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Pulmonology > Pathophys > Flashcards

Pathophys Flashcards

1
Q

Conducting portion of the respiratory tree

A 
Nasal cavity
Larynx
Trachea
Bronchi
Bronchioles (terminal)
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2
Q

Respiratory portion

A

Respiratory bronchioles
Alveolar ducts
Alveoli

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3
Q

How is the R primary bronchi different from the L?

A

It is shorter, wider, and straighter.

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4
Q

What does primary bronchi divide into?

A

Lobar bronchi (5 total)

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5
Q

Define bronchopulmonary segment

A

Tertiary bronchi together with branch of pulmonary AA

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6
Q

What is the order of branching after tertiary bronchi?

A

Terminal bronchi - respiratory bronchi - alveoli - alveolar duct - alveolar sac

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7
Q

What body system is found in the area of the alveolar sac?

A

Lymphatics - removes debris from what you breathe in.

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8
Q

Which 3 tissue/cell types end at the terminal bronchioles?

A
  1. Goblet cells
  2. Glands
  3. Hyaline cartilage
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9
Q

Which tissue type spans the entire bronchial tree?

A

Epithelium

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10
Q

Where do ciliated cells end in the bronchiole tree?

A

Respiratory bronchioles

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11
Q

Which 2 tissues extend into the alveolar ducts and beyond?

A

Smooth muscle & elastic fibers

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12
Q

What are the 2 cells on the surface of the resp. epithelium and what are they coated with?

A

Ciliated cells + goblet cells, coated in mucus

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13
Q

Which cell does smoking harm?

A

Cilia - unable to beat properly, so they can’t move mucus properly.

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14
Q

Gland cell appearance

A

cuboid (vs. squamous appearance of blood vessels)

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15
Q

Define ventilation

A

refers to the movement and distribution of air within the conduction portion of the respiratory tract

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16
Q

Define diffusion

A

refers to the movement of O2 and CO2 between the alveolar space and the capillary blood

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17
Q

Define perfusion

A

refers to the flow and distribution of blood within the pulmonary vascular bed

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18
Q

Where does gas exchange occur?

A

In type I alveolar cells

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19
Q

Where is surfactant produced?

A

In type II alveolar cells

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20
Q

What is the job of the alveolar macrophage?

A

Live outside of the vascular space, when garbage enters the alveolus they can cross between type I alveolar cells, enter the alveolus itself, gobble up the garbage, then move back into the extravascular space where they’ll eventually wind up in the lymphatic channel and exit.

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21
Q

What structures make up the fused basal lamina?

A

The basement lamina of the vasculature and the basement lamina of the alveolar cells.

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22
Q

Where does the lung bud bifurcate?

A

At the carina.

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23
Q

How is negative pressure produced?

A

The parietal pleura absorbs oxygen from the pleural cavity, producing negative pressure within the cavity itself.

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24
Q

What week of gestation do type II alveolar cells appear?

A

Around 24 weeks.

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25
Q

What group of drugs slow/stop uterine contractions?

A

Tocolytics

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26
Q

What is surfactant?

A

“Soap” that lines the alveoli.
It has certain proteins and lipids that keep the surface tension such that the alveoli in the alveolar ducts, when you breath out, don’t collapse on themselves.

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27
Q

What produces respiratory distress syndrome (RDS)?

A

Absence of surfactant

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28
Q

What are the 4 roles of surfactant?

A
  1. To increasepulmonary compliance.
  2. To preventatelectasis(collapse of the lung) at the end of expiration
  3. To facilitate recruitment of collapsed airways
  4. Participates in immunity
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29
Q

What is hyaline membrane disease?

A

An older term for IRDS, based on the pathological findings at autopsy of premature infants.
The hyaline membranes were proteinaceous material in the damaged alveoli.

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30
Q

How is lung maturity determined in pregnancy?

A

In pregnancies >30 weeks – by amniocentesis

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31
Q

What 3 factors are measured for lung maturity?

A
  1. lecithin/sphingomyelin ratio (L/S ratio) – >2:1 ratio is desired
  2. phosphatidylglycerol (PG) – presence indicates maturity
  3. surfactant/albumin (S/A ratio) - < 35 indicates immaturity, 35-55 indeterminant, and >55 indicates maturity (correlates with L/S of 2.2 or greater)
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32
Q

What drug can hasten lung maturity?

A

An IM dose of steroids (commonly given to mothers under 38 weeks if contractions begin)

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33
Q

What are the 5 defense mechanisms of the respiratory system?

A

Vibrissae, mucous, bronchiolar secretions, lymph nodes, and alveolar macrophages.

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34
Q

What particles do vibrissae filter?

A

> 10μm filtered by vibrissae or trapped in the oropharynx

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35
Q

What particles are trapped in mucous and where?

A

< 10μm trapped in mucous in nasal cavity, trachea and bronchi swept by cilia

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36
Q

What characteristics of bronchiolar secretions allows them to participate in defense?

A

they have lysozyme and secretory IgA from lymphatic in connective tissues under the epithelia

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37
Q

How do lymph nodes participate in defense?

A

Lymph nodes surround bronchi at the lung hilum to filter lymph generated in acinus

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38
Q

What particles are “eaten” by alveolar macrophages?

A

1 - 5μm in size may be accessible to the terminal airways and alveoli where they are phagocytized by alveolar macrophages (same size as bacterium)

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39
Q

True/False: the lower respiratory tract contains particles and normal bacterial flora.

A

False: Lower respiratory tract is basically a sterile environment

40
Q

Define Goodpasture syndrome

A

Rare, auto-immune disorder whereby IgG antibodies are directed against Type IV collagen (found in the basement membrane of the lungs, around the alveoli, and in the glomerulus.
Causes: pulmonary dysfunction + renal failure

41
Q

What age groups does Goodpasture syndrome affect?

A

Peak ages on onset 20-30 and 60-70

42
Q

What is the treatment for Goodpasture syndrome?

A

immune suppressants – steroids (first line) and biologics

43
Q

What is systemic lupus erythematosus (SLE)?

A

Common auto-immune disorder
age of onset between 15-35 years old
*mostly women

44
Q

What does SLE affect?

A

skin, lungs (producing a restrictive disease), heart, kidneys, joints, vessels, CNS

45
Q

What tests do you run for SLE?

A

Anti-Smith
Anti-dsDNA (anti-double-stranded DNA)
ANA (anti-nuclear antigen)

46
Q

Describe the difference in fluorescent marker apeparance of Goodpasture’s syndrome and SLE

A

Goodpasture: linear and smooth due to surface bound antigen.
SLE: lumpy and bumpy due to immune complex.

47
Q

What is affected by Cystic Fibrosis?

A

Affects mucus in the lungs & pancreas most often, intestines because of what happens to the pancreas, liver & kidneys less often

48
Q

What inheritance pattern does CF have?

A

Autosomal recessive – gene codes for CF transmembrane conductance regulator protein (CFTR)

49
Q

What bacteria are CF patients colonized with that would not be seen in normal, healthy patient?

A

Pseudomonas aeruginosa

50
Q

How does the mutated protein in CF cause disease?

A

The mutated protein does not fold properly and is degraded by the cell.
It is a transmembrane protein that creates a channel for chloride ion - important for viscosity and salt content of sweat, digestive juices, and mucus

51
Q

What signs are seen in CF infants in the first days of life?

A

GI issues: thick, tarry stools and constipation

52
Q

What causes hyper-salty “taste” in CF patients?

A

In sweat glands, chloride ion is trapped in the ducts, causing sodium to flow out of the cell and upwards towards the skin.

53
Q

Where do airway cilia move?

A

in the Airway Surface Liquid layer (ASL)

54
Q

How is ASL affected by CF?

A

If you move salt out of the ASL (due to lack of channels for chloride ion - defective protein), water is going to go with it, making the ASL more viscous.

55
Q

Define obstructive pulmonary diseases

A

Diseases that produce an obstruction to air flow by narrowed diameter of components of the respiratory tree or by mechanical obstruction by mucus plugging or mass.

56
Q

Characteristics of chronic obstructive pulmonary disease (COPD)
- emphysema

A
  • narrowing with loss of elastic recoil and alveolar structure d/t release of enzymatic digestion by macrophages and neutrophils.
  • air moves in on inspiration, but on expiration, without elastic fibers the distal airways collapse upon themselves trapping air behind.
57
Q

Why are emphysema patients called “pink puffers?”

A

Approximately equal destruction of airways and capillaries, hence not much of a ventilation/perfusion mismatch and so patients stay “pink”. To expel air from the lungs (increased contraction of the diaphragm and chest muscles) and become “puffers”.

58
Q

What are 2 common symptoms in emphysema pts?

A
  • Breathing takes increased energy and causes the patient to lose weight.
  • They will have a hyper-inflated “barrel chest” due to chronic hypoxia and a thin frame
59
Q

Characteristics of chronic bronchitis

A

Excess mucus with chronic cough, air is able to enter around the mucous plugs, but on expiration as the bronchioles collapse around the plugs, and air is trapped.

60
Q

Why are chronic bronchitis pts called “blue bloaters?”

A
  • Patients are not able to get air to the alveolar capillaries (ventilation/perfusion mismatch), the patients become cyanotic (blue).
  • CO2 builds up in the blood to cause an acidosis - promoting pulmonary vasoconstriction. Patients develop pulmonary hypertension with ensuing right heart failure and body-wide edema (bloater).
61
Q

What are complications of chronic bronchitis?

A

Repeated infections, cor pulmonale, peptic ulcers, and respiratory failure.

62
Q

What is the primary cause of COPD?

A

tobacco smoking

63
Q

How does alpha 1-antitrypsin deficiency cause COPD?

A

It’s a protein produced by liver that inhibits neutrophil elastase –> if deficient, elastase breaks down alveolar walls, worsened by tobacco smoking that inactivates alpha 1-antitrypsin

64
Q

If you see emphysema in a young adult, what should be first on your diff dx?

A

Alpha 1-antitrypsin deficiency

65
Q

How is asthma characterized?

A

by constriction of bronchioles and increased mucus production: inflammatory reactions to allergens (worsened by exposure to tobacco smoke)

66
Q

What drugs are used to decrease secretions in asthma?

A

parasympatholytic (Atrovent HFA/ipratropium, Spiriva/tiotropium)

67
Q

What drugs are used to decrease allergic response in asthma?

A
  1. inflammation by steroids (Pulmicort/Flovent HFA, po)
  2. mast cell stabilizers (Intal/cromolyn)
  3. leukotriene inhibitors (Singulair/montelukast, Accolate/zafirlukast)
68
Q

What are restrictive lung diseases?

A

group of disorders is characterized by decreased lung compliance (or increase in the “stiffness” of the lung) due to formation of scar tissue as a result of one several process

69
Q

List the intrinsic causes of restrictive lung diseases

A
  • Pneumoconiosis
  • Radiation
  • Amiodarone, methotrexate
  • ARDS
  • Sarcoidosis
70
Q

List the extrinsic causes of restrictive lung diseases

A
  • Obesity
  • Kyphosis
  • Pleural thickening
71
Q

What is FEV1?

A

forced expiratory volume in one second

72
Q

What is FVC?

A

forced vital capacity

73
Q

How do restrictive lung diseases affect FEV1 and FVC?

A

FEV1 is reduced, however, the decline in FVC is more than that of FEV1, resulting in a higher than 80%FEV1/FVC ratio.

74
Q

How do obstructive lung diseases affect FEV1 and FVC?

A

FEV1 is reduced while FVC remains stable

75
Q

What is pneumoconicosis?

A

occupational diseases caused by the inhalation of inorganic mineral dusts (coal dust, silica, asbestos, talc, etc)

76
Q

What is the disease process of pneumoconicosis? (5 steps)

A
  1. dusts elicit inflammation and pulmonary fibrosis as host response
  2. the more soluble particles tend to elicit MORE of an inflammatory response, while the more insoluble materials tend to elicit a fibrotic response.
  3. size, shape, and concentration of the inhaled material also has a bearing on the resultant damage
  4. particles less than 2μm in size are able to reach the terminal airways where the alveolar macrophage is the primary defense mechanism
  5. Release of chemical mediators from the macrophages and activation of leukocytes are the mechanism of injury to the pulmonary parenchyma.
77
Q

What are other names for adult respiratory distress syndrome?

A

ARDS, RDS Type II, Diffuse Alveolar Damage, “Shock” Lung

78
Q

What is the cause of ARDS?

A

widespread microvascular injury

79
Q

List the 6 things that induce ARDS

A
  1. high altitude exposure
  2. anaphylaxis
  3. chemical or physical irritants
  4. fulminant bacterial or viral infection
  5. drugs/drug reactions
  6. oxygen toxicity
80
Q

Characteristics of ARDS

A

acute onset dyspnea and tachypnea with tachycardia

81
Q

Does hypoxemia in ARDS respond to oxygen therapy?

A

No, cyanosis occurs as oxygen falls. Mortality approaches 50%

82
Q

ARDS inflammatory response

A

includes fibrin rich exudate into alveoli and subsequent hyaline membrane formation

83
Q

What kind of virus is human respiratory syncytial virus?

A

Single stranded RNA virus in the same family as measles and mumps

84
Q

Who does RSV infect and how is it transmitted?

A
  • All kids by 3 years of age

- Transmission is by direct contact with the virus remaining virulent 1-5 hours on external surfaces

85
Q

What does “syncytial” refer to in RSV?

A
  • the clumping of host cells infected with HSV-1, HIV, and paramyxoviruses (RSV)
  • the virus has an F (fusion) protein on its surface that causes neighboring host cells to aggregate into a syncytium
86
Q

How do most clinics diagnose RSV?

A

Rapid antigen detection tests

87
Q

When is “RSV season?”

A

Coincides with flu season.

88
Q

What is the general cause of pulmonary edema (PE)?

A

Intervascular fluid leaking into the alveoli

89
Q

What are some causes of PE?

A

disturbances of the normal hemodynamic equilibrium (congestive heart failure, myocardial infarction, hypertensive heart disease, longstanding mitral stenosis, central nervous system damage) or microvascular injury

90
Q

What causes characteristic pink foam of PE?

A

Intravascular fluid mixing with surfactant

91
Q

Treatment for PE

A

Goal is to decrease vascular pressure in the lungs –> morphine dilates peripheral vessels and shunts blood away from the lungs

92
Q

What is aspiration pneumonia?

A

Pharyngeal content or vomitus into the lung.

93
Q

What patients does aspiration pneumonia frequently occur in?

A
  • unconscious patients or altered mental status
  • those with repeated vomiting episodes
  • those with depressed cough reflexes (alcoholic intoxication, central nervous system malfunction, acute drug intoxication, etc).
94
Q

Aspiration of solid masses…

A

may cause obstruction of the tracheobronchial tree as well as introduce microorganisms

95
Q

Aspiration of liquid gastric contents…

A

causes acute inflammatory reaction, pulmonary edema, and widespread destruction of epithelium with hemorrhage and hyaline membranes

Pulmonology (11 decks)

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