Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pulm > Pathoma Respiratory Part II > Flashcards

Pathoma Respiratory Part II Flashcards

1
Q

Group of diseases characterized by airway obstruction + air trapping; decreased FVC, FEV1, FEV1/FVC ratio; increased TLC, RV, FRC

A

Obstructive lung dz:

  1. chronic bronchitis
  2. emphysema
  3. asthma
  4. bronchiectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Chronic productive cough (due to excessive mucus production) lasting at last 3 months over at least two years; characterized by hypertrophy of bronchial mucinous glands (goblet cells); leads to increased thickness of mucus glands relative to bronchial wall thickness (Reid index > 50%; normal

A

Chronic bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Productive cough
  2. Cyanosis (“blue bloaters”) - mucus plugs trap CO2 –> increased PaCO2 + decreased PaO2
  3. Increased risk of infection and cor pulmonale
A

Chronic bronchitis

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

Highly associated with SMOKING –> pollutants –> irritation and inflammation –> mucinous gland hypertrophy + hyperplasia

A

Chronic bronchitis

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

Destruction of alveolar airs sacs –> loss o f elastic recoil and collapse of airways during exhalation; due to imbalance of proteases and antiproteases

A

Emphysema

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

Smoking –> inflammation + protease-mediated damage

A

CENTRIACINAR emphysema in UPPER lobe

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

Inflammation in the lungs normally leads to

A

release of proteases by neutrophils and macrophages

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

Alpha-1-antitrypsin normally …

A

neutralizes proteases

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

Lack of anti-protease leaves the air sacs vulnerable to protease-mediated damage; mutated protein accumulates in the ER of hepatocytes (pink, PAS+ globules on biopsy_–> cirrhosis; due to PiZ mutation

A

Alpha-1-antitrypsin deficiency –> PANACINAR emphysema in LOWER lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. Dyspnea + cough with minimal sputum
  2. Prolonged expiration w/ pursed lips (“pink puffers”)
  3. Weight loss
  4. Increased AP diameter of chest (“barrel chest”)
  5. Hypoxemia due to destruction of capillaries in the alveolar sac and cor pulmonale are late complications
A

Emphysema

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

Type I HS –> reversible AW bronchoconstriction

A

Atopic asthma

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

Allergens –> TH2 –> IL4 + IL5 + IL10

Re-exposure –> IgE mediated activation of mast cells –> release of preformed histamine granules + LTC4, LTD4, LTE4 –> bronchoconstriction, inflammation and edema

A

Asthma (early phase reaction)

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

Mediates class switch to IgE

A

IL-4

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

Attracts eosinophils

A

IL-5

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

Stimulates TH2 cells and inhibits TH1

A

IL-10

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

Asthma: Allergens –> TH2 –> ?

A

IL4, IL5, IL10

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

Inflammation, especially MAJOR BASIC PROTEIN derived from eosinophils, damages cells and perpetuates bronchoconstriction

A

Late-phase reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q 
Curschmann spirals (spiral-shaped mucus plugs)
Charcot-Leyden crystals (eosinophil-derived)
A

Asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Besides allergens, what else can provoke asthma

A
  1. Exercise
  2. Viral infxn
  3. Aspirin (NASAL POLYPS)
  4. Occupational exposures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Permanent dilatation of bronchioles and bronchioles and bronchi; loss of airway tone results in air trapping; due to necrotizing inflammation with damage to airway walls.

A

Bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of bronchiectasis include:

A
  1. CF
  2. Kartagener syndrome
  3. Tumor or foregoing body
  4. Necrotizing inflection
  5. Allergic bronchopulmonary aspergillosis (ABPA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Kartagener syndrome?

A

Inherited defect of the dynein arm, which is necessary for ciliary movement –> sinus, infertility (poor motility of sperm), + situs inversus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cough, dyspnea, foul-smelling sputum –> hypoxemia w/ cor pulmonale + secondary amyloidosis

A

Bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Characterized by restrictive filling of the lungs; decreased TLC, FEV1, FVC; increased FEV1: FVC ratio; most commonly due to interstitial diseases of the lung; may also arise with chest wall abnormalities (obesity)

A

Restrictive pulmonary dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cyclical lung injury –> TGF-Beta from injured pneumocytes –> Fibrosis of lung interstitium

A

Idiopathic pulmonary fibroiss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the secondary clauses of interstitial fibrosis?

