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Big Ol' Patho. > Respiratory up to Emphysema > Flashcards

Respiratory up to Emphysema Flashcards

1
Q

• Review resp anatomy + functions
o Defense roles of resp tracy
o Gas exchange

A

s

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2
Q

What is considered the “upper respiratory tract”

A

According to google:
The major passages and structures of the upper respiratory tract include the nose or nostrils, nasal cavity, mouth, throat (pharynx), and voice box (larynx)

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3
Q 
What is the "flu"
When does it occur?
Different types?
How long is incubation?
Who is most susceptible?
A

• Acute viral infection in URT
• Seasonal (does not persist throughout the year)
• Types A, B & C (known as “strains”)
o A most prevalent

  • 1-4 days incubation
  • Elder, young, health care workers, chronically ill are more susceptible
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4
Q

Why do we get the flu year after year?

A

The virus mutates

- Different strains

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5
Q

What occurs in the flu?
(patho)

Possible complications?

A
  • Viral injury to epith cells in URT – get in, replicated, lyse these cells
  • Inflm tissue damage
  • If extension to LRT → bronchial and alveolar damage

•Complications
o 2ndry bacterial infection??
o Bronchitis or pneumonia??

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6
Q

• What’s the difference between giving an antibiotic with an infection and without an infection (prophylactically)? Answer this. Related to antibiotic resistance…

A

s

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7
Q

How does antibiotic resistance occur?

A

Bacteria can acquire antibiotic resistance genes from other bacteria in several ways. By undergoing a simple mating process called “conjugation,” bacteria can transfer genetic material, including genes encoding resistance to antibiotics (found on plasmids and transposons) from one bacterium to another.

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8
Q

S&S of flu?

A
  • Fever
  • Lethargy
  • Myalgia
  • Cough
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9
Q

Is a cough beneficial?

A

are coughing at 140-150km/hr (sneezing even greater)

o Cough can help to expectorate fluid building up but can also make things worse by damaging lining, which is already inflamed

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10
Q

How do flu vaccines occur?

A

o Develop antibodies so that when infection occurs doesn’t take as long to have high enough level to bring infection down

o Given more than one strain in the flu vaccine

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11
Q

Tx of flu?

A 
- Vaccine for prophylactic tx
• Prevent spread
• Symptomatic management
• Limit infect to URT
• Antivirals?? (amantadine, relenza) – 99% of time will NOT use these, must be given during specific time period
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12
Q

How do amantadine and relenza work?

A

o Amantadine (first gen) MOA: inhibits the uncoating of the RNA so that it can’t incorporate it into the DNA of the host; is usually more beneficial for A & B types

o Relenza = second generation antiviral prevents replication of DNA & prevents release from host cell?

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13
Q

Pneumonia

  • Aka?
  • Is one of most common…?
  • What is it?
  • What forms does it take?
  • How can it be classified?
A
  • Alternative term = pneumonitis
  • One of the most common socomial infections
  • Inflm of alveoli and bronchioles
  • Infectious and non-infectious forms (toxic pneumonia d/t fumes, etc)
  • Can be classified in one of two ways, either by agent of infection (microbe or chemical) or where in the respiratory tract it infects
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14
Q

Etiology of pneumonia?

A
  • Usually bacteria (often opportunistic)
  • Viruses
  • Fungi – inhalation of spores
  • Aspiration (GI content, etc…anything except air, causing inflm to the lungs)
  • Noxious fumes (such as smoke)
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15
Q

Patho of pneumonia?

A
  • Impaired pulmonary defences
  • Agent enters resp tract + proceeds to lungs
  • Inflm → pulmonary edema → impaired gas exchange
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16
Q

What is typical vs atypical pneumonia?

How does each manifest in terms of area occupied by the infectious agent?

A

Typical = bacterial
- multiply extracellularly in the alveoli and cause inflm and exudation of fluid into the air-filled spaces of the alveoli

Atypical = viral, fungal, noxious fumes
- lack of alveolar infiltration and purulent sputum (as are multiplying within cells)

see figure p 649

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17
Q

2 classifications based on distribution of pneumonia infection?

A

1) lobar
- consolidation in a part or all of a lung lobe (restricted to one lobe)

2) bronchopneumonia
- patchy consolidation involving more than one lobe
(diffused across lung)

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18
Q

Are of consolidation in lung with pneumonia contain what?

A

exudate, inflammatory debris, and cells involved in inflm (host and bacterial)

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19
Q

Manifestations of pneumonia

A
  • Fever and chills
  • Dyspnea
  • Sputum – builds up in lower resp tract, will continually try to cough it out
  • Chest pain
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20
Q

Dx of pneumonia?

