?

Back 305

fine movement (Fingers) > LImbs>Trunk>intercostals>diaphragm
**Recovery in reverse order
**BREATHING recovers first

Front 306

Problems w/ non-depolarzing NMJ blockers?

Back 306

ganglionc blockade = decreased BP
Histamine release = decreased BP, bronchospasm secretions
Muscarinic receptor blocker = tachycardia

Front 307

How is d-tubocurarine eliminated?

Back 307

Renal elimination , 3.5 hour half life (relatively long for NMJ blocker)

Front 308

How increase recovery from paralysis from non-depolarizing NMJ blocker??

Back 308

Administer cholinesterase inhibitor

Front 309

Hepatic metabolism?

Back 309

Vecuronium

Front 310

Hoffman Elimination (spontaneous breakdown)?
Vecuronium
Atracurium
Mivacurium?

Back 310

Atracurium

Front 311

Plasma esterases break it down, shortest duration of action
Vecuronium
Atracurium
Mivacurium?

Back 311

Mivacurium

Front 312

What can be given w/ the anticholinesterase inhibitors (to help minimize side effects NMJ non-depol blockers), to help minimize their side effects?

Back 312

Muscuarinic anticholinergic agents like atropine can minimize bradycardia, bronchoconstriction, and salivation

Front 313

What undergoes spontaneous depolarization, and therefore has more predictable response in all?
Vecuronium
Atracurium
Mivacurium
Pancuronium?

Back 313

Atracurium (recall, Hoffman/spontaneous degradation/elimination)

Front 314

What has much greater differences in the elderly and renal failure --> less predicatable response
Vecuronium
Atracurium
Mivacurium
Pancuronium?

Back 314

Pancuronium

Front 315

Drug interactions of NMJ non-depolarizaing blockers?

Back 315

Calcium channel blockers (decrease release acetylcholine)

Certain inhalation anesthetics (halothane, isoflurane, enflurane, desflurane, sevoflurane) --> action potentiated

Aminoglycoside antibiotics

Front 316

What is the one depolarizing neuromuscular blocker we elarned?

Back 316

Succinylcholine

Front 317

What is the mechanism of succinylcholine?

Back 317

Depolarizing blockade
-agonist that acts like an antagonist

Front 318

How quickly does succinylcholine act?

Back 318

Shortest time to onset (~1 min) and duration of action (5-10 min)

Front 319

Initial response to administration succinylcholine

Back 319

Wave of fasciculation

Front 320

Phase I block (early in block) succinylcholine?

Back 320

cholinesterase inhibitors INTENSIFY BLOCK (prolonged depolarization), no antidote!!

Front 321

Phase II block succinylcholine and chloinesterase inhibotrs?

Back 321

cholinesterase inhbitors may potentially reverse block (use neostigmine)

Front 322

Problems associated with depolarizing Neuromuscular blockade (succinylcholine)

Back 322

Myalgia (muscle soreness)
K+ release from skeletal muscle --> hyperkalemia --> cardiac arrhythmias
**beware in patients w/ extensive burns or soft tissue damage + paraplegics
Atypical pseudocholinesterase-->prolonged paralysis
Malignant hyperthermia (rare)

Front 323

Skeletal muscle relaxants

Back 323

Baclofen
Dantrolene

Front 324

GABAb rececptor agonist?

Back 324

Baclofen
-acts in spinal cords and supraspinal CNS --> inhibit excitation to motor neurons

Front 325

Who use Baclofen for?

Back 325

Treatment of SPASTICITY associated w/ MS
Spinal cord injury
Trigeminal neuralgia (tic de leroux)

Front 326

Inhibits calcium release form sarcoplasmic reticulum in skeletal muscle?

Back 326

Dantrolene

Front 327

Use Dantrolene?

Back 327

tx of malignant HYPERthermia (caused by inhalation of anesthetics (except N2O) and succinylcholine

Front 328

First aid use of dantrolene?

