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NUNP531 Applied Pathophysiology > MIDTERM Resp Illnesses > Flashcards

MIDTERM Resp Illnesses Flashcards

1
Q

How is chronic bronchitis defined?

A

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

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2
Q

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

A

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
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3
Q

Why is someone with chronic bronchitis more prone to infection?

A

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

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4
Q

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

A

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

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5
Q

Are the pathological changes in chronic bronchitis reversible?

A

No but can prevent progression (smoking cessation)

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6
Q

Differentiate chronic bronchitis and emphysema with regard to characteristic airway changes

A

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.

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7
Q

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

A

Classic in CB
Only with infection in Emphysema

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8
Q

Is the following symptom common in CB or emphysema: DYSPNEA

A

CB: late in course
E: common

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9
Q

Is the following symptom common in CB or emphysema: WHEEZING

A

CB: intermittent
E: common

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10
Q

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

A

CB: occassionally
E: CLASSIC

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11
Q

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

A

Always present in both!

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12
Q

Is the following symptom common in CB or emphysema: CYANOSIS

A

CB: common
E: uncommon

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13
Q

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

A

CB: common
E: late in course

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14
Q

Is the following symptom common in CB or emphysema: POLYCYTHEMIA

A

CB: common
E: late in course

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15
Q

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

A

CB: common
E: late in course

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16
Q

What is Cor Pulmonale?

A

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”

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17
Q

What is the key characteristic of changes in emphysema?

A

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.

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18
Q

WHat causes PRIMARY emphysema?

A

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

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19
Q

Patho of emphysema

A

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)

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20
Q

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

A

Pulm Art Hypertension and cor pulmonale

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21
Q

A marked decrease in FEV1 means what?

A

obstruction to gas flow during expiration

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22
Q

What are the 3 obstructive lung diseases?

A

Asthma, chronic bronchitis & emphysema

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23
Q

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

A

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

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24
Q

RIsk factors for asthma?

A

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

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25
Q

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

A

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

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26
Q

Is all asthma similar?

A

No, many different phenotypes

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27
Q

What WBC is most associated with an asthma attack?

A

Eosinophils

eosinophils release toxic neuropeptides that cause tissue injury

28
Q

WHat is happening in asthma? 3 characteristic airway changes?

A

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

29
Q

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

A

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

30
Q

What triggers can create an asthma attack?

A

viral infections
home allergens
tobacco smoke
stress
exercise
Cold air
Laughter

31
Q

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

A

Inhaled corticosteroids

32
Q

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

A

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!

33
Q

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

A

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

34
Q

What is best to establish before starting on controller treatment?

A

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

35
Q

What time of day are asthma symptoms typically worse

A

At night or on waking

36
Q

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

A

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

37
Q

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

A

Withhold meds

38
Q

What are LABAs and SABAs?

A

LABA = long acting beta agonist

SABA = short acting beta agonists

(Bronchodilators)

39
Q

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

A

Often normal, may have expiratory wheeze on auscultation

40
Q

How often is lung function measured following a asthma diagnosis

A

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

41
Q

What 2 meds may cause bronchoconstriction in patients with asmtha

A

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

42
Q

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

A

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

43
Q

What causes acute bronchitis?

A

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

44
Q

What viruses most often cause acute bronchitis?

A

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

45
Q

What are the most common bacterial causes of acute bronchitis?

A

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

46
Q

How long does acute bronchitis last?

A

acute, Usually self-limiting

Clinical course normally lasts 10-14 days

47
Q

S&S of acute bronchitis

A

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

48
Q

What is bronchiolitis?

A

Diffuse, inflammatory obstruction of small airways or bronchioles

49
Q

Who usually gets bronchiolitis?

A

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

50
Q

Most common causes of community acquired pneumonia?

A

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

51
Q

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

A
  • 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
52
Q

Quick patho of CAP

A

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

53
Q

How can viral pneumonia lead to secondary bacterial infection?

A
  • Viruses destroy ciliated epithelial & mucous cells so don’t have intact defense from bacteria either
54
Q

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

A

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).

55
Q

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

A

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

56
Q

S&S of pulmonary embolism

A

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.

57
Q

What changes in the lungs are occurring with a PE?

A

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

58
Q

Pulmonary hypertension has what effect on the heart?

A

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

59
Q

Antigenic drift vs shift

A

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)

60
Q

What is pertussis and who gets it?

A

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

61
Q

Time course of pertussis

A

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
62
Q

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

A

Periods of apnea

63
Q

S&S and progression of Pertussis

A

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

64
Q

What time of day is whooping cough the worst

A

At night

65
Q

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

A

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.

66
Q

Who is most susceptible to a secondary spontaneous pneumo?

A

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.

NUNP531 Applied Pathophysiology (24 decks)

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