Fall'20 A&P III > Respiratory > Flashcards

Respiratory Flashcards

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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
Destruction of alveolar walls and abnormal enlargement of air spaces distal to terminal bronchiole
Chronic pulmonary emphysema
26
Chronic pulmonary emphysema is defined as?
Destruction of alveolar walls and abnormal enlargement of air spaces distal to terminal bronchiole
27
Most common cause of Chronic pulmonary emphysema is?
Smoking
28
Features of Chronic pulmonary emphysema
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
29
What is the pathogenesis of emphysema
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).
30
Features of COPD
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
31
This drug has no receptor, it crosses the cell membrane and its action results in bronchodilation
Nitric oxide via cGMP
32
Patient has a teardrop shaped heart on CXR. What is his most likely diagnosis
COPD
33
This is the 4th leading cause of death in USA
COPD
34
Airway inflammation lasting \>2years
Chronic bronchitis
35
Pathophysiology of smoking in the lungs
increases PMNs (polumorphonucleus cells) and macrophages leading to increased free radicals
36
In COPD diagnosis FE, FEV1 and FEV1/FVC ratio is increased or decreased?
FEV1 and FEV1/FVC ratio is decreased Prolonged FE\>6 seconds
37
In COPD diagnosis CXR findings would show?
Hyperinflated lungs Bullae Flattening diaphragm Decreased vascular markings Decreased lung markings
38
In COPD diagnosis ABG findings would show?
Compensated respiratory acidosis CO2 retention that worsens with supplemental oxygen
39
Residual volume and Total lung capacity in COPD
Residual volume and Total lung capacity are increased due to air trapping
40
Diagnostic signs and symptoms of COPD are?
Chronic dyspnea cough Wheezing sputum production airflow obstruction of PFTs Diminished breathing sounds, wheezing JVD, peripheral edema and hepatomegaly due to Cor pulmonale
41
DLCO in COPD is increased/decreased?
decreased due to emphysema
42
Hematologic finding in COPD
Polycythemia
43
Treatment of COPD
Smoking cessation ABX for H.influenzae, S.pneumoniae Bronchodilators Steroid- demonstrate effectiveness with PFT Supplemental O2 with PO2\<55 -improves survival
44
Complications of COPD
Acute exacerbation after infection Polycythemia Pulmonary HTN Cor pulmonale
45
Anesthetic considerations for COPD
VA anesthetics are potent bronchodilators except for des Protect against reflex bronchoconstriction during intubation/suction in COPD and Asthma Propofol agent of choice
46
This drug can cause pulmonary fibrosis
Bleomycin
47
Pulmonary fibrosis pathophysiology
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
48
This drug can cause Rales,cough, infiltration and fetal fibrosis
Bleomycin
49
Patient has significantly low FEV1 and FV1/FVC and slightly low FVC with High FRC. What is the possible diagnosis
COPD or Asthma (Obstructive condition)
50
Patient has a normal to slightly increased FV1/FVC ratio slightly low FEV1, significantly decrease FVC and low FRC. What is the possible diagnosis
Fibrosis (Restrictive condition)
51
Infection of the alveoli is
Pneumonia
52
Most common cause of pneumonia is?
Gram+ Diplococci in pairs
53
Features of pneumonia
Consolidation; alveoli filled with fluid and cellular debris Impaired gas exchange Low V/Q ratio Hypoxia and hypercapnia
54
Pathophysiology of TB
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
Signs and symptoms of clinical TB
Fever Night sweats Weight loss Hemoptysis
56
Latent TB may reactivate within\_\_\_\_\_ months and be transmitted to others
3 months
57
Development of active tubercles throughout the body is referred to as
Miliary TB
58
Positive montoux test shows
Recent immunization Previous tuberculin test Past exposure to M. tuberculosis Need further tests
59
Multidrug resistance M. tuberculosis is affecting with antibiotics that are used for TB
INH pyrazinamide Rifampin
60
Used in TB immunization
Attenuated M. Bovis
61
Explain why M. Tuberculosis are Apical lessions
They are obligate aerobes that preffer apex of the lung due to its high PO2 and V/Q. Forms cavities- Caseating (cheesy) Granuloma
62
Collapse of alveoli is
Atelectasis
63
Features of Atelectasis
Collapse of alveoli Fever in first 48 hrs post op (95%) Pathogenesis of fever is unknown Minimum decrease in %Sat
64
Atelectasis Can be prevented by
Early mobilization Breathing exercises Incentive spirometry
65
Most common causes of Atelectasis are
* Airways obstruction due to mucous plug or tumor * Lack of surfactant (RDS)
66
Normal pulmonary artery pressure is?
10-14 mmHg
67
Pulmonary hypertension is pressure
≥25 mmHg or ≥35 mmHg during exercise
68
Causes of Pulmonary hypertension are
Atherosclerosis Medial hypertrophy Intimal fibrosis of pulmonary arteries
69
Primary pulmonary hypertension is due to
an inactivating mutation in the BMPR2 gene (normally functions to inhibit vascular smooth muscle proliferation)
70
Secondary pulmonary hypertension is due to
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
What is the course of pulmonary hypertension
Severe respiratory distress -\> cyanosis and RVH -\> DEATH from decompensated cor pulmonale
72
Most PE (95%) originate from?
DVT from leg
73
Non-thrombotic pulmonary emboli are
Septic: endocarditis in IV drug abusers; infected catheters Fat: after long bone fractures Amniotic fluid: During childbirth
74
What are the pathological consequences
Increased PVR Increased PAP Increased Afterload
75
Risk factors for PE
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
PE FAT BAT
FAT BAT: Fat, air, thrombus, bacteria, amniotic fluid and tumor
77
Clinical features of PE
Dyspnea Pleuritic chest pain SOB Signs of RV overload (loud P2 , RV heave) Look for signs of DVT
78
What are the signs of a DVT
1. Leg pain 2. Tenderness 3. warmth 4. redness 5. swelling 6. Homan’s sign: dorsiflexion of foot cause tender calf muscle
79
25% of patients with PE have no suggestive physical findings, making a difficult diagnosis. T/F?
False 50% have no suggestive physical findings, making a difficult diagnosis
80
CXR finding of PE are
Normal Regional oligemia Pleural infarct Pleural effusion
81
Diagnosis of PE is based on
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
ABG diagnostic findings of PE include
Respiratory alkalosis Low PCO2 – pt. is hyperventilating Hypoxemia Increased O2 A-a gradient
83
What causes Elevated D-dimer in PE
Byproduct of intrinsic fibrinolysis
84
The most sensitive and specific test for PE is?
CT arteriography
85
PE treatment
* 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
PEEP Indications
PO2 \< 60 mmHg Widespread alveolar collapse- Atelactasis ARDS Pulmonary edema
87
Dose of PEEP is
5-10 cmH2O
88
What are the benefits of PEEP
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
Complication of PEEP
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
Positive pressure is maintained during both inspiration and expiration
CPAP
91
What is the risk associated with CPAP
Risks of gastric distension and regurgitation
92
CPAP level
\< 14-15 cm H2O (lower than LES pressure)
93
What is the effect of air flow on airway pressure
* 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
At some point during a force expiration, airways begin to close. The volume that can subsequently be exhaled is
the closing volume.
95
Closing capacity=
Closing volume + Residual Volume
96
What factors increase closing volume
Age COPD Airways secretion Anesthesia
97
Lateral Decubitus- Unanesthetized patient
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
Lateral Decubitus - Anesthetized and Paralyzed patient
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
Hypoxemia, hypoxia and ischemia leads to
Oxygen deprivation
100
Causes of Hypoxemia
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
What would be the causes of low PaO2 in a patient with normal A-a gradient
High altitude (normal A-a gradient) Hypoventilation (normal A-a gradient)
102
What are the causes of hypoxia (low O2 delivery to tissue)
Low Cardiac output Hypoxemia Anemia Cyanide poisoning CO (Carbon monoxide) poisoning
103
What are the causes of Ischemia (loss of blood flow)
Impeded blood flow Reduced venous drainage
104
Patient has Chronic necrotizing infection of bronchi resulting in dilatation and destruction of airways, purulent sputum, recurrent infections, hemoptysis. What is the diagnosis
Bronchiectasis
105
Bronchiectasis is associated with what causes?
Bronchial obstruction Cystic fibrosis Poor ciliary motility ( Kartagener's Syndrome)
106
What are the symptoms of Bronchiectasis
Chronic purulent cough with large amount of sputum Clubbing Air fluid levels on chest X-ray
107
What is the Treatment of Bronchiectasis
Treat the infection Bronchodilators Supplemental O2 Postural drainage Surgical resection of localized region of bronchiectasis
108
Non- cardiogenic pulmonary edema; due to damage to alveolar-capillary membrane leading to stiff lungs
ARDS
109
What are the features of ARDS
Severe hypoxemia PO2 \< 60 , FIO2 ≥60, large A-a gradient Bilateral pulmonary infiltrates on CXR Normal or low PA pressure Mortality 50% !!
110
What are the causes of ARDS
Sepsis syndrome Overwhelming pneumonia DIC Major trauma Multiple transfusion Pancreatitis Drowning or near drowning
111
What is the treatment of ARDS
Treat underlying cause Correct hypoxemia but intrapulmonary shunting limits effectiveness of supplemental Oxygen PEEP
112
A collection of air in pleural space leading to lung collapse
Pneumothorax
113
What are the causes of Secondary pneumothorax
COPD TB Trauma PCP Thoracocentesis Central line placement PPV or bronchoscopy
114
pneumothorax caused by Rupture of subpleural belbs
Spontaneous (primary) pneumothorax
115
pneumothorax where a one way valve-like hole develops creating a Life threatening condition
Tension pneumothorax
116
Pneumothorax caused by COPD, TB ,trauma, PCP, thoracocentesis, central line placement , PPV or bronchoscopy
Secondary pneumothorax
117
What are the physical examination findings in a pneumothorax
Tachypnea, Diminished/absent breath sound Hyperresonance Falling O2 sat Hypotension Distended neck vein Tracheal deviation
118
What is the treatment of Pneumothorax
Chest tube, needle decompression
119
Identify A
COPD
120
Identify B
RLD= restrictive lung disease
121
What abnormality is represented
**_Ex_**trathoracic obstruction **_In_**spiration is impaired
122
Identify the abnormality represented
**tracheal obstruction** Both inspiration and expiration are impaired
123
Identify the abnormality represented
**_In_**trathoracic obstruction **_Ex_**piration is impaired
124
What does the curve represent
Maximum expiratory flow
125
Be able to label
Closing volume closing capacity Residual volume Airway closure begins FRC TLC
Fall'20 A&P III
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