Back 328

Treat neuroleptic malignant sydrome (toxicity of antipsychotic drugs)

Front 329

treatment of cardiac arrythmias

Back 329

Lidocaine for ventricular arrhythmias

Front 330

Mucosal vasoconstrictor of upper airway?

Back 330

cocaine

Front 331

obtund pressor resposne to tracheal intubation

Back 331

IV lidocaine

Front 332

drug of abuse

Back 332

cocaine

Front 333

Local anesthetics work at what type of channel?

Back 333

reversibly block nerve conduction through inhibition of sodium channel activity (fast voltage-gated channels)

Front 334

Which form of local anesthetics bind to channel?

Back 334

Ionized drug binds to channel
**but penetrates membrane in uncharged form
**effect of pH is a crucial concept

Front 335

Local anesthetics preferntially bind to ?

Back 335

inactivated sodium channels --> stabilize inactive state
-->block FAST FIRST

Front 336

Primary action local anesthetics

Back 336

Sensory nerves>motor nerves (somatic and autonomic)>CNS>CVS>other smooth muscle>skeletal muscle

Front 337

Sensory nerve sodium gated channel?

Back 337

Nav1.7

Front 338

Order of functional block and recovery local anesthetics?

Back 338

pain, autonomic C-fibers>cold>warmth>touch>deep pressure>motor

Front 339

treatment of cardiac arrythmias

Back 339

Lidocaine for ventricular arrhythmias

Front 340

Mucosal vasoconstrictor of upper airway?

Back 340

cocaine

Front 341

obtund pressor resposne to tracheal intubation

Back 341

IV lidocaine

Front 342

drug of abuse

Back 342

cocaine

Front 343

Local anesthetics work at what type of channel?

Back 343

reversibly block nerve conduction through inhibition of sodium channel activity (fast voltage-gated channels)

Front 344

Which form of local anesthetics bind to channel?

Back 344

Ionized drug binds to channel
**but penetrates membrane in uncharged form
**effect of pH is a crucial concept

Front 345

Local anesthetics preferntially bind to ?

Back 345

inactivated sodium channels --> stabilize inactive state
-->block FAST FIRST

Front 346

Primary action local anesthetics

Back 346

Sensory nerves>motor nerves (somatic and autonomic)>CNS>CVS>other smooth muscle>skeletal muscle

Front 347

Sensory nerve sodium gated channel?

Back 347

Nav1.7

Front 348

Order of functional block and recovery local anesthetics?

Back 348

pain, autonomic C-fibers>cold>warmth>touch>deep pressure>motor

Front 349

oder of action of local anesthetics on fiber size?

Back 349

(autonomic fibers),C, A-delta>>A-alpha,A-beta>A-alpha, motor fibers
**in general, small more suscible than large

Front 350

Crucial concept to remember about order?

Back 350

Autonomic fibers>=pain>sensory>motor

Front 351

Key property of Bupivacine

Back 351

Sensory anesthesia>>>motor blockade

Front 352

2 main types of local anesthetics?

Back 352

amide and ester LAs

Front 353

First aid mnemoic to remeber diffs amides and esters?

Back 353

Amides have 2 I's --> LidocaIne, EtIdocaIne, bupivacaine, mepivacaine

Front 354

degraded by plasma esterases (plasma cholinesterase)?

Back 354

Ester type

Front 355

How can ester types of local anesthetics cause problems?

Back 355

PABA metabolism product can inhibit sulfonamides --> allergic reactions

Front 356

Degraded by hepatic cytochrome P450s?

Back 356

Amide type local anesthetics
-->problems w/ patients w/ severe hepatic disease

Front 357

Longer duration of action?
Bupivacine
Ropivacaine
Tetracaine
Lidocaine
Prilocaine?

Back 357

Bupivacaine
Ropivacaine
Tetracine

Front 358

medium duration of action?
Bupivacine
Ropivacaine
Tetracaine
Lidocaine

Back 358

Lidocaine
Priolocaine

Front 359

How do you increase the duration of action of amide type local anesthetics?

Back 359

protein binding and hydrophobicity

Front 360

where is drug elimination of esters less?

Back 360

CNS --> ester hydrolysis by cholinesterases is less here

Front 361

Most common local anestetic OTC?

Back 361

Benzocaine

Front 362

topical anesthesia ears, noset, throat, only?

Back 362

Cocaine --> vasoconstricting action --> blocks reuptake NE

Front 363

Eutectic mixture (low melting point) of what 2 drugs allows anesthetic action to 5 mm depth after topical administration?

Back 363

Licocaine and Priolcaine
**bridges gap btwn topical and infiltration anesthesia

Front 364

Concerns of Metheoglobinemia?

Back 364

Benzocaine

Front 365

What will prolong duration of action of infiltration anesthesia?

Back 365

Epinephrine

Front 366

Bad fact about infiltration anesthesia?

Back 366

Patient may experience pain immediately after injection

Front 367

Infiltration anesthesia 3 drugs and durations of action?

Back 367

Short: procaine
Moderate: lidocaine
Long: bupivacaine

Front 368

cardiovascular collapse reported after using this drug via IV regional anethesia?

Back 368

Bupivacaine

Front 369

most commonly used drug via IV regional anethesia?

Back 369

Lidocaine w/o epinephrine
some prefer prilocaine for less vasodilation

Front 370

What can be added when doing a peripheral nerve blockade to raise pH and speed onset?

Back 370

Sodium bicarbonate

Front 371

Cardiotoxic potential epidural anesthesia?

Back 371

Bupivacine --> used for long duration surgeries

Front 372

Induces motor block --> good for muscle relaxation with epidural anesthesia

Back 372

Etidocaine

Front 373

Drugs potentially used for spinal anesthesia?

Back 373

Lidocaine
Tetracaine
Bupivacaine

Front 374

potential problem of spinal anesthesia?

Back 374

sympathetic block, vasodilation common, blood pooling, reduced cardiac output, age dependent

Front 375

Toxicity of local anesthetics on heart?

Back 375

decreased conduciton, force of contraction, and excitability
**Bupivacaine more cardiotoxic than lidocaine

Front 376

Hypersensitivity reactions mostly caused by

Back 376

esters, sometimes amides
**also reaction to vasoconstrictors

Front 377

If seizure as result of local anesthetic toxicity can use?

Back 377

thiopental or midazolam

Front 378

Methemoblobinemia potential side effect of?

Back 378

Prilocaine and Benzocaine

Front 379

Hepatic disease?

Back 379

Amides

Front 380

Low esterase activity

Back 380

Esters

Front 381

Neonates

Back 381

Low levels plasma binding proteins

Front 382

Pregancncy

Back 382

Drugs may be more effective in pregnant women (lower CSF protein levela nd higher pH)?

Front 383

Spinal cord dz

Back 383

be careful w/ drug use

Front 384

One page summary list:
Most popular, doses producing CNS toxicity, can cause CV depression?

Back 384

Lidocaine

Front 385

One page summary list:
More toxin in NEONATES!

Back 385

Mepivacaine

Front 386

One page summary list:
-more cardiotoxic than lidocaine
-long-acting
-levo-bupivacaine - S-enatiomer

Back 386

Bupivacaine

Front 387

One page summary list:
-less cardiotxic than bupivacaine
-long acting?

Back 387

Ropivacaine (long rope)

Front 388

One page summary list:
Methemoblobinemia

Back 388

Priolcaine (or benzocaine)

Front 389

One page summary list:
=slow onset, short durtaion
-metabolized to PABA which inhibits sulfonamides

Back 389

Procaine

Front 390

One page summary list:
-slower metabolism w/ more systemic toxicity

Back 390

Tetracaine

Front 391

One page summary list:
-blocks neorepinephrine (catecholamine uptake)
-vasoconstrictor
-abuse potential
-used primarily URT

Back 391

Cocaine

Front 392

One page summary list:
-low solubility
-popular topical agent
-methemegobinemia

Back 392

Benzocaine

Front 393

What is unique about action of estrogen?

Back 393

at critical point in the female cycle the rising leelsof estrogen switch to exert POSITIVE FEEDBACK on secretion of gonadotropic hormones...Timing is everything

Front 394

common cause of infertility?

Back 394

excessive estrogenic inhibition of hypothalamic/pituitary axis

Front 395

Treatment of PCOS?

Back 395

Clomiphene

Front 396

Action of clomiphne?

Back 396

Estrogen receptor antagonist (SERM) --> really a PARTIAL agonist

Front 397

Major action clomiphene?

Back 397

Blocks estrogen inhibition of hypothalamic/pituitary axis
**however, potential overstimulate ovaries and cause multiple births!

Front 398

Nickname of Clomiphene?

Back 398

Fertility drug

Front 399

What are other drugs affecting FSH/LH

Back 399

Clomiphene
Menotropins
hCG
Danazol

Front 400

Stimulates release of FSH and LH?

Back 400

hCG
-inject hCG to induce ovulation
-->mimics "LH surge"

Front 401

Can any sex steroid inhibit the secretion of FSH or LH in either sex?

Back 401

yes!

Front 402

Endometriosus?

Back 402

Danazol

Front 403

Medical castration?

Back 403

Leuprolide (Goserelin, Nafarelin)
GnRH analog --> fertility and chemotherapy

Front 404

How do you use Leuprolide (Goselin, and Nafarelin) for fertility treatment?

Back 404

Intermittent administration
result = ovulation and fertility

Front 405

How do you use Leuprolide (Goselin, and Nafarelin) for infertility treatment?

Back 405

more frequent administration --> suppresses FSH and LH release = infertility

Front 406

First Aid mnemonic leuprolide?

Back 406

Leuprolide can be used in Lieu of GnrH

Front 407

Important point about GnRH receptors

Back 407

Subject to desensitization when overstimulated

Front 408

What kind of cancer can useuse Leuprolide (Goselin, and Nafarelin) for f

Back 408

80% prostate CA androgen dependent
**hormonal control therapy
**leuprolide is a GnRH superagonist
-->desensitizes GnRH receptors on pituitary Gonadotrophs

Front 409

Inhibits FSH/LH release without initial increase?

Back 409

Ganirelix and Abarelix

Front 410

Action of Ganirelix (and Abarelix)

Back 410

Used in management of infertility, especially in IVF b/c prevents prematrue LH surge!

Front 411

What are menotropins?

Back 411

purified prep of FSH, given w/ hCG to mimic lH surge

Front 412

What are urofollitropin and follittropin

Back 412

urofollitropin (purified FSH) and Follitorpin (recombinant product) are similar to menotropins

Front 413

Why do estrogenic drugs have weak oral potency?

Back 413

Strong First-pass hepatic metabolism
-note: highly lipophilic, highly bound, hepatic metabolism

Front 414

Positive effects of synthetic estrogens?

Back 414

Bone Mass and Density

Front 415

What is a major contraindication to bifing sythetic estrogens?

Back 415

>35 y/o and smoke --> history of clot formation

Front 416

What kind of CA is synthetic estrogen use a concer for?

Back 416

Endometrial cancer (w/o progestin), clear cell vaginal and cervical, bresat cancer?

Front 417

Not orally effective, very rapid, t1/2 several minutes?

Back 417

Estradiol

Front 418

Slower, t1/2 12-24 hrs, orally effective?

Back 418

Ethinyl estradiol (not, prodrug is mestranol)

Front 419

conjugated estrogen?

Back 419

Estrone

Front 420

Orally effective PRODRUG, quickly demethylated into Ethinyl estradiol

Back 420

Mestranol (note: also used in oral contraaceptives)

Front 421

Whay are steroidal estrogens available in transdermal patch?

Back 421

Highly lipophilic --> well-absorbed GI tract; easily cross biomembranes

Front 422

All steroidal estrogens are subject to?

Back 422

Enterohepatic circulation
-->contributes significantly to prolonged half-life of ethinyl estradiol
**giving estrogens by oral route may intensify effects on liver

Front 423

What should you give estrogens with to reduce risk of endometrial cancer?

Back 423

Progestin

Front 424

Uses of estrogenic agents?

Back 424

Pre-menopausal hypogonadism (true replacement therapy)

Post-menopausal Hormone Repalcement therapy (HRT)

Front 425

Synthetic estrogen, many side unpleasant side effects (clear cell adenoCA of bagina in f/m exposed in utero)

Back 425

DES (diethylstilbestrol) --> conjugated

Front 426

Non-steroidal compounds from plants w/ estrogen-like structures/activity, weak activity, activity not clear

Back 426

Phytoestrogens

Front 427

HRT (hormone replacement therapy) good for waht types of CA?

Back 427

Breast, prostatic, and endometrial

Front 428

3 non-steroidal estrogenic agents?

Back 428

Clomiphene
Raloxifene
Tamofien

Front 429

Drug of choice in tx of breast CA?

Back 429

Tamoxifen

Front 430

Mechanism of Tamoxifen?

Back 430

Functional competitive estrogen receptor antagonist
**but may exhibit partial agonist activity in some settings and tissues

Front 431

Adverse effects Tamoxifen?

Back 431

Nausea, vomiting **Hot flashes**

Front 432

Problem since Tamoxifen **but may exhibit partial agonist activity in some settings and tissues

Back 432

increased risk of endometrial CA resulting from estrogenic stimulation of uterus

Front 433

Added bonus of Tamoxifen?

Back 433

appears to INCREASE bone density in post-menopausal women

Front 434

Not much action on breast or uterus, therefore also good breast CA (thought to have less clotting issues than tamoxifen)

Back 434

Raloxifene --> however, increased incidence of thromboembolic events early in therapy

Front 435

SERM we learned about --> "Fertiliyt drug" and PCOS

Back 435

Clomiphene

Front 436

What are 3 aromatase inhibitors?

Back 436

Anastrazole
Letrozole
Exemestane

Front 437

Steroidal aromatase inhibitors?
Exemestane
Anastrozole
Letrozole

Back 437

Exemestane

Front 438

Non-steroidal aromatase inhibitors?

Back 438

Anastrozole, Letrozole

Front 439

Why would you use Exemestane
Anastrozole
Letrozole (steroidal aromatase inhibitors)

Back 439

Adjuvant therapy of breast CA w/ tamoxifen AND as first line treatment

Front 440

Unwanted side effect of Aromatase inhibitors (and SERMS)

Back 440

Hot flashes!!!

Front 441

Anastrozole and Letrozole particularly important for what category women?

Back 441

Postmenopausal women w/ breast CA who have + or - lymph nodes and who are at increased risk for recurrent dz

Front 442

Progesterone Analogs (selective progestational activity)

Back 442

Progesterone
Medroxyprogesterone

Front 443

Progestesterone antagonist?

Back 443

Mifepristone (RU-486)

Front 444

19-Nortestestosterone derivatives? (progestational and adrogenic activity)

Back 444

Norethindrone
Drospirenone
Norgestrel, Levonorgestrel

Front 445

Which have the least adrogenic activity of 19-Nortestestosterone derivatives? (progestational and adrogenic activity)
Norethindrone
Drospirenone
Norgestrel, Levonorgestrel

Back 445

Gonanes
Levonorgestrel (norgestrel too)

Front 446

Key action of progestin receptor-mediated action?

Back 446

Maintenance of pregnancy
SUPPRESS MENSTRUATION AND UTERINE CONTRACTILITY

Front 447

Where do progestins have cross-over effects?

Back 447

Androgen receptors

Front 448

"newer" --> anti-androgenic and anti-mineralcorticoid activity; now available in combination types oral contraceptives

Back 448

Drospirenone

Front 449

What is the best way to administerpr progestines?

Back 449

Right now transdermal dosing practical b/c highly lipophilic and easily cross biomembranes, then extensively bound plasma proteins

Front 450

Of Progesterone and 19-Nor compounds, which are orally effective?

Back 450

19-Nor compounds orally effective (t1/2 = 6-24 hours)

Progesterone: plasma t1/2 = 5 min by oral route (first pass effect)

Front 451

Two oral contraceptives?

Back 451

Estrogen and Progestin

Front 452

What is in the combi patch?

Back 452

Estradiol and Norethindrone

Front 453

How do progestins inhibit ovulation?

Back 453

Devrease frequency of GnRH pulses
also decrease penetration cervix of sperm

Front 454

How do combi OCs inhibit ovulation?

Back 454

suppress LH and FSH levels
Eliminate mid-cycle LH surge
-inhibit sperm penetration

Front 455

Beneficial effects of OCs (oral contraceptives?)

Back 455

Reduced risk of endometrial and ovarian cancer

Normalization of menstrual irregularities

Front 456

Contraindications OCs?

Back 456

Cardiovascular --> thromboemoblic disorder
Hormone dependent neoplasia like breast, ovarian, or uterine
Liver tumors/dysfunciton
Pregnancy

Front 457

Slow release OC that is transformed into active progesterone rapidly?

Back 457

Medroxyprogesterone

Front 458

Post coital emergency contraception?

Back 458

RU-486
Mifepristone

Front 459

Mechanism of Mifepristone?

Back 459

Progesterone and glucocorticoid receptor antagonist

Front 460

Who does OC use significantly increase risk in?

Back 460

>35 y/o smoker

smoking, age, DB, HTN, gallbladder dz

Front 461

Key fact about progestin-only contraceptives?

Back 461

Useful for ursing mothers (do not interfere with lactation)

Front 462

What may interfere with metabolism of OC's?

Back 462

Antibiotic treatment --> may block good absorption of drug

Front 463

alternative drug therapy for osteoperosis

Back 463

Alendronate

Front 464

How is testosterone converted to DHT?

Back 464

5 alpha reductase

Front 465

What does DHT do?

Back 465

External genitalia devopment (also associated w/ adulthood prostatic dz)

Hair follicles

Front 466

Direct actions Testosterone?

Back 466

Androgen receptors
-Internal genitalia (Wollffian deveopment), skeletal muscle increase, erythropoeisis

Front 467

Estradiol conversion from testosterone

Back 467

done via CYP19 aromatase
-Estrogen receptor
-->epiphyseal closure
-->increased density
?? libido

Front 468

Legitimate uses testosterone?

Back 468

1. Hypogonadism
2. Breast cancer
3. Stimulation of erythropoiesis
4. Hereditary angioneurotic edema
5. aids related muscle waisting

Front 469

Problem w/ administrationof testosterone?

Back 469

rapidly metabolized (inactive oral route b/c first pass effect)

Front 470

How can testosterone be bioactivated?

Back 470

To DHT in certain target tissues via 5-alpha-reductase

Front 471

Orally effective Androgenic steroids?

Back 471

Oxandrolone and Danazol

Front 472

Problems with Oxandrolone and Danazol

Back 472

Hepatotoxicity, increases LDL, decreased HDL

Front 473

Diff between Oxandrolone and Danazol

Back 473

Oxandrolone (alkylated) and Danazol (synthetic)

Front 474

Steroidal antagonist and antiadrgoen --> weak partial agonist for androgen receptor?

Back 474

Cyproterone acetate

Front 475

Problem w/ Cyproterone acetate?

Back 475

May inhibit spermatogenesis and libido

Front 476

Useful in treatment of Prostatic cancer?

Back 476

Flutamide (non-steroidal antiandrogen)

Front 477

Diff. between Flutamide and Bicalutamide?

Back 477

Bicalumatide has LESS HEPATOTOXCITY and once/day dosing

Front 478

Problems with Flutamide and Bicalutamide?

Back 478

If used alone
-->gyncecomastia and impotence (therefore, use with GnRH analog like Leuprolide to block effect)

Front 479

Inhibitor of 5-alpha-redcutase (type II)

Back 479

Finasteride

Front 480

2 uses of FInasteride?

Back 480

1. BPH
2. Male pattern baldness (caused by excess DHT)

Front 481

Side effect Finasteride

Back 481

Impotence
PREGNANT MUST AVOID
liver problems