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Fall 20' Anatomy III MO > Resp. exam 2 > Flashcards

Resp. exam 2 Flashcards

1
Q

What does Asthma look like on Chest X ray?

A

May be normal

Hyperinflation

Flattening of diaphragm

Mucus plugging

Atelactasis

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2
Q

Pathophysiology of Asthma? (what is happening in the lungs?)

A

increased resistance to airflow due to AIRWAY NARROWING (normal physiology between the attacks)

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3
Q

6 triggering factors to cause asthma?

A

Airway irritants, environmental pollutants (including occupational exposure)

Exercise, cold air , dry air

Upper and lower resp. tract infection

Aspirin (COX inhibition leading to overproduction of leukotriens)

Beta blockers

Gastro esophageal reflux

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4
Q

Clinical Features of Asthma?

A 
SOB
Cough , chest tightness 
Wheezing 
Dyspnea
Worst at night
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5
Q

Physical findings of asthma in between attacks?

A

In between attacks a patients exam will be normal, this is a reversable disease.

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6
Q

Physical findings of asthma during an attack?

A

Tachypnea

Insp. and exp. wheezing

Use of accessory muscles

Pulsus paradoxus

Paradoxical movement of abdomen

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7
Q

Diagnosis of Asthma: what happens to the peak flow expiratory rate?

A

decreased

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8
Q

Diagnosis of Asthma: what happens to the FVC, FEV1, FEV1/FVC?

A

decreased

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9
Q

Diagnosis of Asthma: does Residual volume increase or decrease and why?

A

Increase bc of air trapping

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10
Q

Diagnosis of Asthma: What is the patients diffusion capacity?

A

Normal

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11
Q

**In a patient with Asthma, how can you improve their flow rate?

A

bronchodilators

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12
Q

In Asthma, they have Bronchial hyper-responsiveness to what?

A

histamine

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13
Q

People with Asthma have a high count of what blood component?

A

Eosinophils creating Eosinophilia

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14
Q

What should the CO2 status and O2 status of an asthmatic be?

A

Should be Hypocapnia (low CO2)

mild hypoxemia.

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15
Q

Two medications that can trigger asthma?

A

Aspirin (cox inhibition leading to overproduction of leukotrienes)

Beta blockers

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16
Q

When is asthma the worst?

A

at night

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17
Q

Treatment of asthma? (5 drug types)

A

Anti-inflammatory drugs

Bronchodilators

Anti-leukotrienes-Zileuton

Montelukast (singulair) and Zafirlukast

Anti-IgE monoclonal therapy

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18
Q

Name anti-inflammatory drug types for asthma?

A

inhaled steroids
systemic steroids
Cromolyn

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19
Q

How does the anit-inflammatory drug Cromolyn work?

A

prevents mast cell degranulation, useful in PROPHYLAXIS not for an acute attack of asthma. Also used to prevent exercise induced asthma.

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20
Q

What is a common medication used as part of the therapy for Asthma to try and prevent an attack from reflux?

A

Prilosec (PPI)

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21
Q

How come ASA is a trigger for Asthma?

A

Cox inhibition leads to an overproduction of leukotrienes.

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22
Q

Is asthma considered a reversible or non reversible dz?

A

Reversible bc between attacks they are “normal” or have no symptoms even though their PFTs will not be “normal”

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23
Q

What is paradoxical movement of the abdomen that you sometimes see in patients who are having an asthma attack?

A

opposite movement of the abdominal wall during inspiration and expiration. During inspiration the diaphragm will pull upward which is opposite from normal inspiration when the diaphragm pulls downward.

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24
Q

What kind of lung dz is asthma considered?

A

obstructive

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25
Q

How do the lungs respond to histamine if you have asthma?

A

Bronchial hyper-responsiveness

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26
Q

When is an asthma attack considered a medical emergency?

A

When the patient has normal or elevated carbon dioxide levels while hyperventilating.

40@40 which means CO2 of 40 at 40 RR = medical emergency/respiratory failure bc they are dead spacing and immediate intubation is needed.

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27
Q

When do you use Cromolyn?

A

exercise induced asthma, it is preventative not for acute attack.

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28
Q

Bronchodilators are given for asthma, name some bronchodilators?

A

B2 agonist - inhaled or nebulized

Anticholinergic - atropine and ipratropium

Aminophylline preparation-theophylline

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29
Q

What is ipratropium, what does it help with?

A

anticholinergic for asthma. Blocks Ach from M3 receptor and thus prevents bronchoconstriction

Dry secretions, helpful with excessive mucus formation.

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30
Q

Theophylline is given for asthma, what kind of drug is it? What does it cause to the lungs?
What is an issue with theophylline?

A

Phosphodiesterase inhibitor, increasing cAMP.

Creates bronchodilation.

Narrow therapeutic index - thus people coming into the ER with an asthma attack who use this drug will often overdose on it. Showing up as cardiovascular effects such as tachycardia/high blood pressure.

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31
Q

What asthma medication is a competitive antagonist of leukotriene on cysteinyl-leukotriene receptor?

A

Montelukast (Singulair) and Zafirlukast

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32
Q

Are leukotrienes good or bad? What do they cause?

A

bad, they cause bronchospasm, vasoconstriction, and eosinophil recruitment.

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33
Q

What medication is good for ASA induced asthma?

Why?

A

Montelukast (singulair) and Zafirlukast.

ASA is a cox inhibitor which leads to an overproduction of leukotrienes, Singulair blocks leukotrienes from their receptor and thus they can not exert bronchospasm, vasoconstriction, and eosinophilia.

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34
Q

What medication for asthma blocks the conversion of arachidonic acid to leukotriene?

A

Anti-leukotrienes- Zileuton (zyflo)

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35
Q

What are the adverse effects of Zileuton?

A

dyspepsia (indigestion) arthralgia (joint pain), chest pain, and fever.

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36
Q

What type of drug is Zileuton (zyflo)?

What is the MOA of Zileuton?

A

5-lipoxigenase inhibitor. (asthma medication)

blocks the conversion of arachidonic acid to leukotriene.

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37
Q

What cell does IgE cause to bust open (bad)

A

mast cells

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38
Q

What is Omalizumab, what does it do?

A

Drug therapy for some asthmatics, it binds free IgE, thus less mast cell degeneration.

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39
Q

If someone has IgE related asthma what medication could you give them that is specifically for IgE mediated asthma?

A

Omalizumab

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40
Q

What asthma medication is not helpful in control of sever acute attack?

A

Aminophylline

also cromolyn bc it is only preventative but Mo specified aminophylline in the PPT

41
Q

How to prevent atelectasis?

A

early mobilization, breathing exercises, INSINTIVE SPIROMETRY

42
Q

What is it called when the alveoli collapse and what causes it?

A

Atelectasis is caused by airway obstruction due to mucous plug, tumor or lack of surfactant.

43
Q

A saturation of oxygen drop to 91% would most likely be?

A drop to 78% would most likely be?

A

91% = atelectasis (minimal drop)

78% = pneumonia (decent drop/bad)

44
Q

Management of acute asthma attack would include what drug combination?

A

Beta 2 agonist + steroid + ipratropium (anticholinergic like)

systemic steroid use (IV)

45
Q

Management of chronic asthmatic disease?

A

Inhaled steroid as maintenance + inhaled Beta 2 steroid for symptomatic control.

Add ipratropium

Consider aminophylline

Short course of oral steroid

46
Q

What mechanisms can cause bronchodilation (wanted in asthmatics), or stop bronchoconstriction?

A

Nitric oxide increases cGMP which causes bronchodilation.

Terbutaline (beta 2 agonist) leads to G protein stimulation (Gs) which eventually causes dilation.

Phosphodiesterase inhibitor like Anopheline or theophylline inhibits 5’AMP and allows more cAMP to activate protein kinase and cause dilation.

Ipratropium (atrovent) inhibits Ach on M3 receptors in the lungs which would cause increased calcium and bronchoconstriction, thus by blocking Ach from the Muscarinic receptor it stops bronchoconstriction.

47
Q

How does Nitric oxide cause bronchodilation?

A

nitric oxide can cross the cell membrane without a receptor (lipid soluble) once that happens it increase cGMP which causes bronchodilation.

48
Q

What causes primary pulmonary hypertension?

A

Due an inactivating mutation in the BMPR2 gene (normally functions to inhibit vascular smooth muscle proliferation)

poor prognosis

49
Q

What is normal pulmonary artery pressure?

A

10-14 mmHg

50
Q

What pulmonary artery pressure is considered PHTN at rest and then at exercise?

A

normal (rest) = > or equal to 25 mmHg

exercise = >35 mmHg

51
Q

With a PE, how does V/Q change?

A

ventilation is still good but perfusion is defective, not as good as normal, less perfusion due to the embolus.
= V/Q mismatch, high probability of a clot.

52
Q

95% of PE originate from what?

A

DVT from leg

53
Q

If you have a non-thrombotic PE what three times/situations would that occur in?

A

Septic– endocarditis in IV drug abusers; infected catheters

Fat—after long bone fractures

Amniotic fluid—during child birth

54
Q

Acronym FAT BAT is used to remember what and what does it stand for?

A

Risk factors for pulmonary embolism acronym.

Fat
Air
Thrombus
Bacteria
Amniotic fluid
Tumor
55
Q

What signs are specific to RV overload with a PE?

A

Load P2, RV heave

56
Q

If you are hyperventilating what typically happens to your PCO2?

A

PCO2 should decrease in hyperventilation. You have a medical emergency if someone is hyperventilating and their CO2 is normal or elevated, time to intubate.

57
Q

What does a D-dimer tell you and what could it be indicative of?

A

by product of intrinsic fibrinolysis.

could have a PE

58
Q

What has the V/Q scan been replaced by?

A

CT scan

59
Q

What is the most sensitive and specific test for a PE?

A

CT arteriography

60
Q

**What are the pathological consequences of a PE?

A

Increased pulmonary vascular resistance (big clot is sitting there)

Increased pulmonary artery pressure

Increased RV afterload

Everything increases!

61
Q

Homan’s sign is?

A

dorsiflexion of foot that causes tender calf muscle, sign of PE.

62
Q

ABG’s of a person with PE?

A

Resp. alkalosis

decreased PCO2 - pt. is hyperventilating

hypoxemia

increased O2 A-a gradient

63
Q

If a PE is found, what medication will you put them on right away?

A

Heparin - follow PTT, you want them 1.5-2.5 x normal.

normal is 30 sec.

64
Q

A person who has a PE what is the long term medication they will be on? (like at home)

A

Warfarin, coumadin - follow PT (=12 sec)

65
Q

If you have recurrent PE’s what will they have placed?

A

Inferior vena cava filter

66
Q

If the patient is in the hospital when their PE occurs what thrombolytic therapy might they be placed on? What are the risks?

A

Streptokinase or tPA

risk for bleeding is very high, only use with life-threatening PE

67
Q

Basic difference between PEEP and CPAP?

A

PEEP is positive pressure applied only during expiration.

CPAP is positive pressure applied during inspiration and expiration.

68
Q

When do you want to use PEEP (indications for use)?

A

PO2 < 60
widespread alveolar collapse- atelectasis
ARDS
Pulmonary edema

69
Q

Dose of PEEP that should be used (range)?

A

5-10 cmH2O

70
Q

Why do you need PEEP to inflate completely collapsed alveoli?

A

it is easier to inflate a partially inflated alveoli compared to a completely collapsed alveoli, you need the PEEP to inflate the completely collapsed alveoli (the extra pressure is needed)

71
Q

Complications of PEEP?

A

decreased CO

Barotrauma

fluid retention

redistribution of pulmonary blood flow leading to decrease V/Q and decreased P02

72
Q

Two best exams for diagnosis of PE? (lab and procedure)

A

D-dimer

CT arteriography

73
Q

Is PEEP applied during expiration or inspiration?

A

expiration to keep the alveoli open.

74
Q

CPAP how does it work?

A

Continuous positive airway pressure which means the same amount of pressure is delivered during inspiration and expiration.

75
Q

What should your CPAP level always be below?

A

<14-15 cm H2O bc it needs to be lower than LES pressure.

76
Q

What is a risk with CPAP?

A

Risks of gastric distension and regurgitation

77
Q

Know how to label the flow volume loop.

A 
Vital capacity = length of loop
Inspiratory on bottom
Expiratory on top
TLC left side end of lung volume
RV right side end of lung volume

Effort independent flow occupies most of the expiratory limb of the loop.

78
Q

Effort independent flow on the FV loop is produced by?

A

dynamic compression of the airways during a forced expiration, occupies most of the expiratory limb of the loop

79
Q

F/V loop that has smaller volumes is associated with what type of lung diseases? Tell me some of those diseases.

A 
Restrictive: 
pulmonary fibrosis
Obesity
Scoliosis
Sarcoidosis
Muscular dystrophy, ALS

(restricts the lungs from taking in as much air as they should be)

80
Q

If a F/V loop has a larger volume than normal or a prolonged expiratory limb then it is associated with what type of lung diseases? Tell me some of those diseases.

A 
Obstructive:
COPD (chronic bronchitis and emphysema)
Asthma
Cystic fibrosis
Bronchiectasis
81
Q

Is inspiration or expiration impaired with Extrathoracic obstruction?

A

Inspiration is impaired

82
Q

Is inspiration or expiration impaired with Intrathoracic obstruction?

A

Expiration is impaired

83
Q

If you have a tracheal obstruction what phase of the F/V loop will be impaired?

A

both inspiration and expiration is impaired

84
Q

If intrapleural pressure is greater than airways pressure what happens to the airway?

A

closes

85
Q

What two things can cause intrapleural pressure to increase?

A

forced expiration

valsalva maneuver

86
Q

If you have more force/volume coming out during forced expiration (COPD) then what does this cause?

A

collapse of respiratory passageway at a higher volume. That is why people with COPD hold onto air in their lungs compared to breathing it all out.
Air trapping/CO2 trapping.

87
Q

Which lung is depended and non dependent in the LD position.

A

down lung/ operating table lung is dependent.

The “up” lung is non-dependent.

88
Q

If a lung is well ventilated but poorly perfused that would be called?

A

dead spacing

89
Q

If a lung is poorly ventilated and well perfused that would be called?

A

shunting

90
Q

In the lateral decubitus position, when does the greatest degree of V/Q mismatch occur?

A

When the pt. is anesthetized and/or paralyzed.

91
Q

When a patient is AWAKE/unanethetized and in the lateral decubitus position what changes about ventilation and perfusion?

A

V/Q distribution to dependent and nondependent lung are similar to those found in the upright position.

Dependent lung acts like the base of an upright lung and the nondependent lung acts like the apex of the upright lung.

Blood flow and ventilation to the dependent lung are greater than nondependent lung.

92
Q

closing volume + residual volume = ?

A

closing capacity

93
Q

closing volumes increases with what conditions?

A

increasing age
COPD
airway secretions
anesthesia

94
Q

When anesthetized and/or paralyzed how does the dependent lungs V/Q look?

A

poorly ventilated and well perfused (shunting)

95
Q

When anesthetized and/or paralyzed how does the non-dependent lungs V/Q look?

A

well ventilated but poorly perfused (dead spacing)

96
Q

non-dependent lung: V and Q in the lateral decubitus position when unanesthetized vs anesthetized?

A

unanesthetized: ventilation and perfusion are both decreased
anesthetized: ventilation increases and perfusion decreases.

97
Q

dependent lung: V and Q in the lateral decubitus position when unanesthetized vs anesthetized?

A

unanesthetized: ventilation and perfusion are both increased.
anesthetized: ventilation is decreased and perfusion is increased.

98
Q

If someone has ARDS and you increase PEEP what is the risk?

A

BAROTRAUMA
diminished cardiac output
pneumothorax

Fall 20' Anatomy III MO (5 decks)

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