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Respiratory Tract Pathophysiology > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

What is the most common cause of rhinitis?

A

Rhinovirus

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2
Q

What is the classic triad of aspirin-intolerant asthma?

A

asthma, aspirin-induced bronchospasms and nasal polyps

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3
Q

What are nasal polyps associated with in children and adults?

A

Children- CF

Adults- aspirin-intolerant asthma

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4
Q

What are the characteristics of a nasopharyngeal angiofibroma?

A

benign nasal mucosa tumor that is composed of large blood vessels and fibrous tissue

  • classically seen in adolescent males
  • presents with profuse epistaxis
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5
Q

What are the characteristics of nasopharyngeal carcinoma?

A

malignant tumor of nasopharyngeal epithelium, usually presents with cervical LAD

  • associated with EBV, especially African kids and Chinese young adults
  • Biopsy: pleomorphic keratin+ epithelial cells with lymphocytes
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6
Q

What is the presentation of acute epiglottitis and what is the most common cause?

A

Presents w fever, sore throat, dyphagia, muffled voice, inspiratory stridor

caused by H influenzae type b

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7
Q

Laryngotracheobronchitis (croup)

A

inflammation of upper airway, presents with hoarse cough and inspiratory stridor

-parainfluneza most common cause

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8
Q

vocal cord nodule

A

aka singer’s nodule, on true vocal cord due to overuse

composed of myxoid connective tissue

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9
Q

What are laryngeal papillomas associated with?

A

HPV 6 and 11 - usually single nodule in adults and multiple with kids

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10
Q

What are the three patterns of pneumonia on x-ray?

A

lobar pneumonia - consolidation of entire lobe

bronchopneumonia - scattered patchy consolidation around bronchioles; multifocal and bilateral

interstitial (atypical) pneumonia - diffuse interstitial infiltrates

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11
Q

What are the gross phases of lobar pneumonia?

A
  1. congestion - congested vessels and edema
  2. red hepatization - exudate, PMNs and RBCs fill alveolar air spaces -> solid consistency and red appearance
  3. Gray hepatization - degredation of RBCs within exudate
  4. Resolution -> type II pneumocytes help regenerate
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12
Q

What organisms usually cause lobar pneumonia?

A

strep pneumoniae, klebsiella (aspiration pneumonia)

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13
Q

What bacteria is associated with pneumonia in cystic fibrosis patients?

A

psuedomonas

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14
Q

What are the basic features of COPD?

A

lung can’t empty and air is trapped
-> decreased volume of air that can be forcefully expired is decreased, especially during 1st second –> FEV1:FVC Total lung capacity (TLC) is increased due to air trapping

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15
Q

Chronic bronchitis - clinical features

A

chronic productive cough lasting at least 3 months over at least 2 years due to excess mucus production

‘blue bloaters’ - Cyanosis - mucus prevents adequate diffusion -> low PaO2 and high PaCO2

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16
Q

What are the histological features of chronic bronchitis?

A

Hypertrophy of bronchial mucinous glands -> Reid index increases to > 50% (thickness of mucus glands/bronchial wall thickness)

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17
Q

What are complications of chronic bronchitis?

A

increased risk of infection and cor pulmonale (R heart failure)

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18
Q

What is the pathogenesis of emphysema?

A

Imbalance of proteases and antiproteases-> inflammation in lung leads to protease release by PMNs and macrophages and alpha1-antitrypsin (A1AT) neutralizes protease

–> too much inflammation (from smoking) or too little A1AT (A1AT deficiency) leads to destruction of alveolar air sacs

–>destruction of air sacs causes loss of elastic recoil and collapse of airways during exhalation, increased compliance and decreased diffusing capacity for CO

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19
Q

What usually causes centriacinar emphysema?

A

Smoking; most severe in upper lobes since smoke rises in lungs

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20
Q

Panacinar emphysema is usually caused by what?

A

alpha1-antitrypsin deficiency; most severe in lower lobes

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21
Q

Alpha1-antitrypsin deficiency

A

A1AT deficiency is due to misfolding of protein; can also accumulate in ER of hepatocytes and cause liver cirrhosis

Disease severity based on degree of deficiency

  • PiM= normal allele; usually 2 copies: PiMM
  • PiZ= mutated allele –> PiMZ heterozygotes usually asymptomatic with increase risk of emphysema, PiZZ homozygotes significant risk for panacinar emphysema and cirrhosis
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22
Q

Clinical features of emphysema

A
  • ‘pink-puffer’ prolonged expiration with pursed lips
  • weight loss, cough with minimal sputum
  • ‘barrel-chest’ increased anterior-posterior diameter of chest
  • –> INCREASED FRC (functional reserve capacity)

-CXR: hyperlucency of lung fields and flattening of diaphragm

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23
Q

Pathogenesis of asthma

A

Type I hypersensitivity

Allergen induce Th2 CD4+ cells in susceptible individuals
*Th2 secretes: IL-4 (mediates class switch to IgE), IL-5 (attracts eosinophils) and IL-10 (stimulates Th2 cells and inhibits Th1 cells)

Reexposure to allergen -> IgE-crosslinking mediated activation of mast cells release

  • –> histamine granules (1st phase) and generates leukotrienes C4, D4, and E4 -> bronchoconstriction, inflammation and edema
  • –> Inflammation, especially major basic protein derived from eosinophils, damages cells and perpetuates bronchoconstriction (late phase)
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24
Q

What are the microscopic features of asthma?

A

Curschmann spirals: spiral-shaped mucus plugs

Charcot-Leyden crystals: eosinophil-derived crystals

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25
Q

What is bronchiectasis?

A

permanent dilation of bronchioles and bronchi; loss of airway tone results in air trapping

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26
Q

What are causes of bronchiectasis?

A

Necrotizing inflammation damages airway walls

Causes:
CF- mucus plug -> infection
Kartagener syndrome -> defect of dynein arm causes impaired ciliary movement
Tumor/ foreign body
Necrotizing infection
ABPA (Allergic bronchopulmonary aspergillosis; usually seen in asthma or CF)

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27
Q

What are the features and complications of bronchiectasis?

A

Features: cough, dyspnea, foul-smelling sputum

Complications: cor pulmonale, secondary amyloidosis

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28
Q

What are the general characteristics of restrictive lung diseases?

A

Restricted filling of lung –> decreased TLC and FEV1 and very decreased FVC –> FEV1/FVC > 80%

Commonly due to
- interstitial lung diseases –> DECREASED diffusing capacity of CO, INCREASED A-a gradient

-Poor breathing mechanics (obesity, scoliosis, myasthenia gravis) –> NORMAL A-a gradient

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29
Q

What is the pathogenesis of idiopathic pulmonary fibrosis

A

Likely related to cyclical lung injury and healing; TGF-beta from injured pneumocytes induces fibrosis

Thickening and stiffening of pulm. interstitium -> increased lung elastic recoil -> airway widening due to increased radial traction by surrounding fibrotic tissue –> decrease in airway resistance causes supernormal expiratory flow rates when corrected for lung volume

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30
Q

What drugs can cause interstitial fibrosis?

A

bleomycin, methotrexate, busulfan, amiodarone and radiation therapy

31
Q

what is the pathogenesis of pneumoconioses?

A

exposure to small particles that are fibrogenic, alveolar macrophages engulf particles and induce fibrosis

32
Q

Asbestosis

A

Exposure: asbestos fibers; construction workers, plummers and shipyard workers

Path findings: Affects lower lobes .”ivory white” calcified lung and pleura plaques. Aspestos (ferruginous) bodies- golden/brown fusiform rods in alveolar septum

Associated with increased incidence of lung cancer and mesothelioma; increased risk of cor pulmonale and Caplan syndrome

33
Q

What is Caplan syndrome

A

RA and pneumoconioses with intrapulmonary nodules

Increased risk with asbestosis, coal workers’ pneumoconioses and silicosis

34
Q

Berylliosis

A

Exposure to beryllium in aerospace and manufacturing industries

Affects upper lobes, Noncaseating granulomatous on histology (can be responsive to steroids) in lung, hilar LNs and systemic organs (can look similar to sarcoidosis)

Increased risk for lung cancer

35
Q

Coal worker’s pneumoconiosis

A

carbon dust exposure

Diffuse fibrosis in upper lobes ‘black lung’, associated with RA (Caplan syndrome)

36
Q

Anthracosis

A

asymptomatic condition from mild exposure to carbon

37
Q

Silicosis

A

Silica exposure associated with foundries, sandblasting and mines

Path: fibrotic nodules in upper lobes of lung, ‘eggshell’ calcification of hilar lymph nodes

*Increased risk for TB as silica impairs phagolysosome formation by macrophages

38
Q

Hypersensitivity pneumonitis

A

Mixed type III/IV hypersensitivity reaction to environmental allergen -> usually in farmers (actinomyces, aspergillus) and those who work with birds (avian proteins in bird droppings)

39
Q

Neonatal respiratory distress syndrome (NRDS)

A

surfactant deficiency; Lechithin:sphingomyelin ratio PDA risk, necrotizing enterocolitis

40
Q

What are risk factors for neonatal respiratory distress syndrome (NRDS)?

A

prematurity, maternal diabetes (increased fetal insulin), C-section (decreased release of fetal glucocorticoids)

41
Q

What are complications of supplemental O2 treatment in NRDS?

A

retinopathy, intraventricular hemorrhage, bronchopulmonary dysplasia

42
Q

What are the clinical features of acute respiratory distress syndrome?

A

bilateral lung opacities, decreased PaO2/FiO2

Alveolar damage -> protein rich alveolar fluid and noncardiogenic pulmonary edema (NORMAL PCWP)
Intra-alveolar hyaline membranes

clear frothy alveolar fluid and thick hyaline membranes on histology

43
Q

Sarcoidosis

A
  • noncaseating granulomas in multiple organs- most commonly in hilar lymph nodes and lungs -> restrictive lung disease (decreased lung compliance)
  • usually in African American women
  • steallate inclusions ‘asteroid bodies’ seen within giant cells
  • also commonly causes uveitis, cutaneous nodules, affect salivary and lacrimal glands mimicking Sjogren syndrome
44
Q

What are the clinical features of sarcoidosis?

A

dyspnea/cough
elevated ACE in serum
hypercalcemia (from noncaseating granulomas)
Treat with steroids

45
Q

Pulmonary HTN

A

normal mean pulm artery pressure= 10-14mmHg, pulmonary HTN >/= 25mmHg

Causes arteriosclerosis of pulmonary trunk, smooth muscle hypertrophy of pulmonary arteries and intimal fibrosis

Leads to RV hypertrophy and eventually cor pulmonale

46
Q

Primary pulmonary HTN

A

seen in young adult females, usually due to inactivating mutation in BMPR2 gene which normally inhibits vascular smooth muscle proliferation –> thickened walls –> HTN

47
Q

Secondary pulmonary HTN

A

due to hypoxemia (vessels constrict to shunt blood to better oxygenated areas) or increased volume in pulmonary circuit, recurrent PE

48
Q

Decreased breath sounds, hyperresonant to percussion and tracheal deviation away from side of lesion

A

Tension pneumothorax

49
Q

Bronchial breath sounds; late inspiratory crackles, dullness to percussion and increased fremitus

A

Consolidation (lobar pneumonia, pulmonary edema)

50
Q

Decreased breath sounds, dullness to percussion and fremitus, and tracheal deviation toward the side of lesion

A

atelectasis

51
Q

Decreased breath sounds, dullness to percussion and fremitus, and without tracheal deviation or deviated away from the side of lesion

A

pleural effusion

52
Q

pleural effusion with serum protein/fluid protein

A

transudate; due to increased hydrostatic pressure or decreased oncotic pressure (HF, nephrotic syndrome, cirrhosis)

53
Q

pleural effusion with serum protein/fluid protein >0.5 and serum LDH/fluid LDH >0.6

A

exudate; due to increased vascular permeability (malignancy, pneumonia, trauma, collagen vascular disease)

54
Q

Tension pneumothorax

A

air enters pleural space but cannot exit -> trachea deviates away from affected lung due to increased pressure

55
Q

What is primary spontaneous pneumothorax associated with?

A

rupture of apical blebs or cysts usually in tall, thin, young men

  • Marfan syndrome
  • Ehlers-Danlos syndrome
  • Homocystinuria
56
Q

Fat embolism syndrome - clinical triad

A

acute-onset neuro abnormalities
hypoxemia
petechial rash

In setting of long bone fracture

57
Q

What are the pulmonary effects of Potter syndrome and what causes it?

A

Caused by decreased renal function in fetus (can’t pee) causing oligohydramnios which causes pulmonary hypoplasia along with limb deformities and characteristic facies

58
Q

What are the changes in PaO2, PaCO2, pH and HCO3- at high altitudes

A

PaO2 decreases
PaCO2 decreases
pH increases (respiratory alkylosis)
HCO3- decreases to compensate

59
Q

What happens to the arterial and venous O2 and CO2 during strenuous exercise?

A

PaO2 and PaCO2 are normal

PvO2 decreases and PvCO2 increases

60
Q

Where is V/Q highest and lowest in the lungs?

A

highest at the apex (PA>Pa>Pv), V/Q=3 (wasted ventilation)

lowest at the base (Pa>Pv>PA), V/Q=0.6 (wasted perfusion)

61
Q

What would decrease V/Q?

A

airway obstruction (shunt) ex asthma. 100% O2 does NOT improve PaO2

62
Q

What would increase V/Q?

A

Blood flow obstruction (physiologic dead space), if less than 100% dead space, 100% O2 will improve PaO2

63
Q

What is the A-a gradient?

A

PAO2 - PaO2 = 10-15mmHg normally

64
Q

What can cause an increase in A-a gradient?

A

hypoxemia- shunting, V/Q mismatch, fibrosis

65
Q

What is the alveolar gas equation?

A 
PAO2 = PIO2 (inspired O2) -[PaCO2/R]
R= respiratory quotient CO2 produced/O2 consumed

PAO2= 150mmHg - PaCO2/0.8 at sea level room air

66
Q

What is methemoglobin?

A

oxidized form of Hb (Fe3+ instead of Fe2+), has lower O2 affinity but increased affinity for cyanide

67
Q

How and why is methemoglobinemia induced?

A

Indued to treat cyanide poisoning
Can be done using nitrites, followed by thiosulfate which combines with cyanide to form thicyanite and is excreted by kidneys

68
Q

What drugs and conditions can cause methemoglobinemia? How does it present?

A

Drugs: nitrites, dapsone, benzocaine
Inherited in AR cytochrome b5 reductase deficiency

Presents with cyanosis and chocolate-colored blood; O2 sat lower and PaO2 normal

69
Q

What does CO poisoning do to the Hb concentration, %O2sat of Hb, PaO2, and total O2 content?

A

Hb concentration - normal
%O2sat of Hb - decreases
PaO2 - normal
Total O2 - decreases

70
Q

What factors shift the oxygen-Hb dissociation curve to the right?

A

(lower affinity of O2)

acid, increased CO2, exercise, increased 2,3-BPG, increased altitude, increased temperature

71
Q

Biot’s respiration

A

ataxic respiration

Period breathing: hyperpnea (or normopnea) and then apnea

Poor prognosis, neuron damage

72
Q

Kussmaul breathing

A

Associated with metabolic acidosis in diabetes mellitus

Hyperpnea

K-ketones
U-uremia
S-sepsis
S-salicylates
M-methanol
A-aldehydes
U
L-lactic acid/lactic acidosis
73
Q

Cheyne-Stokes respiration

A

Periodic breathing: gradual hyperpnea/hypopnea (crescendo-decrescendo pattern) and apnea

Caused by hypoperfusion of the brain’s respiratory centers or damage

  • CHF
  • newborns (immature respiratory systems)
  • high altitudes

Respiratory Tract Pathophysiology (1 decks)

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