Nur 235 Pharm Exam 2

Front 1

What are executive functions:

Back 1

make higher level plans, balance checkbook, etc

Front 2

5 drug classes to treat Parkinsons

Back 2

Anticholinergics: block the cholinergic receptors (muscarinic receptors in the striatum)

Dopaminergics: convert to dopamine

Dopamine Agonists: stimulate the dopamine receptors

MAO-B inhibitors: inhibit the MAO-B enzyme which interferes with dopamine

COMT inhibitors: which inhibit the COMT enzyme that inactivates dopamine

Front 3

Therapeutic goal of parkinson tx

Back 3

give patient ability to carry out ADL

Front 4

What is the Beer's Criteria

Back 4

a list of drugs that should not be given to older adults.

Front 5

1 type of drug given to Parkinson's patients on Beer's Criteria

Back 5

Anticholinergic drugs.

Front 6

Amantadine

Back 6

Dopamine Releaser

Front 7

Levodopa

Back 7

Most effective drug for Parkinsons

Only works 2-5 years

75% of patients experience a 50% decrease in symptoms

Front 8

2 types of loss of effect to Levodopa

Back 8

1. Gradual loss

2. Abrupt loss

Front 9

Solutions for treating gradual loss of effect to Levodopa.

Back 9

COMPT inhibitor: Entacapone (Comtan)

Dopamine agonist: Pramaprexol

Front 10

3 ways to manage side effects of Levodopa:

Back 10

decrease dosage, giving amantadine in conjunction with Levodopa, or surgery called deep brain stimulation.

Front 11

% of patients have movement disorder (dyskinesia) side effects from Levodopa

Back 11

80%

Front 12

What does an agonist drug do?

Back 12

Stimulates the receptor & increases the response of the receptor.

Front 13

2 types of receptors

Back 13

-inhibitory

-excitatory

Front 14

What will a dopamine agonist do?

Back 14

Increase the action of Dopamine at the receptor.

Front 15

Early stage treatment of Parkinson's

Back 15

Pramipexole- Mirapex (a dopamine agonist)

Front 16

Pharmacokinetics of Pramipexole-Mirapex

Back 16

Pharmacokinetics, rapidly absorbed, can take with food.

Front 17

Side effects of Pramipexole (Mirapex)

Back 17

Nausea 28%

Dizziness 25%

Daytime somnolence 22%

Insomnia 17%

Constipation 14%

Weakness 14%

Hallucinations 9%

Front 18

Side effects of Mirapex and Sinemet

Back 18

Orthostatic hypotension 54%

Dyskinesia 47%

Hallucinations 17%

Front 19

Adverse effects of levodopa

Back 19

-nausea & vomiting

-dyskinesias (80% of patients)

-Cardiovascular effects: postural hypotension

-Psychosis: 20% of patients

Front 20

Pharmacokinetics of Levodopa: where is it administered & where is it absorbed?

Back 20

Administered orally & rapidly absorbed in intestine.

Front 21

True or False: Food delays absorption by slowing gastric emptying.

Back 21

True. And it competes with dietary proteins for blood brain transport.Nam

Front 22

How much of each Levodopa drug reaches the brain?

Back 22

2%

Front 23

Name 2 inhibitory neurotransmitters used to treat Parkinson's

Back 23

1. Dopamine

2. GABA

Front 24

5 Classifications of Parkinson's

Back 24

1. Dopamine Replacement

2. Dopamine Agonists

3. COMT Inhibitors

4. MAO-B Inhibitors

5. Dopamine Release

Front 25

6 general parts to Pathophysiology of alzheimers

Back 25

1. degenerative

2. vascular

3. infectious

4. metabolic

5. psychiatric

6. development of seniles plaques and neurofibrillary tangles.

Front 26

Only cholinesterase inhibitor used for MILD, MODERATE, SEVERE

Back 26

Donepezil (Aricept)

Front 27

When to start taking Donepezil (Aricept)

Back 27

As soon as symptoms start

Front 28

Side effects of Memantine (Namenda)

Back 28

Dizziness, H/A, confusion, constipation

Front 29

What is difference between seizure and epilepsy

Back 29

seizure is an isolated event, epilepsy is a disorder

Front 30

Define automatism

Back 30

follows complex partial seizure, repetitive, purposeless movements

Front 31

Myoclonic Seizure

Back 31

sudden muscle contraction that last for one second. (Like when your whole body jolts in bed)

Front 32

Name a seizure that persists for 15-30 minutes or longer or a series of seizures during which the patient does not regain consciousness. This is a medical emergency.

