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Step 1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Embryonic stage

A
  • Weeks 4-7
  • Lung bud → trachea → mainstem bronchi → secondary (lobar) bronchi → tertiary (segmental) bronchi
  • Errors at this stage can lead to TE fistula
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2
Q

Pseudoglandular stage

A
  • Weeks 5-16
  • Endodermal tubules → terminal bronchioles
  • Surrounded by modest capillary network
  • Respiration impossible, incompatible with life
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3
Q

Canalicular stage

A
  • Weeks 16-26
  • Terminal bronchioles → respiratory bronchioles → alveolar ducts
  • Surrounded by prominent capillary network
  • Airways increase in diameter
  • Respiration capable at 25 weeks
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4
Q

Saccular stage

A
  • Weeks 26-birth
  • Alveolar ducts → terminal sacs
  • Terminal sacs separated by primary septae
  • Pneumocytes develop
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5
Q

Alveolar stage

A
  • Weeks 32-8 years
  • Terminal sacs → adult alveoli (due to secondary septation)
  • In utero, breathing occurs via aspiration and expulsion of amniotic fluid → ↑ vascular resistance through gestation
  • At birth, fluid gets replaced with air → ↓ pulmonary vascular resistance
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6
Q

Bronchogenic cysts

A
  • Caused by abnormal budding of the foregut and dilation of the terminal or large bronchi
  • Discrete, round, sharply defined and air-filled densities on CXR
  • Drain poorly and cause chronic infections
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7
Q

Club cells

A
  • Non-ciliated
  • Low columnar/cuboidal with secretory granules
  • Secrete component of surfactant
  • Degrade toxins
  • Act as reserve cells
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8
Q

Zone of respiratory tree that has least airway resistance

A

Terminal bronchioles

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9
Q

Where do cartilage and goblet cells extend to on respiratory tree

A

End of bronchi

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10
Q

Where do cilia extend to on respiratory tree

A

Respiratory bronchioles

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11
Q

Inspiratory capacity

A

IRV + TV

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12
Q

Functional residual capacity

A
  • RV + ERV
  • Volume of gas in lungs after normal expiration
  • Includes RV (cannot be measure on spirometry)
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13
Q

Vital capacity

A
  • TV + IRV + ERV

- Maximal volume of gas that can be expired after a maximal inspiration

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14
Q

Physiological dead space

A
  • Anatomic dead space of conducting airways plus alveolar dead space
  • Apex of healthy lung is larges contributor of alveolar dead space
  • Volume of inspired air that does not take part in gas exchange
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15
Q

Physiologic dead space

A
  • Approximately equivalent to anatomic dead space in normal lungs
  • May be greater than anatomic dead space in lung diseases with V/Q defects
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16
Q

Pathologic dead space

A
  • When part of respiratory zone becomes unable to perform gas exchange
  • Ventilated but not perfused
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17
Q

What determines the combined volume of the lungs

A

The elastic properties of both chest wall and lungs

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18
Q

Hysteresis

A

Lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation

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19
Q

How does fetal hemoglobin has an increased affinity for O2

A

Has a decreased affinity for 2,3-BPG

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20
Q

Perfusion limited

A
  • O2 (normal health), CO2, N2O
  • Gas equilibrates early along the length of the capillary
  • Diffusion can only be ↑ if blood flow ↑
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21
Q

Diffusion limited

A
  • O2 (emphysema, fibrosis), CO

- Gas does not equilibrate by the time blood reaches the end of the capillary

22
Q

Haldane and Bohr effects

A

HALDANE EFFECT:

  • Occurs in lungs
  • Oxygenation of Hb promotes dissociation of H+ from Hb
  • This shifts equilibrium toward CO2 formation
  • Therefore, CO2 is released from RBCs

BOHR EFFECT:

  • Occurs in peripheral tissue
  • ↑ H+ from tissue metabolism shifts curve to right, unloading O2
23
Q

Response to high altitude

A
  • ↓ atmospheric O2 → ↓ PaO2 → ↑ ventilation → ↓ PaCO2 → respiratory alkalosis → altitude sickness
  • Chronic ↑ in ventilation
  • ↑ erythropoietin → ↑ hematocrit and Hb (chronic hypoxia)
  • ↑ 2,3-BPG, binds Hb so that Hb releases more O2
  • Cellular changes (↑ mitochondria)
  • ↑ renal excretion of HCO3- to compensate for respiratory alkalosis (can augment with acetazolamide)
  • Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH
24
Q

Response to exercise

A
  • ↑ CO2 production
  • ↑ O2 consumption
  • ↑ ventilation rate to meet O2 demand
  • V/Q ratio from apex to base becomes more uniform
  • ↑ pulmonary blood flow due to ↑ cardiac output
  • ↓ pH during strenuous exercise (secondary to lactic acidosis)
  • No change in PaO2 and PaCO2, but ↑ in venous CO2 content and ↓ in venous O2 content
25
Q

Epistaxis of anterior segment of nostril

A

Kiesselbach plexus

26
Q

Epistaxis of posterior segment of nostril

A

Sphenopalatine artery, branch of maxillary artery

27
Q

Homan sign

A
  • Dorsiflexion of foot → calf pain

- DVT

28
Q

When do cyanosis and hypercapnia occur in chronic bronchitis

A
  • Cyanosis is due to early onset hypoxemia due to shunting

- Late onset dyspnea and CO2 retention (hypercapnia

29
Q

What is associated with peribronchial cuffing

A

Asthma

30
Q

Hypersensitivity pneumonitis

A

Mixed type III/IV hypersensitivity reaction to environmental antigen → dyspnea, cough, chest tightness, headache. Often seen in farmers and those exposed to birds.

31
Q

Caplan syndrome

A

Rheumatoid arthritis and pneumoconioses with intrapulmonary nodules

32
Q

What causes the initial damage in acute respiratory distress syndrome

A

Initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade and oxygen derived free radicals

33
Q

Causes of acute respiratory distress syndrome

A
  • Sepsis
  • Pancreatitis
  • Pneumonia
  • Aspiration
  • uRemia
  • Trauma
  • Amniotic fluid embolism
  • Shock

“SPARTAS”

34
Q

Obstructive sleep apnea in adults

A

Excess parapharyngeal tissue

35
Q

Obstructive sleep apnea in children

A

Adenotonsillar hypertrophy i

36
Q

Obesity hypoventilation syndrome

A

Obesity → hypoventilation → ↓ PaO2 and ↑ PaCO2 during sleep

↑ PaCO2 during waking hours (retention)

37
Q

Nonheritable causes of pulmonary arterial hypertension

A
  • Drugs (eg amphetamines, cocaine)
  • Connective tissue disease
  • HIV infection
  • Portal hypertension
  • Congenital heart disease
  • Schistosomiasis
38
Q

Physical findings of pleural effusion

A
  • ↓ breath sounds
  • Dull to percussion
  • ↓ fremitus
  • No tracheal deviation or might also be away from side of lesion (if large)
39
Q

Physical findings of atelectasis (bronchial obstruction)

A
  • ↓ breath sounds
  • Dull to percussion
  • ↓ fremitus
  • Tracheal deviation toward side of lesion
40
Q

Physical findings of simple pneumothorax

A
  • ↓ breath sounds
  • Hyperresonant to percussion
  • ↓ fremitus
  • No tracheal deviation
41
Q

Physical findings of tension pneumothorax

A
  • ↓ breath sounds
  • Hyperresonant to percussion
  • ↓ fremitus
  • Tracheal deviation away from side of lesion
42
Q

Physical findings of consolidation (lobar pneumonia, pulmonary edema)

A
  • Bronchial breath sounds; late inspiratory crackles
  • Dull to percussion
  • ↑ fremitus (this indicates denser or inflamed lung tissue)
  • No tracheal deviation
43
Q

Sites of metastases from lung cancer

A
  • Adrenals
  • Brain
  • Bone (pathologic fracture)
  • Liver (jaundice, hepatomegaly)
44
Q

Lung metastases

A
  • Usually multiple lesions
  • More common than primary neoplasms
  • Breast
  • Colon
  • Prostate
  • Bladder cancer
45
Q

Antibodies produced by small cell (oat cell) carcinoma are against

A
  • Presynaptic Ca2+ channels (Lamber-Eaton myasthenic syndrome)
  • Neurons (paraneoplastic myelitis, encephalitis, subacute cerebellar degeneration)
46
Q

Small cell (oat cell) carcinoma stains for

A
  • Chromogranin A

- Neuron-specific enolase

47
Q

Adenocarcinoma stains for

A

Mucin

48
Q

Bronchioalveolar subtype (adenocarcinoma in situ)

A
  • CXR often shows hazy infiltrates similar to pneumonia
  • Better prognosis
  • Grows along alveolar septa → apparent “thickening” of alveolar walls
  • Tall columnar cells containing mucus
49
Q

Large cell carcinoma secretes

A

β-hCG

50
Q

Bronchial carcinoid tumor stains for

A

Chromogranin A

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