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Therapeutics 1 Exam 3 > Therapeutics Exam 3 > Flashcards

Therapeutics Exam 3 Flashcards

1
Q

Alveoli

A

Site of gas exchange in lung

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2
Q

What is the function of cilia and mucus in the lung?

A

Clean the lungs from dust and microbes

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3
Q

What factors are part of the Triad of Lung Disease Inducers?

A

Genetic, Environmental, Medications

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4
Q

What are the 7 parts of asthma?

A
  1. wheezing, coughing, shortness of breath
  2. narrowing of airway
  3. inflammation and airway hyperreactivity
  4. release of inflammatory mediators
  5. constriction of airway smooth muscle
  6. excess secretion of mucous
  7. edema of respiratory mucosa
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5
Q

What does the oscillating pressure effect in airways result in?

A

Wheezing

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6
Q

What happens in the EARLY REACTION phase of asthma?

A

-Immediate bronchoconstriction
-Antigen binds to IgE antibodies and triggers release of: histamine, tryptase, LTC4, LTD4, and prostaglandins from mast cells
-Bronchial smooth muscle contraction
-Vascular leakage

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7
Q

What happens in the DELAYED REACTION phase of asthma?

A

-Occurs in 2-8 hours
-Sustained bronchoconstriction
-Activation of TH2 lymphocytes: release of GM-CSF, IL-4, IL-5, IL-13
(other immune cells being recruited besides mast cells)
-Mucus hypersecretion: goblet cells
-Cellular infiltration: eosinophils

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8
Q

IgE is bound to __?

A

FcR on mast cells

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9
Q

Cross-linking of IgE antibodies by multivalent antigens leads to __?

A

Degranulation of mast cells

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10
Q

What does IAR stand for?

A

Immediate asthmatic response

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11
Q

What does LAR stand for?

A

Late asthmatic response

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12
Q

What does FEV1 stand for?

A

Forced expiratory volume

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13
Q

What does ECP stand for?

A

Eosinophil cationic protein
(cytotoxic secretory protein and marker of inflammation)

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14
Q

What does PAF stand for?

A

Platelet activating factor
(hyper-responsiveness)

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15
Q

What is the function of ECP?

A

-Ribonuclease (breaks down RNA)
-Promotes inflammation and fibrosis

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16
Q

What is the function of PAF?

A

-Potent inflammatory mediator

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17
Q

What is the action of neutrophil proteases?

A

Activate eosinophils

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18
Q

What does periostin do?

A

-It is a matrix protein that is an asthma biomarker
-Promotes chronic allergic inflammation in response to TH2 cytokines
-Ligand for alpha/beta integrins to support adhesion and cell migration
-Induced by IL-13 and IL-4

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19
Q

What do EGFR and CLCA cause?

A

Development of hyperplasia

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20
Q

What is the function of Bcl-2?

A

The maintenance of hyperplasia

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21
Q

When stimulated by an allergen, what do TH2 cells release?

A

Cytokines

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22
Q

When stimulated by allergens or irritants, what do neutrophils release?

A

-Proteinases
-Oxidases

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23
Q

Hyperplasia of goblet cells results in __?

A

-Hypersecretion of mucus
-Increased numbers of goblet cells compared to ciliated cells

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24
Q

What does the R576 polymorphism in the IL-4a receptor do?

A

-Mediates enhanced response to IL-13
-Increases inflammation
-Increases goblet cell hyperplasia

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25
Q

What does the Q576R polymorphism in the IL-4a receptor do?

A

Induces hyperreactivity to inhaled antigens

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26
Q

What are the three factors of airway remodeling?

A
  1. Epithelium: mucus hyperplasia and hypersecretion
  2. Basement membrane: thickening
  3. Smooth Muscle: hypertrophy (enlargement)
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27
Q

COPD symptoms

A

-Cough
-Sputum
-Dyspnea (shortness of breath)
-Barrel chest

(Cyelus Sat Down Badly)

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28
Q

How is COPD assessed?

