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Resp Flashcards

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1
Q

Pneumonia

A

aka Pneumonitis

Inflammation of alveoli and bronchioles

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2
Q

Pneumonia: Et?

A

Bacterial
Viruses and fungi
Aspiration
Noxious fumes

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3
Q

Pneumonia: Patho

A

1) Respiratory defenses are compromised
2) Agent enters
3) Inflammatory response > Edema > Impairment of gas exchange d/t production of inflamm. exudate = sputum

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4
Q

Pneumonia: types?

A

Typical - Bacterial (worse d/t presence in alveoli and mucus production inside the air sac)
Atypical - Viral

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5
Q

Consolidation

A

Solification of inflammatory debris, cells, fluid and any other debris (not tissue).

> Impacts fx of lungs and gas exchange

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6
Q

Pneumonia: mnfts?

A 
Fever
Malaise
Dyspnea
Chest pain
Productive cough (with sputum)
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7
Q

Pneumonia: Dx

A

Hx
Px
Chest X-Ray
Sputum analysis to id the microbe

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8
Q

Pneumonia: Tx

A

Antibiotic (if bacterial)

Supportive management

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9
Q

COPD

A

> Obstruction of alveoli, not patent d/t inflammation and increased mucus production
acute during progression of the disease
recurrent and chronic obstruction of airway
may coexist with asthma

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10
Q

COPD: Et and risks

A

Smoking
recurrent respiratory infections
ageing
genetic deficiency of alpha1 antitrypsin

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11
Q

Compliance

A

Refers the ease of which we can breathe and fill the lungs with air.
If elastic tissue is damaged, there is a loss of compliance.

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12
Q

Chronic Bronchitis

A

airway inflammation and obstruction
d/t smoking and recurrent infection
> Increased mucus production

large airway 1st - bronchi
small airway (later) - goblet cells increase mucus production
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13
Q

Chronic Bronchitis: Patho

A

1) increased mucus production
2) Impaired defences and mucociliary blanket
3) Infection
4) Inflammation of airways
5) Alveolar obstruction
6) Alveolar airway collapse &raquo_space;>Air gets trapped in alveolus

Decreased alveolar ventilation > perfusion imbalance > hypoxemia (O2 drops in arterial blood)

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14
Q

Chronic Bronchitis: Mnfts

A

Hx of productive cough (>3 months over 2 consecutive years)
Dyspnea
Impaired respiratory Fx > hypoxemia and hypercapnia
Activity intolerance
Increased sputum
Wheezing and crackles (wet)

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15
Q

Asthma

A

Chronic inflammatory condition of airways with acute episodic obstruction of aw and bronchospams

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16
Q

Asthma: triggers?

A

Allergens
Airway irritants- noxious stimuli (perfume, cold air, smoke, perfume)
Infection
Exercise

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17
Q

Asthma: Et?

A

Complex trait

  • Genetic
  • Environmental factors
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18
Q

Asthma: Atopic

A

Extrinsic pathway
Initiated by a type I hypersensitivity due to allergen exposure
Person usually has other allergic conditions
Mechanism of response:
Early or acute phase- s/s within 10-20 min
Late phase response - 4-8 hours after exposure

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19
Q

Emphysema: definition

A

Loss of elasticity of lung tissue
Abnormal enlargement of airspaces distal to the terminal bronchioles
Alveolar walls and capillary beds get destroyed resulting in loss of compliance

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20
Q

Emphysema: Et

A

smoking

genetic deficiency of alpha 1 antitrypsin (controls proteases in alveoli)

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21
Q

Emphysema: Patho

A
  • smoking inhibits antitrypsin and attracts inflammatory cells (cause damage)
    Increase of proteases damages alveolar walls
    Resulting in permanent distended airspaces that trap the air impairing gas exchange > alveoli merge and surface area decreases

Bullae
Blebs

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22
Q

Emphysema: Mnfts

A

Dyspnea

Increased ventilatory effort

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23
Q

Asthma: definition

A

Chronic inflammatory condition of airways with episodic obstruct and bronchospasm

Various triggers provoke inflammation and airway obstruction (allergens, airway irritants= noxious stimuli, infection, exercise)

