MIDTERM Resp Illnesses

Question 1

How is chronic bronchitis defined?

Answer 1

Hypersecretion of mucus and chronic productive cough for at least 3 months of the year (usu winter months) for at least 2 yrs

Question 2

WHat physical changes are occurring in the airways in chronic bronchitis? What causes the cascade of issues?

Answer 2

Inspired irritants cause airway inflammation

Infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall

Continual bronchial inflammation ->
1) bronchial edema
2) increase in size & # of mucus glands and goblet cells in airway epithelium
3) smooth muscle hypertrophy w/fibrosis
4) narrowing of airways

• thick tenacious mucus

Question 3

Why is someone with chronic bronchitis more prone to infection?

Answer 3

Lung’s defence mechanisms are impaired -> more prone to infection, injury, and ineffective repair

Frequent infectious exacerbations from bacterial colonization of damaged airways plus bronchospasm, dyspnea, productive cough

Question 4

Is inspiration or expiration particularly affected in chronic bronchitis? WHy?

Answer 4

Expiration

Thick mucus + hypertrophied bronchial smooth muscle -> constriction of airways -> obstruction of airways, especially during expiration when airways are narrowed
Airway collapse happens early in expiration, trapping gas in the distal portions of the lung (hyperinflation)

Air trapping -> decreased TV, hypoventilation, hypercapnia

Question 5

Are the pathological changes in chronic bronchitis reversible?

Answer 5

No but can prevent progression (smoking cessation)

Question 6

Differentiate chronic bronchitis and emphysema with regard to characteristic airway changes

Answer 6

CB: bronchial edema, hypersecretion of mucus, bacterial colonization of airways

Emphysema: destruction of alveolar septa and loss of elastic recoil from bronchial walls
***Obstruction from changes in lung tissues rather than mucus production and inflammation as in chronic bronchitis.

Question 7

Is the following symptom common in CB or emphysema:
CHRONIC PRODUCTIVE COUGH

Answer 7

Classic in CB
Only with infection in Emphysema

Question 8

Is the following symptom common in CB or emphysema: DYSPNEA

Answer 8

CB: late in course
E: common

Question 9

Is the following symptom common in CB or emphysema: WHEEZING

Answer 9

CB: intermittent
E: common

Question 10

Is the following symptom common in CB or emphysema: BARREL CHEST

Answer 10

CB: occassionally
E: CLASSIC

Question 11

Is the following symptom common in CB or emphysema: Prolonged expiration

Answer 11

Always present in both!

Question 12

Is the following symptom common in CB or emphysema: CYANOSIS

Answer 12

CB: common
E: uncommon

Question 13

Is the following symptom common in CB or emphysema: CHRONIC HYPOVENTILATION

Answer 13

CB: common
E: late in course

Question 14

Is the following symptom common in CB or emphysema: POLYCYTHEMIA

Answer 14

CB: common
E: late in course

Question 15

Is the following symptom common in CB or emphysema: COR PULMONALE

Answer 15

CB: common
E: late in course

Question 16

What is Cor Pulmonale?

Answer 16

abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels.

Means “pulmonary heart”

Question 17

What is the key characteristic of changes in emphysema?

Answer 17

Abnormal permanent enlargement of gas-exchange airways (acini) accompanied by destruction of alveolar walls without obvious fibrosis.

Major mechanism of airflow limitations is loss of elastic recoil.

Question 18

WHat causes PRIMARY emphysema?

Answer 18

d/t inheritable α1-antitrypsin. Usu for ppl who develop emphysema before age 40 and do not smoke.

Question 19

Patho of emphysema

Answer 19

Breakdown of elastin within septa in alveoli from imbalance of proteases and apoptosis of lung structural cells -> destruction of alveoli

This causes large air spaces within the lung parenchyma (bullae) and air spaces adjacent to pleurae (blebs) -> not effective at gas exchange

Expiration is difficult d/t loss of elastic recoil. Reduction of air that can be expired passively and air trapping occur

Air trapping -> hyperexpansion of chest -> increases workload of breathing

Later on, hypoventilation and hypercapnia

Persistent inflammation in the airways can result in hyper-reactivity of bronchi w/bronchoconstriction

Chronic inflammation -> weight loss, muscle weakness, increased susceptibility to comorbilities (I.e. infection)

Question 20

Destruction of alveolar walls & pulm capillaries leads to what complications in emphysema?

Answer 20

Pulm Art Hypertension and cor pulmonale

Question 21

A marked decrease in FEV1 means what?

Answer 21

obstruction to gas flow during expiration

Question 22

What are the 3 obstructive lung diseases?

Answer 22

Asthma, chronic bronchitis & emphysema

Question 23

When does allergic asthma vs non-allergic asthma present over lifespan?

Answer 23

incidence of allergic asthma is higher in childhood, incidence of non-allergic asthma usually occur after age 40.

Question 24

RIsk factors for asthma?

Answer 24

age at onset of disease, levels of allergen exposure, urban residence, exposure to air pollution, tobacco smoke, recurrent viral resp infections, GERD, obesity

Question 25

T/F there is a genetic component to risk of getting asthma

Answer 25

Yes more than 100 genes identified that play a role in susceptibility, pathogenesis, and treatment respons

Question 26

Is all asthma similar?

Answer 26

No, many different phenotypes

Question 27

What WBC is most associated with an asthma attack?

Answer 27

Eosinophils eosinophils release toxic neuropeptides that cause tissue injury

Question 28

WHat is happening in asthma? 3 characteristic airway changes?

Answer 28

Complex immune response to an allergen that results in: 1) mucosal edema 2) bronchial smooth muscle contraction/spasm 3) mucous secretion End result is bronchial hyper-responsiveness and airway obstruction, expiratory airflow mostly affected and causes air trapping and hyperinflation, VQ mismatch

Question 29

T/F A patient with asthma will likely have an abnormal pulmonary function test between attacks due to permanent damage

Answer 29

False - likely will be normal (though I imagine if it's untreated and frequent, permanent damage will begin to manifest)

Question 30

What triggers can create an asthma attack?

Answer 30

viral infections home allergens tobacco smoke stress exercise Cold air Laughter

Question 31

Treatment with what kind of medication in asthma is key to preventing flareups?

Answer 31

Inhaled corticosteroids

Question 32

Why don't we just give a bronchodilator in an asthma attack? How can this worsen things?

Answer 32

YOu are just opening airways, not actually dealing with the inflammation. Can inc risk of sudden resp failure as swelling worsens and eventually can't compensate GIVE STEROIDS!

Question 33

What two defining characteristics would be necessary for a diagnosis of asthma?

Answer 33

History of resp symptoms (wheeze, SOB, chest tightness, and cough) that vary over time and intensity AND Variable expiratory airflow limitation

Question 34

What is best to establish before starting on controller treatment?

Answer 34

An official asthma diagnosis! It's hard to get an official diagnosis after treatment has started

Question 35

What time of day are asthma symptoms typically worse

Answer 35

At night or on waking

Question 36

What would you expect to see in spirometry results for a diagnosis of asthma?

Answer 36

Need to document at some point that FEV1/FCV ratio is below normal limit Document variation in lung fx is greater than healthy person: FEV1 increases by >200mL and 12% of baseline after inhaling a bronchodilator (for children, just need the 12% inc) = significant bronchodilator responsiveness or reversibility Or same changes are seen after 4 weeks of inflammatory tx *The more variation that's seen, the more confident you can be in asthma diagnosis *May need to repeat testing in the morning, after witholding bronchodilators or during symptoms *May not see this response during a severe attack

Question 37

If controller treatment is already initiated, what might we have to do to confirm an asthma diagnosis?

Answer 37

Withhold meds

Question 38

What are LABAs and SABAs?

Answer 38

LABA = long acting beta agonist SABA = short acting beta agonists (Bronchodilators)

Question 39

What physical exam finding is most likely in a client with asthma (not in acute exacerbation)

Answer 39

Often normal, may have expiratory wheeze on auscultation

Question 40

How often is lung function measured following a asthma diagnosis

Answer 40

Once 3-6 months later, then every 1-2 years (more often in children and those at higher risk of flare ups or lung function decline

Question 41

What 2 meds may cause bronchoconstriction in patients with asmtha

Answer 41

NSAIDs and Beta blockers In contrast to β-agonists, β-blockers have for many years been regarded as contraindicated in patients suffering from asthma due to the potential risk of triggering bronchoconstriction

Question 42

What are the GINA recommendations for treatment of asthmas? Every adult and adolescent with asthma should have 2 things:

Answer 42

1) ICS-containing controller (even those with infrequent symptoms 2) A reliever inhaler: either SABA or low dose ICS-formoterol

Question 43

What causes acute bronchitis?

Answer 43

viral infection, upper respiratory infection, smoking, exposure to cigarette smoke, exposure to other irritants, allergens, chronic aspiration or GERD

Question 44

What viruses most often cause acute bronchitis?

Answer 44

adenovirus, influenza, parainfluenza viruses, respiratory syncytial virus (RSV)

Question 45

What are the most common bacterial causes of acute bronchitis?

Answer 45

Bordetella pertussis, Mycobacterium tuberculosis, Corynebacterium diphtheriae, Mycoplasma pneumonia. Consider B. pertussis in children who are not fully vaccinated.

Question 46

How long does acute bronchitis last?

Answer 46

acute, Usually self-limiting Clinical course normally lasts 10-14 days

Question 47

S&S of acute bronchitis

Answer 47

Fever, cough, chills, malaise, sore throat, rhinorrhea/nasal congestion, rhonchi during respiration Viral bronchitis usually has a non-productive cough, often occurs in paroxysms and is aggravated by cold/dry/dusty air Purulent sputum can be produced in some cases Chest pain (retrosternal) with coughing/deep breathing can develop from coughing S/S similar to pneumonia, but without signs of pulmonary consolidation and chest x-rays do not show infiltrates

Question 48

What is bronchiolitis?

Answer 48

Diffuse, inflammatory obstruction of small airways or bronchioles

Question 49

Who usually gets bronchiolitis?

Answer 49

Mostly children In adults, it usually happens with chronic bronchitis Still can occur with healthy people with upper/lower resp tract infections, inhalation of toxic gases, or unknown etiology

Question 50

Most common causes of community acquired pneumonia?

Answer 50

Streptococcus pneumoniae AKA pneumococcus – most common and most lethal since many virulence factors Influenza virus (haemophilus influenzae) - most common viral causes in adults Respiratory syncytial virus – most common viral causes in children Staphylococcus aureus – MRSA becoming more common Mycoplasma pneumoniae - common cause of atypical pneumonia in those living in dorms/young people

Question 51

How prevalent and dangerous is CAP? Who is most susceptible to getting it?

Answer 51

- 8th leading cause of death in Canada - One of the most common reasons for hospitalization – 36% of those with CAP require CCU admit and have mortality range of 21-58% - More prevalent in the very old and very young - Incidence and mortality are highest in the elderly - viral more common in young

Question 52

Quick patho of CAP

Answer 52

Inflammation and micro-organism toxins can damage respiratory membranes, causing acini and terminal bronchioles to fill with infectious debris & exudate, can lead to CONSOLIDATION of lung tissue, V/Q mismatch and hypoxia

Question 53

How can viral pneumonia lead to secondary bacterial infection?

Answer 53

- Viruses destroy ciliated epithelial & mucous cells so don't have intact defense from bacteria either

Question 54

How do we assess tactile fremitus and what does it indicate?

Answer 54

To assess for tactile fremitus, place the palm of the hand on the chest and have the patient say “ninety-nine” or “one-two-three.” Vibrations are increased over areas of consolidation (e.g., lobar pneumonia).

Question 55

With a chronic PE, what secondary manifestation may eventually cause a patient to present for assessment?

Answer 55

PE slowly develop symptoms of pulmonary hypertension over many years (i.e., chronic thromboembolic pulmonary hypertension)

Question 56

S&S of pulmonary embolism

Answer 56

Acute: sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia, and unexplained anxiety. Massive occlusion causes severe pulmonary hypertension and shock. Occasionally syncope and hemoptysis occur. With large emboli, a pleural friction rub, pleural effusion, fever, and leukocytosis may be noted. Chronic: recurrent small emboli may not be detected until progressive incapacitation, precordial pain, anxiety, dyspnea, and right ventricular enlargement are exhibited.

Question 57

What changes in the lungs are occurring with a PE?

Answer 57

Occlusion leads to.. Hypoxic vasoconstriction Decreased surfactant Release of neurohmornal and inflammatory substances Pulmonary edema Atelectasis

Question 58

Pulmonary hypertension has what effect on the heart?

Answer 58

Fibrosis of constricting artery --> RV hypertrophy --> R side heart failure (cor pulmonale)

Question 59

Antigenic drift vs shift

Answer 59

Antigenic drift refers to minor, progressive mutations in pre-existing combinations of HA and NA antigens, resulting in the frequent emergence of new viral strains (seasonal epidemics). Antigenic shift: major antigenic change (pandemics)

Question 60

What is pertussis and who gets it?

Answer 60

Whooping cough, caused by Bordetella Pertussis (Bacterial infection) Highest incidence in infants and children (up to 14) Infants are most at risk and get the most severe cases Infants who get pertussis are often only partially vaccinated against it

Question 61

Time course of pertussis

Answer 61

Divided into three stages: Catarrhal stage (1-2 weeks) Paroxysmal Stage (2-8 weeks) Convalescent Stage (weeks to months) - Incubation period is generally 7-10 days - Pt is infectious from beginning to 3 weeks after the onset of the cough or after 5 days of antibiotic treatment

Question 62

With respiratory illness it seems that infants have a particularly alarming symptom that is frequently seen?

Answer 62

Periods of apnea

Question 63

S&S and progression of Pertussis

Answer 63

Catarrhal Stage: runny nose, sneezing, low-grade fever, and mild cough (often mistaken for a common cold) Paroxysmal Stage: bursts of rapid coughing ending with an inspiratory whoop, sometimes post-tussive vomiting Infants may have an atypical presentation. They often do not present with symptoms of whooping or post-tussive vomiting but present with episodes of apnea) Diagnostic Symptoms: Non-productive cough that is not improving Watery runny nose Whoop, apnea, posttussive vomiting Sweating between coughing attacks Cyanosis Seizures or poor weight gain (under 4 months) Leukocytosis Pneumonia

Question 64

What time of day is whooping cough the worst

Answer 64

At night

Question 65

What is a primary spontaneous pneumo? Who does this happen most often in?

Answer 65

Usually happens unexpectedly, commonly men between 20-40 yrs. Cause usually unknown, but 80% have emphysema-like changes in their lungs (bullous emphysema) even w/out HX smoking or genetic disorder. 10% have family HX of primary pneumothorax linked mutations in the folliculin gene. Tall, thin frame.

Question 66

Who is most susceptible to a secondary spontaneous pneumo?

Answer 66

Underlying lung condition: COPD w emphysema, cystic fibrosis, lung CA, Marfan syndrome. Later in life More serious than primary as pt already has compromised resp system.