A

-Breathlessness score related to daily activities
-CAT (COPD Assessment Test)
-Degree of airflow limitation
-Comorbidities

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29
Q

What are the comorbidities of COPD?

A

-Smoking
-Diabetes
-Cardiovascular
-Respiratory Infections
-Cancer
(Someone drove Cyelus’s race car)

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30
Q

What are the results of COPD remodeling?

A

-Fibrosis of small airways
-Lung hyperinflation (Alveolar enlargement and Alveolar wall destruction)
-Mucus hypersecretion

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31
Q

What is the result of a genetic deficiency of a1-anti-trypsin?

A

a1-anti-trypsin is a protease inhibitor. Therefore, deficiency results in proteases causing alveolar wall destruction and mucus hypersecretion in COPD remodeling.

-Increased neutrophil migration

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32
Q

What are the functions of a1-anti-trypsin?

A

-Inhibits neutrophil elastase
-Limits lung tissue damage

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33
Q

What is the result of the ZZ allele?

A

Clinically disadvantageous lung function

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34
Q

What is the result of the PI-MZ allele?

A

-Increased height and respiratory function

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35
Q

What factors contribute to EVALI? (E-Cigarette/Vaping Associated Lung Injury)

A

-Sterile exogenous pneumonitis reaction
-Innate immune response
-Vitamin-E acetate
-Hydrocarbons in counterfeit vaping products
-Many compounds are involved in oxidative stress and inflammatory responses in the lungs
-NETosis initiated to trap particles and pathogens but unregulated NETosis can lead to infection

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36
Q

What is Cystic Fibrosis?

A

-Autosomal recessive disease resulting from mutations in the gene for Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)

-Patients excrete mucus that:
-Obstructs airflow
-Harbors pathogens
-Obstructs the pancreatic duct and interferes with digestion

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37
Q

What does CFTR function as?

A

A Cl- channel

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38
Q

What three places are CFTR receptors expressed in?

A

-Airway Epithelium
-Sweat Duct Epithelium
-Pancreatic Duct Epithelium

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39
Q

What is the effect of loss of CTFR function in the sweat duct epithelium?

A

-Increased NaCl concentration in the sweat
(excessively salty sweat)
-NaCl increases extracellularly

Has an opposite effect on sodium in the lungs

40
Q

What is the effect of loss of CFTR function in the airway epithelium?

A

-CFTR works to inhibit ENaC which is a transporter that brings sodium into the cell
-Without CFTR ENaC brings too much sodium into the cell and water follows into the epithelial cell to balance it out
-This dehydrates the mucus outside the cell

41
Q

What do each of the CFTR mutation types affect?

A

1: protein synthesis
2: protein traffic
3: channel gating
4: Channel conductance
5: Protein abundance
6: PM protein stability

1-3= more severe
4-6= milder

42
Q

What asthma drugs cause bronchodilation?

A

-B2 adrenergic agonists
-Methylxanthines
-Anticholinergics

43
Q

What asthma drugs are anti-inflammatory?

A

-Glucocorticoids
-Antileukotriene agents

44
Q

What asthma drugs inhibit mast cell degranulation?

A

-Cromolyn-Type Drugs
-Omalizumab (Xolair)

45
Q

What does LABA stand for?

A

Long-Acting Beta Agonist

46
Q

What does ICS stand for?

A

Inhaled Corticosteroid

47
Q

What does LTRA stand for?

A

Leukotriene Receptor Antagonist

48
Q

What does LAMA stand for?

A

Long-acting Muscarinic Agent

49
Q

What is the primary activity of sympathomimetic amines?

A

B2 adrenergic receptor agonists relax bronchial smooth muscle

50
Q

What are the secondary activities of sympathomimetic amines?

A

-Inhibit release of mediators from mast cells
-Inhibit microvascular leakage
-Increase microciliary transport of mucus

51
Q

What are some examples of SABA’s?

A

-Albuterol (Ventolin)
-Levalbutoral (Xopenex)
-Terbutaline (Brethine)

52
Q

Albuterol Info

A

-Optimal B2 selectivity
Form: Inhalation and Oral

53
Q

Terbutaline Info

A

-Increased palpitations
Form: Inhalation and Oral

54
Q

What are some examples of LABA’s?

A

-Formoterol (Foradil)
-Salmeterol (Serevent)

55
Q

Formoterol Info

A

-Highest receptor affinity
-Increased lipophilicity and resistance to MAO and COMT
-Used morning evening with combination with ICS
Form: Inhalation

56
Q

Salmeterol Info

A

-Greater water solubility and moderate lipophilicity
-Resistant to MAO and COMT
-Used in combination with fluticasone propionate
-Used morning and evening in combinations with ICS
Form: Inhalation

57
Q

SABA’s are resistant to __?

A

COMT

58
Q

LABA’s are resistant to __?

A

COMT and MAO

59
Q

Which form of administration is preferred for acute attacks?

A

Inhalation

60
Q

Are LABA’s prescribed for acute attacks?

A

No, LABA’s are not used for acute attacks and are rarely prescribed by themselves

61
Q

Inhalation Drug Information

A

-Inhalation provides local action on bronchial smooth muscle
-Inhaled drugs have fewer systemic adverse effects

62
Q

What is the maximum amount of times patients should be using albuterol?

A

-Patients should not be using albuterol more than 2x per week
-If they are using it more it may be a sign that their asthma is not well controlled
-This excludes uses for exercise induced asthma

63
Q

What are the adverse effects associated with Selective B2-Adrenergic Agonists?

A

-Skeletal muscle tremors
-Tachycardia and palpitations
-Less with B2 selective agents
-High doses of B2 selective agents may stimulate B1 heart
receptors
-Some reflex tachycardia may occur due to vasodilation caused by
B2 receptor activation
-Vasodilation -> Decreased Blood Pressure -> Increased Heart Rate

64
Q

Can LABA’s be used by themselves?

A

-LABA’s (salmeterol and formoterol) are contraindicated as monotherapy because they increase the risk of asthma related death
-Only use LABA’s in patients who are currently taking long-term control medication but who’s asthma is still uncontrolled

65
Q

What is a glucocorticoid?

A

Inhaled corticosteroid

66
Q

What is the function of glucocorticoids?

A

Alter gene expression of proteins important in the inflammatory process

Reduce the frequency and severity of acute asthma attacks

-Decrease eosinophils, macrophages, and mast cells
-Inhibit prostaglandin and leukotriene synthesis
-Decrease hyperresponsiveness of bronchial smooth muscle cells during asthma

67
Q

How are glucocorticoids usually dosed?

A

A single inhaled dose in the morning
-Usually used in combination products
-4-8 weeks to experience effect

68
Q

What do glucocorticoids increase the risk of?

A

Fungal infections of the mouth and throat

69
Q

What are the actions of theophylline?

A

-Inhibits (phosphodiesterase) PDE 4
-Increases cAMP
-Antagonizes bronchoconstriction produced by adenosine
-HDAC activation
-Increased inflammatory cell apoptosis
-Leads to relaxation of bronchial smooth muscle and airway opening

70
Q

Degranulation of mast cells mechanism

A
  1. IgE antibodies bind to FCeR receptors
  2. Antigen binds to IgE antibody
  3. FCeR receptors cluster
  4. Influx of calcium via CRAC (calcium release activated channels)
71
Q

What two compounds inhibit mast cell degranulation?

A

-Cromolyn Sodium (Intal)
-Nedocromil Sodium (Tilade)

**Stable but insoluble salts
**Must be inhaled, cannot be taken orally

72
Q

What are cromolyn-like drugs used for?

A

-Preventing chronic asthma
-Preventing exercise-induced asthma
-Pre-treatment blocks bronchoconstriction

73
Q

How often are cromolyn-like drugs dosed?

A

Once daily

74
Q

What is biologics therapy?

A

A monoclonal antibody that modulates biological pathways (blocks receptors or cytokines)

75
Q

What are the comorbid conditions associated with biologics therapy?

A

-Obesity
-Smoking
(Obese and Smoking patients are less likely to respond to treatment)
-Some allergies and sensitivities

76
Q

What are the two asthma phenotypes?

A

Type 2 low inflammation
–Neutrophilic
–IL 6, 8, 17
–Harder to treat, more adverse effects

Type 2 high inflammation
–Eosinophilic
–IL 4, 5, 13
–PDG2 stimulation of DP2 receptor
***Treated with monoclonals (biologic therapy)

77
Q

What are the five major types of biologics?

A
  1. IgE antagonist
  2. IL-5 Pathway
  3. IL-5 alpha receptor
  4. IL-4 Receptor
  5. Thymic Stromal Lymphopoietin (TSLP)
78
Q

Omalizumab Information

A

-IgE Antagonist
-Brand: Xolair
-Humanized mouse anti-human IgE antibody
-96% reduction in free IgE levels
-Inhibits binding of IgE antibodies to FCeR1 receptor
-**Decreases numerous cytokine levels
-Inhibits degranulation which suppresses inflammation

79
Q

Interleukin 5 Pathway (IL-5)

A

-IL-5 has a role in recruitment and maturation of eosinophils
-Increased IL-5 levels are associated with severe asthma

80
Q

Interleukin 4 alpha receptor pathway

A

Dupilumab

81
Q

What do eiosinophils release?

A

Leukotrienes

82
Q

What is LTB4?

A

Potent chemotactic agent

83
Q

What is the action of CysLTs?

A

-Increases contraction, secretion, and permeability

84
Q

What are the four parts of non-drug COPD treatment?

A
  1. Smoking cessation
  2. Vaccinations
  3. Pulmonary rehabilitation
  4. Long-term oxygen treatment
85
Q

What is the purpose of drug treatment with COPD?

A

-Drugs will not improve function or decline in function
-They will:
—-Prevent exacerbations
—-Improve symptoms
—-Improve hospitalization rates

86
Q

What is the first line treatment of COPD?

A

Bronchodilators

87
Q

What types of drugs should be used as needed for COPD?

A

SAMA’s and SABA’s

88
Q

When should inhaled corticosteroids be used in COPD treatment?

A

If the patient has high eosinophil counts and exacerbations

89
Q

What drugs should be used if regular use is required in COPD treatment?

A

-LAMA’s
-long-acting B2-adrenergic agonists

90
Q

What is a rare treatment for COPD?

A

a1-antitrypsin replacement
(less than 1% of COPD patients have a deficiency)

-derived from pooled human plasma

91
Q

Muscarinic Antagonist Information

A

-SAMA’s and LAMA’s
-competitively inhibit muscarinic receptors in the lungs
-quaternary ammonium compounds
-limited systemic absorption
*Do not use prn dosing

92
Q

What is the function of ipratropium?

A

-Blocks acetylcholine binding to initiate contraction pathway

93
Q

When are LABA’s contraindicated?

A

LABA’s are contraindicated in asthma treatment but NOT in COPD treatment

94
Q

What are the 4 main targets in asthma treatment?

A
  1. bronchodilation
  2. anti-inflammation
  3. inhibition of mast cell
  4. inhibition of eosinophilia
95
Q

What are the two main targets in COPD treatment?

A
  1. bronchodilation
    (muscarinic and adrenergic receptor based)
  2. Protease inhibitor strategy
96
Q

What are the three main targets of CF treatment?

A
  1. Protein folding/channel correctors
  2. Mucus treatment and pancreatic enzyme (PERT)
  3. Bronchodilation and antibiotics

Therapeutics 1 Exam 3 (1 decks)

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