Mehlman asthma (09-27) (1)

Question 1

What happens?

Answer 1

Bronchospasm that occurs either idiopathically/hereditarily, or in
response to certain allergens or cold air.

Question 2

CP in 1/3 patients? how called?

Answer 2

One-third of patients with asthma only present with a dry cough and no problems breathing. This is called cough-variant asthma. It will often present as a patient with a dry cough that’s worse in the winter.

Question 3

Asthma in atopy. CP?

Answer 3

Can also present as part of atopy constellation – i.e., dry cough in
winter, seasonal allergies / rhinoconjunctivitis / urticaria in spring, and eczema in summer.

Question 4

Aspirin-induced asthma mechanism HY for USMLE. what is it?

Answer 4

inhibition of COX by aspirin –> shunting of arachidonic acid down lipoxygenase pathway –> increased leukotrienes –> increased bronchoconstriction.

Question 5

What is Samter triad?

Answer 5

aspirin allergy, asthma (due to aspirin), nasal polyps.

Question 6

aspirin allergy, asthma (due to aspirin), nasal polyps. how called triad?

Answer 6

Samter triad

Question 7

“Increased expiratory phase” is buzzy word for few asthma vignettes.
It is not specific for asthma and can refer
to any obstructive pathology, but I just make note of it here because you’ll see it quite a bit for asthma.

Answer 7

.

Question 8

“Increased expiratory phase” what does it mean?

Answer 8

in obstructive conditions, it takes us a lot longer to exhale (FEV1 is decr. decr. (2 arrows)).

Question 9

Acutely, asthma causes what dearagements? ph , CO, HCO3?

Answer 9

acute respiratory alkalosis
decr. CO2
incr. pH
non chage bicarb

Question 10

why acute respiratory alkalosis?

Answer 10

Even though the patient is having difficulty
breathing, CO2 diffuses quickly, whereas O2 diffuses slowly, so insofar as the patient’s respiratory rate is ­, CO2 will be decr.

Question 11

why in acute respiratory alkalosis bicars not changed?

Answer 11

Bicarb is unchanged because it takes the kidney about a day to alter excretion

Question 12

in contrast, why CO2 incr. in COPD?

Answer 12

In contrast, CO2 is ­ in COPD because there is large amounts of hypoxic vasoconstriction due to excessive mucous (chronic bronchitis) or decr. alveolar surface area, so CO2 can’t get out, even with faster breathing.

Question 13

Whats about surface in asthma?

Answer 13

In asthma, alveolar surface area is intact, and the degree of mucous production and hypoxic vasoconstriction is not nearly as bad as chronic bronchitis

Question 14

The combination of decr. CO2 and decr. O2 in acute asthma attack is known as what?

Answer 14

Type I respiratory failure.

Eventually, the patient will begin to fatigue and breathing rate will slow.

Question 15

once patient will begin to fatigue and
breathing rate will slow. what changes of O2 and CO2?

Answer 15

This will be observed as CO2 and pH rebounding to normal levels despite O2 remaining low.

This means the patient is in transition to a type II respiratory failure (i.e., hypoventilation), where we have incr.­ CO2 and decr. O2.

Question 16

Worsening asthma. Patient from Type I progresses to type II respiratory failure. What intervention usmle wants?

Answer 16

INTUBATION

Question 17

2CK Q gives vignette of asthma and then asks for best initial step in
diagnosis -> answer = ?

Answer 17

Spirometry

The expiratory component of the curve, as discussed earlier, will appear concave.

Question 18

Should be aware ……. can also be done to diagnose.

Answer 18

methacholine challenge

Question 19

what is metacholine?

Answer 19

This is a muscarinic agonist that bronchoconstricts and can induce
symptoms.

Question 20

never give metacholine in what case?

Answer 20

Never give during acute episode. This can be tried between episodes.

Question 21

Dx. instrumental - spirometry.
medication - metacholine chalange.
if usmle force to choose diagnostic modality - which one?

Answer 21

go with simple spirometry.

Question 22

USMLE cares about both outpatient management of asthma as well as acute attacks

Answer 22

.

Question 23

For outpatient management.
First line Tx for acute attacks?

Answer 23

b2-agonist (albuterol)

Question 24

For outpatient management.
If the Q says the patient has weekly episodes, or they ask for what could decrease risk of future episodes if patient is already on albuterol, the answer is?

Answer 24

the answer is inhaled corticosteroid (ICS; i.e., fluticasone)

Question 25

For outpatient management.
If the combo of albuterol + ICS is insufficient, the next step?

Answer 25

Increasing ICS dose

Question 26

For outpatient management.
Ifc ombo of albuterol + ICS –> incr. ICS –> still not effective, whats the next step?

Answer 26

Adding a LABA (i.e., salmeterol) is the
next step.

Question 27

For outpatient management.
SABA + high dose ICS + LABA –> non effective –> next step?

Answer 27

If insufficient, agents such as mast cell stabilizers, leukotriene blockers, etc., can be tried. If patient has Hx of aspirin allergy,
the latter in particular can be effective.

Question 28

For outpatient management.
If patient has aspirin allergy, what medication can be beneficial?

Answer 28

Leukotriene blockers
If patient has Hx of aspirin allergy, the latter in particular can be effective.

Question 29

For outpatient management.
the last resort Tx?

Answer 29

6) Last resort for outpatient asthma is oral prednisone. It is most effective at decreasing recurrence of episodes, but we want to avoid it if at all possible because of the risk of Cushing syndrome and decr. linear bone growth in Peds.

Question 30

For outpatient management.
what is the most effective at decreasing reccurence?

Answer 30

oral prednisone.

Question 31

Acute management of severe asthma attack (i.e., not outpatient) is …?3

Answer 31

nebulized albuterol, oxygen, and IV methylprednisolone.

Question 32

Inhaled corticosteroids role in acute asthma management?

Answer 32

have no role

Question 33

NBME for 2CK wants you to know that any asthma patient who requires
hospital management for an acute episode must automatically be given
…….. ON DISCHARGE.

Answer 33

ICS (i.e., fluticasone).

In other words, if patient isn’t currently on an ICS, it must be commenced at discharge. I’m explicit here because this particular NBME Q doesn’t mention albuterol anywhere in the stem, but inhaled fluticasone is the answer

Question 34

Another 2CK NBME Q gives a patient who is currently not receiving any asthma medications but who gets 2+ episodes weekly -> answer =?

Answer 34

“inhaled fluticasone + albuterol.”

Students think this is weird because they jump straight to dual management + are even audacious enough to put the ICS before albuterol in the wording of the answer, but it’s what they want.

Question 35

Any patient with 2+ episodes per week needs ICS in addition to the albuterol and can be commenced right away on dual therapy.

Answer 35

.

Question 36

Asthma (outpatient) –> for immediate Mx what?

Answer 36

albuterol (short-acting beta-2 agonist; SABA)

Question 37

outpatient sequence:
1) SABA; then?

Answer 37

low-dose ICS

Question 38

outpatient sequence:
1) SABA; then
2) low-dose ICS; then?

Answer 38

3) maximize dose ICS;

Question 39

outpatient sequence:
1) SABA; then
2) low-dose ICS; then;
3) maximize dose ICS; then?

Answer 39

LABA

That initial order is universal

Question 40

outpatient sequence: last resort?
most effective?

Answer 40

oral corticosteroids

however they are most effective.

Question 41

12M has ongoing wheezing episodes -> Tx?

Answer 41

albuterol inhaler

Question 42

12M has ongoing wheezing episodes + is on albuterol inhaler; next best step? –>?

Answer 42

add low-dose ICS.

Question 43

12M has ongoing wheezing episodes + is on albuterol inhaler; what’s most likely to decrease recurrence –> ?

Answer 43

oral corticosteroids

Question 44

After the LABA and before the oral steroids, any number of agents can be given in any order – i.e., nedocromil or cromolyn sodium, zileuton, montelukast, zafirlukast.

Answer 44

.

Question 45

MOA of nedocromil and cromolyn sodium –> ?

Answer 45

mast cell stabilizers

Question 46

mast cell stabilizers?

Answer 46

nedocromil and cromolyn sodium

Question 47

MOA of zileuton –>?

Answer 47

lipoxygenase inhibitor (enzyme that makes leukotrienes from arachidonic acid).

Question 48

lipoxygenase inhibitor (enzyme that makes leukotrienes from arachidonic acid).?

Answer 48

MOA of zileuton

Question 49

MOA of the -lukasts –>?

Answer 49

leukotriene LTC, D, and E4 inhibitors.

LTB4 receptor agonism is unrelated and induces neutrophilic chemotaxis (LTB4, IL-8, kallikrein, platelet-activating factor, C5a, bacterial proteins).

Question 50

leukotriene LTC, D, and E4 inhibitors.?

Answer 50

MOA of the -lukasts

Question 51

16M goes snowboarding all day + takes pain reliever for sore muscles afterward + next day develops wheezing out on the slopes again; what’s going on?

Answer 51

took aspirin + this is Samter triad (now cumbersomely known as aspirin-exacerbated respiratory disease [AERD])

Just to be clear, other NSAIDs can precipitate Samter triad, but the literature + USMLE will make it explicitly about aspirin.

Question 52

16M takes aspirin + gets wheezing; what are we likely to see on physical exam? –> answer ?

Answer 52

answer on USMLE = nasal polyps.

Question 53

aspirin knock out COX irreversibly by giving aspirin (or reversibly with another NSAID),

Answer 53

.

Question 54

Kid has Hx of AERD; physician considers agent to decrease his recurrence of Sx –> what drugs?

Answer 54

zileuton, or -lukasts (both are correct; and only one will be listed).

Question 55

Kid has Hx of AERD; what agent is most likely to DECREASE HIS RECURRENCE of Sx - what drug?

Answer 55

oral steroids

exceedingly HY

Question 56

oral steroids nasty adverse?

Answer 56

Cushing syndrome

Question 57

Any weird asthma Txs? –> omalizumab.
when use?
what CP/lab?

Answer 57

used for intractable, severe asthma unresponsive to oral steroids + in patients who have eosinophilia + high IgE levels

Question 58

Acute asthma Mx (emergencies) –> most important piece of info straight-up is: what has no role?

Answer 58

USMLE wants you to know that inhaled corticosteroids (ICS) have no role in acute asthma management.

Question 59

Acute asthma Mx (emergencies): first thing we do?

Answer 59

First thing we do is give oxygen (any USMLE Q that shows depressed O2 sats, answer is always O2) +
nebulized albuterol (face mask with mist);
+
IV steroids are THEN administered.

Question 60

Acid-base disturbance in asthma? initially

Answer 60

respiratory alkalosis –> low O2, low CO2, high pH, normal bicarb.

low CO2 is due to high respiratory rate; even if your bronchioles are constricted + filled with secretions, CO2 can diffuse really quickly

in contrast, O2 diffuses slowly and requires healthy airways;

that’s why with a high RR, O2 and CO2 are both low (O2 can’t get in, but CO2 can still get out); 19 times out of 20 on the USMLE, if your respiratory rate is high, CO2 is low.

Question 61

Dry cough in winter + eczema in summer + seasonal allergies in winter; what is the cough? –> Dx?

Answer 61

cough-variant asthma (1/3 of asthmatics only have cough).

Question 62

Young African American woman + dry cough + normal CXR - Dx?

Answer 62

asthma (activation of mast cells), not sarcoidosis.

Question 63

Young African American woman + dry cough + nodularity on CXR –> Dx?

Answer 63

sarcoidosis (non-caseating granulomas).