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2 - CPR (pulmonary) > Respiratory Pathology - 2 > Flashcards

Respiratory Pathology - 2 Flashcards

1
Q

What is the primary description for Restrictive Lung Diseases?

A

DECREASED VOLUME

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2
Q

What is the primary description for Obstructive Lung Diseases?

A

AIR TRAPPING

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3
Q

FEV1/FVC ratio for Restrictive and Obstructive Lung Diseases

A

Restrictive - Normal

Obstructive - Decreased

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4
Q

FVC for Restrictive Lung Diseases is ____

A

Decreased

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5
Q

FEV1 for Obstructive Lung Diseases is ____

A

Decreased

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6
Q

What are 3 Obstructive Lung Diseases?

A

Chronic Bronchitis
Emphysema
Asthmas

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7
Q

Obstructive lung diseases are most often caused by?

A

Smoking

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8
Q

How is Chronic Bronchitis diagnosed?

A

Persistent cough with sputum production for 3 months out of 2 consecutive years

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9
Q

What is the pathophysiologic mechanism for Chronic Bronchitis?

A

Mucus gland hyperplasia –> Damaged epithelium

= Increased mucus and thickened muscle

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10
Q

What is the pathophysiologic mechanism for Chronic Bronchitis?

A

Mucus gland hyperplasia –> Damaged epithelium

= Increased mucus and thickened muscle

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11
Q

What is the term used to describe Chronic Bronchitis patients clinically?

A

Blue Bloaters

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12
Q

Blue Bloaters

A
  • Chronic Bronchitis

= Overweight and Cyanotic, increased hemoglobin and peripheral edema, rhonchi and wheezing

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13
Q

A patient presents as overweight, cyanotic, increased hemoglobin, peripheral edema and with rhonchi and wheezes. What is the likely diagnosis?

A

Chronic Bronchitis

– Blue Bloater

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14
Q

Why do Chronic Bronchitis patients have elevated hemoglobin?

A

Smoking induces carboxy hemoglobin which shifts the O2 dissociation curve to the LEFT and the compensation is to create more hemoglobin

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15
Q

What is Emphysema?

A

Irreversible air space enlargement DISTAL to terminal bronchiole

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16
Q

Air space enlargement distal to terminal bronchiole

A

Emphysema

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17
Q

What are the 2 most common types of Emphysema?

A

Centrilobar - enlargement of resp. bronchioles only

Panlobar/Panacinar - enlargement all distally

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18
Q

What type of emphysema usually presents with smokers that have chronic bronchitis and why?

A

Centrilobar

- chronic bronchitis constricts terminal bronchiole so dilation starts at respiratory bronchioles and moves distally

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19
Q

What is the term used to describe emphysema patients clinically?

A

Pink puffers

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20
Q

Pink Puffers

A
  • Emphysema

= Older, thin, severe dyspnea and quiet chest

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21
Q

A patient presents that is older and thinner with severe dyspnea and a quiet chest. What do you suspect the underlying disease is?

A

Emphysema

- Pink puffer

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22
Q

What will be seen on CXR and chest shape correlation with Emphysema?

A

Enlarged lungs with flattened diaphragm

- Barrel chest with increased AP diameter

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23
Q

What will be heard with auscultation of breath sounds with Emphysema?

A

Diminished breath sounds with prolonged expiratory wheezes

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24
Q

Normally, describe the function of Alpha1 Antitrypsin

A
  • Liver produces and secretes it
  • Coats the lungs to protect them
    = (-) Neutrophil Elastase that is produced by WBCs to breakdown bacteria because it is harmful to lungs
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25
Q

What happens with Alpha1 Antitrypsin Deficiency?

A
  • Alpha 1 AT is stuck in liver and damages it
  • Neutrophil Elastase is NOT (-)
    = Neutrophil Elastase damages the lungs!
26
Q

What is the result of Alpha1 Antitrypsin Deficiency?

A 
Basilar Panacinar (panlobular) Emphysema
-- affects lower lungs and all air spaces distally are enlarged
27
Q

What is the result of Alpha1 Antitrypsin Deficiency?

A 
Basilar Panacinar (panlobular) Emphysema
- affects lower lungs and all air spaces distally are enlarged
28
Q

Alpha1 AT is encoded by what gene/allele on what chromosome?

A

Pi gene on chromosome 14

– Z allele has decreased Alpha1 AT

29
Q

What gene is likely to manifest severe alpha1 AT deficiency?

A

Homozygous PiZZ

30
Q

How do you test for Alpha1 AT deficiency?

A

Serum test for Alpha1 AT

31
Q

What are the 3 components of Asthma?

A
  1. Recurrent airway obstruction with a reversible component
  2. Airway hyper-responsiveness
  3. Airway Inflammation
32
Q

What are the 3 components of Asthma?

A
  1. Recurrent airway obstruction with a reversible component
  2. Airway hyper-responsiveness
  3. Airway inflammation
33
Q

What are the 2 types of Asthma?

A

Atopic (extrinsic)

Non-Atopic (intrinsic)

34
Q

Atopic Asthma is the most common type. When does it present, what are the IgE levels, main inflammatory cells and triggers?

A
  • Presents in childhood
  • ELEVATED IgE levels
  • Eosinophils, mast cells, lymphocytes
  • Triggers = allergens
35
Q

Non-Atopic Asthma is less common. When does it present, what are the IgE levels, main inflammatory cells and triggers?

A
  • Presents in older adults
  • NORMAL IgE levels
  • T lymphocytes and Neutrophils
  • Triggers = cold, exercise, infection
36
Q

Asthma is a combination of what 3 things?

A

Genetics
Immunity
Environment

37
Q

Describe how Asthma is triggered

A
  • Allergen (+) Th2 to secrete IL-4
  • (+) IgE B cell to release IgE to Mast cells
  • Mast cells bind re-exposure to allergen and degranulate IL-5
  • (+) Eosinophils
38
Q

What are the main mediators of the Asthma inflammatory soup?

A

Leukotrienes C4, D4, E4

39
Q

Bronchoconstriction, increased mucus, increased permeability and inflammation is seen with?

A

Asthma

40
Q

With Asthma, what is a possible complication?

A

Airway Remodeling

41
Q

What is involved in the Airway Remodeling if it occurs with Asthma?

A
  • Fibrosis
  • Smooth muscle hyperplasia
  • Increased goblet cells and submucosal glands
42
Q

If Airway Remodeling occurs with Asthma, what does that ultimately mean?

A

Irreversible

= DECREASED response to bronchodilators/corticosteroids!!

43
Q

If an Asthma patient is not responding to bronchodilators/corticosteroids, what has likely occurred?

A

Airway remodeling

- Fibrosis, smooth muscle hyperplasia, increased goblet cells and submucosal glands

44
Q

Status Asthmaticus

A

Unremitting, possible fatal asthma attack

45
Q

What are the findings with Status Asthmaticus?

A
  • Thick mucus plugs with coils = curschmann spirals

- Eosinophils and breakdown product = charcot leyden crystals

46
Q

What are the findings with Status Asthmaticus?

A
  • Thick mucus plugs with coils = curschmann spirals

- Eosinophils and breakdown product = charcot leyden crystals

47
Q

What is the triad seen with Aspirin Sensitive Asthma and how does it occur?

A

Samters triad = asthma, nasal polyps, recurrent rhinitis

– (-) cox so there is increased Leukotrienes C4,D4,E4

48
Q

What is Bronchiectasis?

A

Permanent dilation of airways due to inflammatory destruction

49
Q

Permanent dilation of airways due to inflammatory destruction

A

Bronchiectasis

50
Q

Increased mucus, loss cilia and wall destruction in the airways?

A

Bronchiectasis

51
Q

Bronchiectasis is an end stage process to many things. What are some things it can present with?

A

Infection, Obstruction
Cystic Fibrosis
Ciliary Dyskinesia
ABPA

52
Q

What will be seen on the lung with Bronchiectasis?

A

Dilated Bronchi extend to pleural surface

53
Q

Mutation in Cl- channel causes Na+ and H2O to leave the mucus and cause it to be dehydrated

A

Cystic Fibrosis

54
Q

What is Primary Ciliary Dyskinesia?

A

Dysfunction of dynein arm of microtubules

= Decreased motility of cilia/flagella

55
Q

Primary Ciliary Dyskinesia is often seen with?

A

Kartagener’s Syndrome

56
Q

Kartagener’s Syndrome

A

Sinusitis
Bronchiectasis
Situs Inversus
Male Infertility

57
Q

ABPA

A

Allergic Bronchopulmonary Aspergillosis

58
Q

What is ABPA?

A

Hypersensitivity response to aspergillus infection overlying chronic lung disease

59
Q

What will be signs of ABPA?

A
  • Background of asthma/CF
  • (+) skin test
  • ELEVATED IgE
  • Thick and dark mucus
60
Q

The thick and dark mucus with ABPA will show?

A

Fungal hyphae – Aspergillus

2 - CPR (pulmonary) (26 decks)

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