+

Asthma Case StudyCourtney RamseyJennifer MartinLisa G. CastroNing Huang Stella Cooremans-PenaRosimeire Sawyer

Group 7

+An Asthma Attack

+Background

Jenny, 14 yr old female Spent the night at a friends house Exposures:

Friends father smokes

Current Medications: Fluticasone inhaler BID Albuterol HFA PRN

Allergies: Sulfa (rash)

+Patient Histories

Past Medical History Asthma:

Well controlled Diagnosed at age 10

Sinusitis: Gets 2-3 times per year

Past Surgical History None

Social History Lives at home with parents No regular exposure to 2nd

hand smoke Family History

Grandfather: COPD Secondary to smoking No longer smokes

+November 7, 2013

Patient presented to an emergency walk in clinic in the middle of the night

Chief complaint: “I’m having trouble breathing”

Physical Exam: Neuro: Anxious, Difficulty

Speaking, PERRLA CV: Tachycardia, no murmur Resp: Bilateral high-pitched,

diffuse expiratory wheezing Using accessory muscle Moderate resp. distress

GI/GU/Oral: Mild Oral Thrush All other systems normal

Vital Signs: Temp: 36 C HR 110 BP 124/70 Pulse Ox : 88% on Room Air

Precipitating Events: Patient had spent the night at

a friends house Recent exposure to 2nd hand

smoke Woke up with severe SOB and

nonproductive cough Did not have her

bronchodilator medication with her

+

Question 1

Analyze the pathophysiology of asthma and relate it to the category of obstructive vs. restrictive pulmonary disorder.

+Obstructive vs. Restrictive Pulmonary DiseaseObstructive RestrictiveCharacterized by an increase in resistance to airflow due to partial or complete obstruction

Characterized by reduced expansion of lung parenchyma accompanied by decreased total lung capacity

Total lung capacity normal DecreasedCompliance of the lung is normal

Reduced

FEV1 is decreased Normal or reduced proportionately

FEV1/FVC ratio is decreased Normal Asthma, chronic bronchitis, bronchiectasis, emphysema, and small-airway disease

Chest wall disorders: pleural diseaseChronic interstitial and infiltrative diseases: interstitial fibrosis

+ Pathophysiology of Asthma

• Genetic predisposition to type 1 hypersensitivity

• Exposure to environmental triggers (second hand smoke)

+ Pathophysiology of AsthmaInhaled allergen simulates induction of TH2 cells.

Kumar (2010) et al: Fig 6-11, p195

+ Pathophysiology of Asthma• TH2 cells secrete cytokines that

promote allergic inflammation and stimulate B cells to produce IgE and other antibodies.

TH2 cells

cytokines

IL-4

Stimulates the production of IgE by B cells

IL-5

Activates recruited eosinophil

IL-13

Stimulates mucus secretion and promotes IgE

production by B cells

+ Pathophysiology of AsthmaPriming or sensitization

+ Pathophysiology of Asthma

• IgE coats submucosal mast cells and repeat exposure to the allergen triggers the mast cells to release granules contents and produce cytokines and other mediators which induce the early phase reaction and the last phase reaction.

+Pathophysiology of Asthma Early phase reaction:

• Result within one hour• Mast cells release

mediators (histamine, leukotriene, prostaglandins, enzymes).

• Bronchoconstriction• Increased vascular

permeability• Increased mucus

production

Kumar (2010) et al: Fig 15-10D, p690

+ Pathophysiology of Asthma Late-phase reaction:

• Mast cells, epithelial cells, T cells, and other cytokines produce chemokines to recruit leukocytes

• Inflammation with recruitment of leukocytes

• Mediators released from leukocytes, endothelium and epithelial cells in late reaction

Kumar (2010) et al: Fig 15-10 E, p690

+ Pathophysiology of Asthma

• Repeated bouts of allergen exposure and immune reactions result in structural changes in the bronchial wall called airway remodeling

+ Pathophysiology of Asthma

• Excess mucus• Intense inflammation• Smooth muscle

hyperplasia and hypertrophy

+ Pathophysiology of Asthma• Over thickening of

airway wall• Increase in size of

submucosal glands• Sub-basement

membrane fibrosis• Increased vascularity• Hypertrophy and/or

hyperplasia of the bronchial wall muscle

Kumar (2010) et al: Fig 15-10 B, p690

+

Question 2

Discuss the hypersensitivity trigger of asthma and contrast with the risk factors in this teenager.

+Common Asthma Triggers Tobacco Smoke

Tobacco smoke is unhealthy for everyone, especially people with asthma

If you have asthma, people should never smoke near you Dust Mites Cockroaches Allergen

Cockroaches and their droppings can trigger an asthma attacks

Outdoor air pollution Pets Mold Smoke – burning wood or grass Other Triggers

Infections: Flu, RSV, Sinus Infections Bad Weather, Physical Exercise Acid Reflux, Strong Fragrances Strong Emotions

+Asthma Triggers

History of Asthma Diagnosed at Age 10 Frequent Sinusitis

Exposure to secondhand smoke Spent the night at a friends house whose father is a

smoker

Family History Grandfather: COPD

Secondary to smoking No longer smokes

Patient Risk Factors

+

Question 3

Compare and contrast the typical manifestations of asthma with those seen in this case. Include pathologic etiology of each manifestation.

+Manifestations of Asthma

Wheezing Coughing Chest tightness Shortness of breath

Severe shortness of breath with difficulty speaking

Unproductive cough Tachycardia, heart rate 110 Tachypnea, respiratory rate 24 Anxiety Hypoxia, oxygen saturation on room

air 88% Bilateral high-pitched, diffuse

expiratory wheezing Use of accessory muscles

Typical Manifestations Patient’s Manifestations

Typical manifestations data (Kumar et al., 2010)

+ Etiology of Manifestations

Inflammation is triggered by anything in the environment that causes a person’s airway to hyper-react and make breathing difficult. Jenny’s trigger was tobacco smoke. The inhaled smoke elicited a TH2 dominated response. “TH2 cells secrete cytokines that promote allergic inflammation and

stimulate B cells to produce IgE and other antibodies. These cytokines include IL-4,which stimulates the production of IgE; IL-5, which activates locally recruited eosinophils; and IL-13, which stimulates mucus secretion from bronchial submucosal glands and also promotes IgE production and B cells” (Kumar et al., 2010, p. 689).

Asthma is a disease that inflames and narrows the airways of your lungs.

(1) Inflammation

+Etiology of Manifestations

Early reaction Bronchoconstriction/reversible bronchospasm (triggered by direct

stimulation of subepithelial vagal receptors Increased mucus production Variable degrees of vasodilation with increased vascular permeability

(Kumar et al., 2010)

Asthma is a disease that inflames and narrows the airways of your lungs.

(1) Inflammation

+Etiology of Manifestations

Late reaction Inflammation with recruitment of leukocytes (eosinophils), neutrophils

and T cells Leukocyte recruitment is stimulated by chemokines produced by mast

cells, epithelial cells and T cells Increased airway constriction (Kumar et al., 2010)

Asthma is a disease that inflames and narrows the airways of your lungs.

(1) InflammationImage obtained from www.gene.com

+Etiology of ManifestationsAsthma is a respiratory disease that inflames and narrows the

airways of your lungs.

Image obtained from nlm.nih.gov

(1) Swelling(2) Bronchoconstrictio

n

+Asthma at a glance

Narrowed

airway

•Limited airflow: SOB, wheezing, Tachypnea, tachycardia & anxiety.Tighten

ed muscle

s

•Constricted airway: respiratory distress, difficulty talking, use of accessory muscles.Inflame

d airway

wall

•Inflamed airway wall: mucus production, cough.

+Facts on second hand smoking and asthma Exposure to secondhand smokingcan trigger asthma attacks

and make asthma symptoms more severe (EPA, 2013). Second hand smoking contributes to children/adolescent’s

asthma attacks more than adults due to their narrower airways (Salmun et al., 2007).

Cotinine is a nicotine byproduct that has been found in saliva, urine, and blood of children/adolescent exposed to secondhand smoking (Salmun et al., 2007).

Children with asthma who are exposed to secondhand smoking have asthma that is harder to control, even with medication (Jarvey et al., 2008)

+Question 4

Discuss the results of the diagnostic studies in this case and the relationship to asthma.

+

Patient’s Diagnostic Studies

Chest X-ray Hyperluscent Hyperinflated lungs No infiltrates present

Lab Values : Patient Value :: Normal Value Chemistry : WNL H&H : WNL WBC : 8.0 x 103/mm : 4-10 X

103mm PMN : 56% : 50 – 65% Bands :1% : 0 – 5 % Eosinophils : 4% : 0 – 3 % Basophils : 2 : 1 – 3 % Lymphocytes : 32 % : 25 – 35 % Monocytes : 5% : 2 – 6 %

+

Correlating The Abnormal Lab Values and Patient “Jenny”

Abnormal Chest X-Ray Related to air-trapping due to bronchial

constriction Increased air volume is due to:

Bronchial constriction and air trapping This causes the image to become

hyperluscent

Eosinophils Slightly elevated

Possibly due to allergies These are the predominate inflammatory

cells in allergic reactions Causes of eosinophilia

Allergic reactions Asthma Hay fever Hives

+Question 5What is the FEV1/FVC ratio?  Discuss what these means in this case and analyze the results as they related to obstructive vs. restrictive lung disorders.

+Forced Vital Capacity

FVC (Forced Vital Capacity) -- This is the total volume of air expired after a full inspiration. Patients with obstructive lung disease usually have a normal or only slightly decreased vital capacity. Patients with restrictive lung disease have a decreased vital capacity.

FEV1 (Forced Expiratory Volume in 1 Second) -- This is the volume of air expired in the first second during maximal expiratory effort. The FEV1 is reduced in both obstructive and restrictive lung disease. The FEV1 is reduced in obstructive lung disease because of increased airway resistance. It is reduced in restrictive lung disease because of the low vital capacity.

FEV1/FVC -- This is the percentage of the vital capacity which is expired in the first second of maximal expiration. In healthy patients the FEV1/FVC is usually around 70%. In patients with obstructive lung disease FEV1/FVC decreases and can be as low as 20-30% in severe obstructive airway disease. Restrictive disorders have a near normal FEV1/FVC.

DLCO (Diffusing Capacity of the Lung for Carbon Monoxide) -- Carbon monoxide can be used to measure the diffusing capacity of the lung. The diffusing capacity of the lung is decreased in parenchymal lung disease and COPD (especially emphysema) but is normal in asthma.

+Spirometry

Should be done on: Initial diagnosis After treatment is started & symptoms have stabilized Every 1 to 2 years

Spirometry is used to measure the rate of airflow during maximal expiratory effort after maximal inhalation. Can be useful in differentiating obstructive and restrictive lung disorders. In asthma (obstructive disorder):

forced expiratory volume in 1 second (FEV1) is: decreased forced vital capacity (FVC) is : normal ratio FEV1/FVC is : decreased.

In restrictive disorders: The FEV1 and FVC are both decreased Leaving a normal FEV1/FVC.

With the use of a bronchodilator will demonstrate: An increase in FEV1 of 12% or 200 ml.

Patients with severe asthma may need a short course of oral steroid therapy before they demonstrate reversibility.

Provides an objective assessment of airflow obstruction and is important in staging asthma severity.

+Lab Results

Tidal Volume (TV)                               350 cc Inspiratory Reserved Volume (IRV)    1600 cc Expiratory Reserved Volume (ERV)    400 cc IRV + ERV                                            1900cc Forced Vital Capacity (FVC)                2300 cc  

FEV1                                                     950 cc  

FEV1/FVC ratio                                    0.41     Less than .7 is accepted as being diagnostic

of significant airflow obstruction DLCO                                                   Normal

IRV + ERV   900 cc

Forced Vital Capacity (FVC) 2800 cc

FEV1   2200 cc

FEV1/FVC ratio  0.79

Before Receiving Treatment After receiving bronchodilator :

+Videos

Good, Long, Detailed Asthma Review

An Asthma Attack

Basic Asthma Information

Asthma Animation

+References Allen, J. Interpretation of pulmonary function tests. Retrieved October 17, 2013,

from www2.kumc.edu/internalmedicine/...InterpretofPulmFunctionTests.doc Altinsoy,B., Altintas,N. (2011). Diagnostic approach to unilateral hyperlucent

lung. Journal of the Royal Society of Medicine, 2 (12), 95-98.

Jarvie, J., & Malone, R. (2008). Children’s secondhand smoke exposure in private homes and cars: An ethical analysis. American Journal of Public Health, 98 (12),2140-2145.

Kumar, V., Abbas, A.K., Fausto, N., Aster, J.C. (2010). Robbins and Cotran pathologic basis of disease (8th ed.). Philadelphia, PA: Saunders Elsevier.

Salmun, L., Chilmonczyk, B., Megathlin, K., Haddow, J., & Pulkkinen, A. (2007). Association between exposure to environmental tobacco smoke and exacerbations of asthma in children. Journal of Medicine, 328 (23), 165-169.

+References The Centers for Disease Control and Prevention. (2013). 

Asthma basic information: frequently asked questions. Retrieved from http://www.cdc.gov/asthma/faqs.htm.

UC San Diego School of Medicine. (1998). Pulmonary function tests. Retrieved October 17, 2013, Retrieved from meded.ucsd.edu/isp/1998/asthma/html/spirexp.html

United States Environmental and Protection Agency (EPA). (2013). Secondhand smoke and its affects in children. Retrieved from http://www.epa.gov

Wai, Y.C., Sau, F.N., Emily, T.L., Yiu, Y.C., Kwok, K.C., Yui., Cheuk, T.M., and Yuk, Y.k. (2013). Spirometry is underused in the diagnosis and monitoring of patients with chronic obstructive pulmonary disease (COPD). International Journal of Chronic Obstructive Pulmonary Disease, 8, 389-395.

+References: Images and Videos

Genentech. (n.d.). www.gene.com

Kumar (2010) et al: Fig 6-11, p195

Kumar (2010) et al: Fig 15-10C, p690

Kumar (2010) et al: Fig 15-10D, p690

Kumar (2010) et al: Fig 15-10 E, p690

Kumar (2010) et al: Fig 15-10 A&B, p690

Kumar (2010) et al: Fig 15-10 B, p690

UC San Diego School of Medicine. (1998). Pulmonary function tests. Retrieved October 17, 2013, Retrieved from meded.ucsd.edu/isp/1998/asthma/html/spirexp.html

U.S. National Library of Medicine. (n.d.). nlm.nih.gov

Asad, F. (2010). Asthma- YouTube. Retrieved October 17, 2013, from  www.youtube.com/watch?v=8gimcs19mxq

CPRFreak. (2010). Grace's asthma attack - YouTube. Retrieved October 17, 2013, from www.youtube.com/watch?v=ipg4rkikefq

NHS Choices. (2010). Asthma: An animation – YouTube. Retrieved October 17, 2013, from www.youtube.com/watch?v=7edo9puyvpe

World Medical School. (2012). Asthma- USMLE step 2 review - YouTube. Retrieved October 17, 2013, from www..youtube.com/watch?v=3d6Oyt32gpe

Images Videos