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final from quizlet Flashcards

1
Q

What constitutes the upper respiratory tract?

A

Nose, nasopharynx, oropharynx, laryngopharynx, & pharynx

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2
Q

What constitutes the lower respiratory tract?

A

Trachea, bronchial tree, alveoli & lungs

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3
Q

Common diseases of the respiratory system

A

COPD
Asthma
Chronic Bronchitits
Emphysema

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4
Q

What is COPD

A

Chronic Obstructive Pulmonary Disease. Irreversible decrease in the ability to force air out of the lungs.

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5
Q

What is Asthma

A

Chronic airway inflammation = bronchial constriction
Wheezing and difficulty breathing
Tightness of ches

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6
Q

What is chronic bronchitis

A

Continuous inflammation of bronchi
Excessive secretion of mucus

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7
Q

What is emphysema?

A

Alveolar wall destruction & enlarged air spaces Impaired gas exchanged
Smoking is primary causation

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8
Q

What types of medications are used to treat lower respiratory tract?

A

Bronchodilators such as B-adrenergic agonists, anticholingergic drugs, xanthine derivatives

Non-bronchodilators such as corticosteroids, Leukotriene receptor antagonits (LTRAs)

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9
Q

B-andrenergic agonists indication of use

A

Used to treat severe bronchospasm
For quick relief of symptoms

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10
Q

B-andrenergic agonists mechanism of action

A

Stimulates B2-Adrenergic receptors in the lungs

Relaxes bronchial smooth muscles which causes dilation of the bronchi and bronchioles

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11
Q

B-andrenergic agonist medication examples

A

salbutamol (Ventolin) short acting
Onset of action (inhaled) is immediate
salmeterol xinafoate (Serevent) long acting Combination (steroid and B-Adrnergic - Symbicort or Advair)

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12
Q

B-Andrenergic blockers adverse reactions

A

Tachycardia
Palpitations
Tremor
Anxiety
Hyper/hypotension
headache

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13
Q

Anticholingerics indications for use

A

Maintenance and prevention of bronchospasm

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14
Q

Anticholingerics mechanism of action

A

Prevents bronchial constriction by blocking acetylcholine (Ach) receptors

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15
Q

Anticholinergics medication example

A

ipratropium bromide (Atrovent)
tiotropium bromide monohydrate (Spiriva)
salbutamol and ipratropium combination (Combivent)

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16
Q

Anticholingerics 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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17
Q

Xanthine Derivatives indication for use

A

For prevention of symptoms
Used with mild/moderate asthma
Used with chronic bronchitis & emphysema

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18
Q

Xanthine Derivatives mechanism of action

A

Causes bronchodilation by inhibiting phosphodiesterase enzyme results in smooth muscle dilation

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19
Q

Xanthine Derivatives examples

A

Theophylline
Aminophylline (IV only

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20
Q

Xanthine Derivatives adverse effects

A

Tachycardia
Palpitations
Ventricular dysrhythmias
GERD
nausea
vomiting
anorexia
Increased urination
Hyperglycemia

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21
Q

Corticosteroids indication for use

A

Anti-inflammatory
For management of difficult to treat asthma/respiratory illnesses
Allergic rhinitis

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22
Q

Corticosteroids Mechanism of action

A

Prevent nonspecific inflammatory processes by acting on the 5 types of WBC
Controls inflammatory responses
Increases the effects of B-agonists (bronchodilation)

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23
Q

Corticosteroids medication example

A

Budesonide (Pulmicort)
Fluticasone Propionate (flovent)
Prednisone
Combination with B-AgonistAdvair.

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24
Q

Corticosteroids adverse effects

A

Pharyngeal irritation
Cough and dry mouth
Oral fungal infections
PO Corticosteroids provide more systemic effect and therefore adverse effects are more systemic Susceptibility to infection
Fluid and electrolyte imbalance
Endocrine effects (including hyperglycemia) Osteoporosis

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25
Q

Leukotriene Receptor Antagonist indications for use

A

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

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26
Q

Leukotriene Receptor Antagonist medication examples

A

montelukast (Singulair)
zafirlukast (Accolate)
Both dosed once daily

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27
Q

Leukotriene Receptor Antagonist adverse effects

A

Nausea
Diarrhea
Headache
Nightmares
Liver dysfunction

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28
Q

Nursing assessment variance in oxygenation

A

Respiratory assessment
Environmental exposures & allergens
Smoking habits
Emotional status (anxiety, stress, fear)
Allergies
Caffeine intake

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29
Q

Nursing interventions variance in oxygenation

A
  • Discuss adherence to medication regimen
  • Demonstrate proper administration of inhaled drugs - Reassess respiratory status & breath sounds
  • Instruct patient 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 Q weekly with warm soapy water
  • PATIENT EDUCATION
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30
Q

What constitutes the adrenal system?

A

Adrenal gland Adrenal cortex ( 80-90%) Medications working on it include: Corticosteroids Glucocorticoids Mineralocorticoids Adrenal medulla (10-20%) medications working on it include: Epinephrine Norephinephrine

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31
Q

When are natural corticosteroids sythesized?

A

They are synthesized as needed

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32
Q

What regulates corticosteroid levels?

A

the hypothalamic-pituitary-adrenal gland axis regulates corticosteroids

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33
Q

Physiology of corticosteroid creation

A

Level of corticosteroid low → corticotropin releasing hormone released from hypothalamus → anterior pituitary →ACTH released → adrenal cortex → production of corticosteroids stimulated → corticosteriods reach peak level → signal sent to hypothalamus → HPA inhibited

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34
Q

What are Glucosteroids and what do they do?

A

Major Anti-inflammatory actions
Regulates carbohydrate, protein & lipid metabolism Maintenance of normal BP
Stress effects
Immune response

Examples:
Adrenocorticotropic hormone (ACTH), cortisone, hydrocortisone, methylprednisone, prednisolone

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35
Q

What are Mineralocorticoids and what do they do?

A

BP control
Maintenance of pH levels in blood
Maintenance of serum K levels
Sodium & water reabsorption

Examples:
fludrocortisone 21- acetate (drug replacement

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36
Q

What happens when the adrenal system over-secretes?

A

Cushing’s syndrome

Over secretion of adrenal hormones Glucocorticoid hypersecretion - redistribution of body fat from arms & legs to face, shoulders, trunk, & abdomen
Characteristic ‘moon face’
Aldosterone hypersecretion- increased water & Na retention & muscle weakness from K loss

Causes: tumor, excessive administration of steroids (medication)

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37
Q

Adrenal System under-secretion:

A

Addison’s disease
Under secretion of adrenal hormones
Decreased blood Na and glucose levels, increased K levels Signs & symptoms: Hyperpigmentation, weakness, headache, fatigue, N & V, anorexia, dehydration, weight loss, confusion, fever, abd pain, >hr, diaphoresis, low B/P

Often vague, chronic and nonspecific complaints

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38
Q

Mineralcorticoids mechanism of action

A

Acts on distal kidney tubule → sodium reabsorption into blood → pulls water & fluid with it → help regulate edema & B/P (HTN)
Promotes H & K excretion
Helps regulate blood PH

Used for addison’s disease

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39
Q

Glucocorticoids mechanism of action

A

Inhibition of inflammatory & immune responses

Inhibit or control inflammatory response by:
(1) stabilizing cell membranes of inflammatory cells
(2) decreasing permeability of capillaries to inflammatory cells
(3) decreasing migration of WBCs into inflamed areas Promote breakdown of protein, production of glycogen in liver, & redistribution of fat
Some mineralocorticoid-like activity such as fluid and water retention

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40
Q

Corticosteroids indications

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

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41
Q

What else can Corticosteroids be used for?

A

Bronchospasms (via inhalation route i.e. fluticasone-Flovent)
Allergic rhinitis (via nasal route i.e. fluticasone-flonase) Inflammations of ear, eye, & skin (via topical route i.e. betamethasone)
Exacerbations of chronic respiratory illnesses (asthma & COPD)
PO and IV not interchangeable

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42
Q

What is an Addisonian crisis?

A

This develops when Addison’s Disease isn’t treated. In addisonian crisis, the patient has extremely LOW CORTISOL levels (life threatening).

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43
Q

What is the best time to give glucocorticoids?

A

Early morning (0600-0900) as it minimizes adrenal suppression

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44
Q

Glucocorticoids nursing process

A

Avoid alcohol, caffeine, aspirin, & NSAIDs
Healing may be decreased with long term therapy
Avoid contact with people with infections
Assess therapeutic response & adverse effects to monitor effectiveness

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45
Q

Can you quit corticosteroids cold turkey?

A

God no

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46
Q

Are falls a concern with corticosteroids?

A

Yes

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47
Q

What are anxiolytics and sedative hypnotics?

A

CNS depressants with similar effects

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48
Q

What are anxiolytics used for?

A

Decrease anxiety, promote relaxation

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49
Q

What are sedative hypnotics used for?

A

Promote relaxation, induce sleep

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50
Q

What are anxiolytics used for sleeping referred to as?

A

sedative-hypntoics.

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51
Q

What else differentiates Anxiolytics and sedative hypnotics?

A

Dosage

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52
Q

What are some examples of anxiolytics and sedative hypnotics?

A

Benzos are the main drug used to treat anxiety and insomnia
Antidepressants are becoming more used (trazodone)
Barbituates were used but because they got you a little too turnt and addicted we stopped using them

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53
Q

Can insomnia and anxiety coexist?

A

The clinical presentation of both anxiety and insomnia often coexist
- Daytime anxiety can manifest as a nighttime sleep disturbance
-unable to turn off their worries - And lack of sleep can present as anxiety, fatigue and decreased functioning

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54
Q

What is anxiety?

A

A very common disorder which is on the increase in Western society
Often described as nervousness, tension, worry
Is an unpleasant feeling
It occurs when the individual perceives a situation as threatening to physical, emotional, social or economic well being

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55
Q

Anxiety Pathophysiology

A

Not really understood

Basically there is an excess of excitatory neurotransmitters (e.g. norephinephrine) or a deficiency of inhibitory neurotransmitters (e.g. gamma-aminobutyric acid or GABA)

Neuroendocrine factors also play a role - when under stress, corticotropin releasing factor (CRF) increases release of norephinephrine

Serotonin system is also involved, hence the effectiveness of SSRI’s in treating anxiety

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56
Q

What is sleep?

A

A recurrent period of decreased mental and physical activity

REM sleep is most important for mental and emotional restoration

Non REM is physically restorative

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57
Q

What is insomnia?

A

A prolonged period of difficulty falling asleep

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58
Q

What do benzodiazepines do?

A

They potentiate, or promote the activity of GABA by binding to a specific receptor on the GABA(a) receptor complex.

Gaba is inhibitory, if you’ll recall

The mom neurotransmitter, because I’d like to fu- think about the consequences of actions before I act

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59
Q

Benzodiazepine indications

A

Anti-anxiety
Hypnotic
Anticonvulsant
Prevention of agitation and delirium tremens (DT’s)
Anxiety/agitation associated with depression, psychosis or mania
Often given concurrently with anti-depressants, anti-psychotics and mood stabilizer

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60
Q

What type of sleep do benzos cause?

A

Non REM

Causes effects of CNS depression including
Sedation
Impairment of physical and mental activities
respiratory depression

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61
Q

Benzodiazepine half lives

A

Various benzos have different half lifes

Diazepam, Flurazepam form active metabolites which mess up livers in older adults

Lorazepam, Clonazepam have intermediate half lives which don’t have active metabolites

Trialozam does not accumulate

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62
Q

Which benzos are better for rapid responses?

A

Those with shorter half-lives

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63
Q

What are some commonly used benzos?

A

Diazepam (valium) for GAD, muscle relaxant, alcohol withdrawal

Lorazepam (ativan) for GAD, agitation, alcohol withdrawal

Clonazepam (Rivotril) indicated for seizure disorder, panic disorder, agitation and anxiety (takes longer than ativan, but less addictive)

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64
Q

Benzodiazepine advantages

A

Therapeutic dose has little effect on consciousness

Relatively safe

Few interactions with many other drugs

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65
Q

Benzodiazepine disadvantages

A

Potentially habit forming and addictive -
limit to two weeks use
Some have long half lives and can accumulate Memory and intellectual impairment
Hangover
Reduced motor coordination (driving hazard) Paradoxical confusion
agitation
insomnia

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66
Q

Benzo withdrawal

A

Mild symptoms occur with 6-12 weeks of use
Severe symptoms occur when regularly taken for 4 or more months
Withdrawal symptoms are caused by abrupt removal of benzo molcecules resulting in a decrease of GABA

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67
Q

Mild withdrawal symptoms for benzos

A

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

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68
Q

Severe withdrawal symptoms of benzos

A

irritability, agitation, rage, nervousness, diarrhea, vomiting, sweating

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69
Q

When do symptoms occur with benzos?

A

24 hours for short acting

4-5 days with long acting

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70
Q

Benzo withdrawal treatment

A

Taper the benzodiazepine

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71
Q

What are two non-benzodiazepine hypnotic-sedatives?

A

Chloral Hydrate (Noctec) Zoplicone (imovane)

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72
Q

Tell me about Chloral Hydrate

A

Oldest sedative hypnotic
Relatively safe, inexpensive and effective
Does not suppress REM
Tolerance builds fast
May cause physical dependence

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73
Q

Tell me about Zoplicone

A

Structurally different but functionally the same as Benzos

Indicated for short term insomnia

Delays onset of REM but does not reduce total duration of REM periods

Several drug interactions (suck my squick Carbamazepine)

Dosage: 7.5mg /24 hours half in elderly

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74
Q

Zoplicone considerations

A

Should not be prescribed in quantities larger than one month
- Risk of dependence
- Overdose can be fatal
- Rebound insomnia common
- Taper slowly
- Less side effects than other sedative hypnotics

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75
Q

Non-benzodiazepines: OTC antihistamines

A

Antihistamine with sedative and anti-emetic properties sometimes used to treat anxiety

Primarily hydroxyzine (Atarax), but also diphenhydramine (Benadryl) and dimenhydrinate (Gravol)

Indicated for anxiety, preoperative sedation, nausea and vomiting associated with surgery or motion sickness, pruritus and urticaria associated with allergic dermatoses

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76
Q

Natural health products for: Anxiylotics

A

Kava - Shrub from south america. Suppresses emotional excitability and may produce mild euphoria

Melatonin - Hormone produced in pineal gland, derived from amino acid tryptophan

Valerian - Herb used as a sedative hypnotic

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77
Q

Nursing process patient teaching anxyilotics

A

-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. It just tastes bad
- Pregnancy and breast feeding
- Assessment, Diagnosis, Planning, Implementation, Evaluation

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78
Q

What is Hematopoeisis

A

Formation of blood cells

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79
Q

Hematopoeisis: RBC

A

Manufactured in bone marrow
Immature RBCs are reticulocytes
Lifespan is 120 days
More than 1/3 of RBCs are made of hemoglobin
Heme: Red pigment, contains iron
Globin: Protein chain

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80
Q

Anemia causes

A

Maturation defects: Cytoplasmic, nuclear

Excessive destruction of RBCs (hemolytic anemias): intrinsic RBC abnormalities, extrinsic mechanisms

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81
Q

What is erythropoiesis?

A

production of red blood cells

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82
Q

Erythropoiesis stimulating agents

A

Epoetin alfa (Epogen)

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83
Q

What is epotein alfa?

A

Biosynthetic form of the natural hormone erythropoietin

  • Used for treatment of anemia associated with endstage renal disease, chemotherapy-induced anemia, and anemia associated with zidovudine therapy (antiretroviral medication).
  • Medication is ineffective without adequate body iron stores and bone marrow function.
  • Most patients receiving epoetin alfa need to also receive an oral iron preparation.
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84
Q

What is a longer form of epotein alfa

A

darbepoetin (Aranesp)

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85
Q

Epotein alfa contraindications

A

drug allergy; uncontrolled hypertension
hemoglobin levels that are above 100 mmol/L for cancer patients and 130 mmol/L for patients with kidney disease
head and neck cancers
risk of thrombosis

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86
Q

Epotein alfa adverse effects

A

Most frequent adverse effects: hypertension, fever, headache, pruritus, rash, nausea, vomiting, arthralgia, and injection site reaction

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87
Q

What is iron?

A

Essential mineral in the body
* Oxygen carrier in hemoglobin and myoglobin
* Stored in the liver, spleen, and bone marrow
* Deficiency results in anemia

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88
Q

Iron sources

A

Dietary sources: meats, certain vegetables and grains

Dietary iron must be converted by gastric juices before it can be absorbed.

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89
Q

What foods enhance iron absorption?

A

orange juice, veal, fish, ascorbic acid

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90
Q

What foods impair iron absorption

A

eggs, corn, beans, cereal products containing phytates

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91
Q

Can supplemental iron be added to a multivitamin?

A

Yes, but it’s a touch more rare

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92
Q

What are some Oral iron supplements are available?

A

Ferrous Sulfate
Ferrous Fumarate
Ferrous Gluconate

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93
Q

What are some parenteral iron supplements?

A

iron dextran (Dexiron®, Infufer®)
iron sucrose (Venofer®)
ferric gluconate (Ferrlecit®)
ferumoxytol (Feraheme®)

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94
Q

Iron indications

A

Prevention and treatment of iron-deficiency syndromes

Administration of iron alleviates the symptoms of iron-deficiency anemia, but the underlying cause of the anemia should be corrected

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95
Q

Iron: Adverse Effects

A

Most common cause of pediatric poisoning deaths- what drug schedule is iron? - schedule 2

Causes nausea, vomiting, diarrhea, constipation, and stomach cramps and pain.
Causes black darkened stools.
Liquid oral preparations temporarily discolour teeth.
Injectable forms cause pain upon injection.

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96
Q

What do we do about iron toxicity?

A

Symptomatic and supportive measures

Suction and maintenance of the airway; correction of acidosis; control of shock and dehydration with IV fluids or blood, oxygen, and vasopressors

In patients with severe symptoms of iron intoxication, such as coma, shock, or seizures, chelation therapy with deferoxamine mesylate is initiated.

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97
Q

Parenteral iron: Iron Dextan

A

Iron dextan…
May cause anaphylactic shock!
Used less frequently because it sucks!
More often we use ferric gluconate and iron sucrose!

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98
Q

Parenteral iron: Ferric gluconate

A

Indicated for repletion of total body iron content in patients with iron deficiency anemia who are undergoing hemodialysis!

Risk of anaphylaxis is much less than with iron dextran, and a test dose is not required.!

Doses higher than 125 mg are associated with increased adverse effects including abdominal pain, dyspnea, cramps and itching

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99
Q

What is folic acid?

A

a water soluble, B complex vitamin

Essential for production of red blood cells

Primary use: Folic acid deficiency, during pregnancy (1 month beforehand)

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100
Q

What causes folic acid deficiency?

A

Malabsorption frequently related to alcohol use

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101
Q

Should Folic acid be used if you have anemia?

A

Not until actual cause of anemia is determined

It may mask the symptoms of pernicious anemia which can lead to brain damage

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102
Q

What is Cyanocobalamin (Vitamin B12) used for?

A

Used to treat pernicious anemia and other megaloblastic anemias (large, abnormal, immature RBCs)

  • Administered orally or parentally.
  • Usually administered by deep intramuscular injection to treat pernicious anemia
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103
Q

Nursing process: Assesment for anemia

A

Assess patient history and medication history, including drug allergies.
* Assess potential contraindications.
* Assess baseline laboratory values, especially hemoglobin, hematocrit, reticulocytes, and others.
* Obtain nutritional assessment.

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104
Q

Nursing process: anemia

A

Ferrous salts are contraindicated for patients with ulcerative colitis, peptic ulcer disease, liver disease, and other gastrointestinal disorders.
* Keep away from children, because oral forms may look like candy.
* Iron dextran is contraindicated in all anemias except for iron-deficiency anemia.

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105
Q

Nursing process: anemia interventions

A
  • For liquid iron preparations, follow the manufacturer’s guidelines on dilution and administration.
  • Instruct the patient to take liquid iron preparations through a straw to avoid staining tooth enamel.
  • Oral forms of iron should be taken between meals for maximum absorption but may be taken with meals if gastrointestinal distress occurs.
  • Oral forms should be given with juice but not with milk or antacids. (Milk coats the inside of the absorption place)
  • To avoid esophageal corrosion, patients should remain upright for up to 30 minutes after taking oral iron doses.
  • Patients should be encouraged to eat foods high in iron and folic acid.
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106
Q

What is Hemostasis

A

*General term for any process that stops bleeding *Coagulation is hemostasis that occurs because of the physiological clotting of blood.
*Complex relationship between substances that promote clot formation and either inhibit coagulation or dissolve a formed clot
*Thrombus: technical term for a blood clot
*Embolus: thrombus that moves through blood vessels

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107
Q

How does the coagulation system work?

A

Works as a “Cascade”
Each activated factor serves as a catalyst that amplifies the next reaction.
Result is fibrin, a clot-forming substance
Intrinsic pathway and extrinsic pathway

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108
Q

What is a thrombus?

A

*An aggregation of platelets, fibrin clotting factors and the cellular elements of the blood that is attached to the interior wall of a vein or artery.Tr

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109
Q

What is an embolus?

A

Trouble, usually.

A blood clot that has been dislodged from the wall of a blood vessel and is traveling through the bloodstream.

If an embolus lodges in a coronary artery, it causes a myocardial infarction

If it obstructs a brain vessel, it causes a stroke (a cerebrovascular accident).

If it travels to the lungs, it is a pulmonary embolus.

If it travels to a vein in the leg, it is a deep vein thrombosis (DVT).

Collectively, these complications are called “thromboembolic events.”

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110
Q

What are some coagulation modifier drugs

A

Anticoagulants
- Inhibit action or formation of clotting factors
- Prevent clotting factor

Antiplatelet drugs
- inhibits platelet aggregation
- Prevents platelet plugs

Thrombolytic agents break down formed clots
Antifibirnolytic agents promote blood coagulation and clot formation

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111
Q

Anticoagulant agents

A

*Also known as antithrombotic drugs
*Have no direct effect on a blood clot that is already formed
*Prevent intravascular thrombosis by decreasing blood coagulability
*Used prophylactically to prevent:
Clot formation (thrombus)
An embolus (dislodged clot)

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112
Q

Heparin mechanism of action

A

inhibit clotting factors IIa (thrombin), Xa, and IX

Factors XI and XII are also inactivated but do not play as important of a role as the other three factors

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113
Q

Heparin types

A

Unfractioned heparin is known as “Heparin”

Low-molecular-weight heparins:
enoxaparin (Lovenox)
dalteparin (Fragmin)
nadroparin calcium (Fraxiparine)
tinzaparin sodium (Innohep)

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114
Q

Unfractioned heparin

A

Relatively large molecule that is derived from animal sources
*Frequent laboratory monitoring for bleeding times such as aPTT (how long does it take for a blood clot to form in sec)
*Heparin for catheter flush (10-100 units/mL): no monitoring is needed

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115
Q

Heparin sodium fun facts

A

Natural anticoagulant obtained from the lungs or intestinal mucosa of pigs
10 to 10 000 units/mL

DVT prophylaxis: 5 000 units subcutaneously two or three times a day. Does not need to be monitored when used for prophylaxis.

Weight-based protocol

When heparin is used therapeutically (for treatment), continuous IV infusion.

Measurement of activated partial thromboplastin time (aPTT) (usually every 6 hours until therapeutic effects are seen) is necessary.

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116
Q

Heparin Flushes

A
  • heparin leo
  • small vial of aqueous heparin IV flush solution
  • risk of the development of heparin-induced thrombocytopenia has caused most institutions to use 0.9% normal saline as a flush for heparin-lock IV ports
  • heparin flushes (100 units/mL) are still used for central catheters
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117
Q

Low Molecular Weight Heparin (LMWH)

A

Synthetic smaller molecular structure (fractionated)

More predictable anticoagulant response; more specific for activated factor X

Frequent laboratory monitoring of bleeding times using tests such as aPTT not needed

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118
Q

Direct acting Xa inhibitors

A

Action: Inhibit factor
fondaparinux (Arixtra); rivaroxaban (Xarelto); apixaban (Eliquis)

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119
Q

What is a direct thrombin inhibitor example

A

Dabigatran

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120
Q

Tell me about Warfarin

A

Inhibits vitamin K synthesis by bacteria in the gastrointestinal tract

Action: inhibit vitamin K-dependent clotting factors II, VII, IX, and X which are normally synthesized in the liver

Final effect is the prevention of clot formation

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121
Q

warfarin sodium (Coumadin)

A

Most commonly prescribed oral anticoagulant

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

122
Q

What is normal INR without warfarin?

A

0.8-1.2 seconds

123
Q

What is a normal INR with warfarin?

A

2-3.5 seconds depending on indication for use

124
Q

what IS INR

A

It’s for blood clotting speed because we can’t just say blood clotting speed

125
Q

Warfarin considerations

A

Dietary considerations

Age considerations

Maintenance dose determined by the INR

Natural health product cautions

126
Q

Anticoagulant mechanism of action

A

Vary, depending on drug

Work on different points of the clotting cascade

Prevent intravascular thrombosis by decreasing blood coagulability

Do not lyse existing clots

127
Q

What are some indications for anticoagulants?

A

*Used to prevent clot formation in certain settings in which clot formation is likely

*Myocardial infarction

*Unstable angina

*Atrial fibrillation

  • Indwelling devices, such as mechanical heart valves

*Conditions in which blood flow may be slowed and blood may pool (e.g., major orthopedic surgery, prolonged periods of immobility

128
Q

What are some contraindications for anticoagulants?

A

Drug allergy

*Any acute bleeding process or high risk of such an occurrence

*Warfarin is strongly contraindicated in pregnancy.

*Other anticoagulants are rated in lower pregnancy categories.

*Low-molecular-weight heparins are contraindicated in patients with an indwelling epidural catheter risk of epidural hematoma.

129
Q

Anticoagulants: Adverse Effects

A

Bleeding
-Risk increases with increased dosages
-May be localized or systemic

May also cause:
-Heparin-induced thrombocytopenia
-Nausea, vomiting, abdominal cramps, thrombocytopenia, other effects

130
Q

Treatment: Toxic Effects of Heparin

A

Aimed at reversing the underlying cause

*Symptoms: hematuria, melena (blood in the stool), petechiae, ecchymoses, and gum or mucous membrane bleeding

*Stop drug immediately.

*Intravenous (IV) protamine sulphate: 1 mg of protamine can reverse the effects of 100 units of heparin (1 mg of protamine for each milligram of lowmolecular-weight heparin given).

131
Q

Warfarin adverse effects

A

Bleeding
Lethargy
Muscle pain
Skin necrosis
“Purple toes”
syndrome

132
Q

Treatment: Toxic Effects of Warfarin

A

-Discontinue the warfarin.

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

-Vitamin K1 (phytonadione) can hasten the return to normal coagulation.

-High doses of vitamin K (10 mg) given IV will reverse the anticoagulation within 6 hours.

Severe bleeding: transfusions of human plasma or clotting factor concentrates

Intravenous vitamin K: risk of anaphylaxis. Risk is diminished by diluting it and giving it over 30 minutes.

133
Q

What happens to warfarin when Vitamin K is given?

A

Beyond the fact that Vitamin K is the antidote for anticoagulants? (Vitamin K)

134
Q

Antiplatelet drugs

A

Prevents clot formation by inhibiting platelet adhesion at the beginning of the cascade.

  • Acetylsalicylic acid (ASA) 81-325mg
  • clopidogrel bisulfate (Plavix)
  • ticagrelor (Brilinta)
135
Q

Antiplatelet mechanism of action

A

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

136
Q

Antiplatelet indications

A

Stroke, TIA, and post MI thrombo prevention

*Some antiplatelets used in conjunction with anticoagulant Warfarin as a prophylaxis for CVA, PE, DVT.

137
Q

Antiplatelet side effects

A

ASA Side Effects *nausea, vomiting, GI bleeding, diarrhea, thrombocytopenia, agranulocytosis, anemia

Clopidrogel Side Effects * chest pain, abdominal pain, diarrhea, epistaxis, headache, dizziness, fatigue (flue like symptoms)

138
Q

Nursing Process: Anticoagulants

A

Assess…

Patient history, medication history, allergies
Contraindications
Baseline vital signs, laboratory values (PT/INR or PTT)
Potential drug interactions
History of abnormal bleeding conditions
No IM injections with anticoagulants

139
Q

Heparin nursing process

A

Intravenous doses are usually double-checked with another nurse; high alert

*Ensure that subcutaneous doses are given subcutaneously, not intramuscularly.

*Subcutaneous doses should be given in areas of deep subcutaneous fat, and sites should be rotated

Do not give subcu injection within 5cm of belly-button, incisions, open wounds (HOLES. JUST LEAVE HOLES ALONE)

Do not aspirate or massage subcu site
-First of all it shouldn’t be anywhere NEAR a vein
-Second you’ll make a hematoma

IV doses may be given by bolus or IV infusions.

Anticoagulant effects are seen immediately.

Laboratory values are done daily to monitor coagulation effects (aPTT).

140
Q

What is a heparin antidote

A

*Protamine sulphate

141
Q

Low-Molecular-Weight Heparins: Nursing Process

A

*Given subcutaneously in the abdomen \

*Rotate injection sites.

*Protamine sulphate can be given as an antidote in case of excessive anticoagulation

142
Q

Warfarin (Coumadin): Nursing Process

A

May be started while the patient is still on heparin until PT/INR levels indicate adequate anticoagulation (called cross-over therapy or bridging therapy)

*Full therapeutic effect takes several days.

*Monitor PT/INR regularly; keep follow-up appointments

Many herbal products have potential interactions; increased bleeding may occur including:
Capisicum pepper
Garlic
Ginger
Ginkgo
St John’s Wort
Feverfew

143
Q

Warfarin antidote

A

Vitamin K

144
Q

Anticoagulants and Antiplatelet: Patient Education

A
  • Importance of regular laboratory testing if needed

*Signs of abnormal bleeding

*Measures to prevent bruising, bleeding, and tissue injury *Wearing a medical alert bracelet

*Avoiding foods high in vitamin K (tomatoes, dark leafy green vegetables) if taking Warfarin

145
Q

What are triglycerides and Cholesterol?

A

Two primary forms of lipids in the blood

146
Q

What are triglycerides used for?

A

As an energy source and stored in adipose tissue

147
Q

What is cholesterol used for?

A

Used to make steroid hormones, cell membranes and bile acids

148
Q

What is lipoprotein?

A

combination of triglyceride or cholesterol with apolipoprotein

149
Q

What are the types of lipoprotein?

A

Very-low-density lipoprotein

Produced by the liver
Transports endogenous lipids to peripheral cellsIntermediate-density lipoprotein
*Low-density lipoprotein (LDL)
*High-density lipoprotein (HDL)
Responsible for “recycling” of cholesterol
Also known as “good cholesterol”

150
Q

Cholesterol and coronary artery disease

A

The risk of coronary heart disease in patients with cholesterol levels of 5.2 mmol/L is three to four times greater than that in patients with levels less than 4 mmol/L.

151
Q

Dyslipidemias and Treatment Guidelines

A

*Farmingham Risk Score
*Heart Age Calculator
*Medications to treat dyslipidemia
*Drug choice based on the specific lipid profile of the patient (phenotyping)
All reasonable nondrug means of controlling blood cholesterol levels (e.g., diet, exercise)
*Drug therapy based upon the specific lipid profile of the patient

152
Q

Antilipemics five established classifications of drugs

A

Hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins)
*Bile acid sequestrants
*B vitamin niacin (vitamin B3, nicotinic acid)
*Fibric acid derivatives (fibrates)
*Cholesterol absorption inhibitor ezetimibe (Ezetrol®)

153
Q

What is a statin and what does it do

A

First-line therapy for hypercholesterolemia (elevated LDL)*
Treatment of type IIa and IIb
*Reduces plasma concentrations of LDL cholesterol by 30 to 40%
Decrease in plasma triglycerides by 10 to 30%Increase in HDL cholesterol by 2 to 15%
*Dose dependent

154
Q

Statin mechanism of action

A

Inhibit HMG-CoA reductase enzyme, which is used by the liver to produce cholesterol

*Lower the rate of cholesterol production thereby increasing the amount of LDL receptors in the liver.

155
Q

Statin adverse effects

A

Mild, transient GI disturbances i.e. constipation
*Rash
*Headache
*Myopathy (muscle pain), possibly leading to rhabdomyolysis, a serious condition

156
Q

What is rhabdomyolysis?

A

*Breakdown of muscle protein
*Myoglobinuria: urinary elimination of the muscle protein myoglobin
Can lead to acute kidney injury and even deathWhen recognized reasonably early, rhabdomyolysis is usually reversible with discontinuation of the statin drug.
*Instruct patients to immediately report any signs of toxicity, including muscle soreness or changes in urine colour (tea-coloured).
*Avoid Grapefruit juice

157
Q

Statin drug interactions

A

*oral anticoagulants
*erythromycin
Grapefruit juice

158
Q

What are atorvastatin calcium (Lipitor®) and simvastatin (Zocor®)

A

Two of the most commonly used drugs to lower cholesterol levels

These lower LDLs and trigylcerides while raising HDL

Dosed once daily. Usually at night

159
Q

What are bile acid sequestrants?

A

cholestyramine resin (Olestyr®)
*colestipol hydrochloride
*colesevelam
*Also called bile acid-binding resins and ion-exchange resins

160
Q

Bile acid sequestrants mechanism of action

A

-prevent resorption of bile acids from small intestine
-bile acids are necessary for absorption of cholesterol

161
Q

Can bile acid sequestrants be used with statins?

A

YES

162
Q

What is Niacin

A

Vimtain B3

Lipid-lowering properties require much higher doses than when used as a vitamin.

Effective, inexpensive, often used in combination with other lipid-lowering drugs

163
Q

Niacin indications

A

Reduces the metabolism or catabolism of cholesterol and triglycerides
*Effective in lowering triglyceride, total serum cholesterol, and LDL cholesterol levels
*Increases HDL levels
*Effective in the treatment of types IIa, IIb, III, IV, and V dyslipidemia

164
Q

Niacin adverse effects

A

Flushing (caused by histamine release)
Pruritus
GI distress

165
Q

What are Fibric acid derivatives

A

AKA Fibrates

Bezafibrate
Gemfibrozil
Fenofibrate

166
Q

Fibric Acid Derivatives: Mechanism of Action

A

Believed to work by activating lipoprotein lipase, which breaks down cholesterol

Also suppress the release of free fatty acid from adipose tissue, inhibit the synthesis of triglycerides in the liver, and increase the secretion of cholesterol in the bile

167
Q

Fibric Acid Derivatives: Indications

A

Treatment of types III, IV, and V hyperlipidemias

The fibric acid derivatives bezafibrate, gemfibrozil, and fenofibrate decrease the triglyceride level and increase the HDL cholesterol level by as much as 25%.

All are given with a statin, which increases risk of myositis, myalgia, and rhabdomyolysis

168
Q

Fibric Acid Derivatives: Adverse Effects

A

Abdominal discomfort, diarrhea, nausea
Blurred vision, headache
Increased risk of gallstones
Prolonged prothrombin time
Increased enzyme levels perhaps shown by liver studies

169
Q

What are Cholesterol Absorption Inhibitors

A

ezetimibe (Ezetrol)
Inhibits absorption of cholesterol and related sterols from the small intestine
Results in reduced total cholesterol, LDL cholesterol, apolipoprotein B, and triglyceride levels
Also increases HDL cholesterol levels
Often combined with a statin drug
Can be used as monotherapy

170
Q

Herbal Product: Garlic

A

Used as a antihypertensive, antiplatelet, and lipid reducer
*Adverse effects: dermatitis, vomiting, diarrhea, anorexia, flatulence, antiplatelet activity
*Possible interactions with warfarin, diazepam, and protease inhibitors
*May enhance bleeding when taken with nonsteroidal anti-inflammatory drugs (NSAIDs)

171
Q

Herbal Product: Flax

A

Both the seed and oil of the plant are used.

*Uses: atherosclerosis, hypercholesterolemia, hypertriglyceridemia, gastrointestinal distress, menopausal symptoms, bladder inflammation, others

*May cause diarrhea and allergic reactions

*Possible interactions: antihyperglycemic drugs, anticoagulant drugs

172
Q

Herbal Product: Omega-3Fatty Acids

A

Fish oil products
*Used to reduce cholesterol
*May cause rash, belching, allergic reactions
Potential interactions with anticoagulant drugs
Not good while pregnant. You’ll have fish babies

173
Q

Nursing Process antilpemics: Assessment

A

Obtain health history prior to starting
Assess dietary patterns, substance use, exercise
Assess for contraindications including liver dysfunction, bile concerns
Obtain baseline liver function

174
Q

Nursing Process antilpemics: Interventions

A

Patients on long-term therapy may need supplemental fat-soluble vitamins (A, D, E, K) with Bile Acid Sequestrants
Counsel patient concerning diet and nutrition on an ongoing basis.*
Instruct patient on proper procedure for taking the medications.
*Powder forms must be taken with a liquid, mixed thoroughly but not stirred, and never taken dry.
*Other medications should be taken 1 hour before or 4 to 6 hours after meals to avoid interference with absorption.

175
Q

Niacin interventions

A

To minimize adverse effects of niacin, start on a low initial dose and gradually increase it, and have the patient take the medication with meals.
*Small doses of aspirin or NSAIDs may be taken 30 minutes before niacin to minimize cutaneous flushing.
*Provide teaching regarding the use of NSAIDs and aspirin.
*Inform patients that these medications may take several weeks to show effectiveness

176
Q

Nursing implications antilipemics

A

Instruct patients to report persistent gastrointestinal upset, constipation, abnormal or unusual bleeding, and yellow discoloration of the skin.
*Monitor for adverse effects, including increased liver enzyme studies or signs of myalgias.
*Monitor for therapeutic effects.
*Reduced cholesterol and triglyceride levels

177
Q

What is an antibiotic?

A

Medication that treats bacterial infections

178
Q

Antibiotics: All classes

A

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

179
Q

Sulfonamides: Adverse effects

A

Nausea, vomiting, diarrhea
Photosensitivity, dermatitis
Nercolysis

180
Q

B-lactam Antibiotics

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

181
Q

Penicillin mechanism of action

A

Penicillin enters via the cell wall and binds to cell-wall proteins thus causing destruction of said cell wall

182
Q

Penicillin adverse effects

A

nausea, vomiting, diarrhea, abdominal pain

183
Q

Penicillin interactions

A

Warfarin
Oral contraceptives
NSAIDs

184
Q

Cephalosporins

A

Five generations
Bactericidal
Broad spectrum
Structurally related to penicillin

185
Q

Tetracycline action

A

Bind (chelate) to Ca+++ and Mg++ and Al+++ ions to form insoluble complexes

186
Q

Can dairy be taken with tetracyclines?

A

No. Dairy products, antacids, and iron
salts reduce oral absorption of tetracyclines

187
Q

Can children have tetracyclines?

A

No. It kinda messes up teeth, bones

188
Q

health-care associated infections: prevention

A
  • handwashing (most important)
  • disinfectants
  • antiseptics
189
Q

disinfectants

A

kills organisms

used only on nonliving objects

cidal agent

190
Q

antiseptic

A

inhibits growth of microorganisms = necessarily not kill them

  • applied exclusively to living tissue
  • static agent
191
Q

before antibiotic therapy…

A

cultured to identify organism & potential antibiotic susceptibilities

192
Q

empiric therapy

A

TX of infection b4 specific culture info obtained

193
Q

definitive therapy

A

antibiotic therapy tailored to treat organism identified w/ culture

194
Q

prophylactic therapy

A

TX antibiotics to prevent infection

195
Q

therapeutic response

A

decrease in signs & symptoms of infection

196
Q

subtherapeutic response

A

signs & symptoms of infection DO NOT improve

197
Q

allergic reactions for antibiotics

A

penicillins & sulfonamides 2 classes which ppl allergic too

198
Q

symptoms of allergic reaction to antibiotics

A

difficulty breathing, significant rash, hives, GI intolerance

199
Q

host factors in antibiotic therapy

A

allergies, kidney & liver function, pregnancy status, genetic characteristics, site of infection & host defences

200
Q

4 diff classes in B-lactam

A

penicillins

cephalosporins

carbapenems

monobactams

201
Q

ABX therapy: mechanism of action

A
  • interferences with cell wall & protein synthesis
  • interferences w/ DNA & RNA
  • acting as metabolite to disrupt critical metabolic reactions inside bacterial cell
202
Q

bactericidal

A

kill bacteria

203
Q

bacteriostatic

A

inhibit growth of susceptible bacteria rather than killing them immediately = eventually leads to bacterial death

