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Patho > Q3 Pulm > Flashcards

Q3 Pulm Flashcards

1
Q

Volumes are __________
Capacities are __________

A

Single measure of gas in ONE compartment (IRV, TV, RV, ERV)
Measures of gas in TWO or more volumes (VC=IRV+TV+ERV; IC=IRV+TV; FRC=ERV+RV; TLC=IRV+TV+RV+ERV)

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2
Q

What is the IRV?
ERV?
TV?
RV?
IC?
FRC?
VC?
TLC?

A

IRV = amount of air that can be INHALED beyond a normal TV
ERV = amount of air that can be EXHALED beyond normal TV
RV = amount of air in lungs after an ERV
TV= amount of air inhaled/exhaled during normal breathing
IC= TV+IRV
FRC = ERV+RV
VC = TV+IRV+ERV
TLC = all

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3
Q

What is FVC? FEV1?
What is the purpose of the FEV1/FVC ratio and what is it used for clinically?

A

Forced vital capacity = the maximum gas VOLUME that can be expired when the patient exhales as forcefully and rapidly as possible AFTER MAX inhalation
Forced expiratory volume at 1 second - the volume of air expired after the 1st second of the FVC maneuver.
Ratio = % of FVC expired in 1 second.
Used to measure lung function for example asthma is diagnosed by an FEV1/FVC ratio of <80%.

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4
Q

If a patient expires 5.5L of air forcefully and rapidly after max inspiration, what is the FVC?
If the volume expired after the 1st second of the above maneuver was 4.3L, what was the FEV1? What is the FEV1/FVC ratio? Does this patient have asthma?

A

5.5L
4.3L
78%
Yes less than 80% is asthma

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5
Q

Lung disease classified 3 ways:

How are these related to FEV1/FVC ratios?

A

Obstructive (reduced FEV1/FVC <70%)
Restrictive (reduced TLC -> reduced FVC)
Vascular (reduced lung diffusion)

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6
Q

How would you describe an obstructive lung pattern of respiration?
Examples of obstructive lung diseases?

A

Intake is not affected (same volume expired) and volume of output is not affected (still same volume exhaled) but FLOW is reduced.
Asthma, emphysema, acute/chronic bronchitis, bronchiectasis and bronchiolitis.

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7
Q

What would an increase in 200ml in FVC or an increase in 12% FEV1/FVC ratio indicate?

A

A positive response to bronchodilator therapy.

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8
Q

What does positive response to bronchodilator therapy mean?

A

Patient most likely has asthma

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9
Q

What are some examples of Restrictive pattern lung diseases?

A

CHF, idiopathic pneumonias, Interstitial lung disease, scoliosis, obesity, ALS, Guilian-Barre.

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10
Q

How does a restrictive lung disease affect FEV1 and FVC?

A

Flow is not affected, however there is PROPORTIONATE decrease in FVC AND FEV1 - meaning that the FEV1/FVC ratio stays around the same, however there is a reduced FVC and a reduced FEV1.

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11
Q

What is the most prevalent chronic disease of childhood?

A

Asthma

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12
Q

During asthma attacks, patient is unable to fully expire, so therefore unable to fully inspire leading to _______ and eventually _______. A late sign of impending respiratory failure would be_______

A

Hypoxemia
Acidosis.
Bradycardia, absence of wheezing.

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13
Q

Airway narrowing in asthma is a result of?

A

Smooth muscle contraction, increased mucus and edema.

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14
Q

2 categories of asthma:

A

Intrinsic - NON-allergenic, adult onset. No hx of allergies. Respiratory infections or psychological factors are contributory.
Extrinsic - ALLERGIC, peds onset.
IgE mediated response

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15
Q

One of the best things to do to control asthma?

A

Environmental control (avoiding triggers)

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16
Q

If a patient is 46yo, and suddenly develops symptomology compared to asthma, which no hx of asthma and no allergy hx, what type of asthma is it most likely? What could be contributing to the development?

A

Intrinsic asthma.
Respiratory infections or psychological factors.

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17
Q

Patient states their SOB is limiting their activity, and their PEF is 40-69% of their normal best. What severity is their asthma exacerbation?

A

Moderate.
Mild dyspnea with activity and is PEF at least 70% of normal best
Moderate dyspnea limits activity and PEF 40-69% of normal best
Severe: Dyspnea interferes with conversation and at rest, PEF <40% normal best
Life threatening: pt unable to speak or PEF <25% of normal best.

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18
Q

A patient 18yo has daily asthma symptoms, awakes at night more than 1x/week, uses their SABA daily, has some limitations on normal activity, and has an FEV1 of >60 but <80% and their normal FEV1/FVC is reduced by 5% of their normal. They have had 2 or more exacerbations in the past year requiring oral systemic glucocorticoids. What classification of asthma severity would they be placed in?

A

Persistent moderate.
Intermittent = <2days/week of symptoms, <2x/mo of night time awakenings, SABA <2days/week, no interference with normal activity and normal FEV1 between exacerbations. 0-1 times in the past year requiring systemic glucocorticoids.

Persistent severe = symptoms throughout the day, night time awakenings every night, SABA several times/day, extremely limited activity and FEV1<60% and FEV1/FVC reduced by >5%. 2 or more x/year requiring oral systemic glucocorticoids.

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19
Q

What questions would you ask parents of or patients 0-11 years to ask about their asthma control?

A
  • Daytime asthma symptoms more than a few minutes more than once/week?
  • Night time awakening or coughing due to asthma?
    *SABA needed more than once/week?
  • Activity limitation due to asthma?

If yes to NONE of these = well controlled
If yes to 1-2 = partly controlled
3-4 = uncontrolled.

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20
Q

What is the first thing you do when someone’s asthma is not being well controlled?

A

Assess their understanding and proper use of their medications and avoidance of triggers.

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21
Q

What does prolonged asthma lead to?

A

Remodeling of bronchial tissue

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22
Q

What happens in the early phase of asthma exacerbation?

A

Allergens initiate IgE antibodies released to plasma cells
- these antibodies respond to environmental triggers.
- IgE antibodies bind to Mast cells and basophils
- when triggered, mast cells release cytokines and de-granulate
- de-granulating mast cells release histamine, prostaglandins, Leukotrienes
- smooth muscles tighten and constrict the airway.

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23
Q

What happens in late phase of asthma exacerbation?

A

Eosinophils, basophils, neutrophils, Th, Memory T cells and mast cells all localize to the lungs.
- this causes more bronchoconstriction and inflammation.

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24
Q

T/F: Bronchoconstriction, mucus plug, thickening of basement membrane are examples of immunohistopathologic features.

A

False. They are examples of inflammatory features.

Airway edema, mast-cell activation and infiltration by neutrophils, eosinophils are immunohistopathologic features.

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25
Q

What is the most likely cause of the secondary asthma response that is more resistant to treatment (or late phase)?

A

Neutrophil chemotactic factor.

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26
Q

How does chronic asthma progress pathologically?

A

Normal respiratory epithelium replaced by goblet cells.
Hyper responsiveness of the airway
Leakage from increased permeability.
Increased # and size of mucus glands, hypertrophied muscle, narrowed lumen.

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27
Q

What law explains decreased flow in asthma patients?

A

Poiseuille’s law - decrease in radius = decrease in flow.

28
Q

What are the most important inflammatory mediators?

A

Cytokines

29
Q

What other factors would be present for someone with allergic asthma?

A

Eczema, elevated IgE levels, family hx of allergies, associated with seasonal and environmental triggers.

30
Q

How is EIA different from allergic asthma?

A

Bronchospasm pathology not inflammatory reaction.
W/in 3 mins of end of activity and resolves w/in 60min.
Affected by heat loss, water loss, increased osmolarity of mucosa which cause smooth muscle contraction.

31
Q

T/F: desensitization is an effective tx for occupational asthma.

A

FALSE. It may have the oppositie effect.

32
Q

What respiratory pathology involves oxidative stress and protease-anti protease imbalances?

A

COPD.

33
Q

COPD pathology involves _____ and ______

A

Chronic bronchitis = inflammation and structural changes and increased mucus secretion
Emphysema = destruction and enlargement of air spaces.

34
Q

FRC in COPD is more or less than normal?

A

More?

35
Q

Emphysema is due to excess ______

A

Enzyme lysosomal elastase which destroys elastin.

36
Q

Something other than cigarette smoke that can cause emphysema?

A

Alpha1-antitrypsin deficiency. A1 antitrypsin inactivates enzymes (ANTI) so without it, enzymes run Wild (like lysosomal elastase). And destroy elastin.

37
Q

A loss of radial traction (elastic lung tissue) and the formation of bullae is associated with which disease pathology?

A

Emphysema.

38
Q

2 types of COPD clinical features?

A

Blue bloaters - stocky, overweight, cyanotic, excess body fluids, rales and Rhonchi, cough. Sever hypoxemia and CO2 increases with disease state.
Pink puffers - thin, weight loss, hyperinflation of chest, distant auscultation sounds, use of accessory muscles, minimal or absent cough, barrel chest, clubbing. Mild hypoxemia with little CO2 retention.

39
Q

What happens when you over oxygenate a chronic COPD patient?

A

They lose their respiratory drive. Normally, high CO2 levels are our drive to breath, but since COPDers are used to high levels at baseline, low O2 levels become the drive. If they get too much O2, then their body thinks they dont need to breath anymore.

