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Respiratory Flashcards

1
Q

When in embryonic developpement is survival possible?

A

At 25 weeks

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2
Q

How does breathing in utero work?

A

Aspiration and expulsion of amniotic fluid

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3
Q

How does breathing change at birth?

A

Fluid gets replaced by air and have a decrease in pulmonary vasular resistance

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4
Q

What is pulmonary hypoplasia?

A

Poorly developped bronchial tree with abnormal histology
Usually involves the right lung
Associated with congenital diaphragmatic hernia
Bilateral renal agenesis

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5
Q

What are brochogenic cysts?

A

Abnormal budding of the foregut and dilatation of terminal large bronchi

Show up as discrete, round, sharply defined air filled densities on CXR

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6
Q

What are type 1 cells (pneumocytes)?

A

97% of aleveolar surfaces
Line the alveoli
Squamous, thin for gas diffusion

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7
Q

What are the type 2 cells (penumocytes)

A

Secrete pulmonary surfactant

Decrease in alvelor surface tension

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8
Q

Component of pulmonary surfactant?

A

Complex mix of lecitins and dipalmitoylphospahtidylcholine

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9
Q

Club cells?

A

Non ciliated, low columnar/cuboidal with secretory granules

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10
Q

Causes of neonatal respiratory distress syndrome?
Screening test?
Symptoms?

A

Surfactant deficiency
Increase in surface tension
Alveolar collapse

Screening test: fetal lung maturity lecithin-spingomyelin (L/S) ratio in amnitoic fluid

> 2 is healthy
<1.5 is predictive of NRDS

Presistantly low O2 tension

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11
Q

Risk factors of neonatal respiratory distress syndrome?

Treatement?

A

Prematurity
Maternal diabetes
C-section delivery
Decrease release of fetal glucocorticoids

Treatement:
Maternal steroids before birth
Artificial surfactant for infant

Supplemental O2
(note can result in retinopathy of prematurity, intraventricular hemorrhage, bronchopulmonary dysplasia
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12
Q

What are conduction zone of respiratory tree?

A

Large airways: nose, pharynz, trachea and bronchi
Small airways: bronchioles that divide to terminal bronchioles

Function: warms, humidifies and filters air but doesnt participare in gas exchange

Has pseudostratified ciliated columnar cells that make up epithelium of bronchus

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13
Q

What are respiratory zones of the respiratory tree?

A

Lung parenchycma (bronchioles, alveolar ducts and alveoli)

Participate in gas exchange

Mostly cuboidal cells in respiratory bronchioles

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14
Q

Describe anatomy of the lungs?

A

right lung has three lobes

left lung has 2 lobes

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15
Q

Why right lung more common for inhaled foreign body?

A

Right mainstem bronchus is wider and more vertical then the left

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16
Q

where will a peanut go if aspirated in upright vs supine?

A

Upright enters the inferior segment of the right infereor lobe

Supine: enter the superior segment of the right inferior lobe

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17
Q

why does the left lung only have 2 lobes?

A

That space is occupied by the heart

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18
Q

What are diaphragm structures that perforate?

A 
At T8 (the IVC)
at T10 esophagus and vagus 
At T12: aorta
thoracic duct
Azygous vein
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19
Q

What nerves innervate the diapghgram?

A

Phrenic nerve

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20
Q

where is pain from the diaphgram referred?

A

Shoulder

or Trapezius ridge

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21
Q

What nerves keep the daipggram alive

A

C3
C4
C10

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22
Q

where does cartoid bifucate?
Trachea?
Abdominal aorta?

A

Carotid: C4
Trachea: T4
Abdominal aorta: L4

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23
Q

Inspiratory reserve volume?

A

Air that can still be breathed in after normal inspiration

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24
Q

Tidal volume?

A

Air that moves into lung with each quiet inspiration

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25
Q

Expiratory reserve volume?

A

Air that can still be breathed out after normal expiration

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26
Q

Residual volume?

A

Air in lung after maximal expiration (cannot be measured on spirometry)

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27
Q

Inspiratory capacity?

A

Inspiratory revserve volume + tidal volume

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28
Q

Functional residual capacity?

A

Residual volume + expiratory reserve volume

Can’t be measured by spirometry

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29
Q

Vital capacity?

A

Tidal volume+ inspiratory reserve volume + expired residual volume

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30
Q

Total lung capacity?

A

Inspiratory reserve volume + tidal volume+ expiratory reserve volume + residual volume

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31
Q

what is the dead space

A

Physiologic dead space is equivalent to anatomic dead space in normal lung

Is greater when there is V/Q defects

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32
Q

what is pathologic dead space

A

Part of respiratory zone becomes unable to perform gas exchange (ventilated but not perfused)

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33
Q

Calculation for dead space?

A

Vd = Vt X ( PaCO2- PECp2)/ (PaCO2)

Vt is tidal volume
PaCos arterial co2
PEco2: expired air PCO2

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34
Q

Definition of minute ventilation?

A

Total volume of gas entering lungs per minute

Ve = VT X RR

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35
Q

Definition of alveolar ventilation?

A

Volume of gas per unit of time that reaches the alveoli

Va = (Vt-Vd) xRR

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36
Q

What is elastic recoil?

A

tendency for lungs to collapse inward and the chest to spring outward

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37
Q

What happens to elastic recoil at the functional residual capacity?

A

Inward pull of the lungs is balanced bu the outward pull of the chest wall

Systemic pressure is atmosphereic

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38
Q

What is the airway and alveolar pressure at functional residual capacity?

A

Airway and alveolar pressure are 0

intrapleural pressure is negative

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39
Q

what is the lung compliance?

A

Change in volume for a change in pressure:

Delta V/ delta P

High compliance means the lungs are easier to fill

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40
Q

when is lung compliance decreased?

A

Pulmonary fibrosis
Pneumonia
Pulmonary edema

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41
Q

when is lung compliance increased?

A

Increased in emphysema
Normal aging
Surfactant increases compliance

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42
Q

what is hysteresis?

A

Lung inflation curve follows a different curve then lung deflation curve (due to need to overcome surface tension)

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43
Q

what are the component of hemoglobin?

A

2 alpha and 2 beta unies

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44
Q

What are the forms of hemoglobin?

A

T (deoxygenated)

R elaxed and oxygenated

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45
Q

what does fetal Hb affintiy for O2?

A

Has a higher affinity for O2 then aduld

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46
Q

what factors shift the dissocation curve to the right (increase O2 unloading)

A 
Increase CL
Increase H+
Increase CO2
Increase 2,3 BPG
Increase temperature
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47
Q

Methemoglbin?

A

Oxidixed form of Hb
Does not bind to O2 but has an increased affinity for cyanide
Iron in Hb is reduced state

Presents as chocolate cholored blood

Mehemoglobinemia is induced by nitrates followed by thiosulfates

Can be treated with methmoglobinemia, methylene blue and vitamin C

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48
Q

How do nitrates cause methmeglobin?

A

either from dietary intake or polluted/high altitude H20
and benzocaine

Due to oxidation of Fe 2+ to Fe 3+

Fe 2+ is what binds to O2

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49
Q

what is carboxyhemoglobin?

A

Form of CO that binds to O2
Cause a decrease in binding capacity with a left shift in oxy-hemoglobin dissoaciation curve

Decrease in unloading of O2 in the tissues
CO binds competitively to HB and with 200X greater then O2

Treat with 100% O2 and hyperbaric O2

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50
Q

characteristics of the oxygen-hemoglobin curbe?

A

Sigmoidal shape
Has higher affinity for each susequent O2 molecule that is bound

Myoglobin is monomeric and does not show positive cooperatively

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51
Q

What happens when the curve shifts right?

A

decrease in affinity for Hb and O2 (facilitates unloading of O2 into the tissue)

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52
Q

What is a shift to the left?

A

Decrease in O2 unloading (renal hypoxia) increase in EPO synthesis

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53
Q

How is the fetal curve shifted?

A

Has a higher affinity for O2 then the adult Hb so the curve is shifted to the left

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54
Q

How is the oxygen content of blood measured?

A

o2 content = 1.32 X Hb X Sao2 + 0.003 x PaO2

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55
Q

What happens when there is anemia?

A

Decrease in Hb leads to decrease in O2
No change in O2 saturation and PaO2
O2 delivery to tissue = cardiac output X O2 content of blood

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56
Q

What happens during CO poisoning?

A

Hb: concentration is notmal
Decrease in O2 saturation because the CO competes with the O2
Dissolved O2 is normal
The total O2 content remains normal

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57
Q

What happens during anemia?

A

Hb concentration is decreased
% of O2 saturation of Hb is normal
Dissolved paO2 is notmal
The total O2 content is decreased

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58
Q

What happens during polycythemia?

A

The Hb concentration is incresed
The % of O2 saturation of Hb is normal
Dissolved PaO2 is normal
The total O2 content is increased

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59
Q

Pulmonary circulation, reaction to decrease PaO2?

A

Hypoxic vasocontritction

Shifts blood from poorly ventilated regions of the lung

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60
Q

Decrease in PaO2 due to perfusion limitation-O2?

A

Gas equilibriates along the length of the capillary

Diffusion can only be icnreased if blood flow increases

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61
Q

Decrease in PaO2 due to diffusion limited-O2

A

Emphysema, fibrosis, CO

Gas does not equilibriate by the time it reaches the capillary

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62
Q

What is a consequence of pulmonary HTN?

A

Cor pulmonale and subsequent right ventricular failure (jugular venous distention, edema and hepatomegaly)

63
Q

What is DLCo?

A

The extent to which oxygen passes from the air sacs of lungs into the blood

64
Q

How to measure pulmonary vascular resistance?

A

PVR = Pulmonary artery-PL atrium/ cardiac output

65
Q

What is the alveolar gas equation?

A

PaO2 = pLO2 - PaCo2/R

66
Q

What are causes of Hypoxia?

A

Decrease in cardiac output
Hypoxemia
Anemia
CO poisoning

67
Q

What are causes Hypoxemia (decrease in PaO2)?

A

Normal A-a gradient
High altitude
Hypoventilation

Increase in A-a gradient:
V/Q mismatch
Diffusion is limited (fibrosis)
Right to left shunt

68
Q

what causes ischemia?

A

Impeded arterial flow

Decrease in venous drainage

69
Q

Explain the V/Q mismatch?

A

V/q should be 1 to 1

70
Q

What is the V/Q at apex of lung/at the base?

A

V/Q is equal to 3 (wasted ventilation)
V/Q at the base (0.6) wasted perfusion

Both ventilation and perfusion are greater at the base of the lung then at the apex

(Tuberculosis flourishes at the apex because thrives in high O2 environement)

71
Q

What does V/Q =0 mean?

A

obstruction (shunt) the 100% O2 will not improve the PaO2 (in the case of foreign body aspiration)

72
Q

V/Q = infinity?

A

blood flow obstuction (physiologic dead space)

Assuming less then 100% dead space, 100% O2 will improve PaO2

73
Q

What are the forms that Co2 is transported?

A

HCO3 90%
Carbaminohemoglobine or HbCO2 (5%)
CO2 bound to HB at the N-terminus od globin (not heme)
Dissolced CO2 (5%)

74
Q

What is the Haldane effect?

A

Oxygentation of HB promotes dissociation of H+ from Hb

This shifts equilibrium toward CO2 formation, therefore CO2 is released from RBC

75
Q

What is the Bohr effect?

A

In periphereal tissue, increase in H+ from tissue shits the metabolism to the right, unloading O2

76
Q

How is the majority of CO2 in the blood carried?

A

HCO3 in the plasma

77
Q

What is the response to high altitude?

A

Decrese in atmospheric PO2
Increase in ventilation
Decrease in PaCo2
Respiratory alkalosis
Results in altitiude sickness
Chronic increase in ventilation
Increase in erythroboitin
Increase in 2, 3 BPG (binds to the HB so the HB releases more O2)
Cellular changes in the mitochrondria
Increase renal excretio of HCO3 to compensate for respiratory alkalosis
Chronic hypoxic pulmonary vasoconstrcition leads to pulmonary hypertension and right ventricular hypertrophy

78
Q

Physiologic response to exercise?

A

Increase in CO production
Increase in O2 consumption
Increase in ventilation rate to meet the O2 demand
V/Q ration from the apex to the base becomes more uniform.
Increase in pulmonary blood flow due to increase in cardiac output
Decrease in Ph during exercise (due to lactic acidosis)
No change in PaO2 and PaCO but the CO2 in the venous will increase and there will be a decrease in the O2 content

79
Q

Rhinosinusitis?

A

Obstuction of the sinus cavity and inflammation and pain
Typically the maxillary sinus
Most common is upper respiratory infection
Can have superimposed bacterial infection (usually S pneumonaia, H. Influenzae, M. catarrhalis)

80
Q

Epistaxis?

A

Usually anterior segmane of the nostril (Kiesselback plexus)

Life threatening can occur in the posterior segent (sphenopalatine artery)

81
Q

Head and neck cancer?

What is field cancerization?

A

Usually squamous cell carcinoma
Risk factors include tobacco, ETOH, alchol, HPV-16, EBV

Field cancerization: carcinogen damages wide mucosal area with multiple tumors

82
Q

What is Virchow’s triad?

A

Statsis
Hypercoagulobility (van leiden)
endothelial damage

Do a D-dimer to rule out

83
Q

What are the signs of DVT?

A

Homan sign: dorsiflexion of foot (calf pain)

Most PE arise from deep vein thrombosis

84
Q

Imaging /treatment of DVT?

A 
Choice of compression is U/S
Oral anticoagulants (warfarin and rivaroxaban)
85
Q

Physiology of a PE?

A

V/Q mismatch with leads to hypoxemia and respiratory alkalosis

Will have sudden onsetof dyspnea
Chest pain
Tachypnea
Tachycardia
Large emboli or saddle emboli
86
Q

What are lines of Zahn (PE)?

A

Interdigiting areas of pink (platelets and fibrin) and red RBC found only in thrombi, formed after death

87
Q

Types of PE?

A 
Fat
Air
Thrombus
Bacterial
Amniotic fluid
Tumor
88
Q

Characteristics of fat emboli?

A

Long bone fractures and liposuction

Classic triad of hypozemia, neuro abnormal, and petechial rash

89
Q

Amniotic fluid emboli?

A

Can lead to DIC in the post partum

90
Q

Air emboli?

A

Nitrogen bubbles in divers as they ascend
Leads to decompression sickness
treat with hyperbaric
Can also be due to invasive procedure * central line)

91
Q

What happens to air volumes in obstructive lung disease?

A

Increase in RV and FRC
Increase in TLC
Decrease in FeV1
Decrease in FVC

Decrease in FEV1/FVC ratio is the hallmark

92
Q

Pathology and symptoms of chronic bronchitis>

A

Hyperplasia of mucos secreting glands (the thickness of the wall and epithelium > 50%)

Productve cough for > 3 weeks
Wheexing, crackles, cyanosis (early: hypoxemia due to shunting)

Late onset have CO2 retnetion
Polycythemia

Chronic: pulmonary hypertension or cor pulmonale

93
Q

Emphysema (pink puffer)

A

Enlargement of air spaces
Decrease in recoil, but increase in compliance
Decrease in diffusing capacity for CO (destruction of the alveolar walls)

Centriacinar (associated with smoking)

Panacinar (associtaed with alpha 1 antitrypsin deficinecy)

Barrel shaped chest with flattended daiphgram

Exhalation through pursed lips to increase airway pressure and prevent the collaspse during respiration

94
Q

Asthma?

A

Bronchial hyperresponsiveness
Smooth muscle hypertrophy
Leyden crystaks
Can be triggered by respiratory, allergens, streess

Clinical diagnosis by spirometry and methacholine challenge

Findings: cough, wheezing, dyspnes, hypoxemia, decrease in inspiratory/expiratory ratio
Have mucos plugging
Peribronchia cuffing on CXR

95
Q

What is bronchiectasis?

A

Chronic necrotizing infection of the bronchi
Permenently dilated airways
Recurrent infection
hemoptysis

Associated with bronchial obstruction
Poor ciliary motility
Cystic fibrosis
Allergic bronchopulmonary aspergillosis

96
Q

Characteristics of restrictive lung disease?

A

Decrease in lung volumes
decrease in FVC, TLC
FEV/FVC ratio > 80

Poor breathing mechanics (extrapulmonary, periphereal hypoventilation, normal A-a gradient)

Poor muscular effort (polio, mysanthia gravis, Guillian-Barre syndrome)

Poor structural apparatus (scolisosi, morbid obesity)

Intersitital lung disease: decrease in pulmonary diffusing capacity increase in A-a gradiet)

Neonatal respiratory distress syndrome 
Penumoconisosi 
Sarcoidosis 
Idiopathic pulmonary fibrosis 
Increase in collagen depositon 
Goodpasture syntome
Granulomatosis with polyangiitis
Pulmonary Langerharns
Hypersensitivity pneumonitis
Drug toxicity.
97
Q

Flow volume loops?

A

Obstructive shifts the loops to the left

Restrictive shifts to the right.

98
Q

Hypersensitivity penumonitis?

A

Mixed type III/IV hypersensitivity (reaction to enviromental antigen)

Dyspnea, cough, chest tightness, headache

Often seen in farmers exposed to birds.

99
Q

Pneumoconioses?

A

Coal workers penumoconisosis
Risk of cor pulmonale
Cancer
Caplan syndrome (rheumatoid arthritis, penumoconiosis with intrapulmonary nodules

100
Q

Asbestosis?

A

Associated with ship building
Roofing
Plumbing (Ivory White)
Calcified supradiaphragmatic and pleural plaques

Usually affects the lower lobes
Asbestos bodies are golden brown fusiform dumbells

101
Q

Berylliosis?

A

Exposure to beryllium in aerospace and manufacturing industries

Granulomatosis on histology and therefore occasionlly responsive to steroids

Affects the upper lobes

102
Q

Coal worker’s pneumoconisosi?

A

Prolonged coal dust exposure
Macrophafes with carbon
Known as black lung disease

Affects upper lobes

103
Q

Anthracosis?

A

Asymptomatic condition found in many urban dwellers exposed to sooty air

104
Q

Silicosis?

A

Associated with foundries
Sandblasting
Macrophages respond to silica
Release fibrogenic factors leading to fibrosis

Silica mat disrupt phagolysosomes and impair macrophages
Increases susceptibility to TB

Affects upper lobes

Eggshell calcification of hilar lymph nodes

105
Q

Where are common chemical pathogens to lungs found?

A

Asbestos: Roof (common within insulation)

Silica and Coal: from the earth, but tend to affect the upper lobes of the lungs

106
Q

Acute respiratory distress syndrome?

A

Acute resp failure
Bilarteral lung opacities
Decreased PaO2/FiO2
There is no evidence of heart failure or fluid overload

Causes: 
Sepsis
Pancreatitis
Pneumonai
Aspitation 
Uremia
Trauma 
Amniotic fluid embolism 
Shock
Endothelial damage

There is increase alveolar capillary permeability
Leads to protein rich leakage into the alveolu (diffuse alveoli damage and noncardiogenic pulmonary edema)

Forms intra-alveolar hyaline membranes

Damage is caused by release of neutrophils
substances are toxic to alveolar walls
Cause activation of coagulation cascade

Management: mechanical ventilation with low tidal volumes

Treat the underlying cause

107
Q

Sleep apnea?

A 
Repeated cessation of breathing 
More then 10 seconds
Will have disruption sleep 
Daytime somnolence
Normal PaO2 during the day

Leads to nocturnal hypoxia arrythmias (atial fibrillation/flutter) with sudden death

Hypoxia leads to EPO release with increase in erythopoiesis

108
Q

Obstructive sleep apnea?

A

Respiratory effort against airway obstruction
Associated with obesity and loud snoring
Caused by excess parapharyngeal tissue in adults
Adenotonsillar hypertrophy in children

Treatment: weight loss
CPAP
Surgery

109
Q

Central sleep apnea?

A

No respiratory effort due to CNS injury and toxicity

110
Q

Obesity hypoventilation syndrome?

A

BMI > 30 kg/m2
hypoventilation (decrease in respiratory rate)
Decrease in PaO2 and increase in PaCO2 during sleep
Increase in PaCO2 during waking hours (retention)

111
Q

Pulmonary hypertension?

A

Normal mean artery pressure = 10-14 mmHg
Pulmonary hypertension > 25 mmHg at rest
Results in arteriosclerosis
Medial hypertrophy
Intimal fibrosis of the pulmonary arteries
Severe respiratory distress syndrome with cyanosis and RVH
Death from decompensated cor pulmonale

112
Q

Etiology of pulmonary arterial hypertension?

A

Idiopathic PAH
Heritable PAH often due to mutation of BMPR2 gene
Normally vascular smooth muscle proliferation
Poor prognosis

Other causes:

Amphetamines, cocaine
Connective tissue disease
HIV infection
Portal hypertension 
Congenital heart diease
Schistomiasis

Left heart diease: systole/diastole dysfunction and valvular diease (mitral lung)

Lung disease of hypoxia: destruction of lung parenchyma (COPD) hypoxemia vasoconstriction (obstructive sleep apena) living in high altitude

Chronic thromboemboli: recurrent mircothrombi, with decrease cross section area of the pulmonary vascular bed

Multifactorial: include hematologic, systemic and metabolic disorders

113
Q

Physical findings of pleural effusion?

A

Decrease in breath sounds
Dull percssion
Decrease fremitus
Tracheal deviation can occur (or away from the side of the lesion)

114
Q

Physical findings of atelectasis (bronchial obstruction)

A

Decrease in breath sounds
Dull percussion
Decrease in fremitus
Toward side of the lesion

115
Q

Simple pneumothorax?

A

Decrease in breath sounds
Hyperresonant
Decrease in fremitus

116
Q

Tension pneumothorax?

A

Decrease in breath sounds
Hyperresonant
Decrease in fremitys
Moves away from the side of the leision

117
Q

Findings for lobar pneumonia?

A

Decrease bronchial breath sounds
Late inspiratory crackles
Dull percussion
Increase in fremitus

118
Q

Pleural effusion (transudate)?

A

Decrease in protein content
Due to increase hydrostatic pressure or decrease in oncotic pressure
Can occur in nephrotic syndrome
Cirrhosis

119
Q

Pleural effusion (exudate)

A

Increase in protein content
Cloudy
Due to malignancy (pneumonia, collagen vascular disease, trauma) occurs in a state of vascular permeability

May be drained due to the risk of infection

120
Q

Pleural effusion (lymphatic)

A

Chylothorax
Due to thoracic duct injury from trauma or malignanc
Milky appearing fluid
Increased triglycerides

121
Q

Characteristics of pneumothorax?

A 
Accumulation of air in the pleural spaces
Unilateral chest pain and dyspnea 
Unilateral chest expansion 
Decrease in tactile fremitus 
Hyperresonance
Diminished breath sounds
All on affected side
122
Q

Primary spontaneous pneumothorax?

A

Rupture of apical subpleural bleb or cysts

Occurs within tall, thin, young males

123
Q

Secondary spontaneous pneumothorax?

A

Due to diseased lung *bullae in epmphysemea)
Mechanical ventilation (with use of high pressures)
Barotrauma

124
Q

Traumatic pneumothorax?

A

Blunt (rib fractre)

Penetrating trauma

125
Q

Tension pneumothoraz?

A

Air enters the pleural space but cannot exit
Increased trapped air
Trachea deviates from the affected lung
Needs immediate needle decompression or chest tube displacement

126
Q

Lobar pneumonia?

A

S penumonia
Legionella
Klebsiella

Will have intre-alveolar exudate (consolidation) ma involve the entirelobe or lung

127
Q

Bronchopenumonaia?

A

S. Penumonia
S aureus
H. Influenzae
Klebsielle

Acute inflammatory infiltrates from bronchioles with adjacent alveoli (patchy distribution involving more then 1 lobe)

128
Q

Interstitial pneumonia?

A

Mycoplasma
Chlamydia
Legionella
Viruses (RSV, CMV, influenza, adenovirus)

Diffuse, patchy inflammation loalized to intersitial areas of the alveolar walls

Diffuse distribution (more then 1 lobe) 
Has an indolent course (walking pneumonia)
129
Q

Characteristics of lung abcess?
What is seen on the CXR?
Where abcess found depending on the position?

A

Localized collection of pus within the parenchyma
Caused by aspiration of oropharyngeal contents (usually in patients predisposed to loss of consciousness)

Or with brochial obstruction

Treatment: clindamycin

CXR:
Air fluid levels common in cavities
Due to anaerobes (Bacteriodes, fusobacterium, peptosstreptococcus or S.Aureaus

Upright: basal segments of right lower lobe
Supine: posterior segments of the right upper lobe or superior segement of right lower lobe

130
Q

Mesothelioma?

A

Malignancy of the pleura associated with asbestosis
May result in hemorraghic pleural effusion
Pleural thickening

Psammoma bodies seen on histology
Cytokerain and calretinin + in almost all mesotheliomas
Negatve in most carcinomas
Smoking is not a risk factors

131
Q

Pancost tumor?

A

Carcinoma that occurs at the apex of the lungs
Can cause pancoast syndrome by invading cervical sympathetic chain

Compression of locoregional structures may cause array of findings:

Recurrent laryngeal nerve (hoarseness)
Superior cervial ganglion - Horner’s syndrome (ipsilateral ptosis, misosi, anhidrosis)
Superior vena cava (SVC syndrome)
Sensorimoter deficit

132
Q

Superior vena cava syndrome?

A

Obstruction of the SVC (impairs drainage from the head) face plethora

Will have blanching of the fingertips

Jugular venous distention
Thrombosis from indwelling catheters

Medical emergency: can have raise withn intracranial pressure if obstruction is severe (can cause headaches, dizziness, increase risk of anuerysm, rupture of the intracranial arteries)

133
Q

What are the presentation of lung cancer?

A

Cough
Hemoptysis, bronchial obstruction
Wheezing
Pneumonic coin lesion on CXR

134
Q

what are common sites of metastasis from lung CA?

A

Adrenals
Brain
Bone (pathological fracture)
Liver (jaunedice, heptomegaly)

135
Q

What are possible complications?

A

Superior vena cava syndrome
Pancoast tumor
Horner syndrome
Endocrine (paraneoplastic syndrome)
Recurrent aryngeal nerve compression (horseness)
Effusions (pleural or pericardial )
Risk factors include: smoking, secondhand smoke, radon, asbestos, family history

NOTE: squamous and small cell carcinoma are central and often caused by smoking

136
Q

Characteristics of small cell carcinoma?

A

Usually central
undifferentiated and aggressive
May produce ACTH Cushing syndrome
Antibodies against presynaptic Ca channels or neurons
Lambert-Eaton mysasthenic syndrome or neurons (paraneoplastic myeliis, encephalitis, subacute cerebeller degenertion

Amplification of myc oncogenes common
Managed with chemotherapy +/- radition

Histology: neoplasm of neuroendocrine Kulchitksy cells (small dark blue cells)

Chromogranin A +
Neuron-specific enolase +

137
Q

Characteristics of adenocarcinoma of the lungs?

A

Usually peripheral
Most common lung cancer in non smokers and overall (mets)

Mutations include KRAS. EGFR, ALK

Associated with hypertrophoc osteoarthropathy (clubbing)

Bronchioloalveolar subtype (adenocarcinoma in situ)

CXR shows hazy infiltrates similar to pneumonia (better prognosis)

Bronchial carcinoid and bronchioloalveolar cell carcinoma have lesser association with smoking.

138
Q

Squamous cell carcinoma

A

Central
Hilar mass arising from bronchus
Cavitation
Cigarette, hypercalcemia (produces PTHrP)

139
Q

Large cell carcinoma?

