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PCTH 325 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Conducting airways

A

Responsible for bulk airflow (from nose/mouth to airway system)

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2
Q

Respiratory airways

A

Responsible for gas exchange by diffusion

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3
Q

Asthma

A

Chronic inflammatory disease of the conduction airways

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4
Q

Symptoms of asthma (5)

A
  1. Airway hyper-responsiveness -> airflow limitation
  2. Dyspnea (shortness of breath)
  3. Chest tightness
  4. Wheezing
  5. Sputum production (coughing up mucus from the respiratory system)
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5
Q

Risk factors of asthma (4)

A
  1. Genetics
  2. Occupational exposures
  3. Smoking
  4. Viral infections
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6
Q

Etiology (ie. causes) of asthma

A
  1. Non-allergic asthma (ex. cold temps., occupational asthma, tiring activities like swimming)
  2. Allergic asthma - allergens are proteases (degrades proteins). Ex. house dust mite fecal pellets, cat dander, mold
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7
Q

Cellular mechanisms of hyper-responsiveness

A
  1. Allergens proteolytically degrade the airway epithelium
  2. Allergens cause cross-linking of IgE leading to mast cell activation. Allergic individuals have more IgE on mast cells
  3. Mast cells degranulate, releasing a variety of mediators that cause bronchoconstriction of smooth muscle
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8
Q

3 mediators of asthma

A
  1. Preformed mediators
  2. Newly formed mediators
  3. Cytokines

**idk if we’re supposed to know more

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9
Q

Airway hyper-responsiveness mechanism

A
  1. Allergens activate mast cells -> smooth muscles around the conducting airways contract
  2. Contraction of the smooth muscles limits airflow to the respiratory airways for gas exchange
  3. Inflammation and edema further close off the conducting airways

*Hyper-reactivity (sensitivity) of smooth muscle cells to allergen relates to disease severity

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10
Q

Prevention of smooth muscle contraction (2)

A
  1. Removal of the contractile stimulus
  2. Inhibition of the contractile mechanism (contraction requires Ca2+)
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11
Q

Adrenaline and noradrenaline function related to B2 adrenergic receptor

A

They are endogenous agonists that stimulate the SNS to cause smooth muscle relaxation. B2 adrenergic receptors are expressed on all smooth muscle within the body

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12
Q

B2 adrenergic receptor agonists MOA

A

Bind to B2 adrenergic receptors on smooth muscle cells -> releases of cAMP, leading to:

  • removal of Ca2+ via Ca2+ channels
  • uncoupling of thick and thin filament cross bridging

All of which results in smooth muscle relaxation

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13
Q

Mild asthma treatment

A

Characterized as intermittent mild episodes. Has short-acting B2 adrenergic receptor agonists (SABAs)

Reliever medications are taken when needed and has an onset of 2-3 mins with the duration of action of 4-6 hours

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14
Q

Moderate to severe asthma treatment

A

Characterized as persistent to life threatening episodes. Has long-acting B2 adrenergic receptor agonists (LABAs)

Undergo prophylactic treatment (present all the time) and has an onset of 30 mins and duration of action >12 hours - taken twice a day

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15
Q

True or False: SABAs can be used as a daily asthma control agent

A

False - it is not recommended

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16
Q

Downside to long-term LABA use

A

Can desensitize B2 adrenergic receptors, leading to severe asthma attacks

17
Q

What should LABA be prescribed with?

A

Corticosteroid - reduces inflammation and the dose of LABA required

18
Q

4 side effects of B2 agonists

A
  1. Tachycardia
  2. Tremor
  3. Agitation
  4. Osteoporosis
19
Q

How does inflammation in asthma occur?

A

Release of mast cell inflammatory mediators leads to inflammatory cell recruitment, edema, and mucus secretion

20
Q

2 outcomes of corticosteroid binding to glucocorticoid receptor complex

A
  1. Trans-repression: increases anti-inflammatory cytokines, anti-proteases, and anti-oxidants
  2. Trans-activation: decreases inflammatory cytokines, proteases, and ROS (reactive oxygen species?)
21
Q

Acute side effects of inhaled corticosteroids

A
  1. Upper respiratory tract infection
  2. Dysphonia (hoarseness)
  3. Cough + throat irritation
  4. Headache
22
Q

Long term side effects of inhaled corticosteroids

A
  1. Sleep disturbance
  2. Risk of fractures, osteoporosis
  3. Diabetes
  4. Obesity
  5. Mood changes
  6. Increased appetite
  7. Adrenal suppression
  8. Hypertension
23
Q

2 types of inhaler type and why is the different between them important?

A
  1. Dry powder Inhaler (DPI)
  2. Metered-Dose Inhaler (MDI) - uses propellant to aerosolize the drug

Difference is important because DPI only gives ~3µg of the 50µg stated does while MDI gives ~25µg. This is due to the composition of the inhalers

24
Q

4 consequences of larger drug particles

A
  1. Increased side effects due to more drug ingested
  2. Higher morbidity and poorer control of chronic disease
  3. Risk of exposure to poorly tolerated alternative treatments
  4. Increased cost for additional medications

PCTH 325 (19 decks)

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