204
Q

sulfonamides mechanism of action

A
  • bacteriostatic action
  • prevent bacterial synthesis of folic acid required for synthesis of purines & DNA, RNA
205
Q

sulfonamides only affect organisms that synthesize…

A

own folic acid & does not affect microorganisms that use exogenous folic acid

206
Q

sulfonamides indications

A

effective against gram + & gram -

  • TX of UTI
  • pneumonia
207
Q

sulfonamides used as prophylaxis & TX of pneumonia in HIV pts, upper resp infections, outpt MRSA (t/f)

A

TRUE

208
Q

adverse effects of sulfonamides

A
  • blood: agranulocytosis, thrombocytopenia, hemolytic & aplastic anemia
  • skin: photosensitivity**, stevens-johnson syndrome
  • GI: N & V, diarrhea, hepatotoxicity, pancreatitis
  • toxic nephrosis, headache, convulsions, cough
209
Q

penicillin mechanism action

A
  • enter bacteria via cell wall & bind to penicillin-binding protein
  • then disrupt normal cell wall synthesis = bacteria cell die from lysis
210
Q

bactericidal antibiotics is penicillin? (t/f)

A

TRUE

211
Q

penicillins indications

A
  • prevent & TX of infections caused by (gram + ..)
  • treat health-care acquired infections (pneumonia, intra-abdo infections, sepsis)
212
Q

penicillins contraindications & concerns

A
  • allergy
  • medication errors
213
Q

penicillins adverse effects

A
  • allergic (urticaria, pruritus, angioedema)
  • nausea, vomiting, diarrhea, abdo pain
214
Q

penicillin interactions

A
  • nonsteroidal anti-inflammatory drugs
  • oral contraceptives
  • warfarin
215
Q

cephalosporins

A
  • semisynthetic ABX
  • structure/pharma r/t penicillins
  • broad spectrum
216
Q

cephalosporins have what kind of action

A

bactericidal action

217
Q

cephalosporins are divided into groups according to their…

A

antimicrobial activity

218
Q

cephalosporins 1st gen

A
  • good gram + coverage/ poor gram -
219
Q

cephalosporins 1st gen used for

A

surgical prophylaxis & susceptible staph infections

220
Q

cephalosporins 1st gen examples

A

cefazolin (IV, IM)
cephalexin (PO)

221
Q

cephalosporins 2nd gen

A
  • good gram +/decent gram -
222
Q

cephalosporins 2nd gen cefoxitin (IM, IV) used for

A

prophylactically for abdo or colorectal surgeries

(KILLS ANAEROBES)

223
Q

cephalosporins 2nd gen cefuroxime (PO) used for

A

surgical prophylaxis
DOES NOT KILL ANAEROBES

224
Q

examples of cephalosporins 2nd gen

A
  • cefaclor
  • cefoxitin
  • cefuroxime
  • cefprozil
225
Q

cephalosporins 3rd gen

A
  • most potent against gram -
  • less active against gram +
226
Q

examples cephalosporins 3rd gen

A
  • cefotaxime sodium
  • cefixime
  • cefpodoxime proxetil
  • ceftizoxime
  • ceftazidime
  • ceftriaxone
227
Q

ceftriaxone sodium

A
  • IV and IM, long half-life, once-a-day dosing
  • Elimination is primarily hepatic
  • Easily passes meninges and diffused into cerebrospinal fluid
    to treat central nervous system infections
228
Q

ceftazidime

A
  • IV and IM forms
  • Excellent gram-negative coverage
  • Used for difficult-to-treat organisms such as Pseudomonas
    spp.
  • Excellent spectrum of coverage
229
Q

is resistance to ceftazidime limiting usefulness

A

YES

230
Q

Cephalosporins:
4th Generation

A
  • Broader spectrum of antibacterial activity than thirdgeneration cephalosporins, especially against grampositive bacteria
231
Q

Cephalosporins:
4th Generation used for

A

complicated & uncomplicated UTI

232
Q

cephalosporins adverse effects

A

mild diarrhea, abdo cramps, rash, pruritus, redness, edema

233
Q

carbapenems

A

broadest antibacterial action

bactericidal (gram +/-)

234
Q

carbapenems reserved for

A

complicated body cavity & connective tissue infections in acutely ill hospital pts (MRSA)

235
Q

carbapenems infused over

A

60 mins & may cause drug-induced seizures

236
Q

carbapenems = imipenem used for TX

A

bone, joint, skin, and soft tissue infections

237
Q

carbapenems examples

A
  • imipenem/cilastatin
  • meropenem
  • ertapenem
238
Q

monobactams - aztreonam

A
  • synthetic B-lactam antibiotic
  • bactericidal
  • primarily active against aerobic gram -
239
Q

aztreonam used for

A

management of cystic fibrosis pts w/ chronic pulmonary infections

240
Q

macrolides examples

A
  • erythromycin
  • azithromycin
  • clarithromycin
  • fidaxomicin
241
Q

macrolides mechanism of action

A
  • prevent protein synthesis within bacterial cells
  • bacteriostatic
242
Q

macrolides indications

A
  • strep infections
  • mild to moderate upper & lower resp infection
  • syphilis & lyme disease
  • gonorrhea, chlamydia, mycoplasma
243
Q

macrolides - fidaxomicin adverse effects

A

nausea, vomiting, GI bleed

244
Q

fidaxomicin indicated only for the treatment of

A

c. difficile - associated diarrhea

245
Q

macrolides adverse effects

A
  • N & V, diarrhea, hepatotoxicity, anorexia, heartburn
246
Q

azithromycin & clarithromycin has

A

fewer GI effects, longer duration of action, better efficacy, better tissue penetration

247
Q

with macrolides report immediately..

A

chest pain, palpitations, dizziness, jaundice, hearing loss

248
Q

tetracyclines

A

bacteriostatic: inhibit bacterial growth, inhibit protein synthesis

stop many essential functions of bacteria

249
Q

what reduces absorption of tetracyclines

A

dairy products, antacids, iron salts

250
Q

tetracyclines bind to

A

calcium, magnesium, and Al

251
Q

tetracyclines adverse effects

A
  • strong affinity for calcium = children 8 or less (discolouration teeth)
  • change intestinal flora
  • diarrhea
  • vaginal candidiasis
  • gastric upset
  • enterocolitis
  • coagulation irregularities
252
Q

nursing assessment ABX

A
  • assess allergies, renal liver & cardiac function
  • health history
  • contraindications
  • drug interactions
253
Q

nursing interventions ABX

A
  • obtain cultures from sites BEFORE beginning ABX therapy
  • take ABX exactly as prescribed & until gone
  • watch signs of superinfection or secondary infection (fever, perineal itching, cough)
  • assess adverse effects (N & V, diarrhea)
254
Q

nursing interventions for sulfonamides

A
  • 2,000 to 3000mL fluid/24hr
  • PO w/ food
  • STAT report worsening abdo cramps, stomach pain, diarrhea, hematuria, worsening rash, SOB, fever
255
Q

nursing interventions penicillins

A
  • PO w/ H2O bc acidic fluids may decrease antibacterial action
  • monitor for allergic for 30 mins
  • lactobacillus supplement
256
Q

nursing interventions cephalosporins

A
  • assess allergy (cross allergy w/ pen)
  • PO admin w/ food to decreased GI upset even tho delay absorption
  • acute alcohol intolerance reaction when taken with alcohol
257
Q

nursing interventions macrolides

A
  • highly protein bound & cause severe interactions with protein-bound drugs (carbamazepine, cyclosporine, warfarin)
  • take with meal
258
Q

threat of MRSA becoming resistant to all ABX available (t/f)

