Respiratory Flashcards

1
Q

Asthma meds are aimed at

A

flattening the response to inflammatory mediators

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2
Q

Why is it that steroids that work in asthma have minimal response in COPD?

A

Because the inflammation in COPD is of a different pathway than that of asthma

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3
Q

Inhaled _________ can help reduce the frequency of COPD exacerbations

A

corticosteroids

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4
Q

This type of medication has only a modest ole in increasing air outflow in a patient with COPD with chronic breathlessness that is worsened by exercise

A

Bronchodilators

So basically in COPD, bronchodilators don’t really help and the steroids used in asthma don’t really work either. People with COPD are placed on corticosteroids.

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5
Q

R sided heart failure with COPD

A

Those with CB experience R HF and cor pulmonale as part of the disease process

Those with emphysema experience R heart problems during acute infections

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6
Q

Pink puffers refer to __1___

Blu bloaters refer to __2__

A
1= emphysema
2= CB
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7
Q

PaCO2 in COPD

A

High in CB

Normal in emphysema

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8
Q

Types of bronchodilators used

A

Beta agonists
Anti-cholinergics
Methyxanthines

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9
Q

Problem with using epi for treatment of bronchoconstriction

A

It has B1 and alpha effects as well, which can cause tachycardia, palpitations, and vasoconstriction

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10
Q

Selective B2 agonists

(Short and long acting)

A
Short acting:
- Terbutaline
- Albuterol
- Levalbuterol (the most B2 selective!)
- Salbumatol
^^ We go for the first three of these because we can repeat the dose multiple times

Long-acting

  • Salmeterol (pts on this at home and use albuterol for acute attacks)
  • Formoterol

All of these B2 selective agents have an affinity for B2 200-400 times stronger than that for B1.

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11
Q

What happens at high doses of B2 selective agents?

A

They become less selective and start affecting other receptors

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12
Q

Effect of B2 agonists on electrolytes

A

Hypokalemia**- increased uptake by skeletal muscle. Also there is release of glucose, causing an insulin spike, driving K+ into cells. Also, B2 stimulates the Na/K pump, further driving K+ into cells.

Hypomagnesemia

Hyperglycemia

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13
Q

3 beneficial effects of B2 on the bronchi

A

Smooth muscle relaxation / bronchodilation
Decreased release of histamine from mast cells
Increased ciliary clearance of mucus

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14
Q

Onset of action of B2 agonists

A

15-30 minutes

Levalbuterol may act as soon as 5 minutes

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15
Q

How are B2 agonists given?

A

Inhaled, nebulized, aerosolized, powder, orally, SQ

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16
Q

Only B2 agonist that can be given SQ

A

Terbutaline

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17
Q

Side effects of B2 agonists

A
Muscle tremor (B2)
Increased HR (B1)
Vasodilation (B2)
Metabolic changes (B2)- hypokalemia, hyperglycemia, and mypomagnesemia
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18
Q

How can B2 side effects be minimalized?

A

Inhalation delivery (decreases systemic effects by keeping it in the lungs)

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19
Q

Albuterol dosing

A

100cmg/puff
2 puffs Q4-6 hours
Nebulizer dose: 2.5-5 mg in 5mL of saline

20
Q

Albuterol DOA

A

4-8 hours

21
Q

Albuterol has an additive effect with _______ on bronchomotor tone

A

Anesthetics

22
Q

2 Isomers of albuterol

A

R- This is Levalbuterol and is more B2 selective

S- This type of albuterol has more affinity for B1

23
Q

How to blunt airway hyperresponsiveness prior to anesthesia

A

4 puffs of albuterol

or

2 puff albuterol + 1mg/kg of lidocaine IV

24
Q

Bitolterol

A

B2 selective agent that resembles albuterol but is longer lasting.
CV side effects are rare
Dose is 270mcg/puff
Max of 16-20 puffs/day

25
Q

SQ use of terbutaline

A

SQ use resembles the effects of epinephrine.
Used for status asthmaticus or pre-term labor
Dose for adults in .25mg SQ Q 15 min
Dose for peds is .01mg/kg SQ

26
Q

Terbutaline inhaler dose

A

200mcg/puff

Max of 16-20 puffs/day

27
Q

How can terbutaline be administered?

A

Inhalation
SQ
Oral

28
Q

How do long-acting B2 agonists work?

A

They have a lipophilic side chain that resists degradation. Results in a DOA of 12-24 hours. These are not used for acute attacks.

29
Q

How can the amount of time between asthma flare-ups be avoided?

A

Combined therapy of a long-acting B2 agonist and a steroid

30
Q

Methylxanthines are also called ______

A

Phosphodiesterase inhibitors

31
Q

What is the MAJOR PREVENTATIVE treatment for patients with asthma?

A

Inhaled corticosteroids

32
Q

This is the most important type of drug in the management of asthma

A

Inhaled corticosteroids

33
Q

Do corticosteroids cure asthma?

A

No. They are used as a supportive therapy, not a cure.

34
Q

The degree of bronchoconstriction and hyperresponsiveness in asthma paralleles _____

A

the degree of inflammation

35
Q

Asthma is characterized by these two features

A

Inflammation and hyperresponsiveness

36
Q

Effect of using corticosteroids with a B2 blocker

A

It increases the DOA of the B2 blocker

37
Q

Effect of eosinophil degranulation

A

Interferes with the activity of M2 receptor, causing bronchoconstriction

38
Q

Salmeterol is given as a combination of

A

Salmeterol and fluticasone

39
Q

These are the most important drugs in asthma management

A

Corticosteroids

40
Q

These are the most important drugs in COPD management

A

anticholinergics (tiotropium is best –> only FDA approved anticholinergic for COPD).

Tiotropium has minimal SE because it doesn’t cross the respiratory epithelium

41
Q

Methylxanthines (phosphodiesterase inhibitors) interact with this anesthetic

A

Halothane

42
Q

How long does it take for cromolyn to take effect? How does cromolyn work? What are the SEs?

A

It is a mast cell stabilizer (inhibits antigen-induced histamine release). It is for preventative therapy only!!! Takes 7 days for effect to kick in.

43
Q

Montelukast (Singulair) can interact with ____ and cause ______

A

Warfarin

Prolonged PT

44
Q

The Anti-IgE antibody we know if called

A

Omalizumab

45
Q

Nerves that aren’t part of the ANS can release these substances to induce bronchiole dilation

A

NO and VIP