A 
Peripheral (highly anaplastic) undifferentiated tumor 
Poor prognosis 
Less responsive to chemotherpay
Removed surgically 
Pleomorphic giant cell 
Secrete BHCG
140
Q

Bronchial carcinoid tumor?

A

Excellent prognosis
Mets are rare
Symptoms due to mass effect or carcinoid syndrome (flushing

141
Q

Characteristics of antihistamines?

A

Reversible inhibition of H1 (histamine receptors)
ex. Diphenhydramine, dimenhydrinate, chlorpheniramine

Names contain en/ine or en/ate

Clinical uses:allergy, motion sickness, sleep aid
Sedation, antimuscarinic, anti-alpha adrenergic

142
Q

Second generation of antihistamines?

Clinical uses?

A

Loratadine
Feofenadine
Desloratadine
Cetirizine

Clinical uses are allergt

Adverse effects:
Far less sedating then first generation because of decrease entry into the CNS

143
Q

Expectorants?

A

Thin respiratory secretions
Does not suppress the cough reflex

N-acetylcysteine: mucolytic, liquefies mucus in COPD patients by disrupting disulfide bounds
Also used as an antidote for acetominophen reversal

Examples include:
Gualifensin
N-Acetylcysteine

144
Q

What is dextromethorphan?

A 
Anti-tussive
Antagonizes NMDA glutamate receptors
Synthetic codeine analog 
Has mild opiod effect when used in excess
Naloxone can be given for an overdose 
Mild abuse potential 
May cause serotonin syndrome
145
Q

Pseudoephedrine, phenyllephrine?

A

Mechanism: a-adrenergic agonists (used as nasal decongestants)
Clinical use: reduce hyperemia, edema, nasal congestion

Open obstructed eustachian tibes
Pseudoephedrine illicitly used to make methamephtamine

Adverse effect: HTN
Can also cause CNS stimulation/anxiety

146
Q

What are drugs that can be used for pulmonary HTN?

A

Bosentan: competitively antagonized endothelin-1 receptors
Decreases pulmonary vascular resistence

Adverse effects; Hepatotoxicity

Sildenafil: Inhibits cGMP PDE-5
Prolongs vasodilatory effect of nitric oxide

Adverse: Used to treat erectile dysfunction

147
Q

Epoprostenol, iloprost?

A

PGI2 with direct vasodilatory effects on pulmonary and systemic arterial vascular beds

Inhibits platelet aggregation

Side effects include: flushing and jaw pain

148
Q

Clinical use of B agonists?

A

Albuterol: relazes bronchial smooth muslce (short acting B2-agonsit) used during acute exacerbation

Salmeterol, formoteral: long acting agents for prophylaxis
Adverse effects unclude tremor and arrythmia

149
Q

Inhaled corticosteroids?

A

Fluticasone and budesonide: inhibit sythesis of virtually all cytokines

Inactivates NF-kB (transcription factor for TNF-apha) and other inflammatory agents

First line for chronic asthma

150
Q

Muscarinic antagonists?

A

Ipratropium: competitively blocks muscarinic receptors
Prevents bronchoconstriction
Used for COPD
Tiotropim is long acting

151
Q

Anti-leukotrienes?

A

Montelukast, and zafirlukast
Block leukotriene receptors (CysLT1)
Good for asthma induces by ASA

Zileuton:
5-lipoxygenase pathway inhibitor
Blocks conversion of arachidonic acid to leukotriens
Hepatotoxic

152
Q

Anti-IgE monoclonal therapy?

A

Omalizumab
Binds to unbound serum IgE and blocks binding to FcER1

Used in allergic asthma with increase IgE levels resistant to inhaled steroids

Long acting B2 agonists

153
Q

Methylxanthines

A

Theophylline (causes bronchodilatation by inhibiting phophodieseterase

Narrow therapeutic index (cardiotoxicity and neurotoxicity)

Metabolized by cytochrome

154
Q

Methacholine?

A 
Muscarinic receptor (M3) agonist
Used in bronchial challene to diagnose asthma

US (17 decks)

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