Pulmonary Flashcards

(36 cards)

1
Q

Viral PNA signs/symptoms

A

-nonproductive cough
-low grade fever
-low to normal WBC’s
-contagious as long as symptoms
present

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2
Q

Bacterial PNA Signs/symptoms

A

-productive cough
-purulent sputum
-high fever
-high WBC’s
-infiltrates on xray
-not contagious after 48 hrs on
antibiotics

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3
Q

What is the compensatory mechanism of the lungs in response to hypoxia?

A

intrapulmonary arteries constrict, diverting blood to better oxygenated lung segments-optimizes V/Q ratio

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4
Q

Diseases with decreased V/Q ratio

A

-PNA
-Asthma
-ARDS
-Alveolar collapse
-Pulmonary Edema

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5
Q

Diseases with increased V/Q ratio

A

-PE
-Non-embolic obstruction by tumor
-Emphysema
-radiation therapy
-Cardiovascular shock

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6
Q

V/Q ratio (ventilation/perfusion ratio)

A

adequate ventilation and sufficient perfusion of blood
normal value= 4:5 or 0.8

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7
Q

What are obstructive lung disorders?

A

disorders that obstruct airflow, making it difficult to exhale completely
EX) COPD, Asthma

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8
Q

What are restrictive lung disorders?

A

disorders that reduce total lung capacity by limiting lung expansion
EX) pulmonary fibrosis, hypoventilation syndrome (caused by obesity)

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9
Q

What type of hypersensitivity rxn is responsible for formation of granulomas in TB?

A

Type IV

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10
Q

What causes cavitation in the lungs in active TB infection?

A

tissue necrosis-bacteria eat the tissue; hallmark of advanced disease

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11
Q

What are the characteristics of TB bacteria?

A

-Mycobacterium tuberculosis
-acid fast bacilli (rod shaped)
-has waxy cell wall that prevents
phagocytosis

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12
Q

Initial Pathophysiology of TB

A

-Droplets inhaled/travel to alveoli–> macrophages ingest bacteria –> granulomas form (macrophages, t cells, b cells, other immune cells) –> macrophages merge into giant multinucleated cells to further create barrier

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13
Q

Latent TB

A

-contained in granulomas
-asymptomatic/not contagious
becoming immunocompromised can trigger latent TB and it will turn into active infection

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14
Q

Active TB symtpoms

A

-persistent cough
-hemoptysis
-night sweats
-chest pain
-wt loss
-fatigue

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15
Q

What are the types of asthma?

A

-Allergic (triggered by allergens)
-Non-allergic
-Exercise induced
-Occupational (triggered by irritating substances in certain occupations)

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16
Q

Role of mast cells in asthma

A

-degranulate in response to allergen –>
release inflammatory mediators like
histamine, prostaglandins, and
leukotrienes
-drive the early phase of asthma attack

17
Q

Role of leukotrienes in asthma

A

cause bronchoconstriction, tissue edema (by increasing blood flow & permeability), increase mucus production, attract leukocytes

18
Q

Role of eosinophils in asthma

A

-levels in the blood can help predict severity of asthma
-can damage bronchial walls
-release cytokines that cause inflammation and can lead to remodeling of the airway

19
Q

Pertinent lab values in asthma

A

eosinophils >300
Serum IgE >100
Spirometry= FVC1/FVC ratio < 0.70

20
Q

Acid- Base imbalance in asthma

A

Initially respiratory alkalosis from breathing off too much CO2; progresses to resp. acidosis as pt becomes more tired and cannot ventilate

21
Q

signs/symptoms of asthma

A

Exp. wheezes
chest tightness
SOB
Tachypnea
Anxiety

22
Q

What is pnuemonia

A

infection of lung parenchyma

23
Q

What is the cause of the consolidation appearance on x-ray in PNA

A

d/t increased capillary permeability, fluid, cells, proteins fill alveoli and cause impaired gas exchange- fluid filled alveoli cause consolidation

24
Q

How does Alpha 1 Antitrypsin play a role in emphysema

A

it is an enzyme that prevents elastase from attacking structural fibers in the lung; deficiency causes alveolar destruction

25
Pathophysiology of Emphysema
Chronic progressive lung disease that damages alveoli; loss of alveolar elasticity leading to air trapping and poor gas exchange
26
Pulmonary fxn tests in emphysema
FEVC1/FVC ratio <0.70 low O2; high CO2
27
Risk factors for Emphysema include
smoking, secondhand smoke, air pollution, environmental exposures
28
Complications of emphysema
-Pulmonary HTN leads to Cor pulmonale (right HF) -Pneumothorax-from bullae rupture -Resp failure-advanced stages
29
S/s of Emphysema
chronic cough SOB pink skin "pink puffer" barrel chest cachectic appearance from wt loss
30
Structural changes in Emphysema
-Bullae formation- lrg air filled spaces from destroyed alveoli -Bronchiole collapse-sm airway collapse d/t loss of structural support -Diaphragm flattens- r/t chronic hyperinflation
31
Pathophysiology of Chronic Bronchitis
-persistent inflammation of the bronchi along with excessive mucus production -thickened bronchial walls and hypertrophy of mucus glands -goblet cells hyperplasia
32
S/s of chronic bronchitis
productive cough SOB Chest tightness Frequent resp infections cyanosis "blue bloaters" clubbing
33
Complications of Chronic brochitis
Secondary polycythemia Pulmonary HTN--> Cor Pulmonale reactive vasoconstriction from hypoxia
34
Lab values for Chronic bronchitis
FEV1/FVC ratio <0.70 ABG- hypoxia/increased CO2 CXR-hyperinflation, airway thickening
35
Which inflammatory cells are involved in chronic bronchitis
Neutrophils- contribute to excess mucus Macrophages CD8 t lymphocytes-elevated in smokers
36
Goblet cells
epithelial cells that fxn to produce mucus become hyperplastic in chronic bronchitis