Back 32

Status epilepticus

Front 33

2 seizure meds that suppress calcium influx

Back 33

1. Valproic acid (review)

2. Ethosuximide (traditional)

Front 34

4 traditional seizure meds that block NA influx into the cell

Back 34

1. Phenytoin (traditional)

2. Carbamazepine (traditional)

3. Valproic acid (traditional)

4. Lamotrigine

Front 35

1 medication that promotes potassium efflux: affect of repolarization

Back 35

Ezogabine

Front 36

What does an antagonist of Glutamate do?

Back 36

Works against Glutamate

Front 37

2 anti seizure drugs that antagonize glutamate

Back 37

1. Felbamate

2. Topirimate

Front 38

T or F is Dilantin is used to treat bipolar

Back 38

False.

Front 39

Define Nystagmus

Back 39

Shaky eyeballs

Front 40

Should you use an antipsychotic agent to treat an older adult?

Back 40

NO!

Front 41

Three types of schizophrenia symptoms

Back 41

1. negative

2. positive

3. cognitive symptoms

Front 42

Define labile affect of schizophrenia

Back 42

one minute they are happy, the next they are hostile, the next they are neutral (all over the place.)

Front 43

Define blunted affect of schizophrenia

Back 43

no affect

Front 44

First generation antipsychotics are classified by what?

Back 44

Potency

Front 45

Define Tardive Dyskinesia

Back 45

uncontrolled, repetitive movement of the lounge in and out of the mouth.

Occurs late in treatment of schizophrenia with First generation Antipsychotics- cannot be reversed.

Front 46

What is the most commonly prescribed class of antidepressant?

Back 46

SSRI: Selective Serotonin Reuptake Inhibitors

Front 47

What is the most widely prescribed SSRI in the US?

Back 47

Fluoxetine, trade name Prozac

Front 48

Define Bruxism

Back 48

Grinding your teeth

Front 49

What is serotonin syndrome?

Back 49

adverse effect when patient is taking SSRI combined with MAOI: too much serotonin in the system. 2 to 72 hrs .

Front 50

What is SNRI

Back 50

Serotonin/Norepinephrine Reuptake Inhibitors

Front 51

Important note about MAOI inhibitors

Back 51

Don't take with other drugs.

Front 52

Define Yawngasm

Back 52

When you yawn and at the very end you have an orgasm. Side effect of TCA.

Front 53

Acetylcholine is released by

Back 53

1. all preganglionic neurons

2. parasympathetic postganglionic neurons

note: all motor neurons to skeletal muscles release acetylcholine. (NMJ)

Front 54

Norepinephrine is released by

Back 54

1. sympathetic postganglionic neurons

Front 55

Epinephrine is released by

Back 55

1. Adrenal medulla

Front 56

3 cholinergic receptors

Back 56

1. Nicotinic N

2. Nicotinic M

3. Muscarinic

Front 57

5 adrenergic receptors

Back 57

1. Alpha 1

2. Alpha 2

3. Beta 1

4. Beta 2

5. Dopamine (only responds dopamine)

Front 58

Where are nicotinic n receptors found?

Back 58

The cell bodies of all postganglionic neurons of parasympathetic & sympathetic systems.

-also found on cells of adrenal medulla.

remember: n for neurons

Front 59

Where are nicotinic m receptors found?

Back 59

located on skeletal muscle

remember: m for muscle.

Front 60

Where are muscarinic receptors found?

Back 60

all organs regulated by parasympathetic nervous system.

Front 61

Where are adrenergic receptors found?

(alpha, beta, or both)

Back 61

All organs (except sweat glands) regulated by the sympathetic nervous system.

note: adrenergic receptors are also found on organs regulated by epinephrine released from the adrenal medulla

Front 62

What does activation of muscarinic receptors do to: Heart, lung, bladder, GI tract, sweat glands, sex organs, blood vessels, eye

Back 62

Heart- decrease BP and HR

Lung- contract bronchi sm. muscles

Bladder-relax trigone & sphincter-release urine

GI-increases salivation,secretions, tone & motility

Sweat glands-general sweating

sex organs-erection (vasodilation)

blood vessels- vasodilation

eye- miosis (sm pupil) and focus for near vision

Front 63

What does activation of nicotinic m receptors do?