A

TRUE

259
Q

vancomycin-resistant usually seen in

A

UTI

260
Q

extended-spectrum B lactamases

A
  • organisms that produce ESBL resistant to all B lactam ABX

only be treated with carbapenems or quinolones

261
Q

aminoglycosides

A

not given PO d/t poor oral absorption

very potent ABX w/ serious toxicity

262
Q

aminoglycosides considered what action

A

bactericidal = prevent protein synthesis

kill gram - & some gram +

263
Q

examples of aminoglycosides

A

gentamicin sulphate
streptomycin sulphate
tobramycin sulphate
neomycin sulphate

264
Q

aminoglycosides indications

A
  • kill gram -
  • used in combo w/ other ABX for synergistic effects
  • parenterally
265
Q

neomycin sulphate

A

topical antibacterial

266
Q

aminoglycosides adverse effects

A
  • serious: nephrotoxicity, ototoxicity (auditory impairment & vestibular impairment)
  • headache
  • paresthesia
  • fever
  • vertigo
  • skin rash
267
Q

aminoglycosides therapeutic drug monitoring

A
  • serum levels measured to prevent toxicity
  • serum level needs to be higher than min inhibitory concentration to kill bacteria
268
Q

peak and trough for therapeutic drug monitoring

A
  • peak: highest drug levels for once-daily regimens (not measured)
  • trough: lowest, ensure adequate renal clearance of drug & avoid toxicity
269
Q

quinolones

A
  • oral absorption
  • absorption reduced by antacids, calcium, magnesium, iron
  • effective against gram - & +
270
Q

quinolones

A
  • bactericidal
  • alter DNA of bacteria causing death
  • not affect human DNA
271
Q

quinolones indications

A
  • gram - & +
  • complicated urinary, resp, bone & joint, GI, skin
272
Q

ciprofloxacin & levofloxacin come as

A

PO & injection

273
Q

norfloxacin hydrochloride has limited PO absorption so its used for

A

GU infections

274
Q

quinolones interactions

A
  • antacids, calcium, mag, iron, zinc (take 1hr before/after)
  • dairy
  • enteral tube feedings
  • probenecid
  • nitrofurantoin
  • oral anticoagulants
275
Q

quinolones adverse effects

A

central nervous: headache, dizziness, insomnia, restlessness, convulsions

GI: N & V, diarrhea, constipation, oral candidiasis

skin: rash, pruritis, urticaria, flushing

other: ruptured tendons, tendonitis, blurred vision, tinnitus, fever

276
Q

clindamycin

A

chronic bone infections, GU infections, intra-abdo infectionsc

277
Q

clindamycin may causw

A

pseudomembranous colitis (ABX-associated colitis), c. diff

278
Q

linezolid

A

treat vancomycin resistant (VRE), MRSA

279
Q

linezolid effects

A
  • strenghens effects of vasopressive drugs
  • serotonin syndrome if taken with SSRI
  • reactions if taken with tyramine-containing foods
280
Q

metronidazole

A
  • anaerobic organisms
  • intra-abdo & gynecological infections
  • protozoal infections
  • several drug interactions
281
Q

nitrofurantoin

A
  • used UTO
  • caution w/ kidney impairment
  • drug concentrates in urine
  • may cause heptatotoxicity
282
Q

quinupristin-dalfopristin

A
  • 30:70 combo, works synergistically
  • used bacteremia & infections caused VRE & complicated skin infections (MRSA)
  • may cause arthralgias & myalgias
283
Q

quinupristin-dalfopristin injectable form only?

A

TRUE

284
Q

vancomycin hydrochloride

A
  • TX of choice for MRSA & gram +
  • c. diff
285
Q

vancomycin hydrochloride must montior

A

blood levels to ensure therapeutic levels & prevent toxicity

may cause ototoxicity & nephrotoxicity

286
Q

vancomycin hydrochloride may cause

A

red man syndrome (flushing or itching of head, neck, face)

287
Q

vancomycin hydrochloride infusions

A

over 60 mins

rapid infusions may cause hypotension

288
Q

colistimethate sodium

A
  • polypeptide ABX penetrates & disrupts bacterial membrane of gram -
  • serious adverse effects
  • IV IM inhalation
289
Q

fungi that causes skin infections known as

A

dermatophytes

290
Q

mycotic infections

A
  • cutaneous
  • subcutaneous
  • superficial
  • systemic (life threatening, immunocompromised host)
291
Q

candida albicans

A
  • may follow ABX therapy, corticosteroids
  • may result in overgrowth or systemic infection
292
Q

polyenes: amphotericin B & nystatin mechanism of action

A
  • bind to sterols in cell membrane lining = fungal death
293
Q

imidazoles & triazoles: ketoconazole, fluconazole, itraconazole mechanism of action

A
  • inhibit fungal cell cytochrome P450 enzymes, resuting in cell membrane leaking = altered cell metabolisn & fungal cell death
294
Q

antifungal indication

A
  • systemic & topical fungal infections
295
Q

amphotericin B adverse effects

A
  • cardiac dysrhythmias
  • nephrotoxicity, tinnitus, visual disturbances, convulsions
  • potassium loss
  • pulmonary infiltrates
  • shake & bake fever, headache, nausea, hypotension, tachycardia, anemia
296
Q

fluconazole adverse effects

A

nausea, vomiting, diarrhea, stomach pain, increased liver enzymes

297
Q

nystatin adverse effects

A

nausea, vomiting, anorexia, diarrhea, rash, urticaria

298
Q

nursing assessment antifungal & antibiotics

A
  • allergies, contraindications
  • baseline VS, CBC, liver & renal function, ECG
  • assess meds (OTC & prescribed)
299
Q

nursing interventions antifungal & antibiotics

A
  • follow directions for reconstituation & admin
  • montior VS of pt IV infusions 15-30mins
  • monitor input & output
300
Q

amphotericin B interventions

A
  • reduce severity of infusion reactions = pretreat w/ antipyretic, antihistamines, antiemetics, corticosteroids
  • use IV pumps & most distal veins
  • at home = document weight (gain 1kg or more in 24hr or 2.3kg in week = kidney damage)
301
Q
A

pharm (4 decks)

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