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PHARM 2 > Respiratory Medications And Corticosteroids > Flashcards

Respiratory Medications And Corticosteroids Flashcards

1
Q

What are the 6 types of respiratory medications?

A 
Anticholinergics
Adrenergic agonists
Membrane stabilizer
Xanthines
Related drugs: tocolytics
Corticosteroids
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2
Q

Atropine antagonizes what on airway smooth muscle in large and medium sized airways?

A

Acetylcholine effects

  • affects airways that respond to vagal stimulation
  • decreases airway resistance
  • Increases dead space
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3
Q

This is most effective in treating bronchospasm due to beta antagonists

A

Ipratropium

  • slower onset and less effective than beta agonists in treating bronchial asthma (not useful in acute attacks)
  • more effective than beta agonists in chronic bronchitis or emphysema
  • may use in combo with beta agonists
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4
Q

Is there significant systemic absorption of ipratropim?

A

Minimal systemic absorption (1%)

Limited absorption results in prolonged local site effect

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5
Q

With Ipratropium, blockade of M-2 may cause what?

A

Paradoxical bronchospasm

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6
Q

T/F: tolerance to Ipratropium’s bronchodilator effect has been observed

A

FALSE

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7
Q

What medications contain Ipratropium?

A

Atrovent - Ipratropium alone

Duoneb/combivent - in combo with albuterol

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8
Q

This is a long-acting anticholinergic bronchodilator that blocks muscarinic receptor subtypes M1 and M3

A

Tiotropium (Spiriva)

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9
Q

Tiotrepium (Spireva) does what 2 things?

A

Facilities bronchodilation

Reduces mucous secretion

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10
Q

Tiotropium (Spireva) is used for what conditions?

A

Maintenance treatment of bronchospasm associated with COPD including chronic bronchitis and emphysema

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11
Q

This medication is similar to Spireva except it is given twice daily and has faster onset to peak (2D vs 7D)

A

Aclidinium (Tudorza)

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12
Q

List the 4 Beta agonists

A

Ephedrine
Isoproterenol
Albuterol
Terbutaline

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13
Q

These 2 medications have bronchodilating effects from activation of Beta-2 receptors, and have a significant amount of non-respiratory side effects.

A

Ephedrine and Epinephrine

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14
Q

This medication is a non-selective sympathomimetic (acts on Beta-1 and Beta-2 receptors), and is highly pro-arrhythmic

A

Isoproterenol

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15
Q

What is the action and benefit of Beta-2 agonists?

A

Relax bronchial smooth muscle

Lack stimulating effects on the heart at therapeutic doses

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16
Q

What are 4 uses of Beta-2 agonists?

A
  • preferred treatment for acute episodes of asthma
  • prevention of exercise-induced asthma
  • improve airflow and exercise tolerance in pts with COPD
  • tocolytic to stop premature uterine contractions
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17
Q

What are the 2 classes of Beta-2 agonists?

A

Intermediate acting (3-6 hours)

Long acting (> 12 hours)

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18
Q

What are the routes of administration for Beta-2 Agonists?

A

Inhaled - preferred
Oral
Parenteral - S.Q., IV

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19
Q

What are the 4 steps to the inhalation technique for Beta-2 agonists?

A
  1. Deep breath in, blow it all out
  2. Discharge MDI with a slow deep breath in (over 5-6 seconds)
  3. Hold breath for 10 seconds
  4. Repeat
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20
Q

With inhalation of Beta-2 agonists, what percentage is actually delivered to the lungs?

A

12%

The rest to the mouth, pharynx, and larynx

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21
Q

How does the presence of an ETT affect the amount of inhaled Beta-2 agonist delivered?

A

The presence of an ETT decreases by 50-70% the amount of drug delivered by a MDI that reaches the trachea

*administration during mechanical ventilation increase the amount of drug that passes beyond the dismal end of the ETT

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22
Q

Dose delivered by a nebulizer requires ____x that of a MDI dose to produce the same degree of bronchodilation

A

6-10x

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23
Q

What are the side effects of Beta-2 agonists

A

Tremor: due to stimulation of Beta-2 receptors on skeletal muscle

Tachycardia: direct stimulation of receptors on the heart

Metabolic Response: hyperglycemia, hypokalemia, hypomagnesemia

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24
Q

What is the preferred Beta-2 agonist for acute bronchospasm?