Back 63

contract skeletal muscle

Front 64

Where are nicotinic m receptors located

Back 64

NMJ- neuro muscular junction

Front 65

What does activation of Nicotinic n receptors do?

Back 65

Stimulate parasympathetic and sympathetic postganglionic nerves and release epinephrine from adrenal medulla.

Front 66

Where are Nicotinic n receptors locates

Back 66

all autonomic nervous system ganglia & adrenal medulla

Front 67

What receptors can epinephrine activate?

Back 67

1. all alpha (alpha 1 and alpha 2)

2. all beta (beta 1 and beta 2)

Front 68

What receptors can norepinephrine activate?

Back 68

1. all alpha (alpha 1& alpha 2)

2. beta 1

Front 69

what receptors can dopamine activate?

Back 69

1. alpha 1

2. beta 1

3. dopamine

Front 70

where are alpha 1 receptors located in peripheral system?

Back 70

eye

arterioles of skin, viscera, mucous membrane

veins

sex organs, male

prostatic capsule

bladder

Front 71

what does alpha 1 receptor activation do in peripheral system?

Back 71

eye- increased pupil (mydriasis)

arterioles-skin/viscera/mucusmem- constriction

veins- constriction

sex organs- ejaculation

prostatic capsule- constrict

bladdar- contraction of trigone/sphincter

Front 72

where are alpha 2 receptors located in peripheral system?

Back 72

presynaptic nerve terminals*

*alpha2 receptors in CNS are post sympathetic

Front 73

what does alpha2 receptor activation do in peripheral system?

Back 73

causes inhibition of transmitter release

function: regulate transmitter release

Front 74

where are beta 1 receptors located in peripheral system?

Back 74

-heart

-kidney

Front 75

what does beta 1 activation do in peripheral system?

Back 75

THINK 1 Heart!

heart- increase HR, increased force of contraction, increased AV conduction velocity

Kidney- release of renin

Front 76

where are beta 2 receptors located in peripheral system?

Back 76

Think 2 LUNGS!

arterioles (heart, lung, skeletal muscle)

Bronchi- dilation

Uterus- relaxation

Liver- Glycogenolysis

Skeletal muscle- enhanced contraction, glycogenolysis

Front 77

Where are dopamine receptors located in peripheral system?

Back 77

Kidney

Front 78

What does activation of dopamine receptors do in peripheral system?

Back 78

Dilation of kidney vasculature.

Front 79

Six categories of cholinergic drugs

Back 79

1. Muscarinic agonist

2. Muscarinic antagonist

3. Ganglionic stimulating agents (@nicotinic n)

4. Ganglionic blocking agents (@nicotinic n)

5. Neuromuscular blocking agents(@nicotinic m)

6. Cholinesterase inhibitors (indirect)

Front 80

What does a cholinesterase inhibitor do?

Back 80

Prevents breakdown of acetylcholine by acetylcholinesterase. Increases action of all cholinergic receptors. (INDIRECT)

Front 81

Prototype Muscarinic Agonist

Back 81

Bethanechol (Urecholine)

Front 82

Therapeutic uses for Bethanechol (Urecholine)

Back 82

Urinary retention- receives urinary retention by activating muscarinic receptors of urniary tract

Front 83

Adverse effects of Bethanechol (Urecholine)

Back 83

CV: hypotension & bradycardia

GI/GU: excessive salivation, increased secretion of gastric acid, cramps & diarrhea

Respiratory: exacerbation of asthma

Front 84

Patient teaching for Bethanechol (Urecholine)

Back 84

GI: take 1 hour before or 2 hours after meals to reduce gastric upset.

-Have a bedpan/bathroom readily available, Bethanchol (Urecholine) acts rapidly on intestine and urinary tract.

