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phar 301 > Lecture 18 > Flashcards

Lecture 18 Flashcards

1
Q

What causes Asthma

A

No exact causes but factors
1) Smoking during pregnancy (increases asthma risk in fetus)
2) Obesity
3) Air pollution (environmental)
4) Genetics (family history)
5) Food allergies
6) Antibiotic use and microbiome

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2
Q

Types of Asthma

A

Extrinsic (allergic) and Intrinsic (nonallergic) asthma

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3
Q

What is Extrinsic (allergic) asthma

A

Caused by allergic reaction
Higher levels of IgE present in blood stream
Airway hyperresponsiveness (AHR) (sign of chronic inflammation and immune dysfunction)

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4
Q

What is Intrinsic (nonallergic) asthma

A

Caused by non-allergic factors like:
Stress, anxiety, cold air, dry air, smoke, viruses, infection, etc

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5
Q

Traits of asthma

A

Excess mucous secretion and narrowing of the airway lumen

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6
Q

Symptoms of Asthma

A

Shortness of breath, chest tightness or pain, wheezing when exhaling (children)

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7
Q

Asthma triggers

A

1) Exercised induced (may be worse when air is dry or cold),
2) Occupational asthma (workplace irritants)
3) Allergy-triggered

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8
Q

Pathway of Extrinsic asthma (allergy)

A

Allergen enters airway epithelium–>allergen presented to TH2 cells–>trigger IgE antibody production–>Mast cells bind to IgE and undergo degranulation–>Degranulation produces proinflammatory cytokines, chemokines, histamines, prostaglandins, (cycle of constant immune infiltration

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9
Q

Characteristics of Asthmatic airways

A

Increased number of blood vessels, subepithelial fibrosis (collogen deposition), goblet cell hyperplasia, smooth muscle hyperplasia, hypertrophy, and an increased volume of submucosal glands

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10
Q

What is characterized by airway inflammation, obstruction, and breathlessness

A

Asthma and COPD

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11
Q

Diagnosis for Asthma and COPD

A

Decreased FEV 1 relative to their FVC
Decreased Forced expiratory volume (FEV 1) in comparison to their forced vital capacity (FVC)

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12
Q

Treatment for Asthma

A

Inhalers, Glucocorticoids, Antileukotrienes, Beta-2 agonists, Methylxanthines, Muscarinic receptor antagonists, monoclonal antibody treatment

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13
Q

Types of Inhalers

A

Metered dose inhalers (MDI) and Dry powder inhalers (DPIs)

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14
Q

Mechanism of inhaled form of glucocorticoid

A

ex. Budesonide
Budesonide binds to glucocorticoid receptors (GRs)–> activate histone deacetylase 2 (HDAC2)–>inhibit histone acetyltransferase (HAT)–>inhibit synthesis of inflammatory response mediators and phagocytosis

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15
Q

Overall action of inhaled corticosteroids

A

ex. Budesonide
Maximize local response and avoid system inflammation

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16
Q

Anti-inflammatory action of inhaled glucocorticoids

A

1) Decreased production of prostaglandins, cytokines, and interleukins
2) Decreased proliferation and migration of lymphocytes and macrophages

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17
Q

What are Antileukotrienes

A

ex. Montelukast and Zafirlukast
Competitive antagonists of CysLTR 1
Leukotrienes are bronchoconstrictors and vasoactive lipid mediators so Anti that

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18
Q

What produces Leukotrienes

A

Neutrophils and dendritic cells
Express 5-LO and 5-LO activating protein (FLAP) required for leukotriene biosynthesis

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19
Q

When to use Antileukotrienes

A

Prophylactic treatment to prevent bronchoconstriction, not useful in acute episode

20
Q

Function of Beta-2 agonist

A

Relaxation of smooth muscle in lung and dilation of airways (opening)
May result in fight or flight response in children

21
Q

Mechanism of Beta 2 agonist

A

Open calcium activated potassium channels leading to hyperpolarization of smooth muscle cells

22
Q

What is the current medicine of choice for all types of asthma

A

Beta 2 agonists for their rapid bronchial relaxation with minimal side effects

23
Q

Types of Beta 2 agonists

A

1) Short-acting beta 2 adrenergic receptor agonist (SABA)
2) Long-acting beta 2 adrenergic receptor agonist (LABA)

24
Q

Why use SABA

A

ex. Salbutamol (albuterol) and R-albuterol (decreased tachycardia and palpitations, SNS)
Rapid onset (15-30 minutes)
Duration (4-6 hours)
Good for acute attacks
At high doses–>cardiac stimulation

25
Q

Why use LABA

A

ex. Salmeterol, Formoterol
Long duration due to long, lipophilic side-chain that allows active portion to continuously bind and unbind to receptors of smooth muscle in lung

26
Q

Where are Methylxanthines found

A

Alkaloids found in tea, coffee, chocolate

27
Q

Characteristics of Methylxanthines

A

ex. Theophylline
1) Broncho-dilating and anti-inflammatory
2) Taken orally (cannot be inhaled)
3) Given alongside glucocorticoids (synergy)

28
Q

When to use muscarinic receptor antagonist

A

In chronic inflammatory syndromes (mostly COPD and some asthma)
When parasympathetic reflexes become overactive and easily triggered, leading to bronchoconstriction
Parasympathetic

29
Q

Mechanism of Muscarinic receptor antagonists

A

Cholinergic control of airway in smooth muscle (dominated by muscarinic receptor M3)

30
Q

Types of Muscarinic receptor antagonists

A

Long-acting muscarinic antagonists (LAMAs) and Short-acting muscarinic antagonists (SAMAs)

31
Q

What can monoclonal antibody treatment target in Asthma and COPD

A

ex. Omalizumab (IgE) in age 6+ (have normal IgE levels), Mepolizumab and reslizumab (IL-5)
Antibodies against IgE and IL-5
Only use in sever cases

32
Q

What are the most powerful Asthma controllers (severe cases)

A

Oral corticosteroids, but long term use cause serious toxicity
or Monoclonal antibody therapy

33
Q

Why shouldn’t adults stop inhaled corticosteroid therapy

A

Risk of exacerbation

34
Q

Administration of Asthma treatments

A

Corticosteroids–>inhaled
Antileukotrienes–>Orally and metabolized by P450s
Beta 2 agonist–>inhaled (cannot be taken orally)
Muscarinic receptor antagonists–>inhaled

35
Q

Side effects of glucocorticoids

A

Dysphonia and thrush (fungal infection)
In children–>growth deceleration with high doses
Inhaled is safe during pregnancy

36
Q

Side effects of Antileukotrienes

A

Zileuton–>elevates liver enzymes so inhibits CYP1A2
Oral glucocorticoids + Antileukotrienes–>eosinophilic granulomatosis (Churg-Strauss), potentially fatal

37
Q

Side effects of Beta 2 agonists

A

Skeletal muscle tremor, heart palpitations and tachycardia, nausea, and vomiting
LABA must be accompanied with inhaled glucocorticoids to address underlying inflammation (or else fatal)

38
Q

Side effect of monoclonal antibodies

A

Risk of sensitivity reactions and rarely anaphylaxis

39
Q

Side effect of Theophylline

A

Headache, nausea, vomiting, GI distress, and tremulousness
Can lead to Arrhythmia, seizures, and tachycardia

40
Q

What is the Main cause of Chronic obstructive pulmonary disease (COPD)

A

Smoking, but other causes are environment and Alpha-1 deficiency related emphysema
Affects primarily 65+

41
Q

Marks of COPD

A

Limited Airflow due to emphysema, bronchitis, and bronchiectasis

42
Q

Treatment for COPD

A

LABAs (salmeterol or formoterol), inhaled muscarinic receptor antagonists, ultra long acting beta 2 agonists (indaceterol, olodaterol, and vilanterol)

43
Q

Classes of COPD for diagnosis

A

GOLD 1(mild)- Gold 4 (very severe)
Group A–>low risk, low symptoms
Group B–> low risk, high symptoms
Group C–>high risk, low symptoms
Group D–>high risk, high symptoms
risk = risk of exacerbations (worsening respiratory symptoms)

44
Q

Medical intervention of COPD

A

Lung volume reduction surgery and bronchoscopic intervention and as a last resort lung transplantation

45
Q

Diagnosis of Asthma-COPD overlap syndrome (ACOS)

A

If young patient has COPD like symptoms but incompletely reversible airway constriction

46
Q

Ways to improve ACOS symptoms

A

No treatment
1) Low dose-inhaled corticosteroids
2) LABA (not alone)
3) LAMA

47
Q

What can treat EVALI

A

Influenza cannot be distinguished from EVALI
Corticosteroids may help with EVALI but can worsen respiratory infections

phar 301 (23 decks)

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