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Med 1 UBC Fall 2019 > Week 6-7: Lungs > Flashcards

Week 6-7: Lungs Flashcards

1
Q

3 pathologies of pneumonia

A

1) aspiration
2) droplet transmission
3) hematogenous spread

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2
Q

What colour is gram positive?

A

purple

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3
Q

What colour is gram negative?

A

pink

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4
Q

What sort of shape is a coccobacilli?

A

Rods and spheres and rod/spheres

Ex: haemophilus influenzae

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5
Q

What do diplococci look like?

A

cocci in pairs

Ex: moraxella catarrhalis

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6
Q

Most common pathogens in community-acquired pneumonia?

A

Step pneum
Haemophilus influenzae
Moroxella

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7
Q

Tidal volume

A

the amount you normally breathe in and out (500 mL)

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8
Q

Inspiratory reserve volume

A

The amount you can breathe in if you tried really hard (1900 mL additional)

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9
Q

Expiratory reserve volume

A

The amount you can breathe out if you try really hard (700 mL additional)

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10
Q

Residual volume

A

the amount left in your lungs that will never be breathed out. 1200 mL

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11
Q

Inspiratory capacity

A

the total amount you can forcibly breathe in (TV + IRV)

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12
Q

Functional Residual Capacity

A

Residual Volume + Expiratory reserve volume (the amount left in your lungs if you are just breathing normally)

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13
Q

Vital capacity

A

Inspiratory reserve volume + Tidal Volume + Expiratory Reserve Volume

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14
Q

Total Lung Capacity

A

All lung volumes combined (including residual capacity)

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15
Q

Hyperventilation

A

ventilation exceeds the metabolic demands of the body

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16
Q

Hypoventilation

A

ventilation is insufficient to meet the demands of the body

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17
Q

Minute Ventilation

A

the amount of air inhaled or exhales from the lungs per minute.
Product of Tidal Volume x Resp Rate

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18
Q

Alveolar Ventilation

A

The amount of air reaching the alveolus per minute. This is air that takes part in gas exchange.

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19
Q

Dead Space Ventilation

A

The volume of air inhaled that does not take part in gas exchange because it remains in the conducting airways or it reaches alveoli that are not perfused or poorly perfused.

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20
Q

Anatomic Dead Space

A

Total volume of the conducting airways from the mouth/nose down to the level of the terminal bronchioles.

~150 mL on average in humans

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21
Q

Alveolar Dead Space

A

Volume of air in the alveoli that does not participate in gas exchange (ventilation without perfusion)

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22
Q

Physiologic Dead Space

A

Sum of anatomic and alveolar dead space

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23
Q

Name the factors that affect diffusive transport of gas from alveolar air to pulmonary capillary blood and discuss how these relate to the diffusing capacity of the lungs

A
  1. Membrane thickness
  2. Membrane surface area
  3. Pressure difference across the membrane
  4. Diffusion coefficient of gas
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24
Q

Partial pressures of O2 and CO2 in alveoli

A 
PAO2 = 105 mmHg (compared to 159 in atmospheric air)
PACO2 = 40 mmHg (compared to 0.3 in atmospheric air)
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25
Q

Partial pressures of O2 and CO2 in mixed venous blood

A

PO2 in venous blood = 40 mmHg

PCO2 in venous blood = 45 mmHg

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26
Q

Partial pressures of O2 and CO2 in arterial blood

A 
PaO2 = 100 mmHg
PaCO2 = 40 mmHg
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27
Q

Define pnemonia

A

Pneumonia is a generic term that refers to inflammation of the pulmonary parenchyma. It is often associated with consolidation (solidification) of the lung. Usually infectious etiology.

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28
Q

Predisposing factors for pneumonia

A
  1. suppression of cough reflex (anaesthesia, neuromuscular disorders)
  2. Impaired immunity
  3. Impaired mucociliary apparatus (smoking, syndrome)
  4. Impaired alveolar macrophage function (alcohol, smoking)
  5. Pulmonary edema (cardiac failure)
  6. General debility (alcoholism, post-op, malnourishment)
29
Q

Lobar pneumonia

A

Restricted to lobe; Most common CAP; majority are strep pneum

30
Q

Broncho pneumonia

A
  • patchy infective consolidation of the lung in a predominantly lobular distribution.
  • Common, especially in hospitalized patients; often terminal complication
  • Usually bilateral
  • Pre-existing bronchitis spreads to cause bronchiolitis and extends to involve adjacent lung parenchyma
31
Q

Complications of Bacterial Pneumonia:

A

○ Bacteremia - bacterial dissemination into the blood
○ Lung abscess formation due to destruction of pulmonary parenchyma and suppuration (pus formation)
○ Empyema - extension of inflammation to pleural cavity (pus in pleural cavity –> fibrosis of pleura)
○ Death

32
Q

Interstitial pneumonia

A

the issue isn’t in alveolar lumen. Alveolar walls are thickened by infiltration with mononuclear leukocytes in contrast to the intra-alveolar PMN exudate of bacterial pneumonia

Usually viruses, chlamydia, mycoplasma, pneumocystis

33
Q

Mechanism of cough

A

A reflex. Stimulant of irritant receptors in airway leads to activation of inspiratory muscles including diaphragm, as well as activation of expiratory muscles and larynx.

34
Q

Pathogenesis of asthma

A
  • primarily allergen-driven TH2 response (also viruses and pollutants)
  • APC presents to T cells, which differentiate to TH2. TH2 cells prime B cells with IL-4, IL-5, IL-12 to produce IgE, which are mounted in mast cells —> inflammation
35
Q

Airway remodelling in asthma

A
  • mucous plug containing inflammatory and desquamated epithelial cells
  • smooth muscle hypertrophy
  • thickened basement membrane
  • goblet cell metaplasia
  • inflam cell infiltration
36
Q

How does smoking contribute to pathogenesis of COPD?

A
  • smoke (in combination with genetics, infections, and other exposures) leads to two elements of COPD:
    1) obliteration of parenchyma, destroying recoil and causing emphysema
    2) inflammation of airways, leading to remodelling and thickening and ultimately small airways disease.
  • final outcomes in reduced expiratory flow, hyperinflation, and reduced gas exchange
37
Q

Mechanism of action of nicotine in the CNS

A

Nicotine binds preferentially to nicotine ACh receptors in the CNS - especially the nACh receptor in Central Tegmental Area
- binding of nicotine in nACh receptor in ventral tegmental area results in release of dopamine in nucleus accumbens, which is believed to be linked to reward

38
Q

First line pharmacotherapy for tobacco dependence

A
  • nicotine replacement therapy
  • antidepressant (bupropion)
  • nicotine ACh receptor partial agonist (Varenicline)
39
Q

What is the strongest predictor of all-cause mortality in patients with COPD?

A

Physical activity

40
Q

Define hemoptysis

A

Expectoration of blood

41
Q

Pathology of asthma

A
  • Smooth muscle contraction around central and peripheral airways
  • wall thickening and remodeling
  • increased mucous production and airway obstruction
  • allergic, IgE mediated,
42
Q

Pathology of bronchiectasis

A
  • irreversible dilation of the bronchial tree and obliteration of peripheral small airways
  • due to repetitive/persistent infection
  • wall thickening and remodeling
  • damage undermines mucociliary clearance, resulting in occlusion
43
Q

What is bronchitis?

A
  • chronic inflammation of the bronchi
44
Q

What is bronchiolitis

A
  • infection of bronchioles, mostly in children

- results in wall thickening and obliteration

45
Q

Hydrostatic pressure

A

Pressure exerted by a liquid at equilibrium.

46
Q

Oncotic pressure

A

Due to proteins and osmoles in the plasma. Draws fluid into capillaries

47
Q

Transudate vs exudate

A

Transudate is non-inflammatory pleural fluid (heart failure, cirrhosis, nephrotic syndrome).

Exudate is inflammatory derived pleural fluid. Could be from infection, malignancy, pulmonary embolism, etc.

48
Q

How does pulmonary embolism lead to pleural effusion?