Front 85

Prototype Muscarinic Antagonist (Anticholinergic Drug)

Back 85

Atropine

Front 86

Therapeutic uses for Atropine

Back 86

Pre anesthesia- decreases secretions

During eye surgery- increases pupils (myadraisis)

Reverse Muscarinic Agonist Toxicity

Increases HR

Decrease GI hypertonicity/hypermotility (dysentary)

Front 87

Patient teaching for Atropine/ Anticholinergic Drug

Back 87

Decreased salivation- sip water, chew sugar free gum, avoid sugar

Blurred vision- avoid hazards

Photophobia- wear sunglasses

Urinary retention- void prior to dosing

Constipation- increase fiber and fluid

No sweat- hyperthermia risk

Tachycardia- monitor pulse

Front 88

Drug Drug interactions with Atropine

Back 88

Antihistamines, tricyclic antidepressants, phenothiazines have antimuscarinic action and can cause excessive muscarinic blockade.

Front 89

What does a reversible cholinesterase inhibitor do?

Back 89

Binds reversibly to cholinesterase and prevents its degradation of acetylcholine, causing increase in available acetylcholine and enhancing cholinergic actions.

Front 90

Prototype reversible cholinesterase inhibitor

Back 90

Neostigmine (Bloxiverz, Prostigmin)

Front 91

Neostigmine

Back 91

Bloxiverz, Prostigmin

Front 92

Bloxiverz, Prostigmin

Back 92

Neostigmine- reversible cholinesterase inhibitor

Front 93

Indications for Neostigmine (Bloxiverz, Prostigmin)

Back 93

Tx of myasthenia graves

Front 94

Adverse effects of Neostigmine (Bloxiverz, Prostigmin)

Back 94

Toxic levels result in paralysis of respiratory muscles. Toxicity = SLUDGE and the Killer Bs

Front 95

Cholinesterase Inhibitor Toxicity

Back 95

SLUDGE and the Killer B's:

Salivation

Lacrimation

Urination

Diaphoresis/Diarrhea

Gastrointestinal cramping

Emesis

Bradycardia

Bronchospasm

Bronchorreah (excessive mucous)

Front 96

Irreversible cholinesterase inhibitors

Back 96

Highly toxic, insecticides, used in WWII as nerve agents- only clinical application: glaucoma to reduce intraocular pressure.

Front 97

Neuromuscular Blocking Agent prototype

Back 97

Succinylcholine (Anectine, Quelicin)

Front 98

Succinylcholine (Anectine, Quelicin)

Back 98

Neuromuscular Blocking Agent

Front 99

Indication for Succinylcholine

Back 99

muscle relaxation for surgery, mechanical ventilation, electroconvulsion therapy.

Front 100

Contraindications for Succinylcholine (Anectine, Quelicin)

Back 100

contraindicated for patient with low pseudocholinesterase activity, hx/fx of malignant hyperthermia, predisposition for hyperkalemia

Front 101

Patient education with Succinylcholine (Anectine, Quelicin)

Back 101

Succinylcholine (Anectine, Quelicin) can cause muscle pain, this is not unusual.

Front 102

Four basic mechanisms of drug activation at adrenergic receptors.

Back 102

1. Direct receptor binding

2. Promotion of NE release

3. Inhibition of NE reuptake

4. Inhibition of NE inactivation (inhibit monamine oxidase)

Front 103

What happens when a drug inhibits monamine oxidase?

Back 103

It inhibits NE inactivation and increases activation at adrenergic receptors.

Front 104

2 major classes of adrenergic agonists

Back 104

1. Catecholamines

2. Noncatecholamines

Front 105

3 basic and important aspects of catecholamine class:

Back 105

1. not available for PO

2. short duration of action

3. cannot cross BBB

Front 106

3 basic and important aspects of noncatecholamine class:

Back 106

1. available by PO

2. longer duration of action

3. can cross BBB

Front 107

2 examples of noncatecholamines

Back 107

1. Ephedrine (decongestant)

2. Phenylephedrine (nasal decongestant)

Front 108

Therapeutic application of activation at alpha 1

Back 108

vasoconstriction, hemostasis, nasal decongestions, elevation of blood pressure, mydriasis

Front 109

Therapeutic application of activation at alpha 2

Back 109

none!

Front 110

Therapeutic application of activation at beta 1

Back 110

heart failure, heart block, cardiac arrest, shock, av heart block

Front 111

Therapeutic application of activation of Beta 2

Back 111

asthma, preterm labor

Front 112

Which are more selective, adrenergic agonists or adrenergic antagonists?

Back 112

adrenergic antagonists.

