Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pulmonology > Porth - Obstructive Pulmonary Disorders > Flashcards

Porth - Obstructive Pulmonary Disorders Flashcards

(56 cards)

Start Studying
1
Q

Bronchiectasis - Definition

A
  • Uncommon type of COPD - Permanent dilation of the bronchi and bronchioles (widened airways)

– ^^ Caused by destruction of muscle & elastic supporting tissue as result of cyclical Infection & Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is Bronchiectasis a Primary Disease?

A

No! Occurs 2ndary to persistent infection or obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What was Bronchiectasis associated with in the past?

A

-Used to follow a Necrotizing Bacterial Pneumonia that complicated measles, pertussis, influenza, or TB.

– Has decreased due to Immunizations & Antibiotic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathogenesis of Bronchiectasis

A
  1. Obstruction
  2. Chronic Persistent Infection

*Both damage bronchial walls =’s weakening and dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

2 Presentations of Bronchiectasis:

A
  1. Local obstructive process - involving a lobe or segment of lung
  2. Generalized/Diffuse process - involving much of both lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Localized Bronchiectasis

A

Causes: Tumors, Foreign Bodies, Mucous Plugs =’s cause atelectasis & infection

* Blocks drainage of bronchial secretions

** Local area determined by the site of obstruction or infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Generalized Bronchiectasis

A

Causes: Inherited impairments of host mechanisms; or acquired disorders that introduce bad organisms into airways — Including: Cystic Fibrosis; Lung Infection (TB, lung abscess); congenital/acquired immunodeficient states; exposure to toxic gases * Usually Bilateral ** Most commonly affects lower lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Bronchiectasis Clinical Features

A
  • Atelectasis - Small airway obstruction - Diffuse Bronchitis –Recurrent bronchopulmonary infection: Coughing; production of copious amount of foul-smelling/purulent sputum; hemoptysis — Weight loss & anemia can occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Bronchiectasis Manifestations

A

*Similar to those in Chronic Bronchitis & Emphysema – Marked Dyspnea – Cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Bronchiectasis & Clubbing of the Fingers

A
  • More common in moderate to advanced cases

*Not commonly seen in other types of obstructive lung diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Bronchiectasis Diagnosis & Treatment

A

Diagnosis: -Hx

  • Imaging Studies: evident on Chest Radiographs, High-resolution CT scanning of chest

Treatment: - Early recognition & treatment of infection are key!

– Postural drainage & Chest PT — Remove mucous &good hydration

*Patients benefit from many of the rehabilitation & treatment measures used for Chronic Bronchitis & Emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Emphysema - A Type of COPD!

A

Characterized by: Loss of lung elasticity & abnormal enlargement of air spaces distal to terminal bronchioles w/ destruction of alveloar walls & capillary beds - Enlargement of air spaces & destruction of lung tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Emphysema

Enlargement leads to…

A

Hyperinflation of lungs and increase Total Lung Capacity (TLC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Emphysema

Two Causes

A
  1. Smoking = incites lung injury
  2. deficiency of alpha1-antitrypsin (an enzyme that protects the lung from injury) - Genetic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Emphysema Results from….

A
  • Breakdown of Elastin and other alveolar wall components by enzymes (proteases) that digest proteins
  • Things like smoking cigarettes calls all these inflammatory cells into the lungs, resulting in an influx of these digestive enzymes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Emphysema & alpha1-antitrypsin deficiency

A

1% of COPD cases

  • Found in younger folks w/ emphysema (generally diagnosed before age of 40)

– More common in Scandinavians

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Chronic Bronchitis - A Type of COPD!

A

Airway obstruction of the major and small airways.

  • Increased mucous production; obstruction of small airways, chronic productive cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Chronic Bronchitis is found most commonly in…

A

Middle-aged men & associated with common irritation from smoking & recurrent infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Chronic Bronchitis & Clinical Dx requires…

A
  • History of chronic productive cough that has persisted for at least 3 consecutive months in at least 2 years

– In general, cough has been present for many years w/ increase in exacerbations that produce sputum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Chronic Bronchitis

Earliest Feature

A

Hyper secretion of mucus in the large airways

  • associated with hypertrophy of submucosal glands in the trachea & bronchi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chronic Bronchitis

What’s going on in the Large & Small Airways?

A
  • Large airways: Mucus hyper-secretion/submucosal hypertrophy
  • Small airways: Increase in goblet cells & excess mucous production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Chronic Bronchitis + Viral and Bacterial Infections

A
  • Common in Chronic Bronchitis

– Thought to be a result of, not a cause of CB

— Probably help in maintaining CB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

COPD: Emphysmea & Chronic Bronchitis

Clinical Features

Study These Flashcards
A
  1. Insidious Onset
  • Fatigue
  • Exercise intolerance
  • Sputum Production
  • SOB

* Productive cough more common in the morning

**Dyspnea is more severe as disease progresses

24
Q

COPD: Emphysmea & Chronic Bronchitis

Late Stages

Study These Flashcards
A

Recurrent respiratory infections & Chronic Respiratory failure

*Death occurs during an exacerbation of illness associated with infection & resp. failure

25
COPD: Emphysmea &Chronic Bronchitis Manifestations: "Pink Puffers"
\*Predominant Emphysema \*\*Lack of Cyanosis \*\*\*Use of Accessory Muscles \*\*\*\*Pursed Lipped-Breathing
26
COPD: Emphysmea "Pink Puffers" & their Barrel Chests
- Lung elasticity lost & Lungs Hyper-inflated - - Lungs often collapse during expiration ='s air gets trapped in alveoli and lungs increasing AP-dimension of chest \*Dramatic decrease in breath sounds \*\*Diaphragm fatigue & Acute Respiratory Failure
27
COPD: Chronic Bronchitis Manifestations: "Blue Bloaters"
\*Predominant in Chronic Bronchitis * Reference to: * Cyanosis * Fluid Retention due to Right-Sided Heart Failure :(
28
COPD: Emphysmea &Chronic Bronchitis Is the Obstruction of Airflow worse on Inspiration? or Expiration?
Expiration! - Increased work of breathing & Decreased Effectiveness
29
COPD: Emphysmea & Chronic Bronchitis Late Stage COPD (pt. 1)
- As disease progresses: Expiration is prolonged & Wheezes and Crackles can be heard - Labored Breathing, even at Rest - "Tri-poding" - Pursed Lip Breathing
30
COPD: Emphysmea & Chronic Bronchitis Late State COPD (pt. 2)
- Unable to maintain normal blood gases -- Resulting in: Hypoxemia, hypercapnia, cyanosis \*V/Q imbalance!
31
COPD: Emphysmea & Chronic Bronchitis Severe Hypoxia
- Arterial PO2 levels below 55mmHg -- Vasoconstriction of pulmonary vessels & even less gas exchange in lungs --- Can cause Polycythemia (red blood cell production) --- Increases Right Ventricle work, hence the right-sided heart failure
32
COPD: Emphysmea & Chronic Bronchitis Diagnosis
- History & Physical crucial - PFTs -- FVC & FEV1 decreased - Chest Radiographs - Lab tests
33
COPD: Emphysmea & Chronic Bronchitis Treatment
- Depends on Disease Stage -- Smoking Cessation --- Maintain & Improve Pulmonary Fxning: Pulmonary Rehabilitation (breathing exercises) --- Avoid those who are sick as to not get respiratory infections ---- Vaccines ----- Medications: Bronchodialators: Inhaled B2-agonists; anticholinergic, adrenergic agents; oral Theophylline (measure blood levels) -- Oxygen Therapy
34
Emphysema 2 commonly recognized types: Centriacenar & Panacinar
1. Centriacinar (or Centrilobular): Most common; seen in male smokers; most common in upper lungs -- Affects bronchioles in the central part of the respiratory lobule --- Initial preservation of alveolar ducts & sacs 2. Panacinar: More common in alpha1-antitrypsin deficiency; more common in lower parts of lungs - Initial involvement of the peripheral alveoli & later extends to involve more central bronchioles
35
**Obstructive Airway Disorders:** Asthma
* A chronic disorder of the airways that causes episodes of airway obstruction due to bronchial smooth muscle hyperreactivity and airway inflammation. * Episodes are usually reversible (compare to COPD)
36
**Asthma** Some Factoids
* Affects ~5% of population * Prevalance of asthma has increased * Disease management has gotten better over the years * Decreased hospitalizations & mortality rates
37
**Asthma** Characterized by...
* Variable recurring symptoms * Airflow obstruction * Episodic wheezing * Difficulty breathing * Tight chest * Cough (worse in PM and AM) * Bronchial hyperresponsiveness
38
**Asthma** 2 Types
1. **Extrinsic:** Type I hypersensitivity (atopic) response to extrinsic antigen 2. **Intrinsic:** Initiatied by non-immune mechanisms: * Resp. Tract Infections * Exercise * Ingestion of Aspirin * Emotions * Bronchial Irritants (i.e. smoke)
39
**Asthma** The Common Denominator!
An exaggerated hypersensitivity response to a variety of stimuli. _Contributors:_ * Inflammatory cells & epithelial damage * Mucus hypersecretion * Smooth muscle hypertrophy * Blood vessel proliferation \*Genetic & Evironmental factors play a part!
40
**Asthma** Extrinsic (Atopic)
* Initiated by Type I hypersensitivity reaction * Exposure to antigen or allergen * Childhood/Adolescent onset * Family Hx
41
**Asthma** Extrinsic Asthma
* These folks often have other allergic d/o: * Hay Fever * Urticaria * Eczema * Year-round allergens: * House mites * Cockroach allergens * Animal Danders * *Alternaria (fungus)* ​
42
**Asthma** Extrinsic Asthma & Response Mechanisms Early/Acute Phase
* Early/Acute phase: * 10-20 minutes to develop * Caused by: IgE-mediated release of mediators from sensitized mast cells * Bronchospasm * Mucosal Edema * Increased Mucous Secretions * Can usually be Inhibited or Reversed by: * Bronchodilators (B2-agonists)
43
**Asthma** Extrinsic Asthma & Response Mechanisms Late Phase
* Develops 4-8 hours after exposure * 'Vicious cycle of exacerbations' * Epithelial cell injury w/ decrease mucociliary fxn and accumulation of mucus. * Release of inflammatory mediators * Increased vascular permability & edema * Increased airway responsiveness * Bronchospasm * Edema * Reduced clearance of respiratory tract secretions * Increased airway responsiveness * Can lead to airway remodeling
44
**Asthma** Instrinsic (nonatopic) *Triggers*
* Resp. Tract Infections * Exercise * Hyperventilation * Cold air * Drugs & Chemicals * Hormonal changes & emotional upsets * Air-bourne pollutants * Gastro-esophageal reflux
45
**Asthma** Intrinsic (nonatopic)
Cause epithelial damage and stimulate the production of IgE antibodies directed toward the viral antigens.
46
**Asthma** Intrinsic *Exercise & Cold Enviroments*
* Exercise: Hyperventilation & airway physiology change play a role * Increased ventilation rate challenges ability of airways to condition air before reaching the alveoli * Cold Environment: Exaggerates response of exercise * Warm-up * Wear a mask over mouth & nose
47
**Asthma** Intrinsic *Inhaled Irritants*
* Tobacco smoke/strong odors * Induce Bronchospasm * Irritant receptors & vagal reflex * Children exposed ='s increases severity of asthma * Occupational Asthma: fumes, gases, chemical dusts
48
**Asthma** Intrinsic *Aspirin*
* Clinical Triad: * Nasal Polyps * Chronic Rhinosinusitis * Bronchial Asthma * Mechanism of reaction is unclear, but due in part to: * Acidic metabolism issues * If you have this condition... avoid Aspirin!
49
**Asthma** Clinical Features
* Range of Symptoms: * Wheezing * Tight Chest * Acute Immobilizing Attacks * May be spontaneous, or in response to a trigger * Nocturnal Asthma: Worse @ night
50
**Asthma** Clinical Features
* Bronchospasm * Causes Airways to narrow * Edema of Bronchial Mucosa * Mucus plugging * Prolonged expiration * Decreased FEV and PEF
51
**Asthma** Clinical Features *Prolonged Attack*
* Lung hyperinflate * Decreased Inspiratory Reserve Capacity & Forced Vital Capacity * More energy required to overcome tension & maintain ventilation * Dyspnea & Fatigue * V/Q mismatch * Hypoxemia & Hypercapnia * Increased work demands of the Right Heart
52
**Asthma** Manifestations
* Mild attack: * Chest tightness * Resp. Rate increase w/ prolonged expiration * Mild wheezing (w/w/o cough) * Severe attack: * Accessory muscle use * Distant breath sounds * Loud Wheezing * Progresses: * Fatigue * Moist skin * Anxiety/Apprehension * Decreased breath sounds, decreased wheezing, Ineffective cough * THIS IS NOOOOOOO GOOD!
53
**Asthma** Diagnosis
* Hx * PE * Lab findings * Pulmonary Fxn Studies * Spirometry * Small portable meters measuring PEF are available * Measure 'personal best'
54
**Asthma** Treatment
* Control contributing factors & exposures * Education * Annual Flu Vaccine * Desensitization program * Drugs: * Bronchodialtor * Anti-inflammatory drugs * SABAs * Relax bronchial muscles * Prompt relief * Anticholinergic agents * Blook cholinergic receptors * Reduce intrinsic vagal tone that causes constriction * Bronchodilation * Longer onset of action * Long-term Meds: * inhaled corticosteroids\* * Most effective! * long-acting bronchodialtors * cromolyn, * leukotriene pathway inhibitors * theophylline
55
**Asthma** Severe Asthma
* A sub-group * High medication dose * Persistant * Requires continuous high-dose inhaled or oral corticosteroids * More fatal attacks/rapid deterioration
56
**Asthma** **in Children**
* Most common cause of childhood ER visits, hospitalizations, missed school days * 80% of children are Symptomatic before age 6 * Increasing globally * Ig-E related reaction * Assc. w/ Virus (RSV previously) * Environmental exposures * Often see symptoms at night * Step-wise approach to treatment * Inhaled corticosteroid are 1st-line * Nebulizer therapy for very youngins' Encourage active participation in recreational activities

Pulmonology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions