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SP18: Pharm MT2 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

_________ is normally an allergic response; _________ is normally a response to chemicals.

A

Asthma; COPD

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2
Q

T/F: It is much easier to manage asthma than it is COPD.

A

True

Drugs treating COPD are just trying to keep patient as healthy as possible for as long as they can

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3
Q

T/F: T helper cells are critical mediators of asthma.

A

True

They determine the course of the inflammatory response

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4
Q

Asthma involves the infiltration of ____________.

A

Eosinophils

Allergen -> mast cell -> Th2 -> eosiniphils

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5
Q

_____ cells mediate an inflammatory response in eosinophilic asthma.

A

Th2

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6
Q

What is atopy?

A

A condition where people are predisposed to more Th2 immune response than Th1

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7
Q

Which type of asthma involves a thickening of the basement membrane? What types of drugs does it respond to?

A

Eosinophilic asthma; Inhalational corticosteroids

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8
Q

T/F: Non-eosinophilic asthma involves thickening of the basement membrane.

A

False

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9
Q

_____ may mediate a type of asthma that fills the area with neutrophils.

A

Th17

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10
Q

T/F: Neutrophil (Th17) mediated asthma is responsive to glucocorticoids.

A

False

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11
Q

T/F: Cholinergic stimulation (vagus nerve) is more important in asthma than COPD.

A

False

More important in COPD

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12
Q

What is the major thing causing bronchoconstriction in asthma patients?

A

Leukotrienes

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13
Q

What are the two prominent immediate responses in asthma? What is the long term response?

A

Bronchoconstriction (leukotrienes) and mucus; airway remodeling

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14
Q

What are the three main goals of asthma treatment?

A
  1. Relieve or prevent bronchoconstriction
  2. Inhibit airway inflammation (reduce mucus)
  3. Prevent airway remodling
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15
Q

T/F: The goal of asthma treatment is to cure asthma.

A

FALSE

Manage the disease so patient is as symptom free as possible

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16
Q

While asthma involves allergens and mast cells, what is the mechanism for COPD?

A

Noxious stimuli (cigarette smoke) -> neutrophil, macrophages, Th1 -> proteases eating away lung tissue

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17
Q

What are the goals of COPD treatment?

A
  1. Relieve bronchoconstriction
  2. Improve exercise tolerance
  3. Prevent and treat complications
  4. Slow progress of disease*

*difficult to do

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18
Q

Asthma normally involves ____________, while COPD normally involves ___________.

A

Eosinophils; neutrophils

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19
Q

What is the most important product of mast cell degranulation in asthma?

A

Cystidinyl leukotrienes

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20
Q

What are four ways asthma drugs can work?

A
  1. Stymie allergic response
  2. Diminish number of immune cells in lung
  3. Alter production of bronchoconstrictors
  4. Attenuate activities of bronchoconstrictors
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21
Q

What are the two most important drugs for asthma treatment?

A

Beta2 adrenergic receptor agonists

Corticosteroids

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22
Q

What is the mechanism for bronchodilators?

A

Stimulate PKA -> inhibition of myosin light chain kinase -> no muscle stimulation in smooth muscle cell

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23
Q

T/F: B2 adrenergic receptors activate a G(alpha)s which stimulates cAMP production leading to PKA activity.

A

True

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24
Q

Other than inhibiting MLCK, how else does activated PKA mediate the muscle response?

A

Activates K+ channel leading to less Ca++ in the cell (hyperpolarization)

