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final Flashcards

1
Q

COPD

A

Air in, air gets trapped and they can’t get the air out

Secretions

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2
Q

CPOD & O2

A

Supplemental O2 removes a COPD patient’s hypoxic (low level of oxygen) respiratory drive causing hypoventilation which causes higher carbon dioxide levels, apnea (pauses in breathing), and ultimately respiratory failure.

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3
Q

asthma

A

Chronic airway inflammation = bronchial constriction

Wheezing and difficulty breathing

Tightness of chest

Can’t get CO2 out

Auscultate the lungs: inspiratory wheeze = inflammation & constriction

Appear cyanotic & edema

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4
Q

chronic bronchitis

A

Continuous inflammation of bronchi

Excessive secretion of mucus

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5
Q

emphysema

A

Alveolar wall destruction & enlarged air spaces

Overinflation of air sacs

Decreases working the alveoli and impaired gas exchange between O2 & CO2

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6
Q

bronchodilators

A

B-adrenergic agonists (blue container)

Anticholinergic drugs (green container)

Xanthine derivatives

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7
Q

non-bronchodilators

A

Corticosteroids

Leukotriene receptor antagonists (LTRAs)

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8
Q

B – adrenergic agonists (quick symptoms relieve) indications

A

Used to treat severe bronchospasm

Emergency medication

For quick relief of symptoms

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9
Q

B – adrenergic agonists mechanism of action

A

Relaxes bronchial smooth muscles which causes dilation of bronchi & bronchioles

Imitates norepinephrine on B2 cells = causes vasodilation & increases airflow

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10
Q

B – adrenergic agonists examples

A

Salbutamol (ventolin) short acting (main)

Salmeterol xinafoate (serevent) long acting

Combination (steroid & B-adrenergic – symbicort or advair)

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11
Q

B – adrenergic agonists adverse reactions

A

Tachycardia

Palpitations

Tremor

Nervousness / anxiety

Hypertension / hypotension

Headache

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12
Q

If used too frequently, dose-related adverse effects may be seen because B-adrenergic loses its B2 specific action, especially at larger doses (t/f)

A

TRUE

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13
Q

Anticholinergics (slower) indications for use

A

Maintenance & prevention of bronchospasm

Bronchodilator

Not 1st line treatment for acute symptoms, use after salbutamol!!!

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14
Q

what is the order of medications for respiratory

A

blue (salbutamol) and then green (ipratropium)

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15
Q

anticholinergics mechanism of action

A

Prevents bronchial constriction by blocking acetylcholine (Ach) receptors

Block constriction

Reduce secretions

Onset: 5-15mins, peak 2-3hr

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16
Q

anticholinergic examples

A

Ipratropium bromide (atrovent)

Tiotropium bromide monohydrate (spiriva)

Salbutamol & ipratropium combination (combivent)

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17
Q

anticholinergic adverse effects

A

Dry mouth or throat

Nasal congestion

Heart palpitations

Urinary retention

GI problems

Increased intraocular pressure

Headache

Coughing anxiety

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18
Q

Xanthine derivatives indication of use

A

Used with chronic bronchitis & emphysema

For prevention of symptoms

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19
Q

Xanthine derivatives mechanism of action

A

Causes bronchodilation by inhibiting phosphodiesterase enzyme results in smooth muscle dilation

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20
Q

Xanthine derivatives examples

A

Theophylline (oral medication

Aminophylline (IV only)

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21
Q

Theophylline considerations

A

Short therapeutic window between therapeutic and toxic

Blood work done frequently

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22
Q

Aminophylline special use

A

Used for status asthmaticus

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23
Q

Xanthine derivatives adverse effects

A

Cardiac irregularities

Tachycardia, palpitations, ventricular dysrhythmias

GERD – nausea, vomiting, anorexia

Increased urination

Hyperglycemia

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24
Q

Corticosteroids indications of use

A

Anti-inflammatory (major)

For management of difficult to treat asthma/resp illnesses

Allergic rhinitis

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25
Q

corticosteroids mechanism of action

A

Controls inflammatory responses

Increases the effects of B-agonists (bronchodilation)

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26
Q

corticosteroids examples

A

Budesonide (pulmicort), fluticasone propionate (flovent), prednisone, combination with B-agonist-advair

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27
Q

corticosteroids adverse effects

A

Pharyngeal irritation

Cough & dry mouth

Oral fungal infections

PO corticosteroids provide more systemic effect & therefore adverse effects are more systemic

Susceptibility to infection

Fluid and electrolyte imbalance

Endocrine effects (including hyperglycemia)

Osteoporosis

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28
Q

Leukotriene receptor antagonists indications of use

A

Used for the prophylaxis and long-term treatment and prevention of asthma

Seasonal allergies/asthma

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29
Q

Leukotriene receptor antagonists examples

A

Montelukast (singulair) orally OD

Zafirlukast (accolate) orally BID

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30
Q

Leukotriene receptor antagonists adverse effects

A

Nausea

Diarrhea

Headache

Nightmares

Liver dysfunction

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31
Q

Nursing assessment respiratory

A

Resp assessment

Colour, accessory muscle, O2 sats, resp rate, cough, sputum, cyanotic

Environmental exposures & allergens

Smoking habits

Emotional status (anxiety, stress, fear)

Allergies

Caffeine intake

Increase in adverse effects (salbutamol)

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32
Q

interventions for respiratory

A

Discuss adherence to medication regimen

Demonstrate proper administration of inhaled drugs

Reassess respiratory status & breath sounds

Instruct pt to rinse mouth with water after use of inhaler or nebulized drug
(Esp steroid and anticholinergic to prevent dryness and mucosal irritation)

