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CardioPul 3 > pathology 2 > Flashcards

pathology 2 Flashcards

1
Q

define emphysema

A
  • Irreversible enlargement of airspaces DISTAL to terminal bronchiole

–> accompanied by destruction of airway walls but WITHOUT obvious fibrosis

  • overlap between disease caused by alpha1-AT deficiency and pure chronic bronchitis
  • common pathogenesis = HEAVY CIGARETTE SMOKING
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2
Q

describe the factors associating smoking and emphysema

A
  • smokers have INCREASED neutrophils in the lung

–> neutrophils and macrophages accumulate in alveoli

  • smoking stimulates release of ELASTASE from both neutrophils and macrophages (macrophages elastase is NOT inhibited by alpha1-AT)
  • Oxidants in cigarete smoke and oxygen-derived free radiacls from neutrophils INHIBIT antiprotease

–> FREE RADICALS INCITE TISSUE DAMAGE

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3
Q

Describe centriacinar emphysema

A
  • most common (95%)
  • Portion of acinus formed by RESPIRATORY BRONCHIOLES affected; DISTAL ALVEOLI SPARED
  • GREATEST severeity in APICAL segements of upper lobes
  • assoc. carbon pigment and coal dust suggests MAJOR role of tobacco and coal in genesis
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4
Q

describe panacinar emphysema

A
  • ACINI uniformly enlarged from respiratory bronchioles to terminal blind alveoli
  • Assoc. with ALPHA1-antitypsin deficiency
  • most common in BASILAR PORTIONS OF LUNG

–> often occurs together with centriacinar emphysema

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5
Q

describe Distal acinar emphysema (paraseptal emphysema)

A
  • Enlargement with destruction of DISTAL portion of ACINUS

–> usually worse in upper lung zones

  • usually ADJACENT TO PLEURA, septae, lobule margins; adjacent to areas of scarring, fibrosis, or atelectasis; can form cyst-like structures
  • ASSOC. with SPONTANEOUS PNEUMOTHORAX and bullous disease of lung in young adults

–> not associated with smoking

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6
Q

describe irregular emphysema (airspace enlargement with fibrosis)

A
  • ACINUS IS IRREGULARLY involved
  • associated with SCARRING

–> usually from inflammatory process (called paracicatrical emphysema)

  • most common; usually asymptomatic, insignificant
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7
Q

Define Pink puffers

A
  • SEVERE emphysema
  • over-ventilate and remain relatively well-oxygenated

–> decrease diffusion capacity and relatively normal blood gas values; not much bronchitis

–> barrel chest, DOE; pursed-lip breathing, weight loss

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8
Q

describe blue bloaters

A
  • major component of chronic bronchitis, hypercapnia, abundant purulent sputum and severe hypoxemia (BLUE)
  • may develop cor pulmonale and eventually cardiac failure
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9
Q

Describe Chronic bronchitis

A
  • Persistent cough with production of sputum for AT LEAST 3 MONTHS of a year for at least 2 CONSECUTIVE YEARS

–> may have airflow decrease (decrease FEV1)

  • CIGARETTE SMOKING (most important factor)
  • microbiologic factors important in initiating and maintaing, but 2ndary process; cilia damage
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10
Q

describe the morphologic correlates in chronic bronchitis

A
  • chronic inflammation of airways
  • HYPERTROPHY of submucosal glands of trachea and bronchi (REID INDEX)
  • GOBLET CELL METAPLASIA

–> mucus hypersecretion with plugging

  • bronchial epithelium may show squamous metaplasia and dysplasia
  • marked narrowing of bronchioles; possible BRONCHIOLITIS OBLITERANS
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11
Q

describe the clinical presentation of CHRONIC BRONCHITIS

A
  • Persistent cough and sputum production
  • may lead tos ignificant COPD with outlfow obstruction ; hypercapnia, hypoxemia, possible cyanosis
  • may cause SQUAMOUS METAPLASIA AND DYSPLASIA of bronchial epithelium, providing ground for deelopment of cancer
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12
Q

describe acute exacerbation of chronic bronchitis

A
  • Bacterial infections
  • viral infections
  • cigarette smoke predisposes to infection by:

–> inferfering with ciliary action

–> directly damaging the epithelium

–> inhibiting the ability of bronchial and alveolar leukocytes to clear bacteria

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13
Q
A
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14
Q

describe asthma

A
  • CHRONIC INFLAMMATORY DISORDER OF AIRWAYS

–> recurrent episodes of wheezing, breathlessness, chest tightness and cough (night or early morning)

  • variable bronchoconstriction and airflow limitiation
  • partly reversible
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15
Q

describe the pathophysiology of asthma

A
  • inflammation –> hyperreactive airways –> episodes of reversible bronchoconstriciton

–> unpredictable and disabling with dyspnea, coughing and wheezing

–> patient may be asymptomatic between episodes

  • disease may be unremitting = Status asthmaticus
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16
Q

describe ATOPIC (extrinsic) asthma

A
  • initiated by type I hypersensitivity rxn after exposure to extrinsic allergen
  • Initial sensitization to inhaled antigens stimulate induction of CD4+ cells of Th2 type
  • Th2 cells release cytokines –> IL-4, IL-5
  • subsequent IgE- mediated rxn to inhaled antigens –> acute response and late-phase reaction
  • Induction of Th2 response fundamental
17
Q

describe non-atopic asthma

A
  • initiated by diverse nonimmune mechanisms such as ingestion of aspirin, pulmonary infections, inhalants, and exercise
18
Q

describe the phases of allergic asthma

A
  • Early phase

–> antigen exposure

–> 30 minutes

–> asthmatic attack

–> goes away by itself in hours

  • late phase:

–> 4-8 hours later recruited cell arrive in bronchus

–> binding to left-over IgE triggers another attack

  • Bronchoconstriction: vagal, direct effect of mediators on smooth muscle
19
Q

describe the morphology of asthma

A
  • overdistended, hyperinflated lungs, possible atelectasis
  • occlusion of bronchi and bronchioles by thick, tenacious mucus plugs

–> curschmann sprials = whorls of shed epithelium

–> charcot-leyden crystals = crystalloids made of eosinophilic proteins

20
Q

Describe Bronchiectasis

A
  • permanent dilation of bronchi and bronchioles

–> caused by destruction of muscle and elastic supporting tissue,

–> assoc. with chronic necrotizing infections

**IRREVERSIBLE**

  • TWO CONDITIONS REQUISITE = OBSTRUCTION AND CHRONIC PERSISTENT INFECTION
21
Q

describe kartagener syndrome

A
  • autosomal recessive Disorder that results in a STrUCTURAL DEFECT IN CILIA (DECREASE MOTILITY)

–> loss of radial spokes

  • results in bronchiectasis;; sinusitis; infertility (if male)
22
Q

describe the clinical features

A
  • chronic productive cough, hemoptysis, FOUL SMELLING SPUTUM, can be bloody
  • dyspnea and hypoxemia; pneumonia, lung abscess
  • SYSTEMIC = fever, weight loss, weakness
  • COMPLICATIONS = pulmonary HPT; brain abscesses
23
Q

describe pathogenesis of bronchiectasis

A
  • Two processes necessary
    1) obstruction

–> airway damaged, dilates and distorts

2) chronic persitent infection

–> causes fibrosis around distorted airway and locks it in that position

**IRREVERSIBLE**

CardioPul 3 (15 decks)

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