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RT General Review > Pulmonary Pathophysiology > Flashcards

Pulmonary Pathophysiology Flashcards

1
Q

What is Asthma characterized by?

  • Restrictive vs Obstructive?
A

Characterized by chronic airway inflammation

  • Can develop at any age
  • Obstructive patho, restricts airflow not volume
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2
Q

What are symptoms of Asthma?

A
  • Wheeze
  • SOB
  • Chest tightness
  • Cough
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3
Q

How is asthma diagnosed?

A

PFT reversibility (12% and 200ml) or history of more than 1 symptom of asthma i.e cough and wheeze, or SOB w/chest tigntess

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4
Q

What are asthma triggers?

A
  • Upper respiratory tract infection
  • GERD
  • Exercise
  • Allergen exposure
  • Stress
  • beta blocker/ace inhibitors
  • food allergies
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5
Q

What are 6 phenotypes of asthma?

A
  1. Allergic
  2. Non Allergic
  3. Late Onset
  4. Fixed flow limitation
  5. Obesity
  6. Infant asthma
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6
Q

Describe the characteristics of allergic asthma

A

Commences in childhood

  • Family hx of atopy or increased immune response (eczema, food allergies)
  • Induced sputum
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7
Q

What treatment is very responsive for allergic asthma?

A

Treat w/ICS

  • phenotype is associated with induced sputum and increased ige response
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8
Q

What is non allergic asthma?

A

Neutrophil response

  • less responsive to ICS, higher dose required
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9
Q

What is late onset asthma?

  • which population is most affected
A

Adults (usually women) that present with asthma (no eczema)

  • Less atopy present
  • Asthma remains refractory
  • High levels of ICS needed
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10
Q

What is fixed flow limitation asthma?

A

Long term asthma reshapes airway (airway remodeling)

  • Bronchodilators are no longer helpful
  • Decreased flows
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11
Q

What is obesity related asthma?

A

Little eosinophil action

  • obesity causes inflammatory markers to worsen both asthma and COPD
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12
Q

What is infant asthma?

A

RSV is the cause

  • Increased with second hand smoking
  • Presents as cough, usually nocturnal
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13
Q

Why are Transesophageal echo’s effective for diagnosing/identifying valv disorders?

A

Allows for viewing of the internal structures of of the herat and blood flow patterns

  • helps visualize blood flow, and assesses visually if there is a clot
  • Used to confirm lack of blood clot in the atria in patients w/prolonged afib before performing cardioversion
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14
Q

Why are valve disorders easily identified by auscultations?

A

valve dysfunction results in turbulent flows

  • Depends affected valve, there may be extra heart sounds heard
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15
Q

What are level 1 treatments for GINA Asthma procedure?

A

Low dose ICS to reduce SABA use

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16
Q

What are level 2 treatments for GINA Asthma procedure?

A

Low dose ICS/LABA + SABA

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17
Q

What are level 3 treatments for GINA Asthma procedure?

A
  • Low dose ICS/LABA + LTRA
  • LTRA + SABA
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18
Q

What are level 4 treatments for GINA Asthma procedure?

A

Med-high dose ICS/LABA + LAMA

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19
Q

What are level 5 treatments for GINA Asthma procedure?

A

Severe

  • Anti IgE
  • LTRA
  • ICS+LABA
  • SABA
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20
Q

What is COPD generally characterized by?

A

Persistent airway obstruction and decreased expiratory flow rates

  • Smoking/alpha 1 antitrypsin/CF
  • Greater prevalence in men compared to women
  • Hypoxic resp drive (Since CO2 is always elevated, O2 becomes the primary stimulus for breathing -> SpO2 88-92%)
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21
Q

Clinical Manifestations of COPD?

A
  • Barrel chest
  • Hyperresonsant chest
  • purse lip breathing
  • Flat diaphragms on CxR
  • Decreased VC
  • Increased RV, FRC, TLC
22
Q

How can COPDers compensate/cope with lower pHs?

A

The kidneys compensate for low pH due to high CO2

  • The body than normalizes a new high normal for CO2
23
Q

What is the definition of a acute COPD exacerbation?

A

An acute event characterized by worsening of resp symptoms that is beyond normal and leads to changes in current management plan and meds

24
Q

What are acute COPD exacerbations generally caused by?