Front 113

2 major groups of adrenergic antagonists

Back 113

1. alpha adrenergic blocking agents

2. beta adrenergic blocking agent

Front 114

5 therapeutic applications for alpha blockade

Back 114

1. HTN

2. revers toxicity from alpha 1 agonists

3. BPH

4. Pheochromocytoma

5. Raynaud's Disease

Front 115

4 adverse effects of alpha blockade

Back 115

1. orthostatic hypotension

2. reflex tachycardia

3. nasal congestion

4. inhibition of ejaculation

Front 116

PRAZOSIN

Back 116

prototype alpha blocker/ alpha adrenergic antagonist.

Front 117

Indication for PRAZOSIN

Back 117

only approved for HTN (but can be useful for BPH)

Front 118

Adverse effects of PRAZOSIN

Back 118

FIRST DOSE EFFECT: extreme orthostatic hypotension. Also reflex tachycardia and nasal congestion.

Front 119

Therapeutic application of Beta Blockade (10)

Back 119

-angina

-HTN

-cardiac dysrhthmias

-MI

-reduction of preoperative mortality

-heart failure

-hyperthyroidism

-stage fright

-migraine prophylaxis

Front 120

Adverse effects of beta 1 blockade (4)

Back 120

-bradycardia

-reduced CO

-precipitation of heart failure

-av heart block

-rebound cardiac excitation

Front 121

adverse effects of beta 2 blockade (2)

Back 121

-bronchoconstriction (contraindication in patients w/ asthma)

-hypoglycemia from glycogenolysis inhibition

Front 122

2 adverse effects in neonates from beta 1 and beta 2 blockade

Back 122

1. beta blockers can remain in circulation for several days

2. must be monitored for bradycardia, respiratory distress and hypoglycemia 3 to 5 days after birth

Front 123

what is the indication for dopamine?

Back 123

shock & heart failure (low does, renal perfusion only)

Front 124

what is the indication for Dobutamine?

Back 124

Heart failure only

Front 125

what receptors does Dobutamine act on?

Back 125

Beta 1 only

Front 126

what receptors does Albuterol act on?

Back 126

Beta 2 receptor specific

Front 127

What class is albuterol?

Back 127

noncatecholamine adrenergic agonist

Front 128

what class is PROZOSIN?

Back 128

alpha blocker- alpha adrenergic antagonist

Front 129

what are the indication for PRAZOSIN

Back 129

HTN, but can benefit men with BPH

Front 130

what are the pharmakinetics of PRAZOSIN and TERAZOSIN. What is the main difference?

Back 130

Both:

administered PO

hepatic metabolism

excretion in bile

TERAZOSIN:

prolonged half life, cannot take with food.

Front 131

What should you advise to a patient taking an alpha blocker antagonist? (plus name 2 alpha blocker antagonists)

Back 131

BEWARE FIRST DOSE EFFECT. (Prosazin, Terazosin)

Front 132

-Zosin

Back 132

Alpha Adrenergic Antagonist

Front 133

-Amine

Back 133

catecholamine, adrenergic agonist

Front 134

-Prolol

Back 134

beta blockers

Front 135

First generation nonselective beta blocker

Back 135

Propranolol

Front 136

second generation selective beta blocker

Back 136

Metoprolol

Front 137

2 examples of centrally acting alpha 2 agonist

Back 137

Clonidine & Methyldopa

Front 138

indications for Clonidine

Back 138

HTN, severe pain, ADHD

Front 139

indications for methyldopa

Back 139

HTN in pregnancy

Front 140

contraindications for Methyldopa

Back 140

active liver disease

Front 141

advice for patients taking Clonidine

Back 141

take at bedtime to avoid daytime sedation. advise against rapid discontinuation.

Front 142

contraindications for Clonidine

Back 142

adverse in pregnancy, can be abused.

Front 143

Which class of drugs acting on adrenergic receptors? PO. highly lipid soluble, extensive first pass effect, widely distributed, undergoes hepatic metabolism and urinary excretion.

Back 143

Beta blockers

Front 144

3 cardinal symptoms of parkinson's disease

Back 144

-bradykinesia (slow movement)

-postural instability

-rigidity

-tremors

Front 145

how many new cases of parkinson's disease each year?