A
  1. Bleomycin
  2. Amiodarone
  3. Radiation therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Diffuse fibrosis on CT with end-stage honeycomb lung

A

Idiopathic pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Treatment for pulmonary fibrosis?

A

Transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Interstitial fibrosis due to chronic exposure to small particles that are fibrogenic –> alveolar macrophages engulf foreign particles that induce fibrosis

A

Pneumoconioses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Massive exposures leads to diffuse fibrosis (“black lung”) associated with rheumatoid arthritis (Caplan syndrome)

A

Coal Workers’ Pneumoconiosis (exposure to carbon dust)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Mild exposure to carbon results in WHAT? (collections of carbon laden macrophages that are not clinically significant)

A

Anthracosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Fibrotic nodules in upper lobes of the lung; leads to impaired phagolysosome formation by macrophages + increased risk for TB

A

Silicosis (seen in sandblasters and silica miners)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Noncaseating granulomas in the lung, lilac lymph nodes, and systemic organs –> increased risk for lung cancer

A

Berylliosis, seen in beryllium miners and workers in the aerospace industry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Fibrosis of lung and pleura (plaques) with increased risk for lung carcinoma (MORE COMMON) and mesothelioma; lesions may contain long, golden brown fibers with associated iron (ferruginus body) which confirm exposure

A

Asbestosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Noncaseating granulomas + hilar lymphadenopathy in an African American female due to CD4+ helper T cell response to an unknown antigen –> restrictive lung disease;

A

Sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Uveitis
Cutaneous nodules or erythema nodosum
Dry eyes / mouth (salivary + lacrimal glands)
Restrictive lung disease

A

Sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q
  • Dyspnea or cough (most common presenting sx)
  • Elevated serum ACE
  • Hypercalcemia (1-alpha hydroxyls activity of EPITHELIOD HISTIOCYTES (diagnostic) converts vitamin D to its active form)
  • Stellate inclusions (“asteroid bodies”) are often seen w/i giant cells of the granulomas
A

Sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Treatment for sarcoidosis

A

Steroids, but often resolves spontaneously

39
Q

Granulomatous rxn to inhaled organic antigens (e.g. pigeon-breeder’s lung); presents with fever, cough, and dyspnea hours after exposure; resolves w. removal of the exposure (chronic exposure –> interstitial fibrosis)

A

Hypersensitivity pneumonitis

40
Q

Definition of pulmonary HTN

A

MAP > 25 (normal is 10)

41
Q

Characterized by atherosclerosis of the pulmonary trunk, smooth muscle hypertrophy of pulmonary arteries, and intimal fibrosis; leads to right ventricular hypertrophy with eventual cor pulmonale

A

Pulmonary HTN

42
Q

PLEXIFORM LESIONS

A

Pulmonary HTN

43
Q

Saddle emboli

A

sudden death

44
Q

Classically seen in young adult females; some familial forms related to INACTIVATING mutation in BMPR2 –> proliferation of vascular smooth muscle

A

Primary pulmonary HTN

45
Q

Due to hypoxemia or increased volume in the pulmonary circuit; may also arise with recurrent PE

A

Secondary pulmonary HTN

46
Q

Diffuse damage to the alveolar-capillary interface – leakage of protein-rich fluid –> edema that combines with necrotic epithelial cells to form HYALINE MEMBRANES

A

ARDS

47
Q

“White out” on x ray (diffuse alveolar collapse on expiration)

A

ARDS

48
Q

Hypoxemia and cyanosis with respiratory distress due to thickened diffusion barrier and collapse of air sacs (increased surface tension)

A

ARDS

49
Q

Activation of neutrophils in ARDS induces protease- and free radical mediated damage of

A

type I and type II pneumocytes

50
Q

Respiratory distress due to inadequate surfactant levels

A

Neonatal RDS

51
Q

What produces surfactant?

A

Type II pneumocytes; phosphatidylcholine (lecithin) is the major component

52
Q

Components of surfactant

A

Lecithin (phosphatidylcholine) and sphingomyelin –> L:2 ratio > 2 = mature lungs

53
Q

Risk factors for NRDS

A 
Prematurity
C-section delivery (steroids increase synthesis and release of surfactant)
Maternal diabetes (insulin decreases surfactant)
54
Q

Increased respiratory distress after birth, tachypnea w/ use of accessory muscles; grunting; hypoxemia + cyanosis; diffuse granular (“ground glass”) appearance on CXR

A

NRDS

55
Q

Hypoxemia in infant w/ NRDS increases risk of:

A

persistence of PDA

necrotizing enterocolitis

56
Q

Supplemental O2 given to infant w/ NRDS

A

Blindness

57
Q

Lung damage w. NRDS

A

Bronchopulmonary dysplasia

58
Q

Most common cancers by incidence

A
  1. Breast/prostate
  2. Lung
  3. Colorectal
59
Q

Key risk factors for lung caner

A

Cigarettes, radon, asbestos

60
Q

Coin-lesion on xray

A
  1. Granuloma
  2. Bronchial hamartoma
  3. Small cell
  4. Non-small cell

The firs thing you should do is review previous CXRs.

61
Q

Surgery does not help which lung cancer?

A

Small cell

62
Q

Benigh tumor composed of lung tissue and cartilage; often calcified on imaging

A

Hamartoma

63
Q

Pleural involvement is classically seen with

A

adenocarcinoma

64
Q

Distended head and neck veins with edema and blue discoloration of arms and face

A

Superior vena cava syndrome

65
Q

Hoarseness

A

Involvement of recurrent laryngeal nerve

66
Q

Diaphragmatic paralysis

A

Involvement of the phrenic nerve

67
Q

What are the mutagenic components of cigarettes?

A

Polycyclic aromatic hydrocarbons; arsenic;

68
Q

Horner syndrome

A

Pancoast tumor (apical tumor)

69
Q

Poorly differentiated; arises from neuroendocrine (Kulchisky) cells

A

Small cell carcinoma

70
Q

Keratin pearls or intercellular bridges

A

Squamous cell carcinoma

71
Q

Lung cancer: glands or mucin on histology

A

adenocarcinoma

72
Q

Poorly differentiated large cells (with no keratin bridges intercellular bridges, glands, or mucin)

A

Large cell carcinoma

73
Q

Columnar cells that grown along preexisting bronchioles and alveoli; arises from Clara cells

A

Bronchioalveolar carcinoma

74
Q

Well differentiated neuroendocrine cells; chromogranin positive

A

Carcinoid tumor

75
Q

Multiple “cannon ball” nodules on imaging

A

Metastasis to lung

76
Q

Lung cancers associated with smoking

A

Small cell
Squamous cell
Adenocarcinoma
Large cell carcinoma

77
Q

Lung cancers not associated with smoking

A

Bronchioalveolar carcinoma

Carcinoid tumor

78
Q

Most common tumor in male smokers

A

Squamous cell carcinoma

79
Q

Another (not the most common) tumor associated with male smokers

A

Small cell carcinoma

80
Q

Most common tumor in nonsmokers and female smokers

A

Adenocarcinoma

81
Q

Central tumors

A

Small cell

Squamous cell

82
Q

Peripheral tumors

A

Adenocarcinoma

Bronchioalveolar

83
Q

Can be central or peripheral

A

Large cell

Carcinoid

84
Q

Polyp-like mass in the bronchus

A

Central carcinoid tumor

85
Q

Rapid growth and early metastasis; may produce ADH or ACTH (Cushing) or cause Eaton-Lambert syndrome

A

Small cell

86
Q

May produce PTHrP leading to hypercalcemia

A

squamous cell

87
Q

May present with pneumonia-like consolidation on imaging

A

Bronchioalveolar

88
Q

Pneumothorax in a tall, thin, young man

A

Spontaneous pneumothorax due to rupture of emphysematous bleb, trachea shifts towards collapse

89
Q

Pneumothorax following penetrating chest wall injury

A

Tension pneumothorax; trachea is pushed OPPOSITE to side of injury

90
Q

Trachea shifts away from the pneumothorax

A

Tension pneumothorax

91
Q

Trachea shifts toward the pneumothoraz

A

Spontaneous pneumothoraz

92
Q

Highly associated with occupational exposure to asbestos

A

mesothelioma

93
Q

Recurrent pleural effusions, dyspnea, and chest pain

A

Mesothelioma

Pulm (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions