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Clin Med - Pulmonary > Asthma > Flashcards

Asthma Flashcards

1
Q

Etiology of asthma

A

Conductive airways disease of chronic inflammation

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2
Q

What is the negative pressure in the chest?

How is it created?

A

-4 because in the chest cavity it is 756,and the lungs are 760, so the interpleural space creates a negative 4 with the visceral pleura sticking to the lungs, and the parietal pleura sticking to the expanded chest cavity from the diaphragm contraction (expansion down)

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3
Q

How does the resistance change in the “pipes”

How does it happen in asthma?

A

Resistance is higher on the walls, thus slower, but it is overcomable if the pressure is increased
The higher the resistance, the lower the flow.
But you can increase the force by pushing out air faster to keep the flow the same… this is why asthmatics have to work harder to push the air out, and that extra energy expense can make them more tired, in addition to the increased mucous that blocks oxygen exchange.

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4
Q

The greater the resistance… what does flow do?

A

Flow “slows” which means lower FEV1

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5
Q

A wheeze is what kind of flow

A

Turbulent

More resistance than laminar

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6
Q

Describe the resistance in pipes. Adding up series and parellel, which has more. Use these numbers to tell me why…
3 In series of pipes with each resistance =2
Vs.
3 pipes in parallel each with resistance of 2

A

Parallel has less resistance because to add them, you do the reverse so…
In series: 2+2+2=6resistance
In parallel: 1/2+1/2+1/2= 1.5 resistance

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7
Q

1 trachea, how many small airways

A

Several thousand less than 2mm diameter

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8
Q

Trachea have higher or lower resistance than bronchioles?

A

Higher resistance, because it is not in parallel, but bronchioles are

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9
Q

Air way resistance _________(rises or falls) when the lung is reaching capacity.

A

Falls because we are pulling the airway open to a larger volume

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10
Q

Because even diseased airways are stretched open to a wider size, and that means it is earlier to get air in, or out?

A

Easier in because when they are expanded, they have less surface area to volume, so resistance on the way in is less

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11
Q

Why do people with COPD and asthma purse their lips when they exhale?

A

They’re trying to keep the pressure up in their airways to make exhale easier since that will make the airway stay expanded so they get less resistance.

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12
Q

What can the body do to change the distribution of air flow if a certain area is compromised, say by being filled with blood after a car accident?

A

It can bronchoconstrict with the vagal (parasymp) innervation, using ACh/ methacholine,
Also can use histamine, and it will constrict if it detects a decrease in PACO2.

It can bronchodilate with beta2 adrenergic receptors.

Matching blood flow to perfusion

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13
Q

Asthma is worse during the day!
True or false
Explain the mechanism why

A

False. Less Catecholemines (NE,Epi, DA) at night and early morning hours… the catecholomines are sympathetic, and so they are less active at night so we can rest, but they also bronchidilate… less dilation= more asthma, waking asthmatics up to cough

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14
Q

Why are allergies related to asthma?

A

Because histamines bronchoconstrict, creating wheezing… turbulent breath …aka asthma with exhalation .

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15
Q

Forced vital capacity maneuver is normal if it can be done in…

A

3 seconds… it is really the airway resistance that is normal if they can complete the FVC expiration in 3seconds

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16
Q

Most people just look at FEV1, and FEV, and the ratio of FEV1/FEV, but Dr. Delaney thinks we should also look at…

A

The middle section of the breath, especially if FEV1 and the FEV1/FEV ratio is normal.
This is the MMEFR: maximum mid-expiration flow rate aka FEF25-75.

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17
Q

Why should we also look at MMEFR?

A

Because it is better insight into the small airways, so particularly important for asthma and COPD

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18
Q

FEV= ____-_____= ______

All those acronyms from the breathing graph made by electronic spirometers

A

FEV = FVC=TLC- RV

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19
Q

How do we suspect people have asthma?

A

Compare expected FEV1/FEV to the patient’s, and it will be lower than expected.

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20
Q

How does the residual volume in patients with asthma change during an attack/ in general?

A

The residual volume is increased compared to expected for age and height because they are blowing out hard and fast, so there is more air trapped behind.

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21
Q

In a flow volume loop, why does the slope decrease in the expiration?

A

Loosing the driving pressure, and the airways are getting smaller, so it’s harder to push the last part of the air out.

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22
Q

A peak flow meter can also tell you if they have max effort by…

A

Looking at the initial curve… should go highest at beginning. If not they either didn’t inhale enough, or blew out too slowly.
See slide 21 for graphic

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23
Q

How do you know if someone has an obstructive ventilate defect?

A

FEV1/FEV is lower than 70%

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24
Q

The lower the level of ventilation to perfusion, (V/Q) the _______ hypoxemic, and the _______ the CO2 will be. What are asthmatics?

A

More hypoxemia and higher CO2

As air obstruction grows, more hypoxemic.

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25
Q

Three mechanisms in asthma/ COPD that make it obstructive, and which does asthma have?

A

1) More secretions than can be cleared
2) Inflammation of the wall, swelling and impinging lumen
3) breakdown of surrounding tissue, only in COPD

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26
Q

How does the national asthma education and prevention program classify severity of asthma?

A

Defined as “a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyper-responsiveness, and an underlying inflammation. The interactions of these features determines the clinical manifestations and severity, and response to to treatment.”

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27
Q

What are some common triggers for asthma symptoms

A

Viral infections, cold air, allergens, tobacco smoke, exercise, stress, night/ parasympathetic

28
Q

Our current treatment goals for asthma is to treat symptoms, prevent attacks, and prevent__________

A

Remodeling from scar tissue from long term inflammation. This is done with steroids, and symptomatic treatment is with adrenergics.

29
Q

What wbc is high in asthmatics?

A

Eosinophilia disease. Because… allergies

Maybe also good at attacking parasites. ;)

30
Q

Which th cells are seen in asthma?

A

Th2 are more, but both are present always… the allergic response shifts to a TH2 predominance, and they are producing interlukens, which perpetuate the inflammation cycle and make more eosinophils, which make more interlukens .etc…

31
Q

When a patient is not having an attack their inflammation isn’t present, unlike in COPD.
TRUE OR FALSE.

A

False. Well… kind of.. it is true that COPD has a higher inflammation and obstruction chronically, but asthma varies. however, this is false since the inflammation doesn’t go away completely because there is not cure.

32
Q 
Pathophys of asthma...
Air way resistance is \_\_\_\_\_
In or expiration is limited
Energy expenditure goes \_\_\_\_\_ to breathe
What does the distribution of ventilation do?
A 
Resistance is Up
Expiration is limited
Harder work to breathe from inflammation and increased secretions, and hard to breathe out.
Non uniform distribution of ventilation
(V/Q mismatch, low v/q develop
Localized alveolar hypoxia)
33
Q

What muscles let an asthmatic develop higher force of expiration

A

Scalenes, SCM, intercostals( accessory muscles) which work to expand rib cage and clavicles higher to further expand area of lung.

34
Q

Poiseille’s law is different in the lungs because…

A

the length increases resistance, but the smaller pipes which have higher SA :V are in parallel, so less overall resistance.

35
Q

Why do people with asthma and COPD purse their lips?

A

To maintain a positive pressure to make exhalation easier. More pressure keeps their volume up as they are exhaling. Doesn’t solve the problem, but it helps

36
Q

Hallmark diagnostic for asthma vs. other obstructive diseases

A

allergy related, night time coughing, FEV1/FVC is under 75%, have exasurbations, and feel breathless, and chest tightness.

37
Q

Why do asthmatics cough at night

A

because their constriction is parasympathetic, which is more active at rest, so their bronchioles are constricting under Acetylcholine. Also from histamines.

38
Q

What other things are asthma patients likely to have

A

can be related to nasal polyps, skin allergies, eczema, familial allergies, environmental exposure, sinusitis, GERD, possibly sleep apnea

39
Q

normally it takes ___ seconds to expel FVC

A

3.

40
Q

Why does FEV1/FVC tell us it might be asthma?

A

Because if it is low ratio that means it has a high resistance to get the air out, and there is air trapping.

41
Q

If FEV1/FVC is normal but you still suspect asthma, what can you look at?

A

the second half of forced expiration. aka FEF25-75. aka MMER. That will tell us what is happening in the distal airway

42
Q

When we already know a patient has asthma, why would we use a spirometer

A

To see how bad an attack is… to quantify how bad, and compare it to their normal.

43
Q

Asthma is constrictive. True/false

A

False… it’s obstructive, even though it may feel constrictive in the throat, the real problem is the air trapping in the bronchioles

44
Q

What cellular changes happen with asthma?

A

Eosinophil disease. They mediate inflammation. Also T-lymphocytes. Also the lining of the bronchioles change. Develop larger mucus cells and goblet cells, and constrict, so it’s a double whammy to the lumen’s size. Tripple whammy if asthma not managed, can develop scarring in lungs.

45
Q

What are the triggers for non-alergeic asthma

A

rhinovirus, cold air, exercise, smoke, pollution, parasympathetic stimulation,
Also mouse poop, cockroaches, dust mites could all become allergens… increased asthma in developed countries in urban env’s especially in low income communities.

46
Q

Etiology and Pathophys of asthma

A

obstructive disease of chronic inflammation of the bronchioles. The nature of asthma is that there are periods where FEV1 is fine, and during an acute attack where it falls.

47
Q

Differential diagnosis for Asthma for kids vs. for adults

A

Kids: foreign body inhalation, tumor, bronchiolitis, CF, heart disease

Adults: COPD, COPD/asthma overlap, CFH, Pulmonary embolism, mechanical obstruction (tumor), pulmonary infiltrates wit eosinophils, vocal cord dysfunction, ACE inhibitors, emphysema, Sarcoidoisis, Bronchiectasis

48
Q

What is FEV1/TVC for asthma, vs. restrictive vs. normal

A

FEV/VC is 42% for asthma (during a BAD attack, and obstructive disease), vs. 90% in restrictive, and 80% in normal lungs. MMFR for normal lungs is (change in volume/change in time) in the second half of the breath is 3.5

49
Q

What else can you test if you suspect asthma, and FEV1 is normal?

