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Week 2 Flashcards

1
Q

What proportion of oxygen is dissolved in the plasma? What proportion is carried by Hb?

A

2% in plasma (PO2) 98% with Hb (SO2)

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2
Q

Define O2 content, O2 capacity and O2 saturation

A

O2 content: the total amount of O2 in the blood (dissolved and with Hb)

O2 capacity: the max amount of O2 that can be combined with Hb (20 mL/100mL blood)

02 saturation: is the % of Hb binding sites bound to O2 (oxyHb/O2 capacity)

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3
Q

What is the PO2 and SaO2 of arterial and venous blood?

A

Arterial:

  • PaO2= 100
  • SaO2=100

Venous

  • Pa02=40
  • SaO2=75
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4
Q

What is the oxy-Hb dissociation curve?

A

A curve representing the relationship of oxygen tension and hemoglobin saturation. Each hemoglobin can carry 4 molecules of oxygen that bind cooperatively.

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5
Q

Describe the portions of the Oxy-Hb curve that correspond to oxygen loading and unloading.

A

At the lungs, Hb becomes saturated. At the tissues, a small change in pO2 results in a loarge change in oxygen saturation.

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6
Q

What does a rightward shift of the oxyHb curve mean? A leftward shift?

A

Right: Hb has lower affinity for O2

Left: Hb has higher affinity for O2

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7
Q

What causes a rightward shift of the oxyHb curve?

A
  • Increased temperature
  • increased pCO2
  • decreased pH (Bohr Effect)
  • increased 2,3 BPG (from anaerobic metabolism)

**everything that happens with exercise!

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8
Q

What does the oxyHb curve look like in anemia (with O2 content, as opposed to Sa02 on the y-axis)?

A
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9
Q

What is the effect of CO on oxygen content and oxygen carrying capacity in the blood?

A

Oxygen content decreases (because it is outcompeted by CO) and O2 carrying capacity decreases (?)(because binding spots are taken up by CO)

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10
Q

What is the effect of erythropoeitin (EPO) on the oxygen capacity and content of the blood?

A

Increases both , because you have more RBCs

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11
Q

What color is oxy, deoxy and carboxyHb?

A
  • OxyHb: red
  • deoxyHb: blue
  • carboxyHb (COHb): cherry red (can be seen in deceased according to wikipedia)
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12
Q

What forms does Co2 in the blood exist in, and what is the percentage of each?

A
  1. Bicarbonate (90%)
  2. Disolved (5%)
  3. CarbaminoHb (5%)
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13
Q

What is the role of carbonic anyhydrase in the transport of carbon dioxide?

A

Carbonic anhydrase lives in red blood cells. CO2 diffuses from tissues, into the plasma and into the RBCs. There. it can either combine with Hb (carbaminoHb) or be converted to carbonic acid via carbonic anhydrase. The proton from this reaction binds Hb and does not diffuse. The bicarbonate is transported out of RBCs and Cl- is transported into RBCs to counter the bicarbonate. This is called the chloride shift.

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14
Q

What is the Haldane effect? What produces it?

A
  • Deoxygenation of the blood increases its ability to carry CO2
  • This is good beacuse it permits high loading of CO2 at the tissues (low pO2), and unloading of CO2 at the lungs (high PO2)
  • In high pO2, oxygen binding creates conformational changes that make CO2, H+ binding less favorable
  • In low pO2 (at the tissues), H+ and 2,3 BPG bind to Hb and create conformational changes that make CO2 binding more favorable.
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15
Q

Define bronchiectasis and list possible etiologies

A

Irreversible dilatation of the bronchial tree (bronchi and bronchioles) (vs. the reversible that can accompany infectious pneumonia)

Etiologies:

Congenital:

  • cystic fibrosis
  • primary ciliary dyskenesia
  • kartagener syndromes

Post infectious

  • necrotizing pneumonias (TB, HiB, S. aureus, viral, fungal (e.g. aspergillus)

Obstruction

  • tumour
  • foreign body
  • mucus impaction

Other

  • collagen vascular diseases (rheumatoid arthritis, lupus, scleraderma)
  • post-transplant
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16
Q

Pathophysiology of bronchiectasis

A

Infectious: inflammation, necrosis, fibrosis, dilatation

Obstructive: secretions build up below the obstruction and inflammation ensue

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17
Q

Define bronchiolitis obliterans

A

Irreversible narrowing/compression of small airways by fibrosis, with or without inflammation

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18
Q

Etiology of bronchiolitis obliterans

A

Post-infectious

Envrionmental (fumes, dusts)

Other (post lung transplant, collagen vascular disease, drug-induced)

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19
Q

What is the common pathogenesis of all obstructive lung diseases?

A

Inflammation!

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20
Q

What are common symptoms of chronic obstructive airway disease?

A

Cough

dyspnea

wheeze

sputum production

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21
Q

What are 2 sources of mucus in the lung?

A

1) goblet cells
2) mucous glands found in cartilagenous airways

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22
Q

What are mechanisms of increased lung resistance (x5)?

A
  • lumenal occlusion
  • increased wall thickness
  • loss of elasticity
  • smooth muscle contraction
  • obliteration of airways
23
Q

What are the the mechanisms of increased lung resistance in COPD, bronchiectasis, bronchiolitis obliterans and asthma?

A

COPD: loss of elasticity, obliteration

Bronchiectasis: wall thickening, lumenal occlusion, obliteration

Asthma: smooth muscle spasm, wall thickening

Bronchiolitis obliterans: wall thickening, obliteration

24
Q

What is the natural progression of chronic obstructive airway diseases?

