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Ashly Benson: Path II > Test I: Pumlonary Part I > Flashcards

Test I: Pumlonary Part I Flashcards

1
Q

What factors are required in order to maintain adequate respiration?

A

Adequate intake of air

Rapid diffusion on alveolar ducts/walls

Adequate Perfusion

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2
Q

What is the functional unit of the lung?

A

Acinus: consists of the respiratory bronchiole, alveolar ducts and alveoli.

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3
Q

Where is the blood air interface?

A

The space between the endothelium and the type-1 pneumocyte.

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4
Q

Which lobes of the lungs hold the most air?

A

Upper

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5
Q

Spots found in the upper lung are thought to be……

A

TB or Cancer

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6
Q

When lungs begin to fill with fluid or blood what will be noticed on a chest xray?

A

Costo-phrenic angles will start to get blunted. Base of the lungs will be appear white on X-ray.

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7
Q

What are the classical classifications of pulmonary pathology? (4)

A

Degenerative

Inflammatory

Neoplastic

Pleural

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8
Q

This congenital defect involves defective development of one or both lungs and is found in 10% of neonate death autopsies.

A

Pulmonary Hypoplasia

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9
Q

What is the most common type of tracheo-esophageal fistula? (TE Fistula)

A

Esophageal Atresia and Distral TE Fistula (77%)

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10
Q

What is the primary defect of NRDS (Neonatal Respiratory Distress Syndrome)?

A

Lack of surfactant, which means lungs won’t open and wind up filling with fluid. AKA: Hyaline membrane disease.

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11
Q

Incidence of NRDS is ________ proportional to gestational age.

A

Incidence of NRDS is inversely proportional to gestational age.

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12
Q

Incomplete expansion or collapse of the lung is an anatomical/physiologic/geometric concept called….

A

Atalectasis (often due to failure to breathe deeply)

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13
Q

Atalectasis (incomplete expansion) can occur from…..(3)

A

Reabsorption (bronchial obstruction like tumor)

Compression (from pleural effusion)

Contraction (diffuse lung fibrotic process)

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14
Q

Accumulation of fluid in the lungs leading to impaired gas exchange

A

Pulmonary Edema

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15
Q

Pulmonary edema is generally due to either _______ or ________.

A

Pulmonary edema is generally due to either failure of the heart to remove fluid from lung circulation “cardiogenic pulmonary edema” or direct injury to the lung parenchyma “noncardiogenic pulmonary edema”.

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16
Q

Additional causes of PE include

A

Fluid overload (iatrogenic: IV fluids given too fast)

Lymphatic obstruction (cancer)

Injury to the capillaries of the alveolar septae

Infections agents

Liquid aspiration

Gas inhalation (too much oxygen, smoke)

Chemotherapeutic agents

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17
Q

What is HAPE

A

High Altitude Pulmonary Edema: damage to endothelium due to hypoxia from low oxygen in the air.

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18
Q

Why does hypoalbuminemia (liver disease, nephrotic syndrome) cause PE?

A

Oncotic pressure is necessary to hold plasma in the vascular space.

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19
Q

What is the worst thing about a lung transplant?

A

The first time you cough it’s not your phlem. hahahaha

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20
Q

What are the 4 main pathologic mechanisms of pulmonary edema?

A

Increased venous pressure

Increased oncotic pressure

Lymphatic obstruction

Alveolar injury

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21
Q

In PE gas exchange is compromised because _______breaks the structure of the ____________ cells and fluid entering the ________ spaces reduces or halts ____________.

A

In PE gas exchange is compromised because interstitial fluid breaks the structure of the alveolar epithelial cells and fluid entering the alveolar spaces reduces or halts gas exchange.

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22
Q

Acute PE is usually due to __________.

A

Acute PE is usually due to left ventricular failure.

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23
Q

In which form of PE may there be an absence of pain and sx?

A

Chronic PE

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24
Q

Acute PE s/sx:

A

Tachypnea (rapid breathing)

Extreme dyspnea (shortness of breath SOB)

Restlesness and anxiety (sense of suffocation)

Bronchospasm and wheezing (cardiac asthma)

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25
Q

Pronounced lung markings heading up towards the head =

Pronounced lung markings in the correct pattern, but exaggerated =

A

Pronounced lung markings heading up towards the head = ACUTE PE

Pronounced lung markings in the correct pattern, but exaggerated = CHRONIC PE

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26
Q

In chronic PE alveolar walls become _______

A

fibrotic (Alveolar walls lose their elasticity)

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27
Q

Alveolar fluid may act as a culture medium for bacterial growth: Acute or Chronic?

A

Chronic

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28
Q

Chronic PE is common with what other condition?

A

Congestive Heart Failure Chronic PE: micro-hemorrhages occur, macrophages phagocytize iron from micro hemorrhages - heart failure cells

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29
Q

What is a non-specific pattern of lung injury called?

A

ARDS: Acute Respiratory Distress Syndrome

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30
Q

ARDS results in exudate leaking into the alveoli: cardiogenic or non-cardiogenic?

A

Non-cardiogenic, meaning much more than transudative fluid leaks into the alveoli: fibrin, protein and cells all leak in, resulting in exudate (protein rich)

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31
Q

ARDS results in severe acute lung injury (ALI). What is the process that leads to death of lung cells?

A
  1. low blood oxygen (due to microscopic clots: microthrombi)
  2. increased permeability of pulmonary blood vessels
  3. fluid accumulation in the lungs
  4. death of epithelial and endothelial cells
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32
Q

What are some common causes of ARDS?

A

Sepsis

Widespread lung infections (pneumonia, TB)

Gastric aspiration

Mechanical trauma (lung/head)

Multi-organ failure

Burns from inhaled gases/chemicals

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33
Q

In 20% of ARDS cases there are no identifying risk factors. This is called _______

A

Interstitial pneumonia

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34
Q

Damage to type 2 epithelial cells, resulting in decreased surfactant production is due to……..

A

Damage to type 2 epithelial cells, resulting in decreased surfactant production is due to……..hyaline membranes becomes covered with protein-rich fluid and dead alveolar epithelial cells.

35
Q

Which cells are common in many lung pathologies, especially ARDS?

A

Neutrophils: produce pro-inflammatory products and eat elastin.

36
Q

What is the mortality rate of ARDS?

A

30-70%

37
Q

How does ARDS resolve?

A
  • Resorption of the fluids and removal of debris by alveolar macrophages
  • Replacement of epithelial cells with new functional cells
  • Restoration of capillary endothelial cells
38
Q

Losing elasticity of the lung = ________ = less gas transfer.

Xrays will look more or less opaque?

A

Losing elasticity of the lung = restriction = less gas transfer.

Xrays will look more opaque, with a ground glass appearance

39
Q

_________ = air trapping and wheezing in the (large or small?) airways.

A

Obstruction = air trapping and wheezing in the small airways.

40
Q

Is obstruction a problem of inspiration or expiration?

How will X-rays look?

A

Expiration

Hyper-expansion on X-ray (Lucency and density)

41
Q

What appearance will restriction have on X-ray?

A

Ground glass (Opacity and density)

42
Q

What is the main problem with restriction?

A

Reduced gas transfer.

43
Q

Restrictive Airway Disease (decreased capacity, normal flow rate) has two major classes. What are they?

A

Chest wall disorders: poliomyelitis, severe obesity, pleural diseases and kyphoscoliosis

Acute or chronic interstitial and infiltrative diseases: ARDS, dust inhalation, interstitial fibrosis, pneumoconiosis

44
Q

What is the difference between reactive airway disease and restrictive airway disease?

A

Reactive = sudden bronchial restriction and wheezing

Restrictive = diminished elasticity of the lung = reduced expansion and total lung capacity

45
Q

What are the 3 main diseases of COPD (4th most common cause of morbidity and mortality in the US?

A

Chronic Bronchitis —> Emphysema

Asthma

Bronchiectasis

46
Q

What does Asthma do to the airspaces in the lung?

A

Irreversible enlargement of the airspaces distal to the terminal bronchiole.

47
Q

Is fibrosis seen in obstructive or restrictive lung diseases?

A

Restrictive

48
Q

What are the characteristics of centrilobular emphysema?

A

Central acini affected but distal unharmed

More severe in upper lobes

Predominately in heavy smokers

49
Q

What are the characteristics of panacinar emphysema?

A

Acini uniformly enlarged

More severe in lower lobes and anterior aspect of the lungs

50
Q

Alpha 1 antitrypsin deficiency is present in Centrilobular or Panacinar emphysema?

A

Panacinar

51
Q

Emphysema presents with increased numbers of what cells (3)?

A

Macrophages

T lymphocytes

Neutrophils

52
Q

In emphysema activated inflammatory cells release……(3)

A

Leukotriene

IL-8

TNF

53
Q

Alpha 1-antitrypsin normally presents in serum, tissue fluids and macrophages. What does it do?

A

Inhibits proteases (esp. elastase)

54
Q

_______ and _______ inhibit Alpha 1-antitrypsin, allowing cellular proteases like elastase to cause tissue damage.

A

Oxidants and free radicals (found in smoke) inhibit Alpha 1-antitrypsin, allowing cellular proteases like elastase to cause tissue damage.

55
Q

Nicotine and ROS in smoke activate ______

A

Nicotine and ROS in smoke activate NF-kB

56
Q

NF-kB turns on genes that encode ______ and _____, which attracts and activates ________ (cell type), which release granules rich in ________ which damage lung tissue.

A

NF-kB turns on genes that encode TNF and IL-8, which attracts and activates neutrophils, which release granules rich in elastases which damage lung tissue.

57
Q

Smoking also enhances elastase activity in _________(cell type).

A

Smoking also enhances elastase activity in macrophages.

58
Q

_________ from macrophages and neutrophils also destroys lung tissue.

A

Metalloproteinase (MMP) from macrophages and neutrophils also destroys lung tissue.

