HCP 10: Frances DiAnza Asthma Flashcards

1
Q

What is Hay Fever?

A

Allergic Rhinitis
Causes cold-like symptoms (runny nose, itchy eyes, congestion, sneezing, sinus pressure), but not caused by virus (no fever, body aches, yellow discharge)
Onset is immediately after exposure & lasts for as long as you’re exposed
Causes: Tree/grass pollen, spores, cockroach, dust mites
Risk factors: FHx, nasal polyps, other allergies
Pathogenesis: Type I hypersensitivity IgE
Treatment: Nasal corticosteroids, reduce exposure, anti-histamines

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2
Q

How to Anti-histamines work?

A
Block target tissue response to histamine
1st generation (benadryl): reversibly bind & stabilize inactive form of H1 receptor (more lipophilic, so cross BBB-> drowsiness)
2nd gen (Claritin): Specific for H1 receptor (not lipophilic, doesn't cross BBB)
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3
Q

Why does aspirin sometimes induce asthma?

A

Aspirin inhibits COX2 -> inhibit synthesis of PG -> shunts substrates into 5-lipoxygenase pathway -> increase leukotriene production -> leukotrienes cause potent bronchoconstriction & bronchospasm

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4
Q

How does albuterol cause hypokalemia?

A

Albuterol: Binds to B2 receptor -> activates AC -> increases cAMP -> stimulates activity of Na/K ATPase (Na out, K in), so more K shifted inter cellularly (transient hypokalemia)

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5
Q

What is the MOA of solumedrol? prednisone?

A
It's a steroid...
Binds to cytosolic glucocorticoid receptor
translocates to nucleus
Binds to nuclear response elements
-Lipocortin 1 synthesis -> inhibit PLA2 synthesis -> decrease AA activation
-suppress humoral immunity
-Decrease cytokine gene expression
-Decrease inflammation
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6
Q

Why do we need to taper steroids?

A

Steroids cause suppression of HPA axis, causing decreased ability to make normal amounts of hormones (i.e. cortisol). Tapering prevents adrenal insufficiency.

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7
Q

How should we assess intubation?

A
LEMON score:
L-look for characteristics that predict difficulty
E-Evaluate
M-mallampati score (extend neck, "ah")
O-Obstruction
N-Neck mobility
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8
Q

What are the indications for intubation?

A
Hypoxia/hypercapnia
Respiratory distress
Failure to maintain patent airway
Failure of oxygenation and/or ventilation
Anticipate rapidly deteriorating course
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9
Q

Contraindications for intubation?

A

DNI, difficulty, expanding neck hematoma

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10
Q

Why do we use mechanical ventilation?

A

Used to assist/replace spontaneous breathing
Decrease work of breathing & avoid resp. muscle fatigue
Reverse hypoxia/acidosis
Optimize oxygenation while avoiding overstretch or collapse

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11
Q

What are some different types of mechanical ventilation?

A

Non-invasive - mask
Assist-control: Set TV delivered & additional breaths given if triggered by patient
SIMV: provides breath if patient triggers below set rate or if they don’t breath
Pressure-support: only patient-triggered
Continuous: Set TV no matter what patient does

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12
Q

What is PEEP?

A

Pulmonary expiratory end-pressure

how much pressure left in alveoli at the end of expiration (usually set to 5cm to prevent collapse of airways)

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13
Q

What is FiO2?

A

Fraction of inspired O2

Usually 21% and increases 4% for every 1L O2

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14
Q

What is asthma?

A

Chronic inflammatory disorder causing episodes of wheezing, breathlessness, chest tightness, and cough (esp. at morning/night)
Reversible airflow obstruction w/ contraction of SMC & hyper responsive airways

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15
Q

Why do we see a decreased FEV1/FVC?

A

Bronchoconstriction -> increased resistance -> decrease flow rate

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16
Q

What is the Residual volume in an asthma attack? How is that different from COPD?

A

RV=volume of air in lung left after maximal expiration
Bronchoconstrictiction -> increased resistance -> decreased expiration of air @ typical intrathoracic pressure.
In emphysema, increase in RV due to air trapping in smaller airways (not hypertrophy/bronchoconstriction)

17
Q

Why is wheezing mainly heard on expiration? How is it different from COPD?

A

Increase in intrathoracic pressure during expiration causes further constriction of airways -> more difficult for air to flow -> turbulent & noisy airflow
In COPD, bronchospasm rarely occurs. Extensive parenchymal destruction promotes airway collapse at high intrathoracic pressure

18
Q

Why are albuterol/salmeterol preferred to isopreteronol?

A

they are selective B2 agonists. Isopreteronol is non-selective, so it will have effects on the heart (tachycardia & palpitations).

19
Q

What shouldN’T we give to asthmatics?

A

B-blockers (unless it’s a B1 selective blocker), otherwise we could trigger bronchospasms

20
Q

What is the MOA of theophylline?

A

Non-selective phosphodiesterase inhibitor
Inhibits PDE in SMC
Decrease breakdown of cAMP to AMP
Increased cAMP
Bronchodilation
*Also inhibits adenosine to decrease bronchoconstriction.

21
Q

What is the MOA of Zafirlukast?

A

Leukotriene receptor antagonist
Selectively & reversibly inhibits cysteinyl LT 1 receptor for LTD4/E4
Decrease LTD4/E4 binding
Decrease bronchiolar SMC contraction, airway edema, and eosinophil migration

22
Q

What is the MOA of Zileuton?

A

Leukotriene antagonist
Inhibits 5-lipoxgenase in cells of myeloid origin
inhibit formation of LT from AA
LTB4: Decrease eosinophil/neutrophil migration
LTC4, D4, E4: Decrease SMC contraction, vascular permeability, and mucus secretion

23
Q

What is the MOA of cromolyn sodium?

A

prophylaxis
Binds to mast cell & stabilize, decrease Ca2+ influx, inhibit mast cell degranulation, decrease release of LT, histamine, & SRSA, decrease infl.
Also stabilizes airway nerves to decrease hyperreactivity of bronchi. Decrease response to antigen, environment, or exercise

24
Q

What is the MOA of omalizumab?

A

Monoclonal Ab
Inhibit IgE binding to FCeRI receptor on mast cell, decrease release of infl. mediators
Decrease free IgE in serum
Decrease presentation of IgE receptors on mast cells & basophils