A

Increased R heart pressure leads to increased pulmonary capillary permeability pushing fluid into the pleural space. The fluid may be a transudate (non-inflammatory) or exudate (inflammatory)

49
Q

Small Cell Carcinoma (prevalence and macroscopic features)

A
  • Lung Carcinoma type
  • 15% of lung cancers
  • Predominantly central
  • highly malignant and often disseminated at time of presentation
50
Q

Small cell carcinoma (microscopic features)

A
  • cells have small oval hyperchromatic nuclei and scanty cytoplasm
  • Tumor cells exhibit neuroendocrine differentiation
51
Q

What are the implications of subdividing lung cancer into two categories, small cell and non-small cell

A

Has to do with immunochemistry of the cancers as relevant to therapeutic agents.
Small cell carcinoma is P40 -ve and TTF1 +ve (as is adenocarcinoma)

52
Q

Large cell carcinoma

  • prevalence
  • macroscopic features
  • microscopic features
A
  • 10% lung cancers
  • often peripheral & probably cases of very poorly differentiated adenocarcinoma
  • Large polygonal cells with vesicular nuclei and prominent nucleoli. No specific differentiation.
53
Q

Adenocarcinoma

  • prevalence
  • subcategories
  • macroscopic features
  • microscopic features
A
  • 50%+ lung cancers
  • Subcategories based on bronchiolo-alveolar carcinoma growth patterns and invasive adenocarcinoma growth patterns
  • 2/3 peripheral and 1/3 central lung. Commonest lung cancer in non-smokers. Peripheral tumors cause puckering of pleura
  • Usually cells form glands and/or produce mucin
54
Q

Squamous cell carcinoma

  • Prevalence
  • Macroscopic features
  • microscopic features
A
  • 25% of lung cancers
  • Mostly central growth with cavitations. Adjacent epithelium often displays abnormal growth as well.
  • Variably resemble squamous epithelium with keratin formation and intercellular bridges
55
Q

Massive hemoptysis from a vascular bleed is most likely to come from…

A

Bronchial vessels (95% of the time) over pulmonary vessels (5% of the time). And bronchial artery > vein

56
Q

A normal Alveolar-arterial (Aa) gradient (PAO2 - PaO2) is associated with hypoxia in which situation?

A

Decreased alveolar ventilation (VA)

57
Q

Define empiric therapy

A

○ Presumptive therapy based on the likelihood of pathogen and type of infection
○ Usually “broad spectrum”
○ Goal to decrease morbidity and mortality
Infections where pathogens cannot be diagnosed

58
Q

Targeted antibiotic treatment

A
  • narrow-spectrum
  • based on susceptibility results
  • minimize toxicity to patient and risk of developing resistance
59
Q

define Bacteriostatic

A

drugs slow of stop replication so immune system can eliminate bacteria

60
Q

Bactericidal

A

drugs that kill bacteria directly

61
Q

Antibiotic synergy

A

2 drugs together have high bactericidal activity than either alone (Ex: B-lactam + aminoglycoside)

62
Q

4 mechanisms of antibiotic resistance

A

1) efflux pumps - most common
2) B-lactamases - gram -ve
3) Alteration of penicillin-binding protein
4) Alter porin size

63
Q

How would you treat MRSA

A

Resistant bacteria.
PO: TMP-SMX | Linezolid | doxycycline +/- clindamycin
IV: Vancomycin, daptomycin, ceftaroline

64
Q

How would you treat pseudomonas

A

Resistant bacteria.
PO: ciprofloxacin
IV: Pip-Tazo | Cefepime | Ceftazadime | Merepenem | Imipenem

65
Q

How would you treat ESBL

A

ESBL is extended spectrum beta-lactamase. A resistant bacteria.

Treat with carbapenems

66
Q

What are carbapenems really useful to treat

A

ESBL

67
Q

Which antibiotic doesn’t work in the lungs and why is this?

A

Daptomycin doesn’t work in the lungs because it is inactivated by surfactant.

68
Q

Which pneumonia bacteria are gram +ve

A

The S ones

Strep pneumo and staph aureus

Med 1 UBC Fall 2019 (16 decks)

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