40
Q

What pressure rises with COPD progressive disease? What is the pathology of this?

A

PAP - pulmonary artery pressure.
Vascular remodeling = ^vascular resistance.
Shunting of blood to O2 rich areas further increases the pressure.
Acidosis further increases PVR
When body chronically has low O2, polycythemia happens which increases blood viscosity further reducing flow through the lungs.

41
Q

What is it called with PAP is too high? What happens?

A

Cor pulmonale (mPAP > 20mmHg)
Pulmonary HTN -> R sided HF.

42
Q

How can you distinguish COPD from asthma?

A

Post bronchodilator, only <70% response in FEV1/FVC ratio. Asthma is >80%

43
Q

If a patient has a GOLD grade of 2, what does that mean?

A

Airflow limitation grade FEV1 >50% and <80% = moderate.

1 = FEV1 >80% (mild)
3 = FEV1 >30<50% (severe)
4 = FEV1 <30% (very severe)

44
Q

What could a RBBB indicate on an EKG?

A

Pulmonary HTN.

45
Q

What kind of organisms can reach the lung alveoli and cause PNA?

A

Smaller than 2microns in size.

46
Q

GERD could cause what thype of PNA?

A

Aspiration. Concern for anaerobes with aspiration PNA

47
Q

In AOM (acute otitis media) and OME (otitis media with effusion) which one do abx not work in?

A

OME. It’s not infectious.

48
Q

Most common pathogen in OM?

A

Otitis media
Mostly viral but
H. Influenzae in ~60% of bacterial cases.

49
Q

Indications for abx in AOM

A

Both ears affected
6-23mo old
Severe ear pain or ear pain for at least 2 day
Temp > 102.2

50
Q

Pathogens responsible for sinusitis?
Tx with abx only if?

A

S. Pneumonia, and H. Influenzae = >50% of cases
Symptoms persist for >10 days

51
Q

Most common bacterial cause of pharyngitis?

A

Group A strep.

52
Q

ARDS is usuallly dx within ______ of ______

A

1wk of respiratory insult

53
Q

In ARDS, CXR shows

A

Bilateral opacities NOT related to HF.

54
Q

3 phases of ARDS

A

1 - exudative (inflammatory) - 72hrs release of cytokines, less compliant lungs, increased WOB, hypercapnea, leakage of protein rich fluids out of vasculature.
2 - Proliferative (1-3 weeks). Pulmonary edema resolves and surfactant recoveres
3 - Fibrotic phase (2-3 weeks) - remodeling and fibrosis (hardening). Decreased FRC, V/Q mismatch, severe R-L shunt and R HF.

55
Q

Levels of ARDS severity

A

Mild PaO2/FiO2 >200mmHg
Moderate PaO2/FiO2 > 100mmHg
Severe PaO2/FiO2 <100mmHg

Ex: PaO2 = 105/ FiO2 of 21% (RA) = 714 = mild.
PaO2 100/FiO2 of 60% = 166.6 = moderate

56
Q

What are some things that cause ARDS?

A

Sepsis
Aspiration
PNA
Trauma
Massive Transfusion
Pancreatitis
Medications/ETOH/Drug abuse.

57
Q

Tx for ARDS

A

No FDA approved meds
Conservative fluid strategy
Tx underlying cause
Mechanical ventilation (MAINSTAY!!)

58
Q

What is the mainstay tx for ARDS?
What should settings be at?

A

Mechanical Ventilation
Low TV
Non-invasive if possible
Permissive hypercapnea
Prone positioning.

59
Q

Cystic fibrosis is a dysfunction of what causing what?

A

CFTR chloride transporters
Causes decreased Cl- secretion and increased Na absorption.
Thick mucus, impaired clearance, GI obstruction, DM, pancreatic insufficiency and reproductive issues.

60
Q

TB spread through?

A

Airborne/droplet

61
Q

Different types of Pleural effusion

A

**Transudate (LOW protein and LDH)
Pressure differences cause fluid formation
CHF, low albumin - liver disease or nephrotic syndrome)
**Exudate (HIGH protein, high LDH)
Inflammation causes fluid formation - cancer, infection.

62
Q

Cancer or infection would cause what type of pleural effusion?

A

Exudate.

63
Q

A pleural effusion is an imbalance between

A

Formation and absorption of fluid.

64
Q

What lung pathology contributes to hypoxia without affecting ventilation?

A

Pleural effusion

65
Q

Pleural effusion has a decreased

A

FVC

66
Q

What are some S/s of bronchiectasis?

A

Chronic cough, SOB/CP, hemoptysis , wheezing, nail clubbing, permanent enlargement of parts of the airways of the lung.

67
Q

What type of bacteria is TB?

A

Weakly gram pos Rod-shaped thin aerobic bacteria - acid fast bacilli.

Patho (18 decks)

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