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MHD > pulmpath1 > Flashcards

pulmpath1 Flashcards

1
Q

Type 1 cells (squamous pneumocytes)

A

gas exchange

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2
Q

Type 2 cells (granular pneumocytes)

A

secrete surfactant

-if there is injury repopulate and can turn into type 1

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3
Q

What type of cells line the blood vessels of alveoli, gas exchange?

A

endothelial cells

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4
Q

What cells provide structural support for the alveoli?

A

connective tissue cells (fibroblasts)

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5
Q

What cells are in the interalveolar septa and play immunological role, rare in normal health?

A

neutrophils and lymphocytes

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6
Q

Any process that reduces alveolar surface area, capillary surface area, increases distance from the airspace to the capillary causing what?

A

ventilation-perfusion mismatch–>reduced gas exchange

-in general ventilation perfusion mismatches are more important causes of reduced diffusion capacity than are diseases that damage the alveolar cells

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7
Q

How far do cilia and goblet cells go down the respiratory tract?

A

the end of the respiratory bronchioles

-below the respiratory bronchioles there is no mucociliary escalator

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8
Q

What is agenesis or hypoplasia of the lungs associated with?

A
  1. prolonged oligohydramnios
  2. decreased intrathoracic space
  3. decreased breathing movements
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9
Q

What are some trachea or bronchial anomalies?

A
  1. atresia
  2. stenosis
  3. fistula-abnormal connection (fistula) between the esophagus and the trachea
    - inadequate separation from pharynx and gi tract
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10
Q

What is a bronchogenic cyst?

A

foregut buds that become separated and disconnected from the tracheobronchial tree, progressively enlarging, and forming a cystic mass

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11
Q

What is a congenital cystic adenomatoid malformation CCAM?

A

(congenital pulmonary airway malformation CPAM)

-hamartomatous lesions-usually lower lobes (benign, focal malformation composed of tissue elements normally found at that site, but which are growing in a disorganized mass)

-classified based on size of cysts and level of origin based on histological appearances
type 1-5(1 most common, large cysts, 2-medium cyst)

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12
Q

What is pulmonary sequestration?

A

discrete mass of lung tissue without connection to the airway system

Types: extralobular and interlobular

-doesn’t communicate with tracheobronchial tree so it doesn’t drain-likely to get infected-lot of inflammation-blue cells and mucus

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13
Q

What are some acquired ways to get atelectasis? How does the mediastinum respond?

A
  1. resorption or obstruction
    - asthma, COPD, bronchiectasis, aspiration, post op patients
    - mediastinum shifts towards infected area
  2. compression
    - effusions, air, tumors, CHF
    - mediastinum shifts away from the affected lung
  3. contraction
    - fibrosis of lung/pleura
    - not reversible
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14
Q

What is pneumothorax?

A

causes compression, collapse and atelectasis,leading to respiratory distress
-spontaneous or traumatic

  • most commonly associated with emphysema, asthma, TB
  • spontaneous idiopathic form-in younger people, rupture of peripheral small pleural blebs
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15
Q

What are some causes of edema?

A
  1. increased hydrostatic pressure
  2. reduced osmotic pressure
  3. lymphatic obstruction
  4. na retention
  5. inflammation
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16
Q

What are three that causes of pulmonary edema?

A
  1. hemodynamic or cardiogenic edema
    - left sided heart failure
    - volume overload
  2. edema due to microvascular injury (alveolar injury)
    - infections
    - liquid aspiration, drugs, chemicals, radiation, transfusion
  3. Edema of undetermined origin
    - high altitude, neurogenic
17
Q

How does acute lung injury (non cardiogenic pulmonary edema) present?

A

spectrum of bilateral pulmonary damage

  • acute onset dyspnea
  • hypoxemia
  • development of bilateral pulmonary infiltrates in the absence of cardiac failure

causes: direct-pneumonia, aspiration indirect-sepsis, acute pancreatitis

if severe ALI can progress to ARDS

18
Q

What is ARDS?

A
  • rapid onset of life-threatening respiratory insufficiency
  • cyanosis
  • severe arterial hypoxemia-refractory to oxygen therapy

symptoms: tachypnea and dyspnea
approach to Dx: clinical history, imaging, bronchoscopy(r/o aspiration, hemorrhage, infection, malignancy)
Treatment: treat underlying condition + supportive care

-on X ray you see lots of infiltrates but not cardiomegaly

19
Q

What is the etiology of ARDS?

A

A-aspiration, acute pancreatitis, air/amniotic fluid embolism
R-radiation
D-drug overdose, DIC, drowning
S-shock, sepsis, smoke inhalation

20
Q

histologic ARDS

A

DAD-pathologic term

diffuse alveolar damage

21
Q

How does DAD occur?

A

macrophages give signal of injury
Neutrophils get recruited
Neutrophils degranulate and cause epithelial and endothelial injury
leakage of proteins into alveolar space
protein rich and dead and dying epithelial cells

22
Q

What does DAD result int?

A
  1. pneumocytes and endothelial necrosis
  2. edmea
  3. hyalin membrane formation and widened septa
  4. organization interstitial fibrosis, and type 2 pneumocyte proliferation

50% restore
50% fibrosis-end stage honeycomb fibrosis

23
Q

What are the phases of ARDS?

A
  1. early exudative phase (acute)
  2. subacute proliferative phase (organization)
  3. Fibrotic phase (late)
24
Q

What are the causes for DAD (adult) and Hyaline membrane disease (neonatal)?

A

DAD
-infections, physical/chemical injury, inhaled irritants, hematologic, uremia

Hyaline membrane disease
-deficiency of surfactant-resulting in failure of lungs to inflate after birth

25
Q

WHat are predisposing factors to NRDS/HMD?

A
  • prematurity
  • maternal diabetes
  • c-section
26
Q

What is the function of surfactant?

A
  • stabilizes the lung by reducing surface tension
  • host defense mechanism as a barrier for inhaled particles
  • not produced in sufficient amounts till 34 weeks (can be secreted as early as 20 weeks)
Deficiency:
Increased alveolar surface tension
resistance to inflation
surface collapse
stress on alveolar wall
alveolar injury 
DAD
27
Q

What is surfactant synthesis modulated by?

A 
glucocorticoids-increases production
insulin-decreases production 
labor induces production
prolactin 
thyroxine
tgf-b
28
Q

How do you assess and prevent/treat NRDS/HMD(histology term)?

A
  • delay labor
  • admin exogenous surfactant

Asses:
amniotic fluid assays: lecithin:sphingomyelin ration >2:1
amniotic fluid: lamellar body counts

29
Q

What is acute interstitial pneumonia?

A
  • rapidly progressive disease clinically similar to ARDS with no identifiable cause; death usually within 2 months
  • adults with influenza-like illness followed by SOB
  • microscopically resembles diffuse alveolar damage with brisk interstitial fibroblastic proliferation
  • need to rule out other etiology for ARDS

MHD (81 decks)

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