Obstructive Diseases Flashcards

1
Q

What is a DDx based on these problems?

Wheezing and nighttime breathing problem

Cough productive sputum

Leg edema

Progressive dyspnea

Significant Smoking history (>70 pyhx)

Some hobby and occupational exposures (limited) to respiratory irritants

A
  • COPD
  • Asthma
  • CHF
  • Lung cancer
  • Tracheomalacia
  • Pericardial effusion
  • Pulmonary embolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pt comes in with symtpoms suggestive of obstuctive lung disease, what tests would you order?

A
  • Chest X-ray • EKG
  • CBC
  • BNP

• Pulmonary Function studies

  • Arterial Blood gases
  • Echo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do you see in this image?

A

HYperlucency, Hyperinflated lung, flattened diaphram

will see increased retrosternal space on side view

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Spirometry for obstructed lung disease

A

Scalloped with normal inspiratory and decreased expiratory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

These are all examples of:

  • Emphysema
  • Chronic Bronchitis
  • Bronchiectasis
  • Chronic persistent asthma (FEV1 remains abnormal after therapy)
A

COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Three key determinant of diffusion in lungs

A

The surface area of the lung with contact to diffusing alveoli (VA - Alveolar Volume)

the thickness of the alveolar- capillary membrane (Dm - Membrane Diffusion)

the volume of blood available in the capillary bed of the lung (Vc - Capillary Blood Volume).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What effect does these diseases have on Diffusing capacity?

  • Asthma
  • Alveolar hemorrhage (acute)
  • Intracardiac shunt (left to right)

• Erthyrocytosis

A

Elevation of DLCO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes decrease of DLCO

A

– Significant Anemia

Loss of parenchyma in diseases like emphysema.

– Diseases that scar the lung such as pulmonary fibrosis, or sarcoidosis

– Swelling of lung tissue (pulmonary edema) due to heart failure, or due to an acute inflammatory response to allergens (acute interstitial pneumonitis).

– Diseases of the circulation in the lung, such as pulmonary vasculitis or pulmonary hypertension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Amount of air left in the lungs after a normal expiration. This is a sum of the residual volume which r_equires indirect measurement_ with helium diluation or with body plethysmography)

A

FRC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

____ is the amount of air that can be expired after expiratoin of a tidal volume

____ amount that can be inspired after inspiration of a normal tidal volume

A

ERV

IRV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

___ amount of air inhaled or exhaled in a normal breath

___ the amount of air expired after a maximal inspiration

A

TV

VC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do you calculate forced vital capacity

A

Take TLC - RV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

This pt has restrictive lung disease. What is true of their functional residual capacity?

what about maximum flow rate or total volume exhaled?

A

Decreased functional residual capacity by plethysmography

Decreased maximum flow rate and decreased total lung volume exhaled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is true of the FEV1 and FVC as well as the ratio in restrictive lung disease?

A

In restrictive disease the FEV1 and FVC are reduced but the ratio is normal. A decreased ratio is found in obstructive lung disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

With advanced restrictive disease the _____ level will fall and the _____will rise.

A

arterial oxygen

carbon dioxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens to antatomic dead space and compliance in restrictive lung disease?

A

Anatomic dead space remains relatively constant at different lung inflations

The increased elastic recoil of the lung in restrictive lung disease decrease compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

52 yo man reports worsening productive cough. Present for over 4 years but worsened over last 6 months. Smoked 2 ppd of cigarettes for last 30 years. An increased number of which of the following cell types best accounts for these symptoms?

A

Goblet cells

18
Q

Chronic cough with copious sputum for at least 3 months in 2 consecutive years. Smoking and inhalation of irritating substances including smog are usually associated.

A

Chronic Bronchitis

19
Q

What happens to submucosal glands and goblet cells in chronic bronchitis?

A

Early excess mucus from hypertrophy of submucosal glands in the larger bronchi but later in the course of the disease goblet cell metaplasia of bronchioles and small bronchi also contribute.

20
Q

What are some other microscopic changes we see in pt with chronic bronchitis?

A

infections infiltration of small airways by alveolar macrophages and fibrosis of bronchiolar walls (even obliteration of the lumina

21
Q

What happens to larger bronchi in pt with chornic bronchitis?

A

Smooth muscle hypertrophy can be seen in larger airways related to increased effort to clear bronchi of the mucus but is not the source of the excess mucus

22
Q

What causes increased risk of lung cancer in pts with chronic bronchitis?

A

Squamous cell metaplasia is a reaction to irritation in the larger bronchi and increases risk of lung cancer

23
Q

_____ are normal flat lining cells of alveoli

______ produce surfactant not mucus. The can be increased in a reaction to damage to the lung but does not cause excess mucus.

A

Type 1 pneumocytes

Type 2 pneumocytes

24
Q

What clinical findings are associated with Chronic Bronchitis

A

– Productive cough and dyspnea
– Cyanosis (due to decreased O2 saturation from hypoxemia)

– Expiratory wheezing and rhonchi
– Corpul monale
– clubbing

25
Q

What do we see on CXR in pts with chornic bronchitis

A

– Enlarged heart,horizontally oriented

– Increased bronchial markings

26
Q

51 yo male smoker comes to you with a fevers and productive cough of green yellow sputum up to 1⁄2 cup a day. Also with morning cough the past 5 years. Which of the following findings would be most likely in the patient.

A

increased Reid Index

27
Q

What is an increased REID index mean?

A

Ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and cartilage (Normal is <0.4 ).

The ratio of the gland depth to the total thickness of the bronchial wall is the REID INDEX.

28
Q

Apical cavitary lesions would be seen in ______. Not associated with excessive mucus production.

A

tuberculosis

29
Q

Enlarged hilar lymph nodes suggests

A

sarcoidosis or bronchogenic carcinoma.

30
Q

Elevated sodium chloride level in the sweat is seen in

A

cystic fibrosis

31
Q

37 yo man with SOB and RUQ abdominal pain. DOE with 2 flights of stairs. Smoked 1⁄2 PPH for 10 years. Exam Temp 98.7, RR 22, HR 72. Clubbing. Sclera yellow. Hepatomegaly. Lungs diminished BS bilaterally. Labs. Alk Poh 86, ALT 220, AST 200, T bili 3.8, T bili 3.0. Biopsy of the liver fibrosis in the portal triads, intracellular globular inclusions with eosinophilic material that is PAS stain positive. Which of the following pulmonary findings would be most likely in this patient?

A

Destruction of alveolar walls : anti-trypsin 1 deficiency

32
Q

Where do we see alveolar desctruction in alpha 1 AT deficiency?

what about smoking?

A

Panacinar

Centriacinar

33
Q

Pathophys behind alpha1 antitripsin defiency

A

This is a protease inhibitor which counterbalances substances such as elastase. The normal phenotype is considered PiMM with alpha-1 antitrypsin deficiency a protease antiprotease imbalance leads to unchecked inflammation with neutrophils migrating into alveolar spaces. stimulated cells release elastase from their granules and creates oxygen free radicals which inactive the alpha1 antitrypsin

34
Q

The combination of high elastase activity and increased oxygen free radicals from tobacco smoking in these with low antiprotease activity causes

A

accelerated destruction of the lung tissue.

35
Q

Person presents with symptoms of emphysema and they are 30 with no smking history

A

alpha 1 AT defiency

36
Q

how does alpha 1 antitrypsin defiency cause liver issues?

A

The eosinophilic globular cytoplasmic inclusions are collection of nonfunctional alpha1 antrypsin that accumulates in the hepatocytes and causes hepatic dysfunction and fibrosis leading to cirrhosis and hepatic failure.

37
Q

Interstitial lymphocytic infiltrate are associated with

A

viral infections, myplasma pneumonia and autoimmune conditions.

38
Q

A 16 yo boy presents with earache. He has a history of Recurrent otitis media, ongoing sinus issues, recurrent bronchitis. Exam demonstrates nasal mucosa pale and swollen with yellow to green secretions. Retracted Tympanic membrane and absent mobility with a middle ear effusion. A sweat chloride test is performed and results both times are normal. Microscopic analysis of the boys semen reveals immobile spermatozoa. A defect in which of the following is the most likely for this patient’s condition.

A

Kartageners

39
Q

What is Kartageners

A

is genetic illness as result of immobile cilia (ciliopathy). The cytoskeletal structure of the ciliary and specifically the dynein cellular motors axon the macrotublar doublets at the periphery of the ciliary axoneme.

40
Q

Classic symptoms of Kartageners

A

As a result defects in mucociliary clearance lead to chronic upper and lower respiratory tract disease. Males also demonstrate infertility as a result of immobile spermatozoa.

41
Q

CF is due to CFTR in chrom 7; what GI and pulmonary associations do we see?

A

Respiratory tract disease
– (over 90%), recurrent infections and bronchiectasis with most eventual respiratory failure by age 30-50

GI tract– meconium ileus, malabsorption, pancreatic insufficiency