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Semester 5 PMCP Exam 3 > Oxygen Therapy > Flashcards

Oxygen Therapy Flashcards

1
Q

Asthma results in

A

hyperresponsive rxn to allergen which can then lead to inflammation of airway and bronchospasm

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2
Q

Chemical mediators with asthma

A

Histamine
ECF - A (eosinophilic chemo factor of anaphyl)
Prostaglandins
Leukotrienes

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3
Q

Antihistamines used for asthma

A

usually only a small effect

Histamine is not a major factor

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4
Q

ECF - A as a chemical mediator

A

released from eosinophils and mast cells and will attract more eosinophils

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5
Q

Asthma is worsened by ___ stimulation

A

vagal stimulation

Inc PSNS brought on by anxiety/fear

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6
Q

Vagus/parasympathetics will

A

BC

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7
Q

Sympathetics will

A

BD

Sympathomimetics are first line tx for asthma

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8
Q

Pediatric asthma

A

prevalence is inc

only sx can be cough

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9
Q

pediatric asthma - mechanism

A

events early on (before 3 months) are stimulating the undifferentiated helper T cells which leads to an expression of pro-allergen cytokines which makes them more susceptible to asthma

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10
Q

___ percent of asthma triggers are from ___

A

80% from airborne substances

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11
Q

Quick relief to tx acute asthma attacks

A

short acting B2 agonists

they stimulate adrenergic receptors to cause VD

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12
Q

Long term control to prevent acute asthma attacks

A 
long acting B2 agonists 
corticosteroids
mast cell stabilizers
leukotriene modifers
methylxanthines
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13
Q

Long term control to prevent acute asthma attacks - long acting B2 agonists - con to them

A

excessive reliance can lead to desensitization

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14
Q

Long term control to prevent acute asthma attacks - corticosteroids are

A

first line agents fo rlong term control

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15
Q

Long term control to prevent acute asthma attacks - leukotriene modifers - produced from

A

arachadonic acid

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16
Q

Long term control to prevent acute asthma attacks - methylxanthines - mechanism

A

inhibit cAMP to maintain BD for a while longer

Prolong the sympathetic effect

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17
Q

Long term control to prevent acute asthma attacks - Beta agonist are most effective in

A

relieving acute bronchospasm

relieve sx in 3-15 min

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18
Q

Sole tx for mild episodic asthma and tx of choice for exercise induced asthma

A

B2 agonist

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19
Q

asthma - B agonists - side effects

A 
are transient
mm tremors
tachycardia
nervousness
agitation
hypertension
urinary retention
seizures
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20
Q

B agonist for asthma - best to supplement with

A

other antiinflammatory

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21
Q

B agonist for asthma - examples (3) and their mechanisms

A

levalbuterol - has only the active isomer of albuterol so it lowers side effects
formoterol and salmeterol - long acting for up to 12 hours - good for COPD or chronic sx of asthma

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22
Q

Asthma - corticosteroids - mechanism

A

inhibit inflammatory response by inc number of B receptors and dec mucus production

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23
Q

Asthma - corticosteroids - used for

A

long term suppression, control, reversal of inflammation

NOT for short term attack

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24
Q

Asthma - corticosteroid - how long do you need to take it before see dec in airway inflammation

A

2 to 8 weeks

25
Q

Corticosteroids - early asthma tx

A

If used aggressively early on, may limit progression of asthma

26
Q

Side effects of corticosteroids - asthma

A 
Thrush (fungal mouth infection)
Dysphonia
Appetite stimulation
Inhibits growth up to 1cm per yr
Osteoporosis
HTN
Immune suppression
27
Q

Corticosteroids used for asthma - examples

A

Budesonide
Fluticasone
Combination for long term control could be advair and symbicort

28
Q

ASthma - mast cell stabilizer - mechanism

A

Prevents release of histamine from mast cells which reduces the frequency and severity of the attacks
Has mild antiinflammatory effects
Used to reduce CS usage
No BD activity

29
Q

Asthma - mast cell stabilizer - side effects

A 
transient bronchospasm
cough/dry throat
bitter taste
nausea
vomit
30
Q

Asthma - mast cell stabilizer - how long do you have to take it before see max benefit

A

4-6 weeks

31
Q

Asthma - mast cell stabilizer examples (2)

A

Cromolyn

Nedocromial

32
Q

Asthma - Leukotriene modifier - mechanism

A

blocks LT synthesis or the receptor binding to decrease inflammation

33
Q

Asthma - leukotriene used as

A

an alternative to reduce corticosteroid use

34
Q

ASthma - long term acting ones are never used alone for the tx of asthma T or F

A

TRUE

35
Q

Examples of leukotriene modifiers used for asthma

A

Singulair

Zileuton

36
Q

Asthma - methylxanthines - mechanism

A 
phosphodiesterase inhibitor
Will dec Ca influx and elicit BD by inhibiting cAMP
Dec histamine release 
Narrow therapeutic index 
Weak BD but is long lasting
37
Q

COPD treatment - what is used

A

bronchodilators!!!

  • anticholinergics
  • B2 agonsits (long acting)
  • methylxanthines
38
Q

COPD - only antinflammatory approved for COPD

A

advair

39
Q

For pts who are hypoxemic at rest - only therapy documented to improve progression of COPD is what

A

supplemental oxygen

40
Q

Hypoxemia is what

A

reduced oxygen in blood

41
Q

Hypoxia is what

A

reduced oxygen in tissues

42
Q

Oxygen tx - goals

A

eliminate hypoxia
get SaO2 to 90 percent
Ensures tissue oxygenation
Reduces compensatory hypoxic responses

43
Q

Oxygen tx - if inc in hypoxia can lead to

A

inc in sympathetic tone which causes inc hR, inc contractility, VC

44
Q

Oxygen tx - if hypoxic in lungs can result in

A

pulmonary hypoxic VC

Vessels close down

45
Q

Pros and cons to pulmonary hypoxic VC

A

we can push blood to areas of better gas exchange

inc resistance - harder on heart - inc afterload to R heart

46
Q

Causes of hypoxemia

A

altitude (decrease PO2)
hypoventilation (dec PAO2)
Inadequate oxygenation of blood (dec PaO2)
Impaired transport (poor tissue delivery)
Inadequate of excessive O2 utilization - high metabolic demand

47
Q

Effects of hypoxia

A

Vetilation - inc rate and depth
Cardiovascular function - inc sympathetic activity
Autoregulation of coronary and cerebral vasculature (VD)
Pulmonary hypoxic VC

48
Q

Big problem with hypoxia -

A

loss of ability to respond or loss of consciousness before the recognition of the problem

49
Q

Effects of O2 on arterial blood gases

A

inc dissolved composition (PO2)
High PaO2 impairs CO2 transport - and if CO2 accumulated can lead to acidosis
Absorption atelectasis from nitrogen washout (from giving 100% oxygen)

50
Q

Effects of 100% O2 on normal patient

A 
1 initial mild resp depression
2 CNS can have long term or concurrent stimulation or depression
3 dec sympathetic tone 
4 VC of coronaries and cerebral vessels
5 no change in metabolism
51
Q

Oxygen toxicity - as you lower the oxygen delivery amount a patient can

A

tolerate it for a longer period of time

52
Q

100% oxygen at 1atm is safe for how long

A

24 hours

53
Q

Effects of oxygen toxicity

A

1 absorptive atelectasis
2 resp depression
3 retrolental fibroplasia

54
Q

Nature and severity of oxygen toxicity is determined by

A

degree of hyperoxygenation
duration of exposure
individual cell type

55
Q

Guidelines for oxygen use

A

1 no problems with 100% O2 at 1 atm for 24 hrs
2 no sig problem if concentration of O2 is less than 50% at 1 atm
3 period breaks to dec toxicity
4 toxicity inc if pre existing pulm disease

56
Q

Cause of toxicity is

A

PO2 NOT the concentration

Measure PaO2 and PaCO2 instead of just the saturation

57
Q

Oxygen tx should be aimed at correcting

A

arterial hypoxemia

58
Q

If tissue hypoxia occurs in absence of arterial hypoxemia, then tx should be directed at

A

underlying causes

Semester 5 PMCP Exam 3 (6 decks)

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