Respiratory Flashcards
1
Q
When in embryonic developpement is survival possible?
A
At 25 weeks
2
Q
How does breathing in utero work?
A
Aspiration and expulsion of amniotic fluid
3
Q
How does breathing change at birth?
A
Fluid gets replaced by air and have a decrease in pulmonary vasular resistance
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
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
6
Q
What are type 1 cells (pneumocytes)?
A
97% of aleveolar surfaces
Line the alveoli
Squamous, thin for gas diffusion
7
Q
What are the type 2 cells (penumocytes)
A
Secrete pulmonary surfactant
Decrease in alvelor surface tension
8
Q
Component of pulmonary surfactant?
A
Complex mix of lecitins and dipalmitoylphospahtidylcholine
9
Q
Club cells?
A
Non ciliated, low columnar/cuboidal with secretory granules
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
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
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
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
14
Q
Describe anatomy of the lungs?
A
right lung has three lobes
left lung has 2 lobes
15
Q
Why right lung more common for inhaled foreign body?
A
Right mainstem bronchus is wider and more vertical then the left
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
17
Q
why does the left lung only have 2 lobes?
A
That space is occupied by the heart
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
19
Q
What nerves innervate the diapghgram?
A
Phrenic nerve
20
Q
where is pain from the diaphgram referred?
A
Shoulder
or Trapezius ridge
21
Q
What nerves keep the daipggram alive
A
C3
C4
C10
22
Q
where does cartoid bifucate?
Trachea?
Abdominal aorta?
A
Carotid: C4
Trachea: T4
Abdominal aorta: L4
23
Q
Inspiratory reserve volume?
A
Air that can still be breathed in after normal inspiration
24
Q
Tidal volume?
A
Air that moves into lung with each quiet inspiration
25
Expiratory reserve volume?
Air that can still be breathed out after normal expiration
26
Residual volume?
Air in lung after maximal expiration (cannot be measured on spirometry)
27
Inspiratory capacity?
Inspiratory revserve volume + tidal volume
28
Functional residual capacity?
Residual volume + expiratory reserve volume
| Can't be measured by spirometry
29
Vital capacity?
Tidal volume+ inspiratory reserve volume + expired residual volume
30
Total lung capacity?
Inspiratory reserve volume + tidal volume+ expiratory reserve volume + residual volume
31
what is the dead space
Physiologic dead space is equivalent to anatomic dead space in normal lung
Is greater when there is V/Q defects
32
what is pathologic dead space
Part of respiratory zone becomes unable to perform gas exchange (ventilated but not perfused)
33
Calculation for dead space?
Vd = Vt X ( PaCO2- PECp2)/ (PaCO2)
Vt is tidal volume
PaCos arterial co2
PEco2: expired air PCO2
34
Definition of minute ventilation?
Total volume of gas entering lungs per minute
| Ve = VT X RR
35
Definition of alveolar ventilation?
Volume of gas per unit of time that reaches the alveoli
Va = (Vt-Vd) xRR
36
What is elastic recoil?
tendency for lungs to collapse inward and the chest to spring outward
37
What happens to elastic recoil at the functional residual capacity?
Inward pull of the lungs is balanced bu the outward pull of the chest wall
Systemic pressure is atmosphereic
38
What is the airway and alveolar pressure at functional residual capacity?
Airway and alveolar pressure are 0
| intrapleural pressure is negative
39
what is the lung compliance?
Change in volume for a change in pressure:
Delta V/ delta P
High compliance means the lungs are easier to fill
40
when is lung compliance decreased?
Pulmonary fibrosis
Pneumonia
Pulmonary edema
41
when is lung compliance increased?
Increased in emphysema
Normal aging
Surfactant increases compliance
42
what is hysteresis?
Lung inflation curve follows a different curve then lung deflation curve (due to need to overcome surface tension)
43
what are the component of hemoglobin?
2 alpha and 2 beta unies
44
What are the forms of hemoglobin?
T (deoxygenated)
| R elaxed and oxygenated
45
what does fetal Hb affintiy for O2?
Has a higher affinity for O2 then aduld
46
what factors shift the dissocation curve to the right (increase O2 unloading)
```
Increase CL
Increase H+
Increase CO2
Increase 2,3 BPG
Increase temperature
```
47
Methemoglbin?
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
48
How do nitrates cause methmeglobin?
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
49
what is carboxyhemoglobin?
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
50
characteristics of the oxygen-hemoglobin curbe?
Sigmoidal shape
Has higher affinity for each susequent O2 molecule that is bound
Myoglobin is monomeric and does not show positive cooperatively
51
What happens when the curve shifts right?
decrease in affinity for Hb and O2 (facilitates unloading of O2 into the tissue)
52
What is a shift to the left?
Decrease in O2 unloading (renal hypoxia) increase in EPO synthesis
53
How is the fetal curve shifted?
Has a higher affinity for O2 then the adult Hb so the curve is shifted to the left
54
How is the oxygen content of blood measured?
o2 content = 1.32 X Hb X Sao2 + 0.003 x PaO2
55
What happens when there is anemia?
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
56
What happens during CO poisoning?
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
57
What happens during anemia?
Hb concentration is decreased
% of O2 saturation of Hb is normal
Dissolved paO2 is notmal
The total O2 content is decreased
58
What happens during polycythemia?
The Hb concentration is incresed
The % of O2 saturation of Hb is normal
Dissolved PaO2 is normal
The total O2 content is increased
59
Pulmonary circulation, reaction to decrease PaO2?
Hypoxic vasocontritction
| Shifts blood from poorly ventilated regions of the lung
60
Decrease in PaO2 due to perfusion limitation-O2?
Gas equilibriates along the length of the capillary
| Diffusion can only be icnreased if blood flow increases
61
Decrease in PaO2 due to diffusion limited-O2
Emphysema, fibrosis, CO
| Gas does not equilibriate by the time it reaches the capillary
62
What is a consequence of pulmonary HTN?
Cor pulmonale and subsequent right ventricular failure (jugular venous distention, edema and hepatomegaly)
63
What is DLCo?
The extent to which oxygen passes from the air sacs of lungs into the blood
64
How to measure pulmonary vascular resistance?
PVR = Pulmonary artery-PL atrium/ cardiac output
65
What is the alveolar gas equation?
PaO2 = pLO2 - PaCo2/R
66
What are causes of Hypoxia?
Decrease in cardiac output
Hypoxemia
Anemia
CO poisoning
67
What are causes Hypoxemia (decrease in PaO2)?
Normal A-a gradient
High altitude
Hypoventilation
Increase in A-a gradient:
V/Q mismatch
Diffusion is limited (fibrosis)
Right to left shunt
68
what causes ischemia?
Impeded arterial flow
| Decrease in venous drainage
69
Explain the V/Q mismatch?
V/q should be 1 to 1
70
What is the V/Q at apex of lung/at the base?
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
What does V/Q =0 mean?
obstruction (shunt) the 100% O2 will not improve the PaO2 (in the case of foreign body aspiration)
72
V/Q = infinity?
blood flow obstuction (physiologic dead space)
| Assuming less then 100% dead space, 100% O2 will improve PaO2
73
What are the forms that Co2 is transported?
HCO3 90%
Carbaminohemoglobine or HbCO2 (5%)
CO2 bound to HB at the N-terminus od globin (not heme)
Dissolced CO2 (5%)
74
What is the Haldane effect?
Oxygentation of HB promotes dissociation of H+ from Hb
This shifts equilibrium toward CO2 formation, therefore CO2 is released from RBC
75
What is the Bohr effect?
In periphereal tissue, increase in H+ from tissue shits the metabolism to the right, unloading O2
76
How is the majority of CO2 in the blood carried?
HCO3 in the plasma
77
What is the response to high altitude?
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
Physiologic response to exercise?
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
Rhinosinusitis?
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
Epistaxis?
Usually anterior segmane of the nostril (Kiesselback plexus)
| Life threatening can occur in the posterior segent (sphenopalatine artery)
81
Head and neck cancer?
| What is field cancerization?
Usually squamous cell carcinoma
Risk factors include tobacco, ETOH, alchol, HPV-16, EBV
Field cancerization: carcinogen damages wide mucosal area with multiple tumors
82
What is Virchow's triad?
Statsis
Hypercoagulobility (van leiden)
endothelial damage
Do a D-dimer to rule out
83
What are the signs of DVT?
Homan sign: dorsiflexion of foot (calf pain)
| Most PE arise from deep vein thrombosis
84
Imaging /treatment of DVT?
```
Choice of compression is U/S
Oral anticoagulants (warfarin and rivaroxaban)
```
85
Physiology of a PE?