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Clinical Med (Year 2) > Last Pharm for Exam 1 > Flashcards

Last Pharm for Exam 1 Flashcards

1
Q

What are the 2 delivery options of respiratory meds?

A

Systemic Delivery (Oral or Injection)
Inhaled

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2
Q

Which delivery option is more selective for the respiratory tract? And why?

A

Inhaled because they are much better at delivering drug directly to the lungs

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3
Q

What is one main reason you would choose to use systemic delivery of respiratory meds?

A

They can reach lungs via pulmonary circulation if airway is obstructed (acute asthma, severe COPD)

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4
Q

What are the primary delivery options of inhaled respiratory meds?

A
  • Metered Dose Inhaler (MDI)
  • Nebulizer
  • Dry power inhaler
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5
Q

What are the 4 categories of respiratory meds?

A
  1. Control of respiratory tract irritation & secretion
  2. Bronchodilators
  3. Control of airway inflammation
  4. Other meds
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6
Q

What are some examples of medications that control respiratory tract irritation & secretion?

A
  • Antitussives
  • Antihistamines
  • Decongestants
  • Mucolytics, expectorants `
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7
Q

What is the mechanism of Antitussives: opioids?

A

Suppress cough reflex at brainstem

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8
Q

Antitussives:opioids are often combined with (BLANK) in OTC products

A

Decongestants

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9
Q

What are some examples of Antitussives: opioids ?

A

Codeine
Dextromethorphane
Hydrocodone

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10
Q

What is the mechanism of Benzonatate (antitussive)?
And what does this cause?

A
  • Has an anesthetic effect on vagal nerve endings in the airway
  • Causes a reduction to effects of irritation that starts the cough reflex
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11
Q

What are the primary problems of Antitussives?

A
  • Sedation
  • Dizziness
  • GI upset
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12
Q

What are the rehab concerns when a patient is using Antitussives?

A
  • Overuse, dependence
  • May limit productive cough
  • Not proven to be effective in children
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13
Q

Are cough meds recommended for children?

A

No
- Found to offer no symptomatic relief for acute cough in children
- Use of cough & cod meds place young children at risk for potential side effects & adverse reactions

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14
Q

What is the mechanism of Antihistamines?

A
  • Block H1 receptors which decreased the effects of histamine on upper respiratory tract
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15
Q

What are antihistamines used to treat?

A
  • Histamine mediated coughing, sneezing, & irritation
  • Widespread use: seasonal allergies, colds
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16
Q

What is the main difference between the old agent of antihistamine and the new agent?

A

New agents are non- sedating because the do not cross the blood brain barrier

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17
Q

What are the primary problems of antihistamines if they cross the blood brain barrier?

A
  • Sedation, fatigue
  • Incoordination, blurred vision
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18
Q

What are the rehab concerns in patients using antihistamines?

A
  • Sedative effects
  • Dry out respiratory tract (limit productive cough)
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19
Q

What is the primary drugs used to treat excessive coughing?

A

Opioid derivaties (antitussives)

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20
Q

What are some bronchodilators?

A
  • Beta adrenergic agonist
  • Xanthine derivates
  • Anticholingerics
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21
Q

What is the mechanism of Beta - adrenergic agonists?

A
  • Stimulate beta 2 receptors on airway smooth muscle
  • Increase intracellular production of cyclic AMP (2nd messenger)
  • cAMP initiates smooth muscle relaxation = bronchodilator
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22
Q

What are some Nonselective beta agonists?

A
  • Epinephrine
  • Isoproterenol
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23
Q

What are some selective beta agonists?

A
  • Albuterol
  • Formoterol
  • Metaproterenol
  • Salmeterol
  • Terbutaline
  • Suffix -erol indicates beta 2 agonist*
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24
Q

What is the primary problems of excessive use of beta- adrenergic agonists?

A
  • Bronchial irritation/constriction
  • Cardiac stimulation
  • CNS stimulation
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25
Q

What are the rehab concerns in patients using beta-adrenergic agonist?

A
  • Use before postural drainage
  • Look for signs of overuse
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26
Q

To produce bronchodilation a drug should selectively stimulate (BLANK) receptors in airway smooth muscle

A

beta-2

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27
Q

Xanthine derivatives are chemically similar to (BLANK)

A

caffeine, other methyl xanthines

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28
Q

What are the primary examples of Xanthine derivatives?

A
  • Theophylline
  • Aminophylline
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29
Q

What is the mechanism of Theophylline (powerful bronchodilator)?

A
  • Exact mechanism unclear
  • Probably a combination of:
    • inhibition of cAMP breakdown
    • Blocking adenosine stimulation
    • Inhibit intracellular Ca++ release
    • Anti inflammatory effects
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30
Q

What is the primary problem with Theophylline?

A

Theophylline toxicity
- Toxicity begins if plasma levels >15 micrograms/ml and serious if >20 micrograms/ml

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31
Q

What are the signs of Theophylline toxicity?

A
  • Nausea, confusion, irritability, restlessness
  • Cardia arrhythmias, seizures
32
Q

When does the risk of theophylline toxicity increase?

A

If metabolism is impaired
- Liver disease
- Congestive heart failure
- Patient age > 55
- Infections such as pneumonia
- Concomitant use of other drugs

33
Q

What is the mechanism of anticholinergic drugs?

A
  • They block acetylcholine receptors (acetylcholine stimulates bronchial smooth muscle contraction)
34
Q

What are some examples of Anticholinergic drugs?

A

Ipratropium
Tiotropium

35
Q

Anticholinergic are tolerated well at (BLANK) doses and side effects increase at (BLANK) doses

A
  • tolerated at Lower doses
  • Side effects increase at higher doses
36
Q

Describe the mechanism of decongestants

A
  • Stimulates Alpha 1 receptors agonist (epinephrine, pseudoephedrine, many others) which vasoconstriction nasal mucosa
37
Q

How should decongestants be administered and why?

A
  • Should be administered locally (nasal spray) when possible because oral (systemic) administration may cause serious side effects
38
Q

What are the primary problems of decongestants?

A
  • Headache, nausea, nervousness
  • Cardiovascular stimulation
39
Q

What are some of the rehab concerns for patients on decongestants?

A
  • Dependence, overuse, abuse
  • Cardiac palpitations, increased BP
40
Q

Decongestants used commonly in OTC products are designed to cause (BLANK) in the nasal mucosa, but systemic use can also cause a serious (BLANK) in certain patients.

A

Vasoconstriction
increase in blood pressure

41
Q

What do mucolytics do?

A

Break up, decrease the viscosity of mucous; make it easier to raise & expel secretions

42
Q

What do Expectorants do?

A

Increase production of a thinner, more liquid phlegm; enhance effects of mucolytics

43
Q

What is the mechanism of the primary mucolytics, Acetylcysteine?

A

Breaks up disulfide bounds in mucous which decreases viscosity

44
Q

What is Acetylcysteine an antidote for?

A

acetaminophen poisoning

45
Q

What is the mechanism of the more serious mucolytic, Dornase alfa?

A
  • Breaks up DNA that has been released from inflammatory cells in airway
  • DNA makes mucous very viscous, so this drug reduces the DNA “glue” that holds mucous together
46
Q

What patient population is Dornase alfa very helpful with?

A

People with cystic fibrosis

47
Q

How does the primary expectorants, Guaifenesin work?

A
  • Increases fluid content of phlegm which makes phlegm less viscous and easier to expel
48
Q

Primary expectorants are found in many (BLANK) products

A

OTC

49
Q

What are the primary problems of Mucolytics & Expectorants?

A
  • Usually well tolerated
  • May have nausea, vomiting, irritation of mouth with excessive use
50
Q

What are the rehab concerns in patient using Mucolytics & Expectorants?

A
  • No major concern
  • Beneficial during postural drainage, vibration, percussion
51
Q

What are 3 drugs that can control airway inflammation?

A

Anti- inflammatory steriods
- Cromones
- Leukotriene modifers

52
Q

Anti- inflammatory steroids have powerful effects and inhibit what?

A

Virtually all components of the inflammatory response

53
Q

What can be the issue with systemic administration of anti-inflammatory steroids? What development did this lead to?

A
  • Issue: Many harmful catabolic & metabolic side effects
  • Development: of inhaled agents
54
Q

The development of anti-inflammatory steroids inhaled agents caused what?

A
  • Enabled the use of lower doses b/c drug is applied directly to respiratory tissues
  • Allowed earlier, more extensive use in airway disease
55
Q

What are the rehab concerns when your patients are on anti-inflammatory steroids?

A

Severe side effects minimized if inhaled at limited daily dosage

56
Q

What are anti-inflammatory steroids usually combined with? And what population is this combo useful in?

A
  • Bronchodilator (usually long acting beta 2 agonist)
  • Useful in COPD & asthma
57
Q

What is the mechanism of Cromones?

A

Prevents release of histamine, inflammatory mediators from pulmonary mast cells
- Can prevent attack if taken before exposure to initiating agent/activity

58
Q

What are Leukotrienes?

A
  • Lipid compounds that mediate inflammatory response
  • Play important role in airway inflammation
  • Produced from arachdonic acid by lipoxygenase enzyme
59
Q

How does the Leukotriene modifier, zileuton work?

A

Lipoxygenase inhibitor

60
Q

How does the Leukotriene modifier, montelukast & zafirlukast work?

A

Leukotriene receptor blockers

61
Q

How does supplemental oxygen work?

A

Can reduce hypoxemia whenever alveolar PO2 is unable to provide adequate O2 delivery to pulmonary circulation

62
Q

What are some methods of delivering supplemental oxygen?

A
  • Nasal cannula
  • Mask
  • Tent/hood
  • Direct delivery to endotracheal tube
63
Q

Supplemental O2 is dosed in?

A

Liters per minute
Hours per day

64
Q

What is the typical desired SaO2 in patients with COPD & other patients?

A

COPD: 88-92%
Other patients: 94-98%

65
Q

What are the benefits of supplemental O2?

A
  • Increase exercise tolerance
  • Decrease morbidity due to better oxygenation of tissues
  • Improved quality of life
66
Q

What are the risks of supplemental O2?

A
  • Fire
  • Nasal cannula, face mask can cause dry nose = nose bleeds
  • Tracheal administration: dry out airway, cause irritation & mucous occlusion
  • Oxygen toxicity
67
Q

What is the mechanism of oxygen toxicity?

A
  • O2 increase likelihood of generating free radicals
  • These free radicals damage membranes, proteins & DNA in various cells which lead to cell impairment & tissue/organ damage
68
Q

What are some CNS signs/symptoms of oxygen toxicity?

A
  • Muscle twitching
  • Dizziness
  • Confusion
  • Nausea
  • Incoordination
  • Loss of consciousness
  • Convulsions
69
Q

How is surfactant replacement typically administered?

A

To neonates via endotracheal tube

70
Q

What are the risks of surfactant replacement?

A
  • Pulmonary or intracranial hemorrhage
  • Obstruct airway
  • Decrease O2 saturation during administration
71
Q

What does Nitric oxide do to vascular smooth muscle?

A

Relaxes

72
Q

How is nitric oxide administered?

A

-Inhalation to neonates to facilitate perfusion (improve V/Q ration)

73
Q

Nitric Oxide may (BLANK) chance of survival and (BLANK) risk of developing chronic lung disease in some neonates

A
  • Increase
  • Decrease
74
Q

What are some drugs to help quit smoking?

A
  • Nicotine replacement
  • Bupropion
  • Varenicline
75
Q

How does Bupropion help people quit smoking?

A

Prolongs effects of dopamine, norepinephrine in brain which may decrease nicotine craving

76
Q

How does Varenicline help people quit smoking?

A
  • Partial agonist at nicotine receptors
77
Q

What are some examples of other meds that help in pulmonary disease?

A
  • antianxiety agents & sedatives
  • Opioid analgesics
  • NMJ blockers
  • Treatment & prevention of infections

Clinical Med (Year 2) (17 decks)

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