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General Pathology > Pulmonary Path 1 > Flashcards

Pulmonary Path 1 Flashcards

1
Q

how heavy are the lungs

A

200-250 gms each (right side is slightly heavier)

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2
Q

the act of respiration involves the:

A

upper resp tract, diaphragm and accessory muscles

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3
Q

what makes up the large airways:

A

ex. larynx, trachea and bronchi

lines by pseudostratified, ciliated, columnar epithelium with mucous glands, neuroendocrine cells and cartilage

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4
Q

what are the 2 cells types of the alveoli

A

type 1 (flat) and 2 (cubodial) pneumocytes - type 1 make up 95% and type 2 create the surfactant to keep the alveoli open.

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5
Q

upper airway defense mechanism

A

filtering, hairs in the nasopharynx that block large particles

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6
Q

lower airway defense mechanism

A

mucocilliary units that wave particles up to be swallowed by the trachea

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7
Q

what are the pulmonary defenses?

A

upper resp tract filters, lower resp tract contains mucociliary units, the upper and lower contain lymphoid tissue for cellular immunity and humoral (IgA) and alveolar macrophages (waiting in the air spaces or in the interstitium)

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8
Q

innate “naive” lung compared to a immune lung

A

innate (in children and infants) : mucous blanket, complement (kills bacteria) and neutrophils
immune: antibody response (mainly IgA), macrophages and lymphocytes that activate the antibody response, which will eat up the foreign material

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9
Q

Hemoptysis

A

coughing up blood

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10
Q

Dyspnea

A

difficulty breathing, perception of needing to breathe deeper and faster (shortness of breathe)

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11
Q

Atelectasis

A

collapse of lung volume, reducing the effective volume of the lung - inadequate expansion of airspaces
-either pockets of the lung or the full lung

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12
Q

Pneumothorax

A

air in the pleural space or cavity, leads to collapse of the lung
-a form of atelectasis

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13
Q

Empyema

A

suppuration (pus) in the pleural cavity

- can lead to fibrosis and adhesions that reduce the effectiveness of the lung

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14
Q

Pleural Effusion

A

FLUID in the pleural space
transudate - low molec weight, mild form, caused by an increase in venous pressure ex. CHF
exudate- high protein fluid, with or without inflamm cells, caused by increased vascular permeability (damage to the cells opens up the membrane) ex. pneumonia

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15
Q

Pulmonary Edema

A

accumulation of fluid in the lungs themself (not the pleural space), first in the interstitial tissues (space between the air and blood vessels), then ultimately filling up the air spaces

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16
Q

what causes pulmonary edema

A

increased intravascular pressure (CHF), hypoproteinemia (low protein) and vascular damage (infections, autoimmune diseases)

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17
Q

what is the problem with pulmonary edema?

A

inhibits normal oxygen exchange and predisposes the lung to infection (nutrient filled environment for bacteria)
-need medical tx right away

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18
Q

Thromboemboli

A

usually from the deep veins of the legs or pelvic veins
-small emboli causes minimal damage and larger emboli cause hemorrhage or infarction and very large emboli lodge in the bifurcation of pulmonary aa. (saddle embolus) can cause sudden death

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19
Q

predisposing factors of pulmonary thromboemboli

A

chronic illness (esp infections) , prolonged bed rest (immobile), hypercoagulable states (factor V leidin) or predisposed to deep leg thromboses (DVTS)

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20
Q

hemorrhagic pulmonary infarct

A

dual blood supply into the loose CT of the lung leads to a red infarct because the side of the dual supply that is not blocked bleeds into the space

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21
Q

what are the 4 classic disorders that cause chronic airflow obstruction

A

emphysema, chronic bronchitis, bronchiectasis and asthma (asthma is episodic, but once you have asthma, usually have it for awhile)
-a lot of overlap

22
Q

what are the diseases that “make up” COPD

A

emphysema and chronic bronchitis

23
Q

morbidity and mortality of pulmonary diseases

A

chronic resp disease #3 cause of death and influenza and pneumonia is #8

24
Q

Emphysema

A

PERMANENET enlargmement of the small distal air spaces due to destruction of the alveolar septa (breakage in the walls, recoil gone)
-go from many small air spaces to a large airspace

25
Q

Emphysema clinically

A

dyspnea, cough and prolonged exhalation

“pink puffers” because its easy to get oxygen into the alveoli, but hard to expel