Wash inhaler, spacer, and nebulizer qweekly with warm soapy water

Pt education

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33
Q

how to use medications (puffers)

A

2 puffs of same medications = 1-2 mins b/w each puffs

Can put 2 puff in aerochamber

2 different medications = 2-5 mins b/w medications

Exhale, inhale & puff, hold 10 secs, exhale, repeat

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34
Q

adrenal gland medications

A
  • cortex = corticosteroids (glucocorticoids, mineralocorticoids)
  • medulla = epinephrine, norepinephrine
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35
Q

Corticosteroid levels regulated by

A

hypothalamic-pituitary-adrenal (HPA) axis (give steroids in morning as they reflect HPA)

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36
Q

HPA order

A

Level of cortco low –> corticotropin releasing hormone released from hypothalamus –> anterior pituitary –> ACTH released –> adrenal cortex –> production of corticosteroids reach peak level —> signal sent to hypothalamus –> HPA inhibited

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37
Q

Glucocorticoids

A
  • major inflammatory actions
  • regulates carbo, protein, lipid metabolism
  • maintenance BP
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38
Q

mineralocorticoids

A
  • BP control
  • maintenance pH levels
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39
Q

Adrenal system over-secretion

A

Cushing’s syndrome – over secretion of adrenal hormones

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40
Q

Glucocorticoid hypersecretion

A

redistribution of body fat from arms & legs to face, shoulders, trunk, and abdomen, characteristic “moon face”

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41
Q

Aldosterone hypersecretion

A

increased water & Na retention & muscle weakness from K loss

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42
Q

causes of adrenal over secretion

A

tumor, excessive administration of steroids

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43
Q

Adrenal system under-secretion

A

Addison’s disease

Under secretion of adrenal hormones (Decreased blood Na & glucose levels, increased K levels )

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44
Q

symptoms addisons disease

A

Hyperpigmentation, weakness, headache, fatigue, nausea & vomiting, anorexia, dehydration, weight loss, confusion, fever, abdo pain, diaphoresis, low BP

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45
Q

Mineralocorticoids mechanism of action

A

Acts on distal kidney tubule –> sodium reabsorption into blood –> pulls water & fluid with it –> help regulate edema & BP (HTN)

Promotes H & K excretion

Helps regulate blood pH

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46
Q

mineralocorticoids used for

A

addisons disease

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47
Q

Glucocorticoids examples

A

hydrocorticsone, cortisone, prednisolone, dexamethasone

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48
Q

Glucocorticoids mechanism of action

A

Inhibition of inflammatory & immune responses

Promote breakdown of protein, production of glycogen in liver, & redistribution of fat from peripheral areas to central areas of body

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49
Q

how does glucocorticoids inhibit or control inflammatory response

A
  1. stabilizing cell membranes of inflammatory cells
  2. decreasing permeability of capillaries to inflammatory cells
  3. decreasing migration of WBCs into inflamed areas
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50
Q

Indications of corticosteroids

A

Adrenocortical deficiency

Bacterial meningitis

Cerebral edema

Collagen diseases (systemic lupus erythematosus)

Dermatological diseases

Endocrine diseases (thyroiditis)

GI diseases (ulcerative colitis)

Ocular disorders

Leukemia & lymphoma

Bronchospasms (via inhalation route)

Allergic rhinitis (nasal route)

Inflammations of ear, eye, skin (topical route)

Exacerbation of chronic respiratory illnesses (asthma & COPD)

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51
Q

nursing assessment steroids

A

Assess nutritional & hydration status, baseline weight, intake & output, VS, skin condition, immune status

Assess muscle strength

Baseline lab values

Avoid alcohol, caffeine, aspirin, NSAIDs

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52
Q

nursing interventions steroids

A

Healing may be decreased with long term therapy

Avoid contact with people with infections

Assess therapeutic response & adverse effects to monitor effectiveness

ADDISONIAN CRISIS

Oral given with milk, food, and antacids

IM = administered into large muscle with rotation of sites

Topical = skin clean & dry, gloves worn

Nasal = clear nasal passage first, pt breathes in through nose with administration

Inhaled = fungal infections common, rinse mouth with water

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53
Q

when is the best time to give glucocorticoids

A

Best time to give exogenous glucocorticoids is early in morning = minimizes adrenal suppression

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54
Q

pt education steroids

A

Never stop taking medications abruptly or alter dose

Long term effects of glucocorticoid therapy

Bone health & prevention of falls

Signs and symptoms of acute adrenal insufficiency

Document response to treatment, BP, daily weight, adverse effects

Maintain low sodium & high potassium diet

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55
Q

Anxiolytics

A

promote relaxation, decreased anxiety

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56
Q

Sedatives – hypnotics

A

Promote relaxation and induce sleep

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57
Q

Anxiolytics used for sleeping referred to a

A

sedative-hypnotics

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58
Q

difference b/w anxiolytics & sedatives

A

depends on dose

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59
Q

what kind of drugs used to treat anxiety and insomnia

A

benzos

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60
Q

what is the antidepressants used to treat insomnia

A

trazodone

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61
Q

Daytime anxiety can manifest as a

A

nighttime sleep disturbance – unable to turn off their worries

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62
Q

Lack of sleep can present as anxiety, fatigue, and decreased functioning

A

TRUE

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63
Q

Anxiety – pathophysiology

A

Excess of excitatory neurotransmitters (norepinephrine) or deficiency of inhibitory neurotransmitters (GABA)

Neuroendocrine factors also play role – when under stress, corticotropin releasing factor (CRF) increases release of norepinephrine

Serotonin also involved, hence effectiveness of SSRIs treating anxiety

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64
Q

benzo OD fatal or nonfatal?