Back 145

60,000 new cases / year

Front 146

These patients frequently exhibit sx of dementia, depression, and impaired memory

Back 146

Parkinson's patents

Front 147

Parkinson's is a disorder of the _________system, a complex neuronal network that regulates movement.

Back 147

extrapyramidal system

Front 148

2 neurotransmitters that are off in Parkinson's disease

Back 148

1. not enough dopamine

2. too much acetylcholine

Front 149

What type of transmitter is Dopamine in the CNS?

Back 149

Inhibitory

Front 150

What type of transmitter is Acetylcholine in the CNS?

Back 150

Excitatory.

Front 151

What is the underlying cause of loss of dopamine in CNS in Parkinson's?

Back 151

Loss of Dopamine neurons in substantial negra of brain.

Front 152

What is the cause of Parkinson's?

Back 152

Unknown: environmental and genetic factors

Front 153

What other inhibitory neurotransmitter decreases along with dopamine in Parkinson's disease?

Back 153

GABA

Front 154

In a healthy _________, Dopamine is released from neurons in the __________ ________ and inhibits the firing of neurons that release _____________. Neurons located within the ________release ____________, excite the GABA, and controlled movement results.

Back 154

Striatum

Substantia Nigra

GABA

Striatum

Acetylcholine

Front 155

Safety risks to think about with Parkinson's patients as a nurse

Back 155

-use bed alarms

-fall risk

-non skid shoes

-help with executive function

Front 156

What is COMT inhibitor and what does it do

Back 156

Inhibits Catacholomethyltransferase- keeps it from breaking down dopamine, epinephrine, norepinephrine.

Front 157

What is an MAO-B inhibitor, what does it do?

Back 157

It inhibits the MAO-B enzyme which interferes with dopamine. You will then have more dopamine on hand.

Front 158

First group of drugs used to tx Parkinson's

Back 158

Anticholinergic Agents.

Front 159

Example of anticholinergic agent first used in Parkinson's disease tx.

Back 159

Benztropin (Cogentin)

Front 160

Side effect of anticholinergic agents

Back 160

drowsiness, dizziness, headache, anorexia, dry mouth- on BEERS Criteria list.

Front 161

Drugs used in dopamine replacement (undergoes conversion of dopamine in brain and activates receptors

Back 161

Levodopa and Levodopa/Carbidopa

Front 162

Mose effective drug for tx Parkinson's

Back 162

Levodopa

Front 163

How long will a patient be on Levodopa before it stops working?

Back 163

2 to 5 years

Front 164

2 types of loss associated with loss of effect to Levodopa

Back 164

1. Gradual loss

2. abrupt loss

Front 165

3 solutions to gradual loss of effect from Levodopa

Back 165

-shorten dosing interval

-COMPT inhibitor like Entacapone (Comtan)

-give a direct dopamine agonist- Mirapex, Pramaprexol

Front 166

this Parkinson's drug competes w/ dietary proteins to cross the BBB and thus can't be given with food, especially a high protein diet.

Back 166

Levodopa

Front 167

What fraction of Levodopa reaches the brain?

Back 167

25

Front 168

How is Levodopa administered and how is it absorbed? Where is it metabolized?

Back 168

Orally. Absorbed rapidly in the liver. Metabolized in the periphery.

Front 169

What class of drug is PRAMIPREXOLE?

Back 169

Dopamine agonist

Front 170

Pharmokinetics of Pramipexole

Back 170

PO

Widely distributes

plasma levels peak 1-2 hours

drug eliminated unchanged in urine

Front 171

Nursing assessments for PRAMIPEXOLE

Back 171

-assess for hallucinations/confusion

-monitor BP and ECG

-assess for drowsiness and somnolence

-assess for signs of parkinson

Front 172

Lab considerations for PRAMIPEXOLE

Back 172

increase dosing interval if creatinine clearance is less than 60 mL per min

Front 173

Side effects for PRAMIPEXOLE alone & w/ Levodopa

Back 173

alone: nausea, dizzy, daytime somnolence, insomnia, constipation, weakness, hallucination, IMPULSE CONTROL disorder

w/ levodopa: orthostatic hypotension, dyskinesia

Front 174

Lab considerations for Levodopa/Cardopa (Sinemet)

Back 174

-may increase serum glucose

-monitor hepatic & renal function

-may cause anemia

-may cause high WBC

Front 175

Drug interactions for Levodopa/Cardopa

Back 175

-MAOI- hypertensive crisis

-first generation antipsychotics (block dopamine receptors)

Front 176

This drug may darken sweat or urine

Back 176

Levodopa

Front 177

What class of drug is ENTACAPONE (Comtan)

Back 177

COMPT inhibitor

Front 178

What does ENTACAPONE (Comtan) tx?