A

Albuterol

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25
Q

What are the 3 Short acting Beta agonists (SABA)?

A

Albuterol

Levoalbuterol (xopenex): little or no clinically significant difference in adverse effects compared to albuterol

Metaproterenol: selective Beta-2 agonist

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26
Q

This medication is used to treat asthma and is also a tocololytic

A

Terbutaline

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27
Q

What are the 2 long acting Beta-2 agonists (>12 hrs) (LABA)

A

Salmeterol (serevent): frequently administered with a steroid. What’s in Advair

Vilanterol

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28
Q

Cromolyn Sodium is a ________ ________

A

Membrane stabilizer

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29
Q

Cromolyn Sodium inhibits _______ release of ________ and other mediators from pulmonary mast cells during antibody mediated allergic responses

A

Antigen-induced

Histamine

  • suppresses the secretory response NOT the Ag-Ab interaction
  • does NOT relax bronchial or vascular smooth muscle
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30
Q

T/F: you can use Cromolyn Sodium in an acute asthma attack

A

FALSE

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31
Q

Cromolyn Sodium (Intel) is used for what?

A

Prophylactic treatment of bronchial asthma

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32
Q

What are the 3 methylxanthines?

A

Theophylline/aminomphylline
Caffeine
Therbromine

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33
Q

What are the 4 uses of methylxanthines?

A
  1. Stimulate the CNS
  2. Increase BP
  3. Increase myocardial contractility and HR
  4. Relax smooth muscle (airways)
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34
Q

Methylxanthines are non-selective ______________ inhibitors

A

Phophodiesterase

*inhibit all fraction of PDE isoenzymes

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35
Q

Methylxanthines competitively antagonize _________ receptors

A

Adenosine

*theophylline more active than caffeine or theobromine

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36
Q

Theophylline is used for what?

A
  • Treatment of bronchospasm due to acute exacerbation of asthma
  • CNS stimulant: treat apnea of prematurity in infants
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37
Q

What are the S/S of toxicity of theophylline at:
15-25mcg/ml
25-35:
>35

A

15-25: GI upset, N/V, tremor
25-35: tachycardia, PVCs
>35: Vtach, seizures

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38
Q

What are the 3 effects of caffeine

A

CNS stimulant
Cerebral vasoconstrictor
Secretion of gastric acid

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39
Q

What are the 3 uses of caffeine

A

Apnea of prematurity
Post-Duran puncture HA
Cold remedies (offset sedation from antihistamines)

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40
Q

Ritodrine works on what receptor?

A

It’s a Beta-2 agonist

  • activates adenyl cyclase
  • Some Beta-1 effects - tachycardia
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41
Q

What is Ritodrine used for?

A

It’s a tocolytic. Used to stop uterine contractions of premature labor

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42
Q

T/F: Ritodrine crosses the placenta

A

TRUE

It has cardiac and metabolic effects in both the mother and fetus

  • Dose related tachycardia
  • increased CO
  • Increased renin secretion
  • Exaggerated systemic BP decrease
  • Hyperglycemia in mother may cause reactive hypoglycemia in fetus
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43
Q

This is a low molecular-weight, naturally occurring hydrophilic endogenous amine that produces a variety of physiologic and pathological responses

A

Histamine

-its a chemical mediator of inflammation in allergic disease

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44
Q

What cells contain large amounts of histamine?

A

Mast cells in the skin, lungs, GI tract and circulating basophils

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45
Q

Histamine is released in response to:

A

Certain drugs

AG-AB reactions

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46
Q

T/F: histamine easily crosses the blood-brain barrier

A

False

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47
Q

How many histamine receptors are there?

A

H1
H2
H3
H4

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48
Q

Stimulation of H-1 receptors does what?