A

MEthylcholine challenge test, Shows that the airway smooth muscle is more reactive than normal. Use Methyl Choline (can use histamine) at varying doses, and watch for airway constriction (Falling FEV1). Normal people only get that at very high dosages, asthmatics get very low dose change.

50
Q

What other test with an improvement of symptoms points you towards asthma?

A

Short acting bronchiodialater, and repeat every 15min. Expect 12% improvement in airflow from baseline, plus an absolute improvement of 200ml in both FEV1 or FVC.
(Occasionally can be seen in COPD.)
Flow volume loop should be linear after FEV1 flow, but if asthmatic, there is a concavity to it. Bronchodilator should improve that scoop out.

51
Q

How do you classify severity of patient’s asthma? What can this info be used for?

A

National Asthma Education and Prevention Program: look at the same 4 questions as management to know if step up or step back meds.
1) How often do you have daytime symptoms?
2) How often do you wake at night?
3) How often are you using rescue therapy?
4) Any limitation of activity from asthma?
Shouldn’t have more than 2 of any of these per week.

52
Q

Longterm goal for asthma, and what other things to consider during an assessment.

A

1) control symptoms,
2) normalize function
3) reduce risk of future exasturbation
Consider cost, transportation, culture, health literacy. ALWAYS ask how much they are using and to demonstrate their method

53
Q

NAEPP’s management components

A

1) Do PFT, spirometry, PE (skin, lungs, EENT), Hx, Pt report, to diagnosis/ assess characteristics and severity to monitor if it is being controlled.
2) Educate pt as partnership model in care
3) Control env’tal factors and comorbidity
4) Pharma therapy.
a. Bronchiodilators,
b. Anti-inflammatories

54
Q

what decreases probability of asthma diagnosis?

A

Decreased probability if chronic sputum, chest pain, isolated cough with no other respiratory symptoms, light headedness, peripheral tingling, stridor with exercise-induced dyspnea

55
Q

Tx for exercise asthma

A

prophylaxis Albuterol 10-15min before exercise. Amt of heat energy expended to warm up air and humidify it. Colder air worse.

56
Q

Stepwise management for asthma… primary control

A

1) Consider ICS- low dose
2) Low dose ICS possibly add leukotriene receptor agonist.
3) LD ICS + LABA
4) Med-high ICS/ LABA
5) Refer for add on Anti-E, or Anti-IL5

57
Q

Stepwise for emergency treatment

A

1) SABA
2) SABA
3) SABA/ICS/ Formoterol
4) same as above
5) same as above

58
Q

Secondary Tx in addition or instead of Primary drugs

A

1) nothing else
2) Leukotriene receptor antagonist,
3) low dose theophyline
Med/high ICS, or Low ICS+LTRA/theophyline
4) Add iotropium (anticholinergic), or High dose ICS+LTRA/theophyline
5) Add low dose OCS

59
Q

SABA

A

A. Short Acting Beta Agonists: Albuterol, Levabuterol, Terbutaline, Epinephrine

a. 1st line treatment for acute attacks. 2-5min most effective, fast bronchodilator
b. Works by inhibiting release of bronchospasm mediators, increase ciliary movement, decrease airway resistance and edema

60
Q

Anticholinergics

A

A. central bronchiodilator Iptratropium

a. Good for Acute needs, inhibits nasal secretions, and opens bronchus

61
Q

Corticosteroids

A

1) Oral/IV: Prednisone, Methylprednisone, Prednisolone: Anti-inflammatory
Short use for exacerbations (unless very mild, contraindicated, or just on them recently/ chronically)
2) Inhaled:Long term Beclomethasone, Flunisolide, Trimcinolone
** DRUG OF CHOICE for LONG TERM, CHRONIC MAINTANANCE

62
Q

LABA

A

A. Long-acting bronchodilators/ Beta Agonists Bronchiodilator that prevents nocturnal asthma

a. Salmeterol (also used for emphysema/ COPD)
b. ICS/LABA combos: Symbicort (Budenoside & Formoterol), Advair (Fluticasone & Salmeterol)

63
Q

Anti-inflammatory agents:

A

a. steroids, glucocorticosteroids: inhaled for longterm control of asthma and inflammation
b. Amalizumab: anti-IgE antibody used to control severe uncontrolled asthma.
c. Mast Cell modifiers
1. Cromolyn, Nedocromil
1. Inhibits mast cells and leuukotriene-mediated degranulation. *Prophylaxis only ** helps with cold air, exercise asthma

64
Q

Leukotriene

A

Leukotriene modifiers/ receptor antagonists (LTRA)

a. Montelukast, Zafirlukast, Zileuton helpful for allergic rhinitis/ aspirin induced asthma
1. Blocks leukotriene- mediated neutrophil migration, cap permeability, smooth muscle contraction by inhibiting leukotriene receptors

65
Q

Phosphodiesterase inhibitors

A

all I know is viagra…vasodilator

66
Q

science about LABA used alone

A

no help. have to use with ICS… better than doubling ICS.

Clin Med - Pulmonary (13 decks)

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