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25
What is the difference between SABA and LABA?
SABA — short acting (rescue medication) LABA — long acting (maintenance therapy)
26
What is the gold standard of SABA?
Albuterol
27
T/F: SABA are used as maintenance therapy for COPD.
False LABA
28
What is the importance of the hydrophobic part of LABAs?
They go straight to the membrane and dribble out over time giving a more prolonged effect
29
What are some side effects of B2 agonists?
Muscle tremors are the most common
30
T/F: Both LABAs and SABAs are administered by inhalation.
True
31
T/F: Treatment with inhalation of corticosteroids is critical for managing all asthma types.
False Just eosinophilic
32
____________ act as general immune-suppressant agents.
Corticosteroids
33
How can you measure the effectiveness of corticosteroid treatment of asthma?
Measure reduction in eosinophils
34
All steroids, including cortisol, are derived from _________.
Cholesterol
35
Describe the hypothalamic-pituitary axis.
Stress leads to hypothalamus and pituitary activity -> cortisol and glucocorticoid production -> negative feedback on hypothalamus and pituitary
36
T/F: Cortisol peaks in the morning.
True
37
T/F: Cortisol bound to transport proteins are active.
False Must be unbound to be active
38
T/F: Cortisol will increase blood glucose levels.
True
39
Glucocorticoids reduce the ability of __________ to adhere to vascular endothelium and leave circulation.
Leukocytes Does not allow them to leave vasculature and push inflammation forward
40
T/F: Glucocorticoids inhibit neutrophil apoptosis, but promote eosinophil apoptosis.
True
41
What is the effect of glucocorticoids on pro-inflammatory mediators?
Suppresses production of many of these mediators (protoglandins, leukotrienes, eicosanoids, cytokines Up-regulate ACE and enzymes that degrade bradykinin
42
What is the net result of glucocorticoid use?
Inhibition of vasodilation, chemotaxis, nociception, extravasated. Decrease in inflammation and pain Increase in bronchodilation
43
What is NF(kappa)B?
It is a huge transcription factor in production of inflammatory mediators Glucocorticoids block its action on transcription
44
T/F: Glucocorticoid receptors work through a GPCR.
False They directly stimulate expression of genes and block NF(kappa)B mediated transcription
45
What is Annexin-A1?
A product of glucocorticoid activated genes — attenuates the immune response and eicosanoid production
46
T/F: When glucocorticoid is used to treat adrenal insufficiency it is with much lower doses than for asthma.
True
47
When would glucocorticoids be given systemically?
Acute treatment in emergency room
48
What are some major side effects of inhaled corticosteroids?
Dysphonia, oral candidiasis, adrenal suppression (high does, systemic)
49
T/F: Patients should rinse their mouth after using inhaler.
True
50
What are two groups of people who would not respond to inhaled corticosteroid treatment?
1. Non-eosinophilic asthma patients | 2. Glucocorticoid resistant patients
51
T/F: ICS’s are beneficial to treat COPD
False Research is limited
52
An increase in vagal tone contributes mightily to broncho-constriction in ________.
COPD Produced by AcCh acting on muscarinic receptors
53
How are anti-cholinergenics used in treatment of COPD?
They act as antagonists of muscarinic AcCh receptors
54
__________ is a classic antagonist of muscarinic AcCh receptors.
Atropine
55
What is the first line of defense in treating COPD?
Anti-cholinergics Act as muscarinic antagonists Inhibits smooth muscle contraction and decreases mucus secretion
56
How do most drugs used as anti-cholinergics for asthma differ from atropine?
They have a quaternary amine (positive charge!) that does not allow them to get into the bloodstream as well. Less side effects
57
T/F: Leukotrienes are 1000x more potent at bronchocontriction than histamine in the airway.
True
58
What are the two pathways for arachidonic acid?
1. COX pathway to become prostoglandins | 2. Lipoxygenase to become leukotrienes
59
What are the two ways leukotriene modifiers work?
1. LT receptor antagonist (montelukast, zafirlukast) | 2. lipoxygenase inhibitor (zilueton)
60
When would leukotriene modifiers be used in asthma treatment?
1. Alternative for mild persistent asthma 2. With ICSs 3. Exercise induced asthma prevention
61
What is Omalizumab?
Humanized monoclonal antibody directed against IgE Treat moderate-severe asthma Expensive injections
62
What is allergic rhinitis?
Inflammation of the membrane lining the nose
63
What do nasal passages do?
Warm and humidify air Lots of blood flow, high secretory, rapid movement of water via blood vessels
64
Which glands are more responsible for nasal discharge?
Posterior seromucous glands
65
What is the physiological characterization of a snot-nosed kid, rather than an adult?
Children have the same amount of mucous glands as adults, but they have a smaller nose
66
What are the three major drug classes for treating allergic rhinitis?
1. H1 receptor antagonists (antihistamines) 2. A1-adrenergic receptor agonists (decongestants) 3. Intranasal corticosteroids
67
T/F: Histamine is abundant in mast cells and works through GPCRs.
True
68
Which histamine receptor plays a role in rhinitis?
H1 Activity increases intracellular Ca++ in endothelium
69
What is the major source of histamine?
Degranulation of mast cells and other immune cells
70
How is H1 activated? What are the two effects of activated H1?
Histamine release from degranulation of mast cells 1. Increased Ca+ and NO in endothelium -> NO travels to smooth muscle and causes vasodilation 2. MLCK mediated contraction of endothelium -> leaky endothelium RUNNY NOSE
71
How do anti-histamines work?
Histamine receptor antagonists Block vasodilation and restore the capillary seal
72
What makes 2nd generation H1 antagonists better?
Do not cross BBB, more selective, fewer adverse effect
73
T/F: 1st generation H1 antagonists produce drowsiness.
True
74
What types of drugs are considered decongestants?
Alpha1-adrenergic receptor agonists
75
What is the mechanism that oral decongestants will work through?
Constrict the blood vessels to relieve congestion

SP18: Pharm MT2 (7 decks)

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