Musculoskeletal & Neurologic Drug Therapy

Rheumatoid Arthritis:

1. Chronic, progressive with autoimmune & inflammatory components leading to _____ deterioration

2. ______________ joint stiffness & pain (warm, tender, swollen)

3. More intense in ___ (what part of day?)

1. joint

2. symmetric

3. AM

Rheumatoid Arthritis

Systemic manifestations -

fever, weakness, fatigue, weight ____, _____ thinning, scleritis, corneal ________, vasculitis, __________ under skin

loss, skin, ulcers, nodules

Rheumatoid Arthritis:

Drug therapy relieves symptoms, _____ disease progression, maintain ______ function/ROM, minimize ____________ involvement

slow, joint, systemic

Rheumatoid Arthritis:

1. Gluco____________

2. NSAIDs

3. Disease-modifying antir_________ drugs (DMRDs)

- Conventional/Traditional

- Biologics

- Targeted

1. -corticoids

2. ---

3. -heumatic

Rheumatoid Arthritis: NSAIDS

1. Anti-inflammatory and ___________ actions

2. Does ____ slow disease progression

3. May need to try more than ____ agent to achieve optimal response

1. analgesic

2. NOT

3. one

Rheumatoid Arthritis: NSAIDS - First generation:

1. Salicylates: aspirin, ______________ salicylates, salsalate

2. Nonsalicylates: diclofenac, ___________, indomethacin, meclofenamate, naproxen, sulindac, & more

1. magnesium

2. ibuprofen

Rheumatoid Arthritis: NSAIDS - Second generation (COX-2 inhibitors):

____________ (Celebrex)

Celecobix

Rheumatoid Arthritis: Glucocorticoids

Also used in _______, inflammatory _______ disease, _________ conditions, asthma, _______________ disorders, ________ labor (neonate ______________ distress syndrome)

lupus, bowel, allergic, dermatologic, preterm, respiratory

Rheumatoid Arthritis: Glucocorticoids

1. Powerful anti-_________________/immunosuppressive effects for severe RA & may delay disease progression generally used for ______ exacerbations

2. ______ term therapy recommended only ( _____ term therapy complications can occur)

1. inflammatory, acute

2. short, long

Rheumatoid Arthritis: Glucocorticoids - Routes for symptoms:

1. _____ for generalized symptoms

2. Intraarticular if only two or more _____ affected

1. oral

2. joints

Rheumatoid Arthritis: Glucocorticoids

Short-acting systemic glucocorticoids: ________cortisone & ___________

hydro-, cortisone

Rheumatoid Arthritis: Glucocorticoids

Intermediate-acting systemic glucocorticoids: ______prednisolone, prednisolone, ___________, triamcinol___

methyl-, predisone, -one

Rheumatoid Arthritis: Glucocorticoids

Long-acting systemic glucocorticoids: _________________ & _________________

betamethasone & dexamethasone

Rheumatoid Arthritis: Glucocorticoids Physiology - Corticosteroids produced in the adrenal gland: (2)

1. Mineralocorticoids-modulate _____ & __________ balance

2. Glucocorticoids-influence __________________ metabolism & other process (CV and ____________ integrity, CNS, ______ response, F&E, neonatal _______________ system)

1. salt, water

2. carbohydrate, hematologic, stress, respiratory

Rheumatoid Arthritis: Glucocorticoids Physiology

Regulated by ____________ feedback loop through ____thalamus, anterior pituitary, & _________ cortex

negative, hypo-, adrenal

Glucocorticoids

Corticosteroids produced in the ________ gland

adrenal

Glucocorticoids Physiology:

1. Mineralocorticoids = _____ and _________ balance

2. Glucocorticoids = __________________ metabolism & others; CV and hematologic integrity, CNS, stress response, Fluid & Electrolyte, neonatal respiratory (________________)

3. Regulated via ___________ feedback loop in hypothalamus, _________ pituitary, and adrenal cortex.

1. salt, water

2. carbohydrate, betamethasone

3. negative, anterior

Glucocorticoids Pharmacology MOA:

Penetrate ____ membrane, bind to ____________ receptors (activating it). Receptor-steroid complex moves to cell __________ where it alters target gene activity ( ___________ in DNA)

cell, cytoplasm, nucleus, chromatin

Glucocorticoids Pharmacology:

Causes changes in metabolism and ___________, intense rise in ________, suppression of __________ synthesis, ____ deposits are mobilized (Cushing’s syndrome and _____-face/hump), significant _________ retention and _________ loss in some

electrolytes, glucose, protein, fat, moon, sodium, potassium

Glucocorticoids Pharmacology - Anti-inflammatory and immunosuppressant:

1. Inhibit ____________ mediators reducing swelling, warmth, redness, pain

2. Suppresses ____________ infiltration (dangerous in __________ )

3. Suppresses proliferation of ____________ (reduce _________ inflammation component)

1. chemical

2. phagocytes, infection

3. lymphocytes, immune

Glucocorticoids Pharmacology - ADR REACTIONS:

___________ (Prolonged, systemic), Infection, Impaired ______ healing, ____glycemia, myopathy, F&E Disturbances. ______ delay in children, ___________ disturbances, ________ & glaucoma, PUD, iatrogenic __________ syndrome, _______ suppression over 3 weeks (inability for adrenal gland to produce cortisol/other glucocorticoids)

osteoporosis, wound, hyper-, growth, psychological, cataracts, Cushing's, adrenal

Glucocorticoids Pharmacology - DRUG INTERACTIONS:

_____________ wasting drugs (Thiazide/loop diuretics), _________ (also potassium related); _______ increased r/f GI Bleed/Ulceration; May decrease ___________ antibody response, _____ VIRUSES R/F DEVELOPING/SPREADING VIRAL DISEASE (ABSOLUTE CONTRAINDICATION)

potassium, digoxin, NSAIDS, vaccine, LIVE

Glucocorticoids Pharmacology - CONTRAINDICATIONS:

Systemic _______ infections and _____ virus vaccines

fungal, live

Glucocorticoids Pharmacology - CAUTIONS:

Precautions in _____________, women who are pregnant/_______________

pediatrics, breastfeeding

Glucocorticoids Pharmacology - NURSING:

Dosing is highly individualized and typically given every other ____ (avoid ___________ reactions).

day, adverse

Glucocorticoids Pharmacology - NURSING:

1. Abrupt termination of long-term therapy my unmask adrenal insufficiency (tapper like everything else, duh)...

a. Withdrawal syndrome: ____tension, ____glycemia, myalgia, ___________, fatigue.

b. Administer in ___ to mimic natural ____________ release

a. hypo-, hypo-, arthralgia

b. AM, hormone

Glucocorticoids Pharmacology - NURSING:

2. Administer w/ food or _____

3. Pt needs medical card/ID ________

4. Increased r/f __________

5. S/S ______ retention (sodium imbalances)

6. Assess _______ (cataracts/glaucoma), ___ bleeding, ______________ reactions, CBC ( _________ ), glucose, lipids

2. milk

3. bracelet

4. infection

5. fluid

6. vision, GI, psychological, infection

Methotrexate, sulfasalazine, hydroxychloroquine (Disease modifying antirheumatic drugs/DMARDS):

a. Nursing considerations: largely the _____ for all

b. ____________ (FIRST LINE, 80% success rate)

a. same

b. methotrexate

Methotrexate:

_____ acting (faster than other DMARDS)

fast

Methotrexate MOA:

________ antagonist (needed for ____ synthesis), Benefits from _______suppression of B&T Lymphocytes

folate, DNA, immuno-

Methotrexate CONTRAINDICATIONS:

Pregnancy ( ____________ abnormalities, fetal ____ ), alcoholism/________ impairment, _______suppression, decrease _____ marrow reserve

congenital, death, hepatic, immuno-, bone

Methotrexate ADR REACTIONS:

_________ fibrosis, ______ marrow suppression, ___ ulceration, aplastic ________ (everything is low, related to bone marrow suppression), anemia, leukopenia, thrombocytopenia, N/V/__, anorexia, SJS, alopecia, ______toxicity, infections, secondary ____________ (some others mentioned in the immune section)

hepatic, bone, GI, anemia, D, nephro-, malignancy

Methotrexate:

i. DO NOT EXCEED ___ MG/WEEK, TITRATE DOSE DOWN WHEN _______________

ii. BLACK BOX WARNING: Fatal toxicities of the _____ marrow, liver, lungs, kidneys, _____ reactions, hemorrhagic _________, ___ perforation

i. 20, discontinuing

11. bone, skin, enteritis, GI

Methotrexate:

i. HIGH ALERT MEDICATION! Injection solution requires _________/gown/mask while handling (DO NOT HANDLE IF ___________ ). Monitor for ________ marrow suppression (bleeding _____, bruising, petechiae, guaiac ________ (blood)/urine/emesis)

i. gloves, PREGNANT, bone, gums, stools

Methotrexate:

1. Avoid ____________, ______ temp w/ thrombocytopenia (hemorrhage risk)

2. Assess for _____________ & rash, monitor _____ (I&O, DWT[?], edema), interstitial ___________ (early, dry non-productive ______ ), gout

3. Encourage __ L of fluid intake daily (prevent gout) and assess ___________ periodically.

4. Verify Neg ____________ (HcG), CBC ( _____penia occurs 7-14 days), ______/hepatic labs, ____ acid, serum methotrexate levels _____ during high dose therapy

5. Pt education: AVOID ______ (infection)

1. injections, rectal

2. infection, renal, pneumonitis, cough

3. 2L, nutrition

4. pregnancy, leuko-, renal, uric, DAILY

5. CROWDS

Sulfasalazine – Contraindicated in _____ allergy

sulfa

Hydroxychloroquine – therapeutic effects __-__ months

3-6

Hydroxychloroquine:

i. Toxicity: ____________ leading to blindness. Thorough ____ exam prior and during treatment. ______myopathy, BBB, prolonged ___ interval

ii. Also used as an anti-_________ drug

i. retinopathy, eye, cardio-, QT

ii. malaria

TNF inhibitors (DMARDS), B-lymphocyte depleting agent (DMARDS), & JAK inhibitor Overview:

i. Immunosuppressive drugs targeting ______________ process

ii. Usually used in combination with _____________

iii. Pharmacokinetics somewhat __________

iv. VERY ____________ ($14k-$65k/year) [recombinant DNA technology]

i. inflammatory

ii. methotrexate

iii. unknown

iv. EXPENSIVE

TNF inhibitors (DMARDS), B-lymphocyte depleting agent (DMARDS), & JAK inhibitor Nursing:

Assess relief of RA symptoms, maintain ______ function, minimize ____________ involvement, delay disease _______________.

joint, systemic, progression

TNF inhibitors (DMARDS), B-lymphocyte depleting agent (DMARDS), & JAK inhibitor Nursing:

1. Observe S/S __________(TB, hepatitis, etc.) & _____________

2. ____ with differential, ________ transaminases. Serum creatinine every __-__ weeks for first __ months, then every 8-12 weeks for up to __ months. Rule out ___________ prior to treatment

3. __________ PRIOR TO THERAPY INITIATION (PNA, influenza, Heb b, HPV, herpes zoster). NO _____ VIRUSES WHEN THERAPY HAS STARTED.

1. infection, malignancies

2. CBC, liver 2-4, 3, 6, pregnancy

3. VACCINES, LIVE

Tumor Necrosis Factor (TNF) Inhibitors -

Prototype: ___________ (Enbrel)

Etanercept

Tumor Necrosis Factor (TNF) Inhibitors - Etanercept (Enbrel):

other drugs include adalimu___, certolizu___, golimu___, and inflixi___ (of course our prototype is the only one without the suffix 🙄)

-mab, -mab, -mab, -mab

Tumor Necrosis Factor (TNF) Inhibitors - Etanercept (Enbrel): MOA

Suppresses inflammation by inhibiting ____ (IgG)

TNF

Tumor Necrosis Factor (TNF) Inhibitors - Etanercept (Enbrel) ADR REACTIONS:

___________ site (see methotrexate), cough, __________ pain, lymphoma/_____________ in children/adolescents, serious ______________ (elevated in DM, HIV, immunosuppressed), ___________ reactions, HF, Cancer, hematologic disorders, _______ injury, ____ demyelination disorders, reactivation latent ___

injection, abdominal, malignancies, infections, allergic, liver, CNS, TB

Tumor Necrosis Factor (TNF) Inhibitors - Etanercept (Enbrel) NURSING:

Same as ______________

methotrexate

B-Lymphocyte-Depleting Agents:

Prototype: __________ (only drug in this class)

Rituximab

B-Lymphocyte-Depleting Agents -

Prototype: Rituximab MOA

Reduce number of __-Lymphocytes which play an important role in ______________ responses