A
  • Evokes smooth muscle contraction in the respiratory and GI tracts
  • cause pruritus and sneezing by sensory nerve stimulation
  • slow the HR by decreasing AV nodal conduction
  • mediate epicardial coronary vasoconstriction
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49
Q

Through H-1 and H-2 receptors histamine causes:

A
  • Increased capillary permeability
  • hypotension
  • tachycardia
  • flushing
  • HA
50
Q

Stimulation of H-2 receptors does what?

A
  • activates adenyl cyclase and increases intracellular cAMP
  • increases myocardial contractility and HR
  • with H-1 receptors increase capillary permeability vasodilation
51
Q

What are Cardiovascular effects of H-1 and H-2 stimulation?

A

Dilation or arterioles and capillaries —> flushing, decreased SVR, decreased BP, increased capillary permeability leading to edema

Coronary vasodilation (H2) and vasoconstriction (H1)

Inotropic, chronotropic, andtidromic effects

52
Q

T/F: need H1 and H2 blockers to completely block the vasodilatory effects of histamine

A

TRUE

53
Q

What is the triple response?

A

Wheal and Flare

  • Edema: due to increased permeability
  • Flare: dilated arteries around the edema due to histamine stimulating nerve endings
  • Pruritus: due to histamine in the superficial layers of the skin
54
Q

H-1 receptor activation causes what in the airway?

A

Constricts bronchial smooth muscle

  • in normal pts this action is negligible
  • in pts with asthma or bronchitis, more likely to develop increases in airway resistance
55
Q

What does H-2 receptor stimulation do to airway?

A

Relaxes bronchial smooth muscle

56
Q

Does histamine increase or decrease gastric secretions?

A

Histamine evokes secretion of gastric fluid containing high concentrations of hydrogen ions

  • can occur without enough histamine to alter BP
  • due to H2 receptor stimulation
  • vagal activity also increases H+ secretion
57
Q

Do histamine receptor antagonists reversibility or irreversibly antagonized histamine receptors?

A

REVERSIBLE

58
Q

Do histamine receptor antagonists work by inhibiting the release of histamine?

A

NO

They attach to receptors and prevent the response mediated by histamine
-stabilizes the receptor in the inactive form (inverse agonist)

59
Q

T/F: H1 receptor antagonists are not highly selective for H1 receptors

A

FALSE

60
Q

Which generation of H1 receptors antagonists are sedating and which are non-sedating?

A

First generation: sedating
-may also activate anti-cholinergic, serotonin, or alpha-adrenergic receptors

Second generation: non-sedating

61
Q

Classification that combines and stabilizes the inactive form of the H1 receptor shifting the equilibrium toward the inactive state.

A

Inverse agonists

62
Q

What are the side effects of 1st generation H1 histamine receptor antagonists?

A

CNS: somnolence, decreased alertness, slowed reaction time, and impaired cognitive function

Anticholinergic: dry mouth, blurred vision, urinary retention, and constipation

CV: tachycardia, QT prolongation, heart block, and cardiac dysrhythmias

63
Q

Are you likely to get CNS side effects from 2nd generation H1 histamine receptor antagonists?

A

Unlikely

Enhancement of sedative or ETOH unlikely

64
Q

What are the 5 clinical uses of H1 histamine receptor antagonists?

A
  1. Prevent and relieve symptoms of allergic rhinoconjunctivitis
  2. Pretreatment may provide some protection against bronchospasm induced by various stimuli
  3. Antipruritic
  4. Sedative
  5. Antiemetic
65
Q

What are 2 H1 histamine receptor antagonists?

A

Diphenhydramine (Benadryl)

Dimenhydrinate (Dramamine)

66
Q

What is Benadryl used for?

A

Sedative, antipruritic, antiemetic

Type 1 allergic reactions: anaphylaxis

Anaphylactic reactions (IV contrast, blood products)

67
Q

What is Dramamine used for?

A

Motion sickness and PONV

Inhibits the integrative functions of vestibular nuclei by decreasing vestibular and visual input

68
Q

What are some 2nd generation H1 histamine receptor antagonists?

