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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
Q

What is the difference between SABA and LABA?

A

SABA — short acting (rescue medication)

LABA — long acting (maintenance therapy)

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26
Q

What is the gold standard of SABA?

A

Albuterol

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27
Q

T/F: SABA are used as maintenance therapy for COPD.

A

False

LABA

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28
Q

What is the importance of the hydrophobic part of LABAs?

A

They go straight to the membrane and dribble out over time giving a more prolonged effect

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29
Q

What are some side effects of B2 agonists?

A

Muscle tremors are the most common

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30
Q

T/F: Both LABAs and SABAs are administered by inhalation.

A

True

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31
Q

T/F: Treatment with inhalation of corticosteroids is critical for managing all asthma types.

A

False

Just eosinophilic

32
Q

____________ act as general immune-suppressant agents.

A

Corticosteroids

33
Q

How can you measure the effectiveness of corticosteroid treatment of asthma?

A

Measure reduction in eosinophils

34
Q

All steroids, including cortisol, are derived from _________.

A

Cholesterol

35
Q

Describe the hypothalamic-pituitary axis.

A

Stress leads to hypothalamus and pituitary activity -> cortisol and glucocorticoid production -> negative feedback on hypothalamus and pituitary

36
Q

T/F: Cortisol peaks in the morning.

A

True

37
Q

T/F: Cortisol bound to transport proteins are active.

A

False

Must be unbound to be active

38
Q

T/F: Cortisol will increase blood glucose levels.

A

True

39
Q

Glucocorticoids reduce the ability of __________ to adhere to vascular endothelium and leave circulation.

A

Leukocytes

Does not allow them to leave vasculature and push inflammation forward

40
Q

T/F: Glucocorticoids inhibit neutrophil apoptosis, but promote eosinophil apoptosis.

A

True

41
Q

What is the effect of glucocorticoids on pro-inflammatory mediators?

A

Suppresses production of many of these mediators (protoglandins, leukotrienes, eicosanoids, cytokines

Up-regulate ACE and enzymes that degrade bradykinin

42
Q

What is the net result of glucocorticoid use?

A

Inhibition of vasodilation, chemotaxis, nociception, extravasated.

Decrease in inflammation and pain

Increase in bronchodilation

43
Q

What is NF(kappa)B?

A

It is a huge transcription factor in production of inflammatory mediators

Glucocorticoids block its action on transcription

44
Q

T/F: Glucocorticoid receptors work through a GPCR.

A

False

They directly stimulate expression of genes and block NF(kappa)B mediated transcription

45
Q

What is Annexin-A1?

A

A product of glucocorticoid activated genes — attenuates the immune response and eicosanoid production

46
Q

T/F: When glucocorticoid is used to treat adrenal insufficiency it is with much lower doses than for asthma.

A

True

47
Q

When would glucocorticoids be given systemically?

A

Acute treatment in emergency room

48
Q

What are some major side effects of inhaled corticosteroids?

A

Dysphonia, oral candidiasis, adrenal suppression (high does, systemic)

49
Q

T/F: Patients should rinse their mouth after using inhaler.

A

True

50
Q

What are two groups of people who would not respond to inhaled corticosteroid treatment?

A
  1. Non-eosinophilic asthma patients

2. Glucocorticoid resistant patients

51
Q

T/F: ICS’s are beneficial to treat COPD

A

False

Research is limited

52
Q

An increase in vagal tone contributes mightily to broncho-constriction in ________.

A

COPD

Produced by AcCh acting on muscarinic receptors

53
Q

How are anti-cholinergenics used in treatment of COPD?

A

They act as antagonists of muscarinic AcCh receptors

54
Q

__________ is a classic antagonist of muscarinic AcCh receptors.

A

Atropine

55
Q

What is the first line of defense in treating COPD?

A

Anti-cholinergics

Act as muscarinic antagonists

Inhibits smooth muscle contraction and decreases mucus secretion

56
Q

How do most drugs used as anti-cholinergics for asthma differ from atropine?

A

They have a quaternary amine (positive charge!) that does not allow them to get into the bloodstream as well.

Less side effects

57
Q

T/F: Leukotrienes are 1000x more potent at bronchocontriction than histamine in the airway.

A

True

58
Q

What are the two pathways for arachidonic acid?

A
  1. COX pathway to become prostoglandins

2. Lipoxygenase to become leukotrienes

59
Q

What are the two ways leukotriene modifiers work?

A
  1. LT receptor antagonist (montelukast, zafirlukast)

2. lipoxygenase inhibitor (zilueton)

60
Q

When would leukotriene modifiers be used in asthma treatment?

A
  1. Alternative for mild persistent asthma
  2. With ICSs
  3. Exercise induced asthma prevention
61
Q

What is Omalizumab?

A

Humanized monoclonal antibody directed against IgE

Treat moderate-severe asthma

Expensive injections

62
Q

What is allergic rhinitis?

A

Inflammation of the membrane lining the nose

63
Q

What do nasal passages do?

A

Warm and humidify air

Lots of blood flow, high secretory, rapid movement of water via blood vessels

64
Q

Which glands are more responsible for nasal discharge?

A

Posterior seromucous glands

65
Q

What is the physiological characterization of a snot-nosed kid, rather than an adult?

A

Children have the same amount of mucous glands as adults, but they have a smaller nose

66
Q

What are the three major drug classes for treating allergic rhinitis?

A
  1. H1 receptor antagonists (antihistamines)
  2. A1-adrenergic receptor agonists (decongestants)
  3. Intranasal corticosteroids
67
Q

T/F: Histamine is abundant in mast cells and works through GPCRs.

A

True

68
Q

Which histamine receptor plays a role in rhinitis?

A

H1

Activity increases intracellular Ca++ in endothelium

69
Q

What is the major source of histamine?

A

Degranulation of mast cells and other immune cells

70
Q

How is H1 activated? What are the two effects of activated H1?

A

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
Q

How do anti-histamines work?

A

Histamine receptor antagonists

Block vasodilation and restore the capillary seal

72
Q

What makes 2nd generation H1 antagonists better?

A

Do not cross BBB, more selective, fewer adverse effect

73
Q

T/F: 1st generation H1 antagonists produce drowsiness.

A

True

74
Q

What types of drugs are considered decongestants?

A

Alpha1-adrenergic receptor agonists

75
Q

What is the mechanism that oral decongestants will work through?

A

Constrict the blood vessels to relieve congestion

SP18: Pharm MT2 (7 decks)

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