26
Q

pathogenesis of emphysema

A

imbalance between protease and anti-protease enzymes

  • MAJOR cause is smoking which will promote the destruction and stop the inhibition of the proteases
  • get people to stop smoking before there is complete destruction of distal air ways
27
Q

2 forms of emphysema (pathology of emphy)

A

centriacinar - involves the central portion of the lobule (may progress to a bullae), usually affects the upper lobes **associated with smoking
paracinar - involves the entire resp lobule (rep bronchioles to terminal alveoli) and usually involves the lower lobes MORE **assoc with alpha-1-AT deficiency (genetic)

28
Q

bollus emphysema

A

a large huge pocket in the lung

29
Q

Chronic bronchitis

A

cough with sputum production at least 3 consecutive months for 2 consecutive years (often occurs with empheysema)

30
Q

chronic bronchitis pathogenesis

A

chronic irritation (smoking) and infections

31
Q

chronic bronch clinical appearance

A

“blue bloaters” - hypoxic, cyanotic look

** hard for them to get stuff in to the lungs because there is blockage

32
Q

pathology of chronic bronch

A

increased mucous glands, edema, chronic inflamm, fibrosis (from infections caught in the airway) and narrowing of the airways (the airways narrow because of the all the mucous secretions from the glands that need to go somewhere and in smokers, its worse because they have fewer ciliary units to push the mucous out)

33
Q

COPD patients

A

will get parts of narrowing (chronic bronch) and dilation (emph) in the lung

34
Q

predisposing factors to chronic bronch and emphy

A

cigarette smoking, atmosphere pollutants, infections and genetic factors (Cystic Fibrosis, alpha - 1-at deficiency)

35
Q

what does cigarette smoking do

A

mucous gland hyperplasia, increases smooth mm. tone, inhibits cilia, inhibits phagocytosis and squamous metaplasia

36
Q

Bronchiectasis

A

chronic infection with permanent MAJOR (larger) airway dilation because of infection (ex. bronchitis causes pooling of mucous that leads to bacterial destruction), obstruction (ex. tumors) or both

  • the air space widens because of the destruction of the tissue (from infection or obstruction)
  • not a disease, a result of the other pulmonary diseases
37
Q

clinical bronchiectasis

A

severe cough, bloody mucoid expectoration and dyspena

38
Q

complications with bronchiectasis

A

abscess, pnemonia, bronchopleural fistula (opening between the bronchus and lung) and empyema

39
Q

predisposing factors of bronchiectasis

A

obstructive tumors, foreign bodies, CF (mucous plugs), other COPD, CF; suppurative or necrotizing pneumonia

40
Q

pathology of bronchiectasis

A

dilated distal bronchi and bronchioles, chronic infection with inflammation and variable purulence
-can resolve the infection, but the bronchioles remain wide and are at a constant risk for infection

41
Q

asthma

A

increased irratibility and prominence of SMOOTH MM. in bronchi and bronchioles

  • marked, reversible episodes of contraction and airway constriction (hard for the patient to breathe)
  • episodic in nature, but chronic in longevity
42
Q

initiating factors

A

allergies, infections, exercise, drugs emotion etc..

43
Q

how common is asthma

A

affects 5% of adults and 7 to 10% of kids (esp inner city children)

44
Q

clinical asthma

A

wheezing, long exhalation, hyperinflation of lungs, panic (hard to get air in and out from contraction of the smooth mm. and constriction for the mucous deposits and inflammation)

45
Q

types of asthma

A

atopic and non-atopic

-disease is the same, just try to avoid the trigger

46
Q

atopic asthma

A

allergic, extrinsic

-type 1 hypersensitivty (IgE mediated), environmental antigen and positive family history

47
Q

Non atopic asthma

A

intrinsic

-initiated by viruses or air pollutants

48
Q

asthma pathology

A

increased mucous glands (not as prominent as in chonric bronch), smooth mm. hypertrophy, inflammation with EOSINOPHILS and type 2 helper T cells

49
Q

pathogenesis asthma

A

antigen binds to surface IgE and mast cells releasing a large number of mediators, including histamine and leukotrienes that cause vasodilation and contraction of the smooth mm.

50
Q

asthma tx

A
  • attack may subside spontaneously

- inhalation of bronchodilators for immediate relief (albuterol) and controller medications (corticosteroids)

General Pathology (7 decks)

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