A

Claritin
Allegra
Xyzal

69
Q

Glucocorticoids are produced where?

A

The middle layer of the adrenal cortex - zona fascicula

70
Q

What causes the release of cortisol from the adrenal cortex?

A

Stimulation of the H-P-A axis due to stress

71
Q

What series of metabolic effects are initiated by the release of cortisol?

A

Carbohydrate, protein, and fat metabolism

Fluid and electrolyte balance

CV, CNS, Immune, Endocrine, Renal stabile

Inhibition of inflammatory, allergic response

72
Q

Cortisol is also called what?

A

Hydrocortisone

73
Q

This is secreted secondary to increased potassium, decreased sodium, and decreased BP/fluid volume

A

Aldosterone

74
Q

_______ —> _________ —> __________ —> aldosterone

A

Renin —> AG1 —> AG2 —-> aldosterone

75
Q

What are the 3 effects of aldosterone?

A
  1. Increased K excretion
  2. Increased Na retention
  3. Increased water retention, increased blood volume
76
Q

When are secretory rates of CRH, ACTH, and cortisol are highest____________, and lowest___________

A

Highest in the early morning
Low in the late evening

*changing daily sleeping habits causes a corresponding change in the cycle

77
Q

What is an example fo primary adrenocortical insufficiency?

A

Addison’s disease

Adrenals do not secrete cortisol or aldosterone

Replacement therapy must include glucocorticoid and mineralocorticoid

78
Q

What is secondary adrenocortical insufficiency?

A

Chronic steroid use and suppression fo the H-P-A axis

  • aldosterone secretion maintained
  • replacement usually requires only glucocorticoid
79
Q

Make slide for physiological effects after lecture

A

Don’t know

80
Q

What is the glucocorticoid effect?

A

Anti-inflammatory response

81
Q

What is the mineralocorticoid effect?

A

Evoke dismal renal tubular re-absorption of Na+ in exchange for K+

82
Q

What are the 5 naturally occurring corticosteroids?

A 
Cortisol (hydrocortisone)
Cortisone
Corticosterone
Desoxycorticosterone
Aldosterone
83
Q

What are the synthetic glucocorticoids?

A 
Prednisone
Prednisolone
Methylprednisolone
Betamethasone
Dexamethasone
Triamcinolone
84
Q

What is the synthetic mineralocorticoid?

A

Fludrocortisone

85
Q

What methods of administration are effective for steroids?

A

Oral

IV: Water soluble forms can be administered IV

IM: prolonged effects with IM administration

Topical or aerosol

86
Q

Can steroids cross the placenta?

A

YES

87
Q

Endocrine side effects of corticosteroids

A

Adrenal atrophy, HPA axis suppression/secondary adrenal insufficiency, cushing’s syndrome, diabetes/hyperglycemia

88
Q

Cardio side effects of corticosteroids

A

Dyslipidemia, HTN, thrombosis, vas Ulithi summer

89
Q

CNS side effects of corticosteroids

A

Cataracts, glaucoma, changes in mood/behavior/cognition/memory, HA, psychosis, cerebral atrophy

90
Q

Immune side effects of corticosteroids

A

Immunosuppression, increased infection risk, latent viral activation

91
Q

Renal side effects of corticosteroids

A

Increased sodium and water retention, increased K+ and H+ ion secretion, edema

92
Q

GI side effects of corticosteroids

A

PUD, GI bleed, pancreatitis

93
Q

Musculoskeletal side effects of corticosteroids

A

OP, osteonecrosis, atrophy, myopathy, retardation of normal bone growth

94
Q

Skin side effects of corticosteroids

A

Atrophy, acne, dermatitis, delayed wound healing, erythema, ecchymosis, hirsutism, hyperpigmentation

95
Q

GU side effects of corticosteroids

A

Delayed puberty, hypogonadism, fetal growth inhibition, menstrual disorders

96
Q

Use of corticosteroids caucuses what electrolyte and metabolic changes?