B, autoimmune

B-Lymphocyte-Depleting Agents -

Prototype: Rituximab MOA

1. Monoclonal antibody against _____(Found exclusively on the __-lymphocyte) causing B-lymphocyte Lysis ( _____ )

2. Also used in combination with _______________, typically for those who are unresponsive to ____ inhibitors

1. CD20, B, death

2. methotrexate, TNF

B-Lymphocyte-Depleting Agents -

Prototype: Rituximab ADR REACTIONS:

____ like s/s; SEVERE _________ reactions. Post infusion _____ failure/toxicity. Death occurring w/I ___ hours (80% w/I first infusion). Hep __ reactivation leading to hepatic failure, progressive multifocal _____encephalopathy, transient neutropenia.

flu, infusion, renal, 24, B, leuko-

B-Lymphocyte-Depleting Agents -

Prototype: Rituximab NURSING

See _____________

methotrexate

Jannus Kinase (JAK) Inhibitors

Prototype: Tofacitinib

only 1 other drug Bariciti___

-nib

Jannus Kinase (JAK) Inhibitors

Prototype: Tofacitinib

1. Newest RA drug, ______ term safety not established

2. Typically only used in those with moderate to severe RA who cannot take ______________.

1. long

2. methotrexate

Jannus Kinase (JAK) Inhibitors

Prototype: Tofacitinib MOA

inhibits the Intracellular enzymes that signal for ___________ (JAK enzyme) signaling (STAT pathway). _____ pathway involved in inflammatory/immune responses; thus, this inhibits that process.

cytokine, STAT

Jannus Kinase (JAK) Inhibitors

Prototype: Tofacitinib ADR REACTIONS:

~20% will develop ______________. ____pharyngitis, herpes zoster, gastroenteritis, increased serum _____________, bradycardia, prolonged ___ interval, ___ perforation, ______ injury, malignancies. FATAL INFECTIONS ( ___ ), ___________ lymphocytes, neutrophils, platelet count, erythrocytes.

infection, naso-, cholesterol, PR, GI, liver, TB, decreased

Gout- identify anti-inflammatory vs hyperuricemia drugs - Anti-inflammatory

First line: _______ [alternatively glucocorticoids). If tolerant, __________ (more on this drug later)

NSAIDS, Colchicine

Gout- identify anti-inflammatory vs hyperuricemia drugs - Anti-inflammatory

Lowering Uric Acid: Long-term drugs ____purinol & ____xostat (Inhibit ______ acid formation)

allo-, febu-, uric

Lowering Uric Acid: Long-term drugs Allopurinol & Febuxostat (Inhibit uric acid formation):

1. Also includes (but probably will not need to know): Lesinurad & probenecid ( ______________ uric acid excretion), pegloticase & rasburicase (convert _____ acid to allantoin)

2. Lacks anti-______________ & analgesic properties.

1. accelerates, uric

2. inflammatory

Colchicine:

1. Anti-Inflam specific for _____

2. Short term for ______ attacks (at _____ doses) or longer term for maintenance/prevention at ________ doses

3. ____: We don’t know fam.

4. Avoid during ___________ but not necessarily teratogenic (we kinda just don’t know)

5. Adjust dosing for older adults w/ cardia/_____/hepatic/___ diseases

1. gout

2. acute, high, lower

3. MOA

4. pregnancy

5. renal, GI

Colchicine ADR REACTIONS: 1/2

__________ therapeutic index, ________ to any tissue that has a large # of proliferating cells. ___ Tract, ______ marrow disruption causes much of the drugs major toxicity. _____suppression (causing leukopenia, granulocytopenia, thrombocytopenia, pancytopenia.

narrow, toxic, GI, bone, myelo-

Colchicine ADR REACTIONS: 2/2

_________ (rhabdomyolysis [increases with ______/hepatic impairment, _____ drugs]) Monitor _______ pain, tenderness, weakness.

MYOPATHY, renal, statin, muscle

Colchicine - drug interactions:

______ (rhabdo), P-glyco_________ (PGP) inhibs [cyclosporine, ranolazine] and inhibs of ___3A4 (ketoconazole, clarithromycin, HIB protease inhibs) can cause _____ threatening increased colchicine levels.

statins, -protien, CYP-, life

Allopurinol (Xanthine Oxidase Inhibitor) - First line for chronic tophaceous gout:

Maintenance dose recommended as initial therapy can precipitate a _____ attack ( ___________ or low-dose ______ decrease this risk)

gout, colchicine, NSAID

Allopurinol (Xanthine Oxidase Inhibitor) MOA:

Inhibits xanthine _________ (XO) needed for ____ acid formation. Prevents new tophi formation and regression of current _____, lowers r/f ________ urate crystal deposits

oxidase, uric, tophi, kidney

Allopurinol (Xanthine Oxidase Inhibitor) ADR REACTIONS: 1/2

Well tolerated! Mild ___ (N/V/D, abd discomfort), neuro (drowsiness, headache, ___________ taste). ________ (prolonged use), _____ marrow suppression (rare) ______toxicity, hypersensitivity. Most serious – Fatal _________________ syndrome (fever, rash, eosinophilia, liver/kidney dysfunction.

GI, metallic, cataracts, bone, hepato-, hypersensitivity

Allopurinol (Xanthine Oxidase Inhibitor) ADR REACTIONS: 2/2

Korean, Chinese, Thai ancestry should be tested for ____-B*5081 as severe cutaneious adverse reaction ( _____ ) syndrome can occur (same class as ___ )

HLA, SCAR, SJS

How to diagnosis osteoporosis and drug treatment needed:

Risk factors: Female, _______ age, lower ___, hx of ___________, family hx ____ fracture, _____ glucocorticoid use

FRAX tool evaluates ___-year risk

older, BMI, fracture, hip, oral

10

How to diagnosis osteoporosis and drug treatment needed:

S/S: Loss of ______! _____ deformity, chronic _____ pain, impaired ___________

height, spinal, back, breathing

How to diagnosis osteoporosis and drug treatment needed:

Diagnosing: _____-mineral Density (BMD) testing [all women ___ and over and younger post__________ women at risk. Test all men after age ___ ]

bone, 65, -menopausal, 70

How to diagnosis osteoporosis and drug treatment needed: DIAGNOSING

1. Dual-________ x-ray absorptiometry (DEXA)

2. Osteopenia: 1 SD below the mean ( ___% bone loss) or T score -1

3. Osteoporosis: ____ SD below the mean (20% bone loss) or T score -2.5

1. energy

2. 10%

3. 2.5

How to diagnosis osteoporosis and drug treatment needed

a. Goal for treatment: maintain or increase _____ strength

b. _______________- (pay extra attention to bolded as they are most likely to reduce fractures)

a. bone

b. medications

How to diagnosis osteoporosis and drug treatment needed MEDICATIONS:

Female: reabsorption agents (estrogen, raloxifene, bis_______nates [ ___________ (Prototype)], risedronate, ibandronate, zoledronic ____, calcitonin, denosu___. Reformation agents like teriparatide

Men: _____________, risedronate, zoledronic acid, teriparatide, denosumab

phospho-, alendronate, acid, -mab

Alendronate

Alendronate CONTRAINDICATIONS:

____________ abnormalities, inability to stand/sit upright for ___ minutes, _____ impairment, __________ (OB)

esophageal, 30, renal, pregnancy

Alendronate ADR REACTIONS:

Generally well tolerated; _____________ (BIGGEST CONCERN DUE TO CONTRAINDICATION), atypical ________ fractures, esophageal _______, musculoskeletal _____, ________ problems (blurred vision, scleritis, eye pain), osteonecrosis of ____ (most common ___ bisphosphonates), ____parathyroidism, ______ fibrillation

esophagitis, femoral, cancer, pain, ocular, jaw, IV, hyper-, atrial

Alendronate NURSING:

50% of this med is rapidly absorbed into the _____ and remains there for _____ (up to a decade). Suppresses reabsorption by inhibiting ___________.

bone, years, OSTEOCLASTS

Alendronate NURSING:

1. FOOD, ___, CAFFINE, MINERAL ________ can _________ absorption

2. Administer first thing in the ___ with 6-8oz of _______, ___ minutes apart from any other medication.

3. REMAIN _________ FOR ___ MINUTES AFTER TAKING

4. No __________ dosing; notify HCP of side effects (eye pain, blurred vision, prior to ________ surgery (necrosis), or ______________ (OB)

1. OJ, WATER, decrease

2. AM, water, 30

3. upright, 30

4. double, dental, pregnancy

Cholinesterase inhibitor names and adverse effects (Dementia drugs):

1. Donepezil ( _____________ inhibition)

2. Galantamine ( _____________ inhibition)

3. Rivastigmine ( ________________ inhibition)

1. reversible

2. reversible

3. irreversible

Cholinesterase inhibitor MOA *all 3*:

Prevent the breakdown of _________________ increasing availability (enhances transmission to _________ that are still intact)

acetylcholine, neurons

Cholinesterase inhibitor INDICATIONS:

1. Indicated for mild-__________ symptoms ( ____________ can be used for severe)

2. 1/12 pts will benefit with modest and ______-lasting improvements

1. moderate, donepezil

2. short

Cholinesterase inhibitor ADR REACTIONS:

Typical ___________ (Dryyyyy), ___ (N/V/D dyspepsia), dizziness, headache, broncho____________ (use cautiously in asthma/COPD), CV (rare _____cardia, fainting, falls leading to fall related injuries [ __________ ], ____________ placement)

cholinergic, GI, -constriction, brady-, fractures, pacemaker

Cholinesterase inhibitor ADR REACTIONS:

____stigmine only – 7% weight _____ in 18-28% of males vs females; route IR/ER tablet, solution & _________ patch

Riva-, loss, topical

NMDA antagonist action- Memantine:

Modulates the effects of _____________ (major excitatory CNS transmitter) at the NMDA receptors (critical for ____________ and learning) by blocking __________ influx

glutamate, memory, calcium

NMDA antagonist action- Memantine:

Basically, it causes NMDA receptors to prevent ____________ from entering the cells of the brain which helps normalize ____________ levels.

calcium, glutamate

Parkinson’s disease:

S/S: resting __________, ___________, postural _______________, slowed movement ( _____kinesia)

tremor, rigidity, instability, brady-

Parkinson’s disease:

Other s/s: Micrographia (text getting _____________ as you write), hypophonia, loss of ______, excessive _____________, autonomic dysfunction ( ____________ is the first sign, followed by urinary ______________, dysphasia, ________________)

smaller, smell, salivation, constipation, retention, incontinence

Parkinson’s disease - Drug classes:

1. Dopaminergic Agents – Carbid___/Levod___ (FIRST LINE DRUG)

2. Anti____________ Agents

1. -opa, -opa

2. -cholinergic

Carbidopa/levodopa ACTION:

Increases ______________ synthesis. Conversion of levodopa to ______________ through enzymes. NOT A _____. Can’t treat w/ dopamine alone bc dopamine doesn’t cross ____. Half-life of dopamine is short in the ______ and could not reach the brain.

dopamine, dopamine, CURE, BBB, blood

Carbidopa/levodopa Acute Loss Effects:

Gradual “__________ off” at end of drug dosing ( ___therapeutic level)

wearing, sub-

Carbidopa/levodopa Acute Loss Effects:

Abrupt ____ of effect: “on-off phenomenon lasting minutes/_____ even when drug levels are _____”

loss, hours, high

Carbidopa/levodopa:

Rapidly absorbed ( _________ ), _____ delays absorption ( _________ ESPECIALLY).

orally, food, PROTEINS

Carbidopa/levodopa:

Levodopa must be combined with _____________ or entacapone to decrease the amount of ____rboxylation in the periphery (allows more drug to enter the ____ )

carbidopa, deca-, CNS

Carbidopa/levodopa:

Onset ___________, peak __ hrs, duration ___ hrs, therapeutic effect 2-3 _______ /up to __ months

unknown, 2, 12, weeks, 6

Carbidopa/levodopa ADR REACTIONS:

Dose Dependent; ____ (very common), annoying/disabling ________ (80% in 1st year), postural hypotension, dysrhythmias, psychosis (20%), CNS effects (anxiety, agitation, ____________ , _____ [gambling, sexual]), dark _____ /urine (harmless), activate malignant _____________

N/V, dyskinesia, depression, urges, sweat, melanoma

Carbidopa/levodopa DRUG FOOD:

____ generation antipsychotics block ____________ receptors ( _____________ effects of dopa) MAO-I (just never take these…like ever)

High ________ meals could trigger abrupt loss effect; high ____ foods decrease absorption

1st, dopamine, decreases

PROTIEN, fat

Carbidopa/levodopa NURSING:

Administer on an ________ stomach, DO NOT change dosing regimen (be _____________ )

empty, consistent

Carbidopa/levodopa NURSING:

1. High _________foods impair effects, daily __________ should be spread throughout the day

2. Notify provider of any skin changes ( ____________ )

3. Large amounts of vitamin ___ (pyridoxine) and _____ may interfere with levodopa action

1. protein, proteins

2. melanoma

3. B6, iron