COPD

Question 1

COPD Spirometry

Answer 1

Decreased FVC, even more decreased FEV1, leading to decreased FEV1:FVC ratio (<80%)
Also increased TLC

Question 2

Chronic Bronchitis (definition, characterized by, classic presentation)

Answer 2

Chronic productive cough lasting at least 3 months over 2 years, heavily associated with smoking
Characterized by hypertrophy/hyperplasia of bronchial mucinous glands taking up >50% of the wall (Reid index)
“Blue bloaters” - mucous traps CO2, so increase in PaCO2 and decrease PaO2 and get cyanosis. At risk for cor pulmonale

Question 3

2 General Causes of Emphysema

Answer 3

Balance of proteases and antiproteases, so:
Excessive inflammation (leading to excessive protease production from nphils and macs), like from smoking
Antiprotease deficiency like alpha-1 antitrypsin (A1AT)

Question 4

Smoking Emphysema (micro and gross location)

Answer 4

From excessive inflammation, centriacinar and upper lobes (because that’s where the smoke hits most)

Question 5

A1AT Deficiency Emphysema (micro and gross location, as well as extra-pulmonary complication/histo finding)

Answer 5

Panacinar and lower lobes
Also liver cirrhosis because misfolded protein builds up in ER of hepatocytes, revealing pink, PAS-positive globules in hepatocytes

Question 6

A1AT 4 Genotypes

Answer 6

PiM - normal allele
PiZ - most common clinically relevant, significantly low levels of A1AT and buildup in ER
PiMZ - heterozygotes, usually asymptomatic but big risk if smoke
PiZZ - Significant risk

Question 7

Emphysema Classic Presentation

Answer 7

Dyspnea and cough with MINIMAL sputum, and “pink puffer” - purse lips to create some back pressure to keep airways open. Difficult breathing yields weight loss
Also increase in AP diameter because now lung doesn’t have recoil to counter chest wall expansion as well, so increased FRC
Hypoxemia and cor pulmonale late

Question 8

Asthma Pathogenesis (5)

Answer 8

TH2 CD4 T cells stimulated by allergens in genetically susceptible individuals.
Secrete IL4, IL5, and IL10
Re-exposure to Ag leads to IgE mediated activation of mast cells, which release preformed histamine granules and produce leukotrienes C4, D4, and E4 causing bronchoaconstriction, inflammation, edema (early phase reaction)
Inflammation, especially major basic protein from ephils, damages cells and perpetuates (late phase reaction)

Question 9

IL4, 5, and 10 actions

Answer 9

IL4 - mediates class switch to IgE
IL5 - attracts eosinophils
IL10 - stimulates TH2 cells and inhibits TH1

Question 10

Sputum Findings in Asthma (2)

Answer 10

Curschmann spirals - spiral shaped mucus plugs

**Charcot-Leyden Crystals - eosinophil derived crystals

Question 11

Bronchiectasis 3 Notable Causes (& others)

Answer 11

Cystic Fibrosis
Kartagener’s Syndrome - defect of dynein arm in cilia also causing sinusitis/infertility/situs inversus
Allergic bronchopulmonary aspergillosis - Hypersensitivity reaction to Aspergillus causing chronic inflammatory damage
Also any tumor or foreign body or necrotizing infection or anything can cause

Question 12

Bronchiectasis Sputum

Answer 12

Foul-smelling

Question 13

Bronchiectasis Complication

Answer 13

Secondary (AA) amyloidosis, because chronic inflammation leads to acute phase reactant SAA which deposits AA