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Fall'20 A&P III > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Describe the pathophysiology of asthma

A

Reversible increased resistance to airflow due to airway narrowing during attack. Patients have normal physiology between the attacks. Caused by bronchospasm or inflammation.

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2
Q

Airway narrowing in asthma is caused by?

A
  • bronchospasm
  • inflammation
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3
Q

What are the triggering factors for Asthma

A
  • Airway irritants
  • Exercise, cold air, dry air
  • Resp infection; upper/lower
  • ASA from overproduction of leukotriens
  • Beta blockers
  • GERD
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4
Q

Identify the clinical features of asthma

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

What are the physical exam findings of Asthma between attacks

A
  • Normal physical examination
  • Abnormal PFT
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6
Q

What are the physical exam findings of Asthma during attacks

A
  • Tachypnea
  • Inspiratory and expiratory wheezing
  • Use of accessory muscles
  • pulsus paradoxus
  • Paradoxical movement of abdomen
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7
Q

Identify the diagnosis criteria for asthma

A

Decreased Peak flow expiratory rate

FVC, FEV1 and FEV1/FVC decreases

  • Increased RV
  • Normal diffusion capacity
  • Improvement of flow rate with bronchodilators
  • Bronchial hyperesponsiveness to histamine
  • Eosinophilia
  • CXR: hypeinflation; flatening of diaphragm; mucus plug; atelectasis
  • ABG: Hypocapnia; Mild hypoxemia; Hypocarbia is common
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8
Q

What are CXR diagnostic findings for asthma

A
  • Hypeinflation
  • Flatening of diaphragm
  • Mucus plug .
  • Atelectasis
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9
Q

What are the ABG diagnostic findings for asthma

A

Hypocapnia

Mild hypoxemia

Hypocarbia is common

Tachypnea in presence of normal or high CO2 (40@40) = Respiratory Emergency, respiratory failure will occur. Intubation is indicated.

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10
Q

Describe the treatment of asthma

A

Anti-inflamatory drugs

Bronchodilators

Anti-leukotrienes- Zileuton(Zyflo)

Montelukast (Singulair) and Zafirlukast

Anti-IgE monoclonal therapy

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11
Q

Describe the use of Anti-inflamatory drugs for treatment of Asthma

A
  • Inhaled Steroids
  • Systemic Steroids
  • Cromolyn to prevent mast cell degranulation
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12
Q

This drug is used only for prophylaxis and not acute asthma attacks. It can also be used to prevent exercise induced asthma

A

Cromolyn

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13
Q

Describe the use of bronchodilators for treatment of Asthma

A
  • Beta 2 agonists
  • Anticholinergics
  • Aminophyline preparations
  • theophyline: PDE inhibitor with narrow therapeutic index
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14
Q

This drug is a PDE inhibitor with a narrow therapeutic index, used as a bronchodilator

A

theophyline

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15
Q

Describe the use of Anti-leukotrienes- Zileuton(Zyflo) for treatment of Asthma

A
  • 5-lipoxigenase inhibitor
  • Blocks conversion of arachidonic acid to leukotriene
  • Adverse effects; Dyspnea, arthralgia, chest pain, fever
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16
Q

This drug can cause Dyspnea, arthralgia, chest pain, and fever

A

Anti-leukotrienes- Zileuton(Zyflo)

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17
Q

Describe the use of Montelukast (Singulair) and Zafirlukast for treatment of Asthma

A
  • Competitive antagonist of leukotriene on cysteinyl-leukotriene1 receptor.
  • Prevent bronchospasm, vasoconstriction and eosinophil recruitment.
  • Good for aspirin induced asthma
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18
Q

Blocks the conversion of arachidonic acid to leukotriene

A

Zileuton (zyflo): 5-lipoxygenase inhibitor

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19
Q

Competitive antagonist of leukotriene on cysteinyl-leukotriene1 receptor

A

Montelukast (singulair) and Zafirlukast

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20
Q

Describe the use of Anti-IgE monoclonal therapy for treatment of Asthma

A

Use Omalizumab which binds free IgE

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21
Q

This drug binds free IgE

A

Omalizumab

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22
Q

Describe the management of acute asthma attack

A
  • Beta agonist + steroid + ipatropium
  • Systemic steroids IV
  • Aminophyline not effective in severe acute attack
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23
Q

Describe the management of chronic asthma

A

Inhaled steroids as maintenance + beta 2 agonist for symptomatic control

Add ipatropium

Consider aminophyline

Short course steroids

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24
Q

3 messenger systems for bronchial smooth muscle tone are?

A

Beta 2 stimulant via Gs Protein

Nitric oxide via cGMP

Cholinergic muscarinic via IP3

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25
Q

Destruction of alveolar walls and abnormal enlargement of air spaces distal to terminal bronchiole

A

Chronic pulmonary emphysema

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26
Q

Chronic pulmonary emphysema is defined as?

A

Destruction of alveolar walls and abnormal enlargement of air spaces distal to terminal bronchiole

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27
Q

Most common cause of Chronic pulmonary emphysema is?

A

Smoking

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28
Q

Features of Chronic pulmonary emphysema

A

Chronic infection

Chronic obstruction

Co2 retention due to decreased diffusion capacity

Hypoxia and hypercapnia due to V/Q mismatch

Cor pulmonale due to pulmonary hypertension

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29
Q

What is the pathogenesis of emphysema

A

Inflamatory cells are recruited to the lungs due to long term exposure to smoking.

They release proteinases in excess of inhibitors

If repair is abnormal, airspace destruction and enlargement results (Emphysema).

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30
Q

Features of COPD

A

Fourth leading cause of death in US

Emphysema

Chronic bronchitis

Both characterized by chronic airway obstruction, dyspnea, caugh, sputum production

MCC is smoking -> PMNs (polumorphonucleus cells) and macrophages -> increased free radicals

Other causes apha1 antitrypsin deficiency- antiprotease, second hand smoking, chronic asthma

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31
Q

This drug has no receptor, it crosses the cell membrane and its action results in bronchodilation

A

Nitric oxide via cGMP

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32
Q

Patient has a teardrop shaped heart on CXR. What is his most likely diagnosis

A

COPD

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33
Q

This is the 4th leading cause of death in USA

A

COPD

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34
Q

Airway inflammation lasting >2years

A

Chronic bronchitis

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35
Q

Pathophysiology of smoking in the lungs

A

increases PMNs (polumorphonucleus cells) and macrophages leading to increased free radicals

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36
Q

In COPD diagnosis FE, FEV1 and FEV1/FVC ratio is increased or decreased?

A

FEV1 and FEV1/FVC ratio is decreased

Prolonged FE>6 seconds

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37
Q

In COPD diagnosis CXR findings would show?

A

Hyperinflated lungs

Bullae

Flattening diaphragm

Decreased vascular markings

Decreased lung markings

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38
Q

In COPD diagnosis ABG findings would show?

A

Compensated respiratory acidosis

CO2 retention that worsens with supplemental oxygen

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39
Q

Residual volume and Total lung capacity in COPD

A

Residual volume and Total lung capacity are increased due to air trapping

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40
Q

Diagnostic signs and symptoms of COPD are?

A

Chronic dyspnea cough

Wheezing

sputum production

airflow obstruction of PFTs

Diminished breathing sounds, wheezing

JVD, peripheral edema and hepatomegaly due to Cor pulmonale

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41
Q

DLCO in COPD is increased/decreased?

A

decreased due to emphysema

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42
Q

Hematologic finding in COPD

A

Polycythemia

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43
Q

Treatment of COPD

A

Smoking cessation

ABX for H.influenzae, S.pneumoniae

Bronchodilators

Steroid- demonstrate effectiveness with PFT

Supplemental O2 with PO2<55 -improves survival

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44
Q

Complications of COPD

A

Acute exacerbation after infection

Polycythemia

Pulmonary HTN

Cor pulmonale

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45
Q

Anesthetic considerations for COPD

A

VA anesthetics are potent bronchodilators except for des

Protect against reflex bronchoconstriction during intubation/suction in COPD and Asthma

Propofol agent of choice

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46
Q

This drug can cause pulmonary fibrosis

A

Bleomycin

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47
Q

Pulmonary fibrosis pathophysiology

A

Is a restrictive disease with decreased lung compliance in which inspiration is impaired due to scarring of lungs with increased collagen

Decreased lung volumes

Increased or normal FEV1/FVC ratio because FEV1 is only slightly low whereas FVCis significantly low

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48
Q

This drug can cause Rales,cough, infiltration and fetal fibrosis

A

Bleomycin

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49
Q

Patient has significantly low FEV1 and FV1/FVC and slightly low FVC with High FRC. What is the possible diagnosis

A

COPD or Asthma (Obstructive condition)

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50
Q

Patient has a normal to slightly increased FV1/FVC ratio slightly low FEV1, significantly decrease FVC and low FRC. What is the possible diagnosis

A

Fibrosis (Restrictive condition)

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51
Q

Infection of the alveoli is

52
Q

Most common cause of pneumonia is?

A

Gram+ Diplococci in pairs

53
Q

Features of pneumonia

A

Consolidation; alveoli filled with fluid and cellular debris

Impaired gas exchange

Low V/Q ratio

Hypoxia and hypercapnia

54
Q

Pathophysiology of TB

A
  1. Mycobacterium tuberculosis (Acid fast) enters the respiratory tract in small aerosolized droplets
  2. Macrophages accumulate in the lung forming a tubercle that harbors M. Tuberculosis
  3. Bacteria spread throughout body when tubercle breaks apart
55
Q

Signs and symptoms of clinical TB

A

Fever

Night sweats

Weight loss

Hemoptysis

56
Q

Latent TB may reactivate within_____ months and be transmitted to others

57
Q

Development of active tubercles throughout the body is referred to as

A

Miliary TB

58
Q

Positive montoux test shows

A

Recent immunization

Previous tuberculin test

Past exposure to M. tuberculosis

Need further tests

59
Q

Multidrug resistance M. tuberculosis is affecting with antibiotics that are used for TB

A

INH

pyrazinamide

Rifampin

60
Q

Used in TB immunization

A

Attenuated M. Bovis

61
Q

Explain why M. Tuberculosis are Apical lessions

A

They are obligate aerobes that preffer apex of the lung due to its high PO2 and V/Q.

Forms cavities- Caseating (cheesy) Granuloma

62
Q

Collapse of alveoli is

A

Atelectasis

63
Q

Features of Atelectasis

A

Collapse of alveoli

Fever in first 48 hrs post op (95%) Pathogenesis of fever is unknown

Minimum decrease in %Sat

64
Q

Atelectasis Can be prevented by

A

Early mobilization

Breathing exercises

Incentive spirometry

65
Q

Most common causes of Atelectasis are

A
  • Airways obstruction due to mucous plug or tumor
  • Lack of surfactant (RDS)
66
Q

Normal pulmonary artery pressure is?

A

10-14 mmHg

67
Q

Pulmonary hypertension is pressure

A

≥25 mmHg or ≥35 mmHg during exercise

68
Q

Causes of Pulmonary hypertension are

A

Atherosclerosis

Medial hypertrophy

Intimal fibrosis of pulmonary arteries

69
Q

Primary pulmonary hypertension is due to

A

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

70
Q

Secondary pulmonary hypertension is due to

A

Due to COPD (destruction of lung parenchyma)

Mitral stenosis (Increased resistance leading to high pressure)

Recurrent thromboemboli (reduced cross-sectional area of pulmonary vascular bed)

Autoimmune disease (e.g. systemic sclerosis ; inflammation leading to intimal fibrosis hence medial hypertrophy )

Left-to-right shunt (High shear stress leading to endothelial injury )

Sleep apnea or living at high altitude (hypoxic vasoconstriction)

71
Q

What is the course of pulmonary hypertension

A

Severe respiratory distress -> cyanosis and RVH -> DEATH from decompensated cor pulmonale

72
Q

Most PE (95%) originate from?

A

DVT from leg

73
Q

Non-thrombotic pulmonary emboli are

A

Septic: endocarditis in IV drug abusers; infected catheters

Fat: after long bone fractures

Amniotic fluid: During childbirth

74
Q

What are the pathological consequences

A

Increased PVR

Increased PAP

Increased Afterload

75
Q

Risk factors for PE

A
  1. Immobilization (esp. post op)
  2. Pelvic/leg surgery or trauma
  3. Malignancy
  4. Obesity
  5. CHF ( predisposes to vascular stasis)
  6. OCPs ( Oral contraceptives)
  7. Hypercoagulability
  8. Endothelial damage
76
Q

PE FAT BAT

A

FAT BAT: Fat, air, thrombus, bacteria, amniotic fluid and tumor

77
Q

Clinical features of PE

A

Dyspnea

Pleuritic chest pain

SOB

Signs of RV overload (loud P2 , RV heave)

Look for signs of DVT

78
Q

What are the signs of a DVT

A
  1. Leg pain
  2. Tenderness
  3. warmth
  4. redness
  5. swelling
  6. Homan’s sign: dorsiflexion of foot cause tender calf muscle
79
Q

25% of patients with PE have no suggestive physical findings, making a difficult diagnosis. T/F?

A

False

50% have no suggestive physical findings, making a difficult diagnosis

80
Q

CXR finding of PE are

A

Normal

Regional oligemia

Pleural infarct

Pleural effusion

81
Q

Diagnosis of PE is based on

A
  1. H&P
  2. CXR
  3. ABG
  4. Elevated D- dimer
  5. V/Q Scan- replaced by CT
  6. CT arteriography
  7. Pulmonary angiography- rarely needed
  8. Lower extremities duplex US for DVT
82
Q

ABG diagnostic findings of PE include

A

Respiratory alkalosis

Low PCO2 – pt. is hyperventilating

Hypoxemia

Increased O2 A-a gradient

83
Q

What causes Elevated D-dimer in PE

A

Byproduct of intrinsic fibrinolysis

84
Q

The most sensitive and specific test for PE is?

A

CT arteriography

85
Q

PE treatment

A
  • Heparin– follow PTT(1.5-2.5 X, normal = 30 sec)
  • Warfarin, coumadin– follow PT (=12 sec)
  • Inferior vena cava filter
  • Thrombolytic therapy—streptokinase, tPA Risk of bleeding is very high. Use only with life-threatening PE
86
Q

PEEP Indications

A

PO2 < 60 mmHg

Widespread alveolar collapse- Atelactasis

ARDS

Pulmonary edema

87
Q

Dose of PEEP is

A

5-10 cmH2O

88
Q

What are the benefits of PEEP

A
  1. Prevent collapse of alveoli
  2. Helps to maintain patency of alveoli
  3. Helps to recruit more alveoli
  4. Increases FRC by expanding previously collapsed alveoli
  5. Decreases intrapulmonary shunting
  6. Improves V/Q ratio => increased PO2
89
Q

Complication of PEEP

A
  1. Decreased Cardiac Output due to interference with Venous return
  2. Barotrauma e.g. pneumothorax, air in mediastinum, and subcutaneous emphysema
  3. Fluid retention due to obstruction of lymph flow and capillary damage
  4. Redistribution of pulmonary blood flow leading to decrease V/Q resulting in decrease PO2
90
Q

Positive pressure is maintained during both inspiration and expiration

91
Q

What is the risk associated with CPAP

A

Risks of gastric distension and regurgitation

92
Q

CPAP level

A

< 14-15 cm H2O (lower than LES pressure)

93
Q

What is the effect of air flow on airway pressure

A
  • Increased flow causes decreased pressure
  • If intrapleural pressure > air ways pressure, the air ways closes
  • Intrapleural pressure increases in force expiration or Valsalva maneuver
94
Q

At some point during a force expiration, airways begin to close. The volume that can subsequently be exhaled is

A

the closing volume.

95
Q

Closing capacity=

A

Closing volume + Residual Volume

96
Q

What factors increase closing volume

A

Age

COPD

Airways secretion

Anesthesia

97
Q

Lateral Decubitus- Unanesthetized patient

A

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

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

Thus the dependent lung is similar to the dependent areas of the upright lung (near the diaphragm) under normal conditions

98
Q

Lateral Decubitus - Anesthetized and Paralyzed patient

A

Dependent lung is “compressed” by the weight of abdominal contents

The nondependent lung is well ventilated but poorly perfused (dead spacing)

Depending lung is poorly ventilated and well perfused (shunting) Greatest degree of V/Q mismatch occurs

99
Q

Hypoxemia, hypoxia and ischemia leads to

A

Oxygen deprivation

100
Q

Causes of Hypoxemia

A

High altitude (normal A-a gradient)

Hypoventilation (normal A-a gradient)

V/Q mismatch (high A-a gradient)

Diffusion limitation (high A-a gradient)

Right-to-left shunt (high A-a gradient)

101
Q

What would be the causes of low PaO2 in a patient with normal A-a gradient

A

High altitude (normal A-a gradient)

Hypoventilation (normal A-a gradient)

102
Q

What are the causes of hypoxia (low O2 delivery to tissue)

A

Low Cardiac output

Hypoxemia

Anemia

Cyanide poisoning

CO (Carbon monoxide) poisoning

103
Q

What are the causes of Ischemia (loss of blood flow)

A

Impeded blood flow

Reduced venous drainage

104
Q

Patient has Chronic necrotizing infection of bronchi resulting in dilatation and destruction of airways, purulent sputum, recurrent infections, hemoptysis. What is the diagnosis

A

Bronchiectasis

105
Q

Bronchiectasis is associated with what causes?

A

Bronchial obstruction

Cystic fibrosis

Poor ciliary motility ( Kartagener’s Syndrome)

106
Q

What are the symptoms of Bronchiectasis

A

Chronic purulent cough with large amount of sputum

Clubbing

Air fluid levels on chest X-ray

107
Q

What is the Treatment of Bronchiectasis

A

Treat the infection

Bronchodilators

Supplemental O2

Postural drainage

Surgical resection of localized region of bronchiectasis

108
Q

Non- cardiogenic pulmonary edema; due to damage to alveolar-capillary membrane leading to stiff lungs

109
Q

What are the features of ARDS

A

Severe hypoxemia PO2 < 60 , FIO2 ≥60,

large A-a gradient

Bilateral pulmonary infiltrates on CXR

Normal or low PA pressure

Mortality 50% !!

110
Q

What are the causes of ARDS

A

Sepsis syndrome

Overwhelming pneumonia

DIC

Major trauma

Multiple transfusion

Pancreatitis

Drowning or near drowning

111
Q

What is the treatment of ARDS

A

Treat underlying cause

Correct hypoxemia but intrapulmonary shunting limits effectiveness of supplemental Oxygen

PEEP

112
Q

A collection of air in pleural space leading to lung collapse

A

Pneumothorax

113
Q

What are the causes of Secondary pneumothorax

A

COPD

TB

Trauma

PCP

Thoracocentesis

Central line placement

PPV or bronchoscopy

114
Q

pneumothorax caused by Rupture of subpleural belbs

A

Spontaneous (primary) pneumothorax

115
Q

pneumothorax where a one way valve-like hole develops creating a Life threatening condition

A

Tension pneumothorax

116
Q

Pneumothorax caused by COPD, TB ,trauma, PCP, thoracocentesis, central line placement , PPV or bronchoscopy

A

Secondary pneumothorax

117
Q

What are the physical examination findings in a pneumothorax

A

Tachypnea,

Diminished/absent breath sound

Hyperresonance

Falling O2 sat

Hypotension

Distended neck vein

Tracheal deviation

118
Q

What is the treatment of Pneumothorax

A

Chest tube, needle decompression

119
Q

Identify A

120
Q

Identify B

A

RLD= restrictive lung disease

121
Q

What abnormality is represented

A

Extrathoracic obstruction

Inspiration is impaired

122
Q

Identify the abnormality represented

A

tracheal obstruction

Both inspiration and expiration are impaired

123
Q

Identify the abnormality represented

A

Intrathoracic obstruction

Expiration is impaired

124
Q

What does the curve represent

A

Maximum expiratory flow

125
Q

Be able to label

A

Closing volume

closing capacity

Residual volume

Airway closure begins

FRC

TLC

Fall'20 A&P III (13 decks)

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