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Patho 2 > Resp > Flashcards

Resp Flashcards

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

A

Complex trait

  • genetic (familial)
  • environmental factors

Goals:
> Reduce inflammation
> Avoid triggers

25
Q

Asthma: Patho

A

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
Q

Asthma: Types

A
  • Extrinsic (atopic) — External factors: allergens

- Intrinsic (topic) – Resp Tract Infections, exercise, hyperventilation, cold air, exercise,..

27
Q

Asthma: Mnfts

A 
Dyspnea
wheezing
coughing in attempt to open airway
bronchospasm
increase in the respiratory effort - use of accessory muscles
Hypoxemia?
Immobilization?
28
Q

Asthma: Dx

A 
Hx
Px
Pulm Fx Tests - spirometry
Labs
Inhalation Challenge tests to decrease hypersensitivity
29
Q

Asthma: Tx

A

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
Q

Atelectasis: def

A

Partial collapse of lung

Incomplete expansion of lung or portion of a lung

31
Q

Atelectasis: Et

A 
Airway obstruction
Lung compression (pneumothorax or pleural effusion)
Contraction - increased recoil of the lung d/t loss of surfactant or secretions
32
Q

Atelectasis: Mnfts

A

Dyspnea
Tachypnea and tachycardia (compensatory)
Decrease chest expansion (or not equal)
tracheal midline shift on inhalation

33
Q

Atelectasis: Dx

A 
Hx
Px
Chest X ray
CT (if small)
Bronchoscopy
34
Q

Atelectasis: Tx

A

Treat underlying cause

Respiratory support

35
Q

Pleural Effusion

A

Fluid accumulation in pleural cavity/space d/t abnormal fluid seepage and/or drainage

Rate of fluid formation exceeds the removal rate

36
Q

Pleural Effusion: Types

A

1) Exudate (more proteins)
2) Transudate
3) Empyema
4) Chylothorax
5) Hemothorax

37
Q

Pleural Effusion: Et

A

usually CHF

when not cardiogenic: infection, CA, pulmonary infarction

38
Q

Pleural Effusion: Patho

A
  • Normal fluid entry via parietal capillaries
  • Drainage into parietal lymphatics
  • if entry exceeds drainage > pleural effusion
39
Q

Pleural Effusion: Dx

A

Hx
Px
US
CT

40
Q

Pleural Effusion: Tx

A

Treat underlying cause
Thoracocentesis (+fluid analysis to identify type and cause)
Chest tube to drain?

41
Q

Pulmonary Edema

A

Accumulation of fluid IN the alveoli

42
Q

Pulmonary Edema: Et

A

mostly Left Heart Failure

When non-cardiogenic > IV fluid overload, smoke inhalation, aspiration, IV drug use (increases vessel permeability)

43
Q

Pulmonary Edema: Patho

A
  • 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
Q

Pulmonary Edema: Mnfts

A

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
Q

Pulmonary Edema: Tx

A

Address underlying cause
If Cardiogenic- inotrope
Respiratory support: O2, mechanical ventilation?

46
Q

Paranasal sinuses (air sacs)

A

Frontal
Ethmoid
Maxillary

47
Q

Rhinosinusitis

A

Inflammation of paranasal sinuses

Aka sinusitis

48
Q

Rhinosinusitis: Patho

A

Low oxygen content in the sinuses facilitate the growth of microorganisms
Impairs local defenses
Alters the functions of the Immune Response cells

49
Q

Rhinosinusitis: Et

A 
Obstruction of the narrow ostia that drain the sinuses
URT viruses - infections
Allergic Rhinitis
Nasal Polyps
Changes in barometric pressure
50
Q

Rhinosinusitis: Mnfts

A 
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
Q

Rhinosinusitis: Dx

A 
Hx
Px
Differentiate headache type
Transillumination
CT scan
MRI if neoplasms are suspected
52
Q

Rhinosinusitis: Tx

A

Usually mnfts improve after 7 days

If not > 2/3 improve with antibiotic

53
Q

Tuberculosis

A

Infectious disease caused by Mycobacterium tuberculosis

  • M tuberculosis hominis: airborne spread by inhalation of droplet nuclei
  • M tuberculosis avian
54
Q

Primary TB

A
  • Develops in unexposed previously & unsensitized individuals
  • Initiated by inhalation of droplet nuclei that contains the tuberculosis bacillus
55
Q

Secondary TB

A

Reinfection from inhaled droplet nuclei or reactivation of a previous “healed” primary infection
Occurs when IR is impaired

56
Q

TB: Patho

A
  • 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
Q

TB: Dx

A

Screening:

  • TB Skin test
  • CXR

Definitive Dx:

  • Culture
  • Genotyping
58
Q

TB: Tx

A

Multidrug regimen d/t high rate of mutation
INH, Rifampin, Pyrazinamide
> 6 months tx

Patho 2 (7 decks)

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