A
  • A long asymptomatic period because the changes occur primarily in the small airways, and the most physiological resistance is at gen. 4/5 ish, so it takes a long time for the pathophysiological resistance to show up.
  • exertional dyspnea usually comes first and progresses to dyspnea at rest.
25
What are the primary inflammatory triggers for COPD, bronchiectasis, asthma and bronchiolitis obliterans?
COPD: smoke Bronchiectasis: bacteria Asthma: allergen drive Th2 response Bronchiolitis obliterans: various, including fumes and transplant rejection
26
What is the importance of the immune system in asthma?
An allergen causes a Th2 mediated response, mast cells unload IgE, everything together cause bronchoconstriction and inflammation.
27
What is the role of smoking in COPD development?
Cigarette smoke, along with genetic susceptibility and environmental exposure combines to cause: 1. parenchyma inflammation---\> emphysema 2. airway inflammation--\> remodelling and thickening--\>small airway disease Together these decrease expiratory flow, and cause hyperinflation of the lung with gas exchange abnormalities
28
centroacinar vs panacinar emphysema
centroacinar: starts in centre of lobule and works its way out panacinar: occurs throughout the lobule
29
Define COPD
Chronic obstructive pulmonary disease (COPD), a common preventable and treatable disease, is characterized by airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.
30
Define asthma
a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation.
31
Classes of bronchodilators, and the indications for each
* Beta agonists: asthma and COPD * anticholinergics: COPD (chronic and acute exacerbation) and acute asthma (but not commonly used) * methylxanthines: 2nd or 3rd line for asthma and COPD
32
What is the MOA of beta-agonists?
GPCReceptors on smooth muscle cells, cAMP 2nd messenger, bronchodilation
33
What are the different kinds of beta-agonists used for bronchodilation?
Short acting (SABA) Long acting (LABA) Ultra long acting
34
What is in a blue puffer, when is it used, and what are possible side-effects?
Salbutamol * SABA * Rescue puffer SE: tremors, tachycardia. If these appear after the puffer has been used for some time it could be a sign that the asthma is getting worse because the patient is using the puffer more often.
35
What is an example of a LABA? What is it used for?
Salme*terol* * long duration bronchodilator * NOT a rescue puffer * should be used in conjunction with corticosteroids
36
What is are 2 examples of anticholinergics used for asthma, COPD?
Ipratropium * It's a modified version of atropine designed to be more lipophobic so it doesn't cross membranes Tiotropium * It's a selective M3 anticholinergic
37
What is the MOA of Ipratropium?
Acts on M2 (bronchial secretion) and M3 (bronchoconstriction) receptors in the lung
38
What are side effects of anticholinergics in their use in asthma/COPD?
Dry mouth: causes cavities, and is annoying Nasal irritation Nose Bleeds
39
What is an example of a methylxanthine? What is the MOA? What are SE? When is it used?
Theophylline Poorly define MOA, inhibits phosphodiesterase and supports bronchodilation SE: nausea, vomiting, stimulation (insomnia, anxiety, tremor), arrhythmias Used as a last line for asthma because the SE are so serious
40
How do corticosteroids work?
They act in the nucleus to inhibit the transcription of some genes and promote the transcription of other gene Inhibit expression: * pro-inflammatory cytokines * COX-2 They are immunosuppressants and metabolic modulators
41
What is an example of a systemic corticosteroid? What are side effects
Prednisone SE * obesity, hyperglycemia, osteoporosis etc....
42
What are 2 examples of inhaled corticosteroids? What are side effects?
budeso*nide*, flutaca*sone* SE: * oral thrush * dysphonia * sore throat
43
What are broad categories of drugs that can be used to treat asthma/COPD?
* Bronchodilators * Corticosteroids * Leuktriene receptor antagonists * Monoclonal antibodies
44
What is the MOA of leukotriene receptor antagonists?
they block leukotriene receptors (LT2) and prevent bronchoconstriction and inflammation in the airways and mucus hypersecretion.
45
What is an example of a leukotriene receptor antagonist? Indication? What is the advantage? What is the disadvantage?
* Montelukast - used for management of chronic asthma (not for acute) * Oral dosing * Not as effective as other treatments
46
What is an example of a monoclonal antibody? When is it used? What is the route?
Omalizu*mab* binds up IgE, used in asthma. Injected subcutaneously.
47
What is combination therapy and what is the rationale for it?
* Usually a LABA and corticosteroid * long term beta-agonist use downregulates B2 receptors. Corticosteroids upregulate them * Advair (salmeterol + fluticasone) * Symbicort (formeterol + budesonide) * Zenhale (formoterol + mometasone)
48
Types of inhalation administration of drugs?
MDI (metered dose inhaler) (AKA puffer) dry powder inhaler nebulizer
49
When not to use beta-agonists?
In anyone who tachycardia could pose a problem (pre-existing arrhythmia, coronary artery disease, aortic stenosis)
50
When to not use anticholinergics?
In any patient who has a condition that would be exacerbated by cholinergic antagonism (e.g. glaucoma, urinary retention)
51
What is the mode of delivery for: * corticosteroids (fluticasone, budesonide) * montelukast * ipratropium * salbutemol/indacaterol/salmeterol
* corticosteroids (fluticasone, budesonide)--\> inhaled * montelukast--\> oral * ipratropium--\>inhaled * salbutemol/indacaterol/salmeterol--\> inhaled
52
What is the natural history of COPD in smokers and non-smokers, vs. a healthy age-matched subject (in terms of FEV1)?
53
Is inspiratory flow effort dependent? Is expiratory flow effort dependent?
Inspiratory flow is effort dependent, but expiratory flow is almost entirely effort independent.

Pulm Block (10 decks)

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