A
  • Px
  • Chest x-ray (very effective)
  • Sputum analysis
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21
Q

Tx of pneumonia

A
  • Supportive (for dyspnea, hypoxia, etc)

* Abx if bacterial

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22
Q

COPD
What does it include?
What is it?

A
  • Several disorders – includes chronic bronchitis and emphysema
  • May coexist with asthma (was previously also considered under COPD but not any longer)

• Persistent inflm of air way, parenchyma, and vasculature
–> Acute, recurrent and chronic obstruction of a/

•Leading cause of death

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23
Q

Et/Risk factors for COPD?

A
  • Smoking (80-90%)
  • Recurrent resp infections (ex: sinusitis)
  • Ageing
  • Genetic def of alpha 1 antitrypsin
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24
Q

How is aging a risk factor for COPD?

A

drop in compliance in airways and lungs

25
Q

By what mechanisms does smoking damage the resp tract

A
  • Causes increase in secretion of mucus (becomes problematic as is now too much)
  • To much mucus overwhelmes the cilia → now mucous wont move
  • Damages cilia
  • Causes inflammation
  • Causes coughing (which aggrevates and worsens damage to the resp tract)
  • Substantial damage to walls of the airways and walls of the alveoli
26
Q

How does the Mucociliary blanket work?

A

Goblet cells produce mucus – this mucus traps debris, cilia bring it up to expectorate

27
Q

Outline mechanisms by which COPD causes airway obstruction

*see fig 29-7, p. 687

A
  • In normal bronchial airway has elastic fibres provide traction and hold the airway open

1) Hypertrophy of bronchial wall (lumen smaller, compromises air flow)
2) Inflm and hypersecretion of mucus
3) Loss of elastic fibres that hold airway open

*All of these linked to chronic bronchitis

28
Q

What is chronic bronchitis?

What causes it?

A

• Inflm & obstruction of airway
–> Exudate fills lumen (area of least resistance)

• D/t smoking & chronic/recurrent infection – each time you have infection, have inflm and damge to the lining

29
Q

Characteristics of changes seen in chronic bronchitis?

A

• Affect larger airways first
–> Hypertrophy of submucosal glands (attempting to meet increased demand as smoking irritates the airways, causing inc mucus, which causes increased workload of the glands…inc in size…too much mucus)

•Changes affect smaller airways later
–> Inc in goblet cells (number and size; substantial inc in mucous → airway obstruction

30
Q

Patho of chronic bronchitis?

A

Is primarily damage to the airway itself….not the alveoli so much

  • Excess mucus → mucociliary defenses impaired → infections form (mucous is nutritive, moist, warm…bacteria thrive here)
  • Bronchial walls inflm → lumen obstructed (by mucus, exudate, thickening of bronchial walls) → a/w collapse as air diffuses from alveoli into surrounding capillaries
  • Air trapped in parts of lung → dec alveolar ventilation → ventilation: perfusion imbalance → hypoxemia
31
Q

Difference between hypoxemia and hypoxia?

A
  • hypoxemia = deficiency of oxygen in ARTERIAL blood)

- Hypoxia = deficiency in the amount of oxygen reaching the tissues.

32
Q

Ventilation-Perfusion ratio

A

resp system + cardio work in concert with one another

o Approx 4.2L/min of air enter the lung
o In each minute, entire blood volume (~5.5L) will flow to the lungs
o Ratio = ~0.8 = normal ventilation-perfusion ratio
o Ratio – doesn’t matter if you double or half both numbers, will always get same ratio – this is problem because if you only have half of both values, this will appear to be the same ratio but is not actually normal
o When ventilation component is obstructed, will have 4.2 decrease…ratio will change

33
Q

Dx of chronic bronchitis?

A
  • Look for presence of chronic productive coughing for at least 3 months of year for 2 consecutive years
    • lots of other diagnostics
34
Q

Manifestations of chronic bronchitis?

A 
IPADSHOW (without O)
o	Impaired resp fx (o2 + co2)
o	Prolonged expiration
o	Activity intolerance
o	Dyspnea
o	Sputum (lots! d/t exudate + mucus)
o	Hypoxemia + Hypercariba
o	Wheezing + crackles
35
Q

What constitutes respiration?

A

ventilation (inhalation, exhalation) + gas exchange

36
Q

Why do you see activity intolerance in chronic bronchitis?

A

Not enough energy produced (because oxygen not adequate), can’t carry out basic functions

37
Q

Why do wheezes and crackles occur?

A

o Wheezing b/c breathing forcefully through obstructed airways
o Crackles are wet b/c air is moving over + through fluids (heard with stethoscope)

38
Q

**What are the normal and accessory muscles used in inspiration?

A

Normal = diaphragm + external intercostals

Accessory = sternocleidomastoid, pectoralis minor, serratus anterior, latissimus dorsi…more?

39
Q

**• Look at process of ventilation – are both processes active or passive…which is more than the other?

A 
Inspiration = active
Expiration = passive
40
Q

Why do you see prolonged expiration?

A

More resistance with exhalation? Is passive process so will move more slowly?

41
Q

What’s a possible complication of chronic bronchitis?

A

Secondary bacterial infection

42
Q

Which is more severe, chronic bronchitis or emphysema?

Why?

A

Emphysema

partially b/c irreversible damage? In chronic bronchitis can still get gas if air reaches alveoli?

43
Q

What is emphysema?

A

• Destruction of alveolar tissue and capillary beds causing:

1) Loss of lung compliance
2) Enlarged distal spaces (alveoli)

44
Q

What is lung compliance?

A

Simplified….is ease with which lungs fill and empty

45
Q

Why does loss of lung compliance occur in emphysema?

A

the elastic tissue is damaged by enzymes. These enzymes are secreted by leukocytes (white blood cells) in response to a variety of inhaled irritants, such as cigarette smoke. Patients with emphysema have a very high lung compliance due to the poor elastic recoil, they have no problem inflating the lungs but have extreme difficulty exhaling air

46
Q

Et of emphysema?

A
  • Smoking – responsible for almost ALL emphysema

* Genetic def of alpha 1 (a1) antitrypsin - accounts for less than 1% of cases

47
Q

How does a deficiency in a1 antitrypsin result in emphysema?

A

o Antitrypsin = enzyme inhibitor; these enzymes break down structural components in the lungs in a controlled fashion when this breakdown is needed.
o A1 antitrypsin controls these enzymes by regulating their activity…those with this cannot form or synthesize a1 antitrypsin so don’t have this regulation → proteases free to cause structural damage

48
Q

In what two ways does smoking act in the patho of emphysema?

A

1) Inhibits a1 antitrypsin – This applies to those with classic emphysema (chronic smokers) – they are producing a1 antitrypsin but smoking inhibits this regulator
2) Attracts inflm cells - Components in smoking attract inflammatory cells AND these cells release proteases (double whammy) → damage d/t inflm process + extra protease release

49
Q

Patho of emphysema?

A

*impacts both alveoli and vasculature

  • Inc proteases (d/t 2 mechanisms of smoking or a1 deficiency) → destruction of alveolar walls → alveoli merge → dec in surface area → permanent distended air spaces → ventilation impaired
  • Air traps in between alveoli → inc dead space → inc in work of breathing
  • Capillary wall destroyed (by proteases) → impaired perfusion
50
Q

3 factors seen in inc work of breathing

A

Nasal flaring, Pursed lip breathing, Use of accessory muscles

51
Q

See Fig 29-9 flow chart of effects of smoking **

A

s

52
Q

What are the two forms of emphysema in terms of the kind of damage they cause?

A

o Centriacinar emphysema = most common type; topography of alveoli is similar to normal but substantial damage to the terminal airways

o Panacinar = walls of alveoli essentially gone; terminal airways impacted as well; is far worse than centriacinar form

  • See fig 29-10
53
Q

Manifesations of emphysema?

A
  • Dyspnea
  • Inc in ventilatory effort
  • Barrel chest
54
Q

Dx of COPD?

A
  • Hx, px
  • Labs (lactate dehydrogenase and other specific markers that will discuss later)
  • Chest X-Ray
  • Pulm function tests (lung capacity, tidal volume, etc)
55
Q

Are all chronic diseases progressive?

A

No, not IBD (and others)

56
Q

Tx of COPD?

A
  • Limit progression through: smoking cessation + avoiding irritants
  • Flu and pneumococcal vaccines
  • DRUGS (stage based(
    1) First line: Short acting B-agonists and anticholinergics
    2) If above doesn’t suffice, add inhaled steroids
    3) If that doesn’t work, change short acting B-agonist for long-acting B-agonist
    4) Theophylline – is bronchodilator; also has added benefit of minimal inflammatory effects; used to be used as first line
57
Q

What kind of irritants may exist for the client with COPD?

A

b/c airways are compromised are more affected by irritants that aren’t bad for normal people: cold air, pollen, perfumes, etc

58
Q

Why are Flu and pneumococcal vaccines important for pt with COPD?

A

important prophylactic measure b/c are at high risk of infection d/t having compromised airway

59
Q

o Look up what alpha and beta receptors are and the subclasses of each; determine what binds to each of these receptors physiologically, and what is achieved by this binding normally (physiologically); then look at drug and whether it blocks or acts on the receptor

A

xx

Big Ol' Patho. (17 decks)

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