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24
Q

Asthma: Et

Study These Flashcards
A

Complex trait

  • genetic (familial)
  • environmental factors

Goals:
> Reduce inflammation
> Avoid triggers

25
Asthma: Patho
Activated T-lymphocytes direct further release of inflammatory mediators from eosinophils, mast cells and helper T lymphocytes produce interleukins Mediators increase vascular permeability and edema Increase airway responsiveness > bronchospasm
26
Asthma: Types
- Extrinsic (atopic) --- External factors: allergens | - Intrinsic (topic) -- Resp Tract Infections, exercise, hyperventilation, cold air, exercise,..
27
Asthma: Mnfts
``` Dyspnea wheezing coughing in attempt to open airway bronchospasm increase in the respiratory effort - use of accessory muscles Hypoxemia? Immobilization? ```
28
Asthma: Dx
``` Hx Px Pulm Fx Tests - spirometry Labs Inhalation Challenge tests to decrease hypersensitivity ```
29
Asthma: Tx
Goal: Control with minimal meds Preventative: avoid allergens, irritants, avoid smoking and exposure Drugs: Step 1: short acting inhaled bronchodilators Step 2: inhaled steroid Step 3: long acting bronchodilator with steroid Step 4: short course steroid (PO) and 3rd drug - leukotriene or Theophyline
30
Atelectasis: def
Partial collapse of lung | Incomplete expansion of lung or portion of a lung
31
Atelectasis: Et
``` Airway obstruction Lung compression (pneumothorax or pleural effusion) Contraction - increased recoil of the lung d/t loss of surfactant or secretions ```
32
Atelectasis: Mnfts
Dyspnea Tachypnea and tachycardia (compensatory) Decrease chest expansion (or not equal) tracheal midline shift on inhalation
33
Atelectasis: Dx
``` Hx Px Chest X ray CT (if small) Bronchoscopy ```
34
Atelectasis: Tx
Treat underlying cause | Respiratory support
35
Pleural Effusion
Fluid accumulation in pleural cavity/space d/t abnormal fluid seepage and/or drainage Rate of fluid formation exceeds the removal rate
36
Pleural Effusion: Types
1) Exudate (more proteins) 2) Transudate 3) Empyema 4) Chylothorax 5) Hemothorax
37
Pleural Effusion: Et
usually CHF | when not cardiogenic: infection, CA, pulmonary infarction
38
Pleural Effusion: Patho
- Normal fluid entry via parietal capillaries - Drainage into parietal lymphatics - if entry exceeds drainage > pleural effusion
39
Pleural Effusion: Dx
Hx Px US CT
40
Pleural Effusion: Tx
Treat underlying cause Thoracocentesis (+fluid analysis to identify type and cause) Chest tube to drain?
41
Pulmonary Edema
Accumulation of fluid IN the alveoli
42
Pulmonary Edema: Et
mostly Left Heart Failure | When non-cardiogenic > IV fluid overload, smoke inhalation, aspiration, IV drug use (increases vessel permeability)
43
Pulmonary Edema: Patho
- Vascular fluid into interstitial space to alveoli - Leads to impaired gas exchange d/t greater alveolar-vessel membrane distance - Less compliance d/t space available
44
Pulmonary Edema: Mnfts
Dyspnea r/t hypoxia Coughing to expectorate extra fluid (frothy, productive cough) Blood tinged sputum d/t capillaries damage Less compliance Crackles in LS
45
Pulmonary Edema: Tx
Address underlying cause If Cardiogenic- inotrope Respiratory support: O2, mechanical ventilation?
46
Paranasal sinuses (air sacs)
Frontal Ethmoid Maxillary
47
Rhinosinusitis
Inflammation of paranasal sinuses | Aka sinusitis
48
Rhinosinusitis: Patho
Low oxygen content in the sinuses facilitate the growth of microorganisms Impairs local defenses Alters the functions of the Immune Response cells
49
Rhinosinusitis: Et
``` Obstruction of the narrow ostia that drain the sinuses URT viruses - infections Allergic Rhinitis Nasal Polyps Changes in barometric pressure ```
50
Rhinosinusitis: Mnfts
``` Difficult to differentiate from those of the common cold & allergic rhinitis - facial pain - headache - pain on bending - unilateral maxillary pain - pain in teeth - purulent nasal drainage ``` Symptoms usually resolve within 5 to 7 days without medical is immuno compromised pts, often there are no signs of inflammation such as purulent drainage are absent.
51
Rhinosinusitis: Dx
``` Hx Px Differentiate headache type Transillumination CT scan MRI if neoplasms are suspected ```
52
Rhinosinusitis: Tx
Usually mnfts improve after 7 days | If not > 2/3 improve with antibiotic
53
Tuberculosis
Infectious disease caused by Mycobacterium tuberculosis - M tuberculosis hominis: airborne spread by inhalation of droplet nuclei - M tuberculosis avian
54
Primary TB
- Develops in unexposed previously & unsensitized individuals - Initiated by inhalation of droplet nuclei that contains the tuberculosis bacillus
55
Secondary TB
Reinfection from inhaled droplet nuclei or reactivation of a previous “healed” primary infection Occurs when IR is impaired
56
TB: Patho
- Inhaled droplet nuclei enters and deposits in the alveoli - Alveolar macrophages phagocytize but are unable to kill the mycobacteria d/t lipid coated cell wall - Tubercle bacilli proliferate & multiply - Infected macrophages expose the antigen and a delayed cell-mediated response is activated - T-cells - Sensitized T-cells stimulate the production of lytic enzymes in the macrophages (proteases) - When released proteases damage lung tissue - Ghon focus - granulomatous lesions that result from cell-mediated IR (usually in upper segments of lower lobes - O2 concentration is higher) - Ghon complex when lymphatics spread infection > dormant?
57
TB: Dx
Screening: - TB Skin test - CXR Definitive Dx: - Culture - Genotyping
58
TB: Tx
Multidrug regimen d/t high rate of mutation INH, Rifampin, Pyrazinamide > 6 months tx

Patho 2 (7 decks)

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