59
Q

What are the antioxidants normally found in the lung that are depleted by tobacco smoke? (2)

A

Superoxide dismutase

Glutathione

60
Q

Emphysema manifests after at least _____ of functioning of the lung has been lost.

A

Emphysema manifests after at least 1/3 of functioning of the lung has been lost.

61
Q

What, shown here, is a hallmark of COPD that can often lead to a pneumothorax?

A

Blebs or bullae whose walls are paper thin and easily rupture, forming a pneumothorax.

62
Q

What are symptoms commonly found in emphysema patients who don’t have a history of chronic bronchitis?

A

Weight loss

Barrel-chested (hunched over)

Limited expiratory airflow

Pulse ox normal

Pts. over ventilate PINK PUFFER

Develop cor pulmonale and CHF

  • Cor pulmonale is failure of the right side of the heart brought on by long-term high blood pressure in the pulmonary arteries and right ventricle of the heart.

Death often due to

Respiratory acidosis and coma

R sided heart failure (collapse of lungs due to pneumothorax)

63
Q

Chronic Bronchitis is defined clinically by persistent cough with sputum production for at least ____ months in at least ____ consecutive years in the absence of any other identifiable cause.

A

Chronic Bronchitis is defined clinically by persistent cough with sputum production for at least 3 months in at least 2 consecutive years in the absence of any other identifiable cause.

64
Q

Etiology of chronic bronchitis is due to:

A

tobacco smoke

breathing smog dust from grains, cotton and silica

65
Q

What is the major morphology of chronic bronchitis?

A

Hyper-secretion of mucus.

Cigarette smoke predisposes to infection b/c of loss of ciliary function of the epithelium = mucus production = inhibition of bronchial and alveolar macrophages.

66
Q

In chronic bronchitis, there is increased mucus production because of increased number of ______ cells; proteases _____ and _____ released from _________ (cell type) stimulate hyper-secretion.

A

In chronic bronchitis, there is increased mucus production because of increased number of goblet cells; proteases MMP and Elastase released from neutrophils stimulate hyper-secretion.

67
Q

Can you see acute bronchitis on Xray?

A

No. In acute bronchitis you hear honks and wheezes which clear with coughing.

68
Q

What are the 4 classical histological findings in bronchial asthma?

A

1) Inflammation
2) Bronchial (luminal) narrowing
3) Increased mucous (looks like chronic bronchitis)
4) Smooth muscle hyperplasia

69
Q

If the asthma etiology is from allergy what other histological finding will there be?

A

Eosinophils.

70
Q

Chronic bronchitis has sputum production, where Asthma has ______.

A

Chronic bronchitis has sputum production, where Asthma has wheezing and no sputum.

71
Q

A hallmark of asthma is increased or decreased airway responsiveness to a variety of stimuli?

A

A hallmark of asthma is increased airway responsiveness to a variety of stimuli. This leads to bronchoconstriction/spasm, inflammation and increased mucus production.

72
Q

What is status asthmaticus?

A

Unremitting asthma attacks

73
Q

What is asthma hygiene theory?

A

Incidence of asthma is lower in populations exposed to an abundance of microbes.

74
Q

Which type of asthma is most common, atopic of non-atopic?

A

Atopic: Type I IgE mediated, often begins in childhood

75
Q

What is Sampter’s triad? (Hint: involves aspirin)

A

Asthma

Rhinitis and nasal polyps

Hives

76
Q

Exposures to caustic agents from fumes, dusts , gases or chemicals are triggers for ___________ asthma.

A

Occupational

77
Q

Exercise induced asthma may be due to extreme sensitivity to changes in _________ and ________ of air entering the lungs.

A

Exercise induced asthma may be due to extreme sensitivity to changes in humidity and temperature of air entering the lungs. (exercise induced asthma lacks inflammatory changes)

78
Q

What are the early phase characteristics of asthma (3)?

A

Bronchoconstriction

Increased mucus production

Vasodilation/increased vascular permeability

79
Q

In the late phase of asthma secretions of _____ cells, _______ cells and T cells recruit _________, _________ and T cells, causing inflammation.

A

In the late phase of asthma secretions of mast cells, epithelial cells and T cells recruit eosinophils, neutrophils and T cells, causing inflammation.

80
Q

What chemo-attractant and activator of eosinophils is produced by airway epithelium?

A

Eotaxin

81
Q

Over time, asthma changes the structure of the bronchial wall by hypertrophy and hyperplasia of both the ______ layer and the ______ glands.

A

Over time, asthma changes the structure of the bronchial wall by hypertrophy and hyperplasia of both the muscle layer and the mucus glands.

82
Q

Does asthma cause increased or decreased airway vascularity over time?

A

Increased

83
Q

What are triggers of asthma?

A

Irritants

Cold air

Stress

Exercise

Infections

84
Q

What are the gross morphologies of asthma? (3)

A

Mucus plugs: occlude bronchi and bronchioles

Hyperinflation of the lungs

Bronchoconstriction

Ashly Benson: Path II (1 decks)

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