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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
Q

GOLD A Treatment for COPD?

A

SAAC prn or SABA prn

26
Q

GOLD B Treatment for COPD?

A

LAAC or LABA

27
Q

GOLD C Treatment for COPD?

A
  • LAAC + ICS
  • LABA + ICS
28
Q

GOLD D Treatment for COPD?

A

LAAC + ICS + mucomyst + xanthine

29
Q

What is Emphysema characterized by? (3)

A
  1. Enlargement of the air spaces distal to the terminal bronchioles
  2. Loss of elastic tissue
  3. Destruction of alveolar septal walls
30
Q

What are the 3 phenotypes of Emphysema?

A
  1. Centrilobular
  2. Panlobular
  3. Bollus
31
Q

What is Centrilobular Emphysema characterized by?

A
  • Destruction of the bronchioles
  • Lesions to the upper lobes
  • Rarely occurs in non smokers, more common in men
32
Q

What is Panlobular Emphysema characterized by?

A

Generalized distribution

  • Septal destruction
  • Seen in antitrypsin and aging
33
Q

What is Bollus Emphysema?

A

Damage at the alveolar level

  • Blebs form
  • Bullae present on CxR
34
Q

General treatments for Emphysema (non-pharmalogical options)?

A
  • Relieve symptoms
  • Home O2
  • Increase exercise tolerance (pulmonary rehab)
35
Q

What are treatments for acute emphysema exacerbations?

A
  • SABA/SAAC -> Combivent (neb or mdi)
  • Diuretics/fluid balance
  • Prednisone
  • BiPAP if required
36
Q

What is SpO2/PaO2 would be considered an acute emphysema exacerbation?

A

SpO2 88-92 (COPD range)

  • PaO2 > 60
37
Q

Patho of Pleural Effusions?

A

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
Q

Treatment options for pleural effusions

A
  • Supportive (O2 and Tx underlying causes)
  • 5th ICS thoracentesis
  • Pleurodesis
  • Lung expansion
39
Q

Chest x ray findings for Pleural effusion?

A

Curved meniscus sign

  • fluid in fissures
  • 75 ml can blunt costophrenic angles
40
Q

Patho of Exudative pleural effusions?

A

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
Q

Patho of Transudative pleural effusions

A

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
Q

What conditions would be associated with transudative pleural effusions?

A

Any leaky condition

  • CHF
  • Hepatic cirrhosis
  • Peritoneal dialysis
  • PE
  • Pulmonary infarction
  • Increased HP
  • Decreased OP
43
Q

What pathologies would be associated with exudative pleural effusions?

A

Any fluids associated with injury

  • Malignancy
  • Burns
  • Infection
  • GI disease
  • lupus
44
Q

General ARDS pathology

A

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
Q

Most common cause of ARDS?

A

Sepsis

46
Q

Most common cause of ARDS?

A

Sepsis

47
Q

General pathophysiology of Pulmonary edema

A

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
Q

Causes of cardiogenic pulmonary edema

A

Hydrostatic pressure issue caused by:

  • LVF/pump failure
  • HP is increased
  • Excessive fluids
  • MI
  • Renal failure
49
Q

Chest x ray indicators of Pulmonary edema?

A

Kelley a and b lines (non hydrostatic does have this)

50
Q

pathophysiology of Non hydrostatic pulmonary edema?

A

Increased capillary permeability

  • lymphatic insufficiency
  • Decreased intrapleural pressure
  • Decreased oncotic pressure
51
Q

Causes of non hydrostatic pulmonary edema?

A
  • Alveolar hypoxia
  • ARDS
  • Pulmonary infections
52
Q

Treatments for pulmonary edema?

A
  • Inotrope and vasodilators
  • Diuretics
  • Oxygen
  • NIV - BiPAP to off load work on heart

RT General Review (42 decks)

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