A

not fatal unless combo w/ CNS depressants

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65
Q

benzo used for

A

sedation, reduce anxiety, muscle skeletal relaxation, anticonvulsant effects

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66
Q

benzo potentiates

A

GABA

GABA calms you, calms down dopamine

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67
Q

do benzo supress rem sleep

A

NOOOOOOO

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68
Q

Diazepam, flurazepam, and chlordiazepoxide form active metabolites that have long-acting half-lives (>24hrs) & tend to

A

accumulate, especially in older adults or those with impaired liver function

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69
Q

Alprazolam, lorazepam, clonazepam, oxazepam, and temazepam have intermediate acting ½ lives 6-24hrs which

A

don’t have active metabolites and generally do not accumulate

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70
Q

Midazolam & triazolam have short acting ½ lives <6 hours(t/f)

A

TRUE

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71
Q

diazepam used effectively in TX

A

GAD, muscle relaxant, alcohol withdrawal

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72
Q

lorazepan used to TX

A

GAD, agitation, alcohol withdrawal

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73
Q

midazolam

A

IV only (sedation, anaesthesia)

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74
Q

clonazepam

A

seizures, panic, agitation, mood stabilizer

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75
Q

benzo disadvantages

A

Potentially habit forming & addictive – limit to 2 week use

Shouldn’t be used beyond 4 weeks

Some have long ½ life & can accumulate

Memory & intellectual impairment

Hangover

Reduced motor coordination

Paradoxical confusion, agitation, insomnia especially with pediatric & other adult clients

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76
Q

adverse effects benzo

A

CNS effects (Diplopia, tremors, ataxia (impaired coordination), drowsiness, headache, nausea, vomiting)

Autonomic effects
(Changes in libido, constipation, incontinence, urinary retention, hypotension, tachycardia, nasal congestion)

Accumulations effects
(Confusion, hypoactivity, intellectual impairment)

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77
Q

Mild withdrawal symptoms occur within

A

6-12 weeks

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78
Q

mild withdrawal sx

A

Anxiety, panic, hand tremors, sweating restlessness, insomnia, weakness, aches, pains, blurred vision, palpitations

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79
Q

severe withdrawal sx

A

Irritability, agitation, rage, nervousness, diarrhea, vomiting, sweating, seizures

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80
Q

TX of withdrawal of benzo w/

A

benzo

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81
Q

to prevent withdrawal of benzo

A

taper drug by 10-25% every 1-2 weeks over 4-16 weeks

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82
Q

drug to reverse benzo toxicity

A

flumazenil

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83
Q

chloral hydrate suppress rem

A

NO

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84
Q

chloral hydrate mechanism of action

A

GABA

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85
Q

chloral hydrate s/e

A

drowsiness, N & V. stomach pain, headache

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86
Q

zopiclone

A

Differs structurally from benzos but has a similar effects, binds with benzo receptors

Indicated for symptomatic relief of transient & short term (7-10 days) insomnia characterized by difficulty falling and remaining asleep, and/or early morning awakenings

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87
Q

zopiclone and REM sleep

A

Delayed onset of REM sleep, does not reduce total duration of REM periods

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88
Q

considerations with zopiclone

A

Should not be prescribed in quantities larger than 1 month

Risk of dependence

Overdose can be fatal

Rebound insomnia common

Taper slowly

Less side effects than other sedative hypnotics

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89
Q

antihistamine mechanism of action

A

bind to HA receptor to reduce negative symptoms

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90
Q

antihistamines s/e

A
  • drowsiness, dry mouth, urinary retention, blurred vision, paradoxical effects
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91
Q

dimenhydrinate

A

gravol

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92
Q

diphenhydramine

A

benadryl

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93
Q

Nursing process, patient teaching sedatives

A

Nursing Implications for all sedative/hypnotics:

Use with caution in the elderly and pediatric populations

Baseline vitals – including postural B/P

Hypnotics: 15-30 minutes pre bedtime for maximum effectiveness

Avoid ETOH and other CNS depressants

Avoid grapefruit juice

Pregnancy and breast feeding

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94
Q

hematopoiesis

A

Formation new blood cells (red, white, platelets)

Hemoglobin = O2 and remove CO2

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95
Q

Hematocrit

A

Important marker for anemia

Percentage of WBC & RBC in blood

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96
Q

lifespan of RBC

A

Lifespan = 120 days (significant)

More than 1/3 made of hemoglobin

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97
Q

anemias

A

Maturation defects (120 days (lifespan))

Excessive destruction of RBCs (hemolytic anemias)

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98
Q

maturation defects

A

Lack of B12 or folic acid

Blood loss, child birth, GI bleeding, periods

Cytoplasmic

Nuclear

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99
Q

Excessive destruction of RBCs (hemolytic anemias)

A

Genetic deficit = sickle cell disease (immature RBC)

Intrinsic RBC abnormalities = Sickle cell

Extrinsic mechanisms = Mechanical (blood loss)

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100
Q

Erythropoiesis – stimulating agents (stimulates RBC production from bone marrow)

A

Epoetin alfa

Biosynthetic form of hormone erythropoietin (produced in kidney)

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101
Q

Erythropoiesis – stimulating agents treat

A

anemia associated end-stage renal disease, chemo – induced anemia, anemia associated with antiretroviral medications

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102
Q

Erythropoiesis – stimulating agents ineffective w/o adequate

A

iron stores & bone marrow function

You must be able to be able to store iron (ferritin)