A

Hypokalemia metabolic alkalosis

-mineralocorticoid effect of cortisol on distal renal tubules leading to enhanced absorption of Na+ and loss of K+

97
Q

Corticosteroids inhibit or enhance glucose use in peripheral tissues?

A

They inhibit glucose use in peripheral tissues

Also promote hepatic gluconeogenesis

98
Q

What changes to oral hypoglycemics or insulin may need to be made when corticosteroids are given to type II diabetics?

A

May need to increase dose

99
Q

How does fat redistribute with corticosteroid use?

A

Buffalo hump

Moon face

Loss of fat from the extremities

100
Q

What are the catabolic effects seen with corticosteroids?

A

Peripherally, they mobilize amino acids from tissues

  • decreased skeletal muscles mass
  • osteoporosis
  • thinning of the skin
  • negative nitrogen balance
101
Q

T/F: Steroid use is associated with a decreased incidence of neurosis and psychosis

A

FALSE

102
Q

Behavioral changes include __________ and ___________

A

Manic depression

Suicidal tendencies

103
Q

Cataracts can develop with _______ years of usage

A

> 4 years

104
Q

Long term corticosteroids tend to increase ______ and number of _________ in blood

A

Hematocrit

Leukocytes

105
Q

Single dose of cortisol decreases circulating:
Lymphocytes by
Monocytes by

A

Lymphocytes by 70%
Monocytes by 90%

*cells are sequestered rather than destroyed

106
Q

How do glucocorticoids affect growth in children?

A

Arrest of growth can result from the administration of relatively small doses

107
Q

Corticosteroids inhibits _______ synthesis and _______ division

A

DNA

Cell

108
Q

What are some relative contraindications for corticosteroids?

A 
Active systemic infection
Immunosuppression
Acute psychosis
Primary glaucoma
Hypokalemia
CHF
Cushing’s syndrome
Diabetes
HTN
Osteoporosis
Hyperthyroidism
109
Q

What are 4 concerns surgeons have with intraoperative use of corticosteroids?

A
  1. Masking infection or further complicating surgery intended to treat infection
  2. Altering glucose control in diabetes
  3. Aseptic necrosis of the femoral head
  4. Failure of bone fusion
110
Q

Likelihood is increased for HPA axis suppression by:

A

Longer the duration

Larger the dose

111
Q

What is associated more commonly with H-P-A axis suppression?

A

Prednisone or dexamethasone (even physiological doses) given as a single daily dose at bedtime is associated more commonly with HPA axis suppression

112
Q

What therapies are unlikely to suppress HPA axis?

A
  • Prednisone 5mg/day or less
  • long term every other day dosing
  • glucocorticoids, any dose < 3 weeks
113
Q

What therapies are assumed to suppress HPA axis?

A
  • Prednisone 20mg.day > 3 weeks within previous year
  • Pt with clinical signs of Cushing syndrome from any steroid dose

*no need to the the HPA axis in these patients, just supplement with stress dose steroids

114
Q

After cessation of therapy, how long can it take the HPA axis to recover?

A

12 months or longer

115
Q

H-P function returns to normal ______ adrenal function

A

BEFORE

116
Q

What test checks adrenal function?

A

Cosyntropin (ACTH) stimulation test

117
Q

Goal is to __________ the plasma concentration of cortisol _______ normal during majorly surgery in pts receiving chronic treatment with corticosteroid and manifesting a subnormal response to the preoperative infusion of ACTH

A

Maintain

Above

118
Q

It’s here a need for addition corticosteroid coverage for minor operations?

A

Minimal or no addition coverage

119
Q

T/F: you can base dose of corticosteroid supplementation based on the magnitude of the planned surgical procedure

A

TRUE

120
Q

What can exaggerate the need for exogenous corticosteroid supplementation

A

Burns or sepsis

121
Q

What are some S/S of acute adrenal crisis?

A
  • hypotension unresponsive to vasopressors
  • hyperdynamic circulation
  • hypoglycemia
  • hyperkalemia
  • hyponatremia
  • hypovolemia
  • metabolic acidosis
  • decreased LOC

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