Chronic Obstructive Pulmonary Disease Flashcards

1
Q

Spirometry results in obstructive diseases

A

low FVC

very low FEV1

low FEV1:FVC

(all three must be present)

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2
Q

Total lung capacity in obstructive diseases

A

increases

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3
Q

Chronic bronchitis lasts for how long

A

3+ months of coughing over a minimum of 2+ years

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4
Q

Histological findings of chronic bonchitis

A

hypertrophy of bronchial mucinous glands

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5
Q

Most prominent feature of chronic bronchitis

A

large amounts of mucous production

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6
Q

Mucus in chronic bronchitis

A

goes up: cough it up

goes down: plugs bronchioles

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7
Q

“Blue bloaters”

A

chronic bronchitis

cyanosis, due to mucus plugs

increase pCO2 and decrease pO2

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8
Q

Infection in chronic bronchitis

A

more likely

infections love to hide behind plugged tubes

plugged with mucus

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9
Q

Cor pulmonale

A

right heart failure

after right ventricular hypertrophy

due to pulmonary HTN

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10
Q

Reid index

A

used to determine thickness of mucus glands in chronic bronchitis

if >50% → chronic bronchitis

normal < 40%

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11
Q

Basic pathophysiology of emphysema

A
  1. loss of elastic recoil of alveoli
  2. air way collapse

*bronchioles normally have alveoli on them and their elastic recoil keeps the bronchioles open

*when they are consolidated, they don’t hold up as well and the bronchioles collapse under the vaccum-type pressure

*obstruction of the airway

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12
Q

How are the alveoli damaged in emphysema

A

usually there is a balance of

proteases ⇔ anti-proteases

proteases clean up debris that ends up in the alveoli

anti-proteases inactivate these so things don’t get out of hand

by increasing particulate matter (smoking) or losing antiproteases (A1AT deficiency)

macrophages go crazy either way and destroy the alveoli

⇒ emphysema

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13
Q

α1 anti-trypsin

tell me about it

A

A1AT synthesized in liver

put in blood, travels to lungs to act as anti-protease and keep balance in macrophages

proteases ⇔ anti-proteases

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14
Q

Problems in A1AT deficiency

A

liver cirrhosis

⇒ buildup of A1AT in liver, where it is synthesized

⇒ pink, PAS+ granules

emphysema

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15
Q

Type of emphysema seen in smoking

A

centriacinar emphysema

b/c damage most where convection ends (bronchioles)

upper lobs preferentially

smoke → up

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16
Q

Type of emphysema found in A1AT deficiency

A

panacinar emphysema

all over

because deficiency is all over

17
Q

“Pink puffer”

A

emphysema

pursed lips to build back pressure

18
Q

Genes in A1AT deficiency

A

PiM is normal

PiZ is pathologic

homozygous = bad

heterozygous = not as bad

19
Q

Why total lung capacity increases in emphysema

A

loss of lung elasticity

lung doesn’t pull in like it wants to collapse as much

chest wall still wants to expand it

20
Q

Hypoxemia in emphysema

A

loss of capillaries in alveolar walls

alveolar destruction

21
Q

CD4+ involved in asthma

A

Th2 cells

IL-4: IgE class-switching

IL-5: eosinophil recruitment

IL-10: stimulates Th2 cells over Th1

22
Q

Late phase of asthma

A

Major Basic Protein

damages alveoli

23
Q

Crystals in asthma sputum

A

Charcot-Leyden crystals

24
Q

Someone coughs this up and gives it to you

A

Charot-Leyden crystals

Major Basic Protein cystals

asthma

25
Q

Molecules that lead to bronchoconstriction in asthma

A

leukotrienes C4, D4, E4

26
Q

ASA-intolerant asthma

classic triad

A

nasal polyps

asthma

ASA-induced bronchospasms

27
Q

Death cause is asthma

A

status asthmaticus

does not respond to drugs

28
Q

Bronchiectasis basic pathology

A

premenent dilation of bronchioles and bronchi

loss of airway tone

air trapping

29
Q

Air trapping in bronchiectasis

A

turbulant air flow

airways are too large, laminar flow is disrupted

30
Q

Common causes of bronchiectasis

A

CF

Kartagener syndrome

Tumor of foreign body

Necrotizing infection

Allergic bronchopulmonary aspergillosis

31
Q

Kartagener syndrome pathophysiology

A

dynein arm defect

cilia

32
Q

Sputum in bronchiectasis

A

foul smelling!

loaded with inflammatory junk

sitting in the lungs and rotting in the big airways

33
Q

Allergic bronchopulmonary aspergillosis

A

seen most often in CF and bronchiectasis