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103
Q

Erythropoiesis – stimulating agents contraindications

A

Allergy

Hypertension

Hemoglobin levels

Head and neck cancers

Thrombosis

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104
Q

hemoglobin levels for Erythropoiesis – stimulating agents

A

100mmol/L for cancer pt

130mmol/L for pt w/ kidney disease (Don’t want pt to have if hemoglobin too high = Too high = viscosity)

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105
Q

adverse effects Erythropoiesis – stimulating agents

A

Hypertension, fever, headache, pruritus, rash, N & V, arthralgia (joint stiffness), injection site reaction

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106
Q

iron

A

O2 carrier in hemoglobin & myoglobin

Iron & oxygen binding protein in the muscle

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107
Q

Foods enhance absorption iron

A

Orange juice, veal, fish, ascorbic acid

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108
Q

Foods impair absorption iron

A

Eggs, corn, beans, cereal products containing phytates

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109
Q

Oral iron are available as ferrous salts

A

(fumarate (33% iron), sulphate (20% iron), gluconate (11.6% most common))

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110
Q

iron indications

A

Prevention & treatment of deficiency

Admin alleviates symptoms of anemia but underlying cause of anemia needs to be corrected

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111
Q

adverse effects of iron

A

Nausea, vomiting, diarrhea, constipation, stomach cramps, pain

Most common cause of pediatric poisoning (Schedule 2)

Black darkened stools (dark green)

Temp discolour teeth (liquid oral)

Injectable (pain upon injection)

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112
Q

Toxicity iron

Symptomatic & supportive measures

A

Suction & maintenance of airway

Correction of acidosis

Control of shock & dehydration with IV fluids or blood

Oxygen

Vasopressors

Severe symptoms (coma, shock, seizures) = Chelation therapy w/ deferoxamine mesylate

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113
Q

dextran

A

Anaphylactic reactions (major orthostatic hypotension & fatal)

Test dose of 25mg admin before full dose then remainder given 1 hr after

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114
Q

Ferric gluconate

A

Indicated for repletion of total iron content in pt w/ iron deficiency anemia undergoing hemodialysis

Risk of anaphylaxis is much less than dextran

Doses higher than 125mg associated with increased adverse effects = Abdominal pain, dyspnea, cramps, itching

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115
Q

Folic acid

A

B-complex vitamin (B9)

Essential for erythropoiesis

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116
Q

primary uses folic acid

A

Deficiency

During pregnancy = prevent neural tube defects (Trying to get prego = take 1 month before)

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117
Q

Cyanocobalamin – vitamin B12

A

Treat pernicious anemia & other megaloblastic anemias (large, abnormal, immature RBCs)

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118
Q

B12 & folic acid = building blocks for RBC (t/f)

A

TRUE

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119
Q

Nursing process: assessment anemia

A

Pt history & medications, allergies

Assess potential contraindications

Assess baseline lab values, especially hemoglobin, hematocrit

Obtain nutritional assessment

Hematochezia = Frank or fresh blood in stool

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120
Q

Dextran contraindicated in all anemias except for

A

iron-deficiency anemia

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121
Q

Interventions anemia

A

Liquid preparations = follow manufacturer’s guidelines on dilution & administration

Instruct pt to take liquid iron through a straw to avoid staining tooth enamel

Oral forms taken b/w meals for max absorption by can be taken with meals if GI distress occurs (Given with juice NOT milk or antacids = Because milk & antacids create a barrier)

Avoid esophageal corrosion = remain upright for 30 mins after

Pt encouraged to eat foods high in iron & folic acid

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122
Q

Triglycerides

A

energy sources & stored in adipose tissue

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123
Q

Cholesterol

A

used to make steroid hormones, cell membranes, bile acids

124
Q

Low-density lipoprotein

A

Produced by liver

Transports endogenous lipids to peripheral cells

125
Q

High-density lipoprotein (HDL)

A

Responsible for “recycling” of cholesterol

“good cholesterol”

126
Q

1st line therapy for hypercholesterolemia (elevated LDL)

A

Hydroxymethylglutaryl – coenzyme A (HMG-CoA) reductase inhibitors (statins)

127
Q

Most potent LDL reduces

A

Pravastatin sodium

Simvastatin

Atorvastatin

Fluvastatin sodium

Rosuvastatin calcium

Lovastatin

128
Q

statin mechnism of action

A

Inhibit enzyme which used by liver to produce cholesterol

Lower rate of cholesterol production = increasing the amount of LDL receptors in liver

129
Q

statin adverse effects

A

Mild, transient GI disturbances (constipation)

Rash

Headache

Myopathy (muscle pain), possibly leading to rhabdomyolysis (serious condition)

Do not use for patients with elevated liver enzymes or liver disease

130
Q

Rhabdomyolysis

A

Breakdown of muscle protein

Lead to acute kidney injury

Early intervention = reversible with discontinuation of drug

Report STAT signs of toxicity (muscle soreness or urine colour (tea-coloured))

131
Q

avoid grapejuice for rhabdomyolysis

A

YES

132
Q

Atorvastatin calcium & simvastatin

A

Lowers total & LDL cholesterol levels & triglyceride levels

Raises HDL (good cholesterol)

Dosed once daily, evening meal or bedtime to correlate diurnal rhythm (liver produces most cholesterol)

133
Q

Bile acid sequestrants examples

A

Cholestyramine resin, colestipol hydrochloride, colesevelam

134
Q

Bile acid sequestrants mechanism of action

A

Prevent resorption of bile acids from small intestine

Bile acids necessary for absorption cholesterol

135
Q

can Bile acid sequestrants be used with statins

A

YES

136
Q

adverse effects Bile acid sequestrants

A

Constipation

Heartburn, nausea, belching, bloating = Tend to disappear over time

Mild increases in triglyceride levels

137
Q

B vitamin niacin (vitamin B3, nicotinic acid) adverse effects

A

Flushing (caused by histamine release)

Pruritus

GI distress

138
Q

Fibric acid derivatives (fibrates) examples

A

Bezafibrate, gemfibrozil, fenofibrate

139
Q

Fibric acid derivatives (fibrates) be given with statin

A

YES increase risk of myositis, myalgia, rhabdomyolysis

140
Q

Fibric acid derivatives (fibrates) adverse effects

A

Abdominal discomfort, diarrhea, nausea,

Blurred vision, headache

Increased risk of gallstones

Prolonged prothrombin time

Increased enzyme levels??

141
Q

Cholesterol absorption inhibitor (ezetimibe)

A

Inhibits absorption of cholesterol & related sterols from small intestine

142
Q

Cholesterol absorption inhibitor (ezetimibe) used with statin

A

YES

143
Q

garlic

A

antispasmodic, antiseptic, antibacterial, antiviral, antihypertensive, antiplatelet, lipid reducer

144
Q

garlic possible interactions

A

warfarin, diazepam, protease inhibitors

145
Q

garlic may enhance

A

bleeding with nonsteroidal anti-inflammatory drugs (NSAIDs)

146
Q

Assessment lipids

A

Before therapy, health & medication history

Dietary patterns, exercise level, weight, height, VS, tobacco & alcohol

Contraindications, conditions that require caution, drug interactions

Results of baseline liver function

147
Q

lipids contraindicated

A

Biliary obstruction

Liver dysfunction

Active liver dysfunction

148
Q

interventions lipids

A

Long term therapy = supplemental fat-soluble vitamins (A, D, E, K) with bile acid sequestrants

Refer to guidelines for admin time & meals

Educate diet & nutrition

Educate on proper procedure for taking meds

Powder forms = mixed thoroughly with liquid (NOT STIRRED)

Other meds taken 1 hr before or 4-6 hours after meals to avoid interference with absorption

Minimize effects of niacin = start low & gradually increase & take with meals

Inform meds take several weeks to show effectiveness

149
Q

niacin = Small doses aspirin or NSAIDs may be 30mins to minimize flushing

Provide education about NSAIDs & aspirin

A

TRUE

150
Q

Evaluation lipids

A

Instruct to report persistent GI upset, constipation, abnormal bleeding, yellowing skin

Monitor for adverse effects (increased liver enzyme labs & signs of myalgias)

Monitor for therapeutic effects = Reduced cholesterol & triglyceride levels

151
Q

Coagulation system “cascade”

A

Each activated factor serves as catalyst that amplifies next reaction

Results = fibrin (clot-forming substance)

152
Q

Thrombus

A

Aggregation of platelets, fibrin clotting factors & cellular elements of blood that is attached to interior wall of vein or artery

153
Q

Anticoagulants

A

Inhibit action or formation of clotting factors

Prevent clot formation

No direct effect on blood clot that is already formed

Prevent intravascular thrombosis by decreasing blood coagulability

Used prophylactically to prevent

154
Q

Antiplatelet drugs

A

Inhibit platelet aggregation

Prevent platelet plugs

155
Q

Thrombolytic agents

A

breaks down formed clots)

156
Q

Antifibrinolytics agents

A

(promote blood coagulation & clot formation)

157
Q

action of heparin

A

Inhibit clotting factors IIa (thrombin), Xa, IX

158
Q

Low-molecular-weight heparins examples

A

Enoxaparin

Dalteparin

Nadroparin calcium

Tinzaparin sodium

159
Q

Unfractionated heparin sodium

A

Frequent lab monitoring for bleeding times (aPTT – how long does it take for blood clot to form in sec) - normal time = 25-35 secs

Weight-based protocol

160
Q

lab monitoring needed for low molecular heparins

A

NO

161
Q

Direct acting Xa inhibitors action

A

nhibit factor

Fondaparinux, rivaroxaban, apixaban

162
Q

Warfarin

A

Inhibit vitamin K synthesis by bacteria in GI tract

163
Q

warfarin action

A

Inhibit vitamin K-dependent clotting factors II, VII, IX, and X which normally synthesized in liver

164
Q

final effect of warfarin

A

prevention of clot formation

165
Q

lab monitoring for warfarin

A

Careful monitoring of prothrombin time(PT)/international normalized ratio (INR)

166
Q

therapeutic INR warfarin

A

2-3.5 sec

167
Q

maintenance dose of warfarin determined by

A

INR

168
Q

mechanism of action warfarin

A

Work on different points of clotting cascade

Prevent intravascular thrombosis by decreasing blood coagulability

Do not lyse existing clots

169
Q

warfarin indications

A

Prevent clot formation in certain settings in which clot formation is likely (Unstable angina, Atrial fibrillation, Indwelling devices (mechanical heart valves), Conditions in which blood flow may be slowed & blood may pool (prolonged periods of immobility))

170
Q

contraindications warfarin

A

Allergy

Acute bleeding process or high risk of

Warfarin strongly contraindicated in pregnancy

Low-molecular-weight heparins = indwelling epidural catheter risk of epidural hematoma

171
Q

adverse effects warfarin

A

Bleeding = Risk increases with increased dosages (May be localized or systemic)

Heparin-induced thrombocytopenia

Nausea, vomiting, abdominal cramps, thrombocytopenia

172
Q

symptoms of toxic effects of heparin

A

Hematuria

Melena (blood in stool)

Petechiae

Ecchymoses

Gum or mucous membrane bleeding

173
Q

antidote for toxic effects of heparin

A

protamine sulphate (reverse 100 units)

174
Q

warfarin adverse effects

A

Bleeding, lethargy, muscle pain, skin necrosis, “purple toes” syndrome

175
Q

toxic effects of warfarin mayy take

A

May take 36-42 hours before liver can resynthesize enough clotting factors to reverse warfarin effects

176
Q

antidote for warfarin

A

vitamin K

Vitamin K can quicken return to normal coagulation

Vitamin K given, warfarin resistance will occur for up to 7 days

177
Q

Antiplatelet drugs

A

Prevents clot formation by inhibiting platelet adhesion at beginning of cascade

178
Q

antiplatelet examples

A

Acetylsalicylic acid

Clopidogrel bisulfate

Ticagrelor

179
Q

mechanism of action antiplatelet

A

Affect normal function of platelets to prevent platelet adhesion to site of blood vessel injury

180
Q

indications antiplatelet

A

Stroke, TIA, post MI thrombo prevention

Some used in conjunction with anticoagulant warfarin as prophylaxis for CVA, PE, DVT

181
Q

ASA s/e

A

Nausea, vomiting, GI bleeding, diarrhea, thrombocytopenia, agranulocytosis, anemia

182
Q

clopidogrel s/e

A

Chest pain, abdo pain, diarrhea, epistaxis, headache, dizziness, fatigue

183
Q

assessment coagulants

A

History, medications, allergies

Contraindications

Baseline VS, lab values (PT, INR, PTT)

Potential drug interactions

History of abnormal bleeding conditions

No IM injections with anticoagulants

184
Q

Heparin nursing process

A

IV doses double-checked (high alert)

Ensure subcut dose given SC

Subcut given areas of deep subcut fat & sites rotated

Don’t give within 5cm of umbilicus, abdo incisions, open wounds, scars, drainage tubes, stomas, areas of bruising

Don’t aspirate (hematoma)

IV = bolus or IV infusions

Anticoagulants effects seen immediately

Lab values done daily to monitor coagulation effects (aPTT)

Protamine sulphate given as antidote in case of excessive anticoagulation

185
Q

Low-molecular-weight heparins nursing process

A

SC in abdo

Rotate sites

Protamine sulphate given as antidote

186
Q

Warfarin nursing process

A

May start if pt still on heparin until PT/INR level indicate adequate anticoagulation (cross-over therapy or bridging therapy)

Full therapeutic effects take days

Antidote is vitamin K

Many herbal products potential interactions = increased bleeding may occur

Capsicum pepper, garlic, ginger, ginkgo, st. John’s wort, feverfew

187
Q

Anticoagulants & antiplatelet: nursing education

A

Importance of reg lab testing

Signs of abnormal bleeding

Measures of prevent bruising & tissue injury

Wearing medical alert bracelet

Avoid foods high in vitamin K (tomatoes, dark leafy green)

Consulting the physician before taking other drugs or OTC products

188
Q

Antibiotics: All classes

A

Sulfonamides
B-Lactam (4 diff classes)
macrolides
Tetracyclines
Aminoglycosides
Quinolones
Miscellaneous

189
Q

sulfonamide action

A

Bacteriostatic
Prevent bacterial synthesis of folic acid (B-complex vitamin) required for synthesis of purines and nucleic acid (DNA & RNA)

190
Q

sulfa uses

A

Gram-positive and negative bacteria;
Treatment of urinary tract infections; pneumonia; UTI

191
Q

sulfa adverse effects

A

Common allergic reactions including photophobia and skin rash; see Adverse Effects

Superinfection

192
Q

b-lactams penicillin action

A

Bactericidal
Enter the bacteria via the cell wall then bind to penicillin-binding protein.
Broad spectrum

193
Q

penicillin uses

A

Gram-positive and negative; Health care-acquired infections, including pneumonias, intra-abdominal infections and sepsis.

194
Q

penicillin adverse effects

A

Nausea, vomiting, diarrhea, abdominal pain

Superinfection

195
Q

penicillin nursing process

A

An allergic reaction to penicillin may also have an allergic reaction to other B- Lactam antibiotics.

196
Q

B-Lactams: Cephalosporin
(5 generations available) action

A

Bactericidal Structurally and pharmacologically related
to penicillin;
Broad spectrum

197
Q

B-Lactams: Cephalosporin
(5 generations available) uses

A

Gram-positive and negative; surgical prophylaxis and for susceptible staphylococcal infections; 4th generation difficult to treat UTI

198
Q

cephalosporin adverse effects

A

Mild diarrhea, abdominal cramps, rash, pruritus, redness, edema

Superinfection

199
Q

cephalosporin nursing process

A

Penicillin cross- sensitivity; Incidence between 1 and 4%.

200
Q

B-Lactams Carbapenem
(broadest antibacterial action of any abx to date) action

A

Bactericidal
Binds to penicillin-binding proteins inside bacteria, which in turn inhibits bacterial cell wall synthesis.

201
Q

B-Lactams Carbapenem
(broadest antibacterial action of any abx to date) uses

A

Reserved for complicated body infections; treatment of severe or high-risk bacterial infections such as multidrug-resistant (MDR) bacterial infections i.e. MRSA.

202
Q

B-Lactams Carbapenem
(broadest antibacterial action of any abx to date) adverse effects

A

most serious adverse effect is seizures; 1.5% for <500mg q 6hrs and 10% > 500mg q 6hrs
Superinfection

203
Q

nursing process B-Lactams Carbapenem
(broadest antibacterial action of any abx to date)

A

Cross sensitivity to PCN; Must be infused over 60 minutes

204
Q

Macrolides action

A

Bacteriostatic
Prevent protein synthesis within bacterial cells

205
Q

macrolides uses

A

“Strep” infections
Streptococcus ;
Mild to moderate URI and LRI; Haemophilus influenza;
Spirochetal infections-
Syphilis and Lyme disease;
Gonorrhea; Chlamydia.

206
Q

adverse effects macrolides

A

GI effects (primarily erythromycin)
N & V, diarrhea.
Fidaxomicin (Dificid): N & V, and GI bleed.
Superinfection

207
Q

nrusing process macrolides

A

**Fidaxomicin (Dificid) is the newest macrolide antibiotic. It is indicated only for the treatment of diarrhea associated with Clostridium difficile.

208
Q

tetracyclines action

A

Bacteriostatic
inhibit bacterial growth
Inhibit protein synthesis; Bind (chelate) to Ca, Mg and Al ions to form insoluble complexes

209
Q

tetracycline uses

A

Gram-negative and gram-positive organisms; acne in adults and adolescents; chlamydia, mycoplasma pneumonia; h.pylori; syphilis; resistant to gonorrhea.

210
Q

tetracycline adverse effects

A

Diarrhea
Vaginal candidiasis
Gastric upset
Enterocolitis
Photophobia
Superinfection

211
Q

nursing process tetracycline

A

Dairy products, antacids, and iron
salts reduce oral absorption of tetracycline; discolors of teeth

212
Q

aminoglycoside action

A

Bactericidal
Prevent protein synthesis; Often used in combination with other antibiotics for synergistic effects.

213
Q

aminoglycosides uses

A

Kill mostly gram-negative bacteria, some
gram-positive bacteria; Used for certain gram-positive infections that are resistant to other antibiotics such as Enterococcus spp., S. aureus. MRSA, ESBL

214
Q

adverse effects aminoglycosides

A

Nephrotoxicity; Ototoxicity [eighth cranial nerve])

Superinfection

215
Q

nursing process aminoglycosides

A

Must monitor drug levels to prevent toxicities

216
Q

quinolones action

A

Bactericidal
Alter deoxyribonucleic acid (DNA) of bacteria, causing death

217
Q

quinolones uses

A

Effective against gram-negative organisms and some gram-positive organisms; Potent and broad-spectrum for complicated urinary tract, respiratory, bone and joint, gastrointestinal, and skin infections.

218
Q

quinolones adverse effects

A

Nausea, vomiting, diarrhea, constipation, oral candidiasis, dysphagia, increased liver function
Superinfection

219
Q

quinolones nursing process

A

Absorption reduced by antacids, calcium, magnesium, iron, others

220
Q

gram - & +

A

+ = thick cell wall & outer capsule

  • = small capsule w/ 2 membranes (harder time treating due to 2 membranes)
221
Q

can disinfectants be used on humans

A

no – nonliving objects only

222
Q

when do you take a culture and sensitivity

A

BEFORE TX

223
Q

empiric therapy

A

tx of infection before culture information obtained

224
Q

definitive therapy

A

once culture obtained, abx tailored the best abx for specific bacteria

225
Q

what is the order of. medicaitons for abx

A

broad (wait 3 days for culture to be returned) narrow medicaiton

226
Q

subtherapeutic response

A

s/s not improve

227
Q

secondary infection

A

superinfection occurs when second infection closely follows intitial infection & comes from external source (colds, coughs)

228
Q

host factors

A

comorbidities & things increase suspectibility

229
Q

anaphylaxis s/s

A

hives, flushing, itching, anxiety, fast heart rate, tongue throat swelling

230
Q

bactericidal

A

kill

231
Q

bacteriostatic

A

inhibit growth

232
Q

sulfonamides used for

A

UTI

233
Q

sulfo action

A

prevent bacterial synthesis of folic acid which is required for synthesis (bacteriostatic)

234
Q

sulfo can be used for UTI but what else

A

pneumonia, MRSA

235
Q

sulfo is a 2 combo drug that causes what kind of effect

A

synergistic

236
Q

most common side effects sulfo

A

N & V diarrhea photosensitivity

237
Q

b lactams 4 categories

A

penicillins

cephalosporins

carbapenems

monobactams

238
Q

pencillin action

A

bactericidal (kill)

239
Q

penicillin used

A

pneumonias, abdo infections, sepsis

240
Q

ppl allergic to penicillin are at increase risk of allergy to

A

other b lactams abx

241
Q

common s/e penicillin

A

N & V diarrhea abdo pain

242
Q

cross sensitivity

A

cephalosporins chemically similar to penicillin thus ppl with allergic to penicillin may have allergy to ^^

243
Q

1st gen cephalo used fr

A

surgical prophylaxis & staph infections

244
Q

2nd gen cephalo used for

A

surgical prophylaxis

245
Q

3rd gen cephalo

A

broad spectrum

246
Q

4th gen cephalo used for

A

un/complicated uti

247
Q

cephalo s/e

A

ando cramps rash redness edema itchy

248
Q

which med used for MRSA in carbapenems

A

imipenem

249
Q

how long does carbapenems be infused over

A

60 mins

250
Q

monobactams used for

A

cystic fibrosis

251
Q

which med usded for c diff

A

macrolides = fidaxomicin

252
Q

which med ruins teeth

A

tetracycline
8 years or young = tooth discolouration occurs if abx binds to calcium in teeth

253
Q

during assessment process of abx what some things need to look for

A
  • allergics
  • hx
  • labs
  • interactiions’
  • superinfections (yeast infections)
  • tetracycline reduce effectiveness of contraceptives
254
Q

with abx you need to avoid

A

antacids, antidiarrheal, dairy, calcium, iron = reduce tetracycline absorption

consume drug 2 hr before or 3 hrs after ^^^

255
Q

which sulfo how much fluid?

A

2-3L

256
Q

penicillins may require pt to supplemental

A

probiotics as it kills all gut bacteria

257
Q

VRE is usually seen in

A

UTI

258
Q

aminoglycosides considerations

A

trough levels to prevent toxicities

12 hrs after dose

30 mins before morning dose

259
Q

aminoglycosides adverse effects

A

nephrotoxicity, ototoxicity

260
Q

giving 2 abx, which one given first

A

ex: b lactam given first as it breaks down cell wall of bacteria & allow aminoglycosides to gain access to ribosomes to kill

261
Q

quinolones work good for

A

complicated uti

262
Q

vancomycin considerations

A

trough levels d/t heptatoxicity

MRSA

263
Q

what abx does red man syndrome occur

A

vancomycin

264
Q

what is red man snydrome

A

flushing erythema itching of head face neck upper truck

265
Q

why does red man syndrome occur

A

infusing abx too quickly

266
Q

how do you assess for ototoxicity & nephrotoxicity

A

o - hearing loss, tinnitus, fullness in ear

n - BUN & Cr

267
Q

what do you assess in linezolid

A

concurrent use of ssri risk of serotonin syndrome

268
Q

fluconazole s/e

A
  • n & v, diarrhea, stomach pain, increased liver enzymes
269
Q

nystatin s/e

A

n & v, anorexia, diarrhea, rash, hives

270
Q

how to admin nystatin

A

oral = dropped directly on tongue & held in mouth as long as possible & then swallowed = swish med thoroughly in mouth before swallowing

271
Q

WBC levels

A

5,000 - 11,000

272
Q

PLTs levels

A

150,000 - 400,000

273
Q

INR sec levels

A

0.8-1.2

274
Q

NA levels

A

136-145

275
Q

lithium maintenance <66yrs

A

0.6-1.0

276
Q

LFT

A

ALT (enzyme)

277
Q

H A1C

A

< 7%

278
Q

creatinine

A

f = 44-97
m = 53-106

279
Q

valporic acid

A

350 - 830

280
Q

hemoglobin

A

m = 140-180
f = 120-160

281
Q

k+

A

3.5-5

282
Q

fasting glucose nondiabetic

A

4-6

283
Q

GFR

A

> 90 ml/min

284
Q

c-reactive protein

A

< 0.3 - 1.0

285
Q

extrapyramidal symptoms include

A

dystonia
akathisia
akinesia
parkinsonism
rabbit syndrome
pisa syndrome
tardive dyskinesia

286
Q

anticholinergic side effects

A

blurred vision
dry mouth
urinary retention
psychomotor agitation
tachycardia
dizziness
decreased BP

287
Q

1st gen antpsychotics

A
  • loxapine
  • haloperidol (haldol)
  • flupenthixol (long acting)
  • trifluoperazine
  • methotrimeprazine (nozinan)
  • chlorpromazine (largectil)
288
Q

2nd gen AP

A

clozapine (clozaril)
risperidone (risperdal)
olanzapine (zyprexa)
quetiapine (seroquel)

289
Q

acute dystonic reaction

A
  • severe involuntary muscle spasms
  • difficulty swallowing
  • stiff neck
  • thick tongue
  • extreme facial grimacing
290
Q

akathisia

A
  • need for movement
  • restlessness/pacing
  • “my nerves are jumping”
  • nervous energy
291
Q

akinesia

A

immobility, weakness

complaints of fatigue

lack of muscle movement

292
Q

parkinsonism

A

resting tremor

shuffling gait

mask-like face

drooling

293
Q

TD

A

uncontrollable, abnormal, and repetitive movements of the face, torso, and/or other body parts.

294
Q

hypernatremia leads to

A

decreased lithium concentrations

295
Q

hyponatremia leads to

A

increased lithium concentrations

296
Q

caffeine, metamucil, bronchial dilators do what to lithium

A

decrease

297
Q

N & V, diarrhea, sweating, ACE inhibitors, ARBS, CCBs, NSAIDs do what to kidneys

A

sodium loss = retain more lithium (increase)

298
Q

target levels of lithium in acute phase mania

A

0.8-1.2mmol/L

299
Q

maintenance levels of lithium

A

0.6-1mEq/L

300
Q

elderly levels of lithium

A

0.4-0.6mEq/L

301
Q

mild to moderate lithium toxicity levels

A

1-2mEq/L

302
Q

side effects of mild to moderate lithium toxicitiy levels

A

diarrhea, vomiting, fatigue, tremors, increased drowisness, uncontrolled movement, blurred vision

303
Q

symptomsof severe lithium toxicity

A

delirium, slurred speech, seziuers, rapid heart rate, hyperthermia, nystagmus, confusion, kidney failure, coma

304
Q

Choice triad:

A

Choice triad:

3 step process to determine pt’s medication interest

Communication model, shared learning, rapport

Where the patient is at in that moment with medication interest & choice

  1. has insight, believe something is wrong = wants relief
  2. motivated to use medication as they believe it will help relieve the symptoms they are experiencing
  3. client believes the benefits of taking the medication are greater than the adverse effects (weighing the pros & cons)
305
Q

Medication interest model:

A

Medication interest model:

Communication, collaborated listening

Framework of interviewing techniques used to elicit & explore the clients beliefs/feelings regarding each step in the choice triad

pharm (4 decks)

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