  • Treatment options (step ups?)
A

Usually caused by resp infection

  • Use LABA/LAAC over SABA/SAAC
  • If LABA isn’t enough, combine w/ICS
25
GOLD A Treatment for COPD?
SAAC prn or SABA prn
26
GOLD B Treatment for COPD?
LAAC or LABA
27
GOLD C Treatment for COPD?
- LAAC + ICS - LABA + ICS
28
GOLD D Treatment for COPD?
LAAC + ICS + mucomyst + xanthine
29
What is Emphysema characterized by? (3)
1. Enlargement of the air spaces distal to the terminal bronchioles 2. Loss of elastic tissue 3. Destruction of alveolar septal walls
30
What are the 3 phenotypes of Emphysema?
1. Centrilobular 2. Panlobular 3. Bollus
31
What is Centrilobular Emphysema characterized by?
- Destruction of the bronchioles - Lesions to the upper lobes - Rarely occurs in non smokers, more common in men
32
What is Panlobular Emphysema characterized by?
Generalized distribution - Septal destruction - Seen in antitrypsin and aging
33
What is Bollus Emphysema?
Damage at the alveolar level - Blebs form - Bullae present on CxR
34
General treatments for Emphysema (non-pharmalogical options)?
- Relieve symptoms - Home O2 - Increase exercise tolerance (pulmonary rehab)
35
What are treatments for acute emphysema exacerbations?
- SABA/SAAC -> Combivent (neb or mdi) - Diuretics/fluid balance - Prednisone - BiPAP if required
36
What is SpO2/PaO2 would be considered an acute emphysema exacerbation?
SpO2 88-92 (COPD range) - PaO2 > 60
37
Patho of Pleural Effusions?
Accumulation of fluid in pleural space: two variants Transudative and Exudative Causes: - Lung compression and atelectasis - Compression of pulmonary vasculature - Overall **decreasing venous return**
38
Treatment options for pleural effusions
- Supportive (O2 and Tx underlying causes) - 5th ICS thoracentesis - Pleurodesis - Lung expansion
39
Chest x ray findings for Pleural effusion?
Curved meniscus sign - fluid in fissures - 75 ml can blunt costophrenic angles
40
Patho of Exudative pleural effusions?
Caused by damage (wounds) to pleural membranes: Pleural fluid built up due to **inflammation** - Serous fluid from debriefed 2nd degree burn or infection - Exu = out of = has more stuff - Contains proteins,WBC, Firbin in fluid
41
Patho of Transudative pleural effusions
Pleural fluid collecting as a consequence of **passive capillary leak** - Trans = cross - Increased Hydrostatic pressure across capillary membranes or hypoalbuminemia - Proteins don’t cross over, just fluid - Usually caused by imbalance in pressure between blood vessels and the pleural space - CHF is the most common
42
What conditions would be associated with transudative pleural effusions?
Any leaky condition - CHF - Hepatic cirrhosis - Peritoneal dialysis - PE - Pulmonary infarction - Increased HP - Decreased OP
43
What pathologies would be associated with exudative pleural effusions?
Any fluids associated with injury - Malignancy - Burns - Infection - GI disease - lupus
44
General ARDS pathology
Initial injury leads to exduative stage: it is restrictive in nature causing: - Shunt (v/q mismatch) - Impaired gas exchange - Decreased lung compliance - Inhomogenous distribution - Increases density of lug
45
Most common cause of ARDS?
Sepsis
46
Most common cause of ARDS?
Sepsis
47
General pathophysiology of Pulmonary edema
Accumulation of fluid from vasculature and alveolar lung spaces - Alveolar wall and interstitial spaces swell - SVT can cause it - Can present as cardiogenic (hydrostatic pressure) and non cardiogenic in origin.
48
Causes of cardiogenic pulmonary edema
Hydrostatic pressure issue caused by: - LVF/pump failure - HP is increased - Excessive fluids - MI - Renal failure
49
Chest x ray indicators of Pulmonary edema?
Kelley a and b lines (non hydrostatic does have this)
50
pathophysiology of Non hydrostatic pulmonary edema?
Increased capillary permeability - lymphatic insufficiency - Decreased intrapleural pressure - Decreased oncotic pressure
51
Causes of non hydrostatic pulmonary edema?
- Alveolar hypoxia - ARDS - Pulmonary infections
52
Treatments for pulmonary edema?
- Inotrope and vasodilators - Diuretics - Oxygen - NIV - BiPAP to off load work on heart

RT General Review (42 decks)

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