Back 178

Parkinson's

Front 179

True or False- You can use ENTACAPONE (Comtan) alone to tx Parkinson's

Back 179

False- it is only indicated for use with Levodopa/Carbidopa. It has no effect on its own.

Front 180

These two drugs used to tx Parkinson's may not be used on their own- have no effect on their own

Back 180

Carbidopa and Entacapone

Front 181

How does ENTACAPONE work in the body?

Back 181

It decreases metabolism of levodopa in peripheral tissues by inhibiting COMT. Increases half life of levodopa by 50 to 70%

Front 182

This drug increases half life of Levodopa by 50 to 75%

Back 182

ENTACAPONE (Comtan)

Front 183

Nursing interventions for use of ENTACAPONE (Comtan) in Parkinson's tx

Back 183

-assess Parkinson's sx

-monitor for neuroleptic malignant syndrome

Front 184

What is neuroleptic malignant syndrome & what Parkinson's drug is it associated with?

Back 184

-elevated temp

-muscular rigidity

-altered concouslness

-elevated CPK

-ENTACAPONE (Comtan)

Front 185

This Parkinson's drug increases risk of hallucinations in geriatric patients

Back 185

PRAMIPEXOLE (Mirapex)

Front 186

% of patients on Levodopa that experience dyskinesias

Back 186

80%

Front 187

% of patients on Levodopa that experience psychosis

Back 187

20%- visual hallucinations, vivid dreams , paranoia

Front 188

What class of drug is SELEGILINE (Eldepryl, Zelapar) ? What is it used to treat?

Back 188

MAO-B inhibitor used to tx Parkinson's

Front 189

Can SELEGILINE (Eldepryl, Zelapar) be used alone or must it be used in combination with Levodopa?

Back 189

SELEGILINE (Eldepryl, Zelapar) can be used alone or in combination with Levodopa.

Front 190

How does SELEGILINE (Eldepryl, Zelapar) work in the body?

Back 190

It causes selective, irreversible inhibition of MAO-B, the enzyme that normal deactivates dopamine in the striatum. It suppress the destruction of dopamine, thus prolonging the effects of levodopa.

Front 191

What are the pharmakinetics of SELEGILINE (Eldepryl, Zelapar)

Back 191

SELEGILINE (Eldepryl, Zelapar) is available as an oral tablet/capsule, undergoes rapid GI absorption, can cross BBB, undergoes hepatic metabolism and renal excretion.

Front 192

2 metabolites of SELEGILINE (Eldepryl, Zelapar) that are CNS stimulants

Back 192

-1 amphetamine

-1- methamphetamine

Front 193

drug drug interactions with SELEGILINE (Eldepryl, Zelapar)

Back 193

-concurrent use with meperidine or other opiod analgesics may result in fatal reaction- sweating, rigidity, hypotension, coma.

-SSRI- may cause serotonin syndrome

-tricyclic antidepressants-systole, diaphoresis, HTN, seizures

-may initially increase risk of side effects of levodopa/carbidopa

-drug + tyramine continent foods can causeHTN reaction

Front 194

Education for patients on SELEGILINE (Eldepryl, Zelapar)- taking more than 20mg per day

Back 194

avoid tyramine containing foods- alcoholic beverages, caffeine, OTC cold/cough meds.

Front 195

What class of drug is Benztropine (Cogentin) & what does it treat?

Back 195

Centrally acting anticholinergic drug tx Parkinson's

Front 196

This is the oldest med used to tx Parkinson's, now second line.

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Benztropine (Cogentin)

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What does Benztropine (Cogent) do in the body?

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Blocks muscarinic receptors in striatum which improves balance bt dopamine and Ach. Reduces tremor and rigidity but not bradykinesia

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What cardinal sx of parkinson's can Benztropine (Cogent) relieve

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-tremor

-rigidity

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This parkinson's drug is on BEERS list for its CNS side effects of sedation and confusion for geriatric patients

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Benztropine (Cogent)