• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/34

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

34 Cards in this Set

  • Front
  • Back
These two respiratory processes usually co-exist and are lumped together under COPD.
Emphysema and chronic bronchitis
What does an alveolar sac consist of?
2-3 alveoli
What does an acinus consist of?
A single terminal bronchiole, its respiratory bronchioles, alveolar ducts, and alveolar sacs
What defines emphysema?
Permanent enlargement of airspaces distal to terminal bronchiole (acinus)

Thinning an destruction of alveolar walls, large airspaces forme dby confluence of adjacent alveoli

In pure emphysema, fibrosis is absent
Which types of emphysema are most important clinically? Which is more common?
Centriacinar--20X more common than panacinar
Panacinar
Who is affected by centriacinar emphysema?

Where is it distributed?
AKA centrilobular or proximal acinar

Occurs in heavy smokers who are also likely to have chronic bronchitis; rarely seen in nonsmokers

Distal alveoli spared. Lesions present in apices.

Also present in coal worker's pneumoniosis
Who is affected by panlobular emphysema?

Where is it distributed?
AKA Panlobular emphysema

Most prominent in bases; uniform enlargement throughout the acinus

Hardest to diagnose

Occurs in alpha-AT deficiency
Who is affected by distal acinar emphysema?

Where is it distributed?
Results in pneumothorax in otherwise healthy people

Affects distal acinus with proximal acini spared; often adjacent to to areas of scarring.
What is the most comon form of emphysema?

Where is it distributed?
Irregular emphysema (most common, least clinically significant)

Results in irregular enlargement throughout acinus; seen frequently in areas of scarring
List and describe the three types of localized air expansion.
Bleb: collection of air within pleura

Cyst: closed cavity lined by bronchial/bronchiolar epithelium or fibrous tissue

Bulla: emphysematous space w/lung parenchema >1cm in diameter.
alpha1-antitrypsin:
Function
When does deficiency result?
Consequences of deficiency?
Antiprotease

There are many variants that still undergo normal folding, but the PiZZ variant results in severe deficiency, manifesting as slow, abnl protein folding in the ER of the hepatocyte

al-AT aggregates do not migrate to Golgi apparatus and lack of secretion into circulation

Results in liver dz and/or emphysema
How does a1-AT deficiency result in emphysema?
imbalance of elastase (wants to destroy elastic tissue) and antiprotease (wants to destroy elastase) results in net destruction of alveolar wall

Principal anti-elastase factor is alpha1-AT
Elastase is produced by _____.
Nphils and macs
How does smoking result in emphysema?
1)Increases elastase activity, decreases anti-elastase activity:
-Inc'd alveolar nphils and macs
-Release of nphil chemotactic factors from macs
-Stimulated Signs of hyperinflation--seen in COPD, asthma (air-trapping)
-Release of elastase from nphils
-Inc'd elastase activity of macs; mac elastase NOT inhibited by alpha1-AT
-Oxidants in smoke inhibit alpha1-AT


2) Free radicals present in tobacco smoke overwhelm antioxidant protection in lungs (antioxidants: superoxide dismutase and glutathione)
-Oxidation also inactivates antiproteases
Why does emphysema due to smoking affect the ______ lobes?
Emphysema affects lower lobes bc there is greater perfusion and quantity of nphils in the lower lungs. Results in panacinar emphysema.
Why does emphysema due to a1-AT deficiency affect the ______ lobes?
a1-AT deficiency localized to upper lobes; bc relatively smaller amount of a1-AT delivered to that region.

Resutls in centriacinar emphysema.
Who does chronic bronchitis tend to affect?

General symptoms?

Pathophysiology?
City dwellers and smokers

Productive cough, degree hypoxemia (blue bloaters)

Excess mucus in large airways; hypertrophy of submucosal glands and alterations in small bronchi/oles produce obstruction.

If much obstruction present-->emphysema
Pathologic features of chronic bronchitis.
Mucosa is hyperemic (enhanced blood supply_ an dswollen w/copious mucous or mucopurulent secretions

Mucous glands large with many goblet cells
Sometimes squamous metaplasia (smoking)
Narrowed bronchiole lumens due to goblet cell hyperplasia, inflammn, mucus plugging, fibrosis
What is the Reid Index of gland size?

Utility?
Ratio of thickness of gland layer to thickness of bronchial wall to depth of cartilage

Normal ratio <0.4

If over 0.4-->chronic bronchitis
Briefly describe a Type I hypersensitivity reaction.
Rapidly developing immunologic reaction occurring iwthin minutes after combination of antigen w/Ab bound to mast cells in individual that has been PREVIOUSLY SENSITIZED.

Susceptible individuals make strong TH2 (helper cells--recruitment) response to allergens.
What is bronchial asthma?
Chronic inflammatory disorder of airways that cause recurrent episodes of wheezing, dyspnea, chest tightness, and cough, particularly at night or in the early morning.

Results in chronic airway inflammn and hyperresponsive bronchi; mostly assocd with atopy (type I hypersens rxn)
Extrinsic vs Intrinsic Bronchial Asthma:
General
Provide Examples
Extrinsic:
Atopic (allergic) asthma
Occupational asthma
Bronchopulmonary aspergillosis

Intrinsic:
ASA ingestion, viral infections, exposure to cold, inhaled irritants, stress, or exercise
Inhaled allergens elicit a Th__-dominated response favoring production of _____ and recruitment of ________.
Inhaled allergens elicit TH2 dominated response favoring IgE production and eosinophil recruitment.
Describe the TH2 and ADAM-33 theories of atopic asthma.
-TH1 and TH2 dcells usually inhibited by cytokines released by each other. In atopic asthma, may have imbalance in which TH2 cells not inhibited by IFN-gamma released by TH1 cells, thus resulting in promotion of inflammn.

-ADAM-33 is a matrix metalloproteinase expressed by fibroblasts and bronchial SM; may play role in remodeling of airways that occur prior to onset of asthma.
What occurs during the immediate phase of asthma? Manifesting symptoms?
Immediate phase = re-exposure to allergen

Mast cells on mucosal surface simulated by IgE, release chemical mediators and directly stimulate subepithelial psymp receptors resulting in bronchoconstriction, edema from inc'd cap perm, mucus secretion, and hypotn in severe cases.
What occurs during the late phase of asthma?
Mast cells releasing cytokines have recruited ephils, nphils, monocytes, lymphocyts, and bphils.

Bronchial epithelial cells release EOTAXIN which attracts and activates ephils. Ephils dump MAJOR BASIC PROTEIN which causes epithelial damage and bronchoconstriction.

Occurs a few hours after re-exposure, persists for a day.
Gross and histologic pathologic features of asthma.
Gross: overinflated lungs; bronchi and bronchioles occluded by mucus plugs

Histologic: edema and inflammn of bronchial walls, thick BMs, inc'd size of submucosal glands, SM hypertrophy
What are Curshmann's spirals?

What do they indicate?
Curschmann's spirals refers to a finding in the sputum of spiral shaped mucus plugs (inspissates mucous). Indicative of asthma.
What is Charcot-Leyden protein?

What does it indicate?
Charcot-Leyden protein is a major autocystallizing constitutent of human ephils and bphils; indicative of asthma.
What is bronchiectasis?

Associations?
Chronic, necrotizing infection of bronchi with permanent dilation

Assocd w/:
Bronchial obstruction, tumors, foreign bodies

Necrotizing pneumonia, TB, staph

Hereditary conditions:
Cystic fibrosis
Congenital bronchiectasis
Intralobar sequestration
Immunodeficiency states
IMMOTILE CILIA
Gross and histologic appearance of bronchiectasis.
Gross; Saccular, fusiform, or cylindroid dilations in airways.

Microscopic: Dilated airways with thin, inflamed wall with areas of necrosis and squamous metaplasia. Fibrosis if chronic.
What does bronchiectasis appear like in cystic fibrosis?
Squamous metaplasia, impaired ciliary motion, necrosis of walls
What is Kartegener Syndrome?
Absence of dynein in arms; immotile cilia
Lung changes of aging.
Changes of mild emphysema
Alveoli and capillaries decrease in quantity-->decreased diffusion capacity
-->Dec'd muscle mass of diaphragm

Results in dec'd mucociliary action, blunted cough reflex, disorders of swallowing and esophageal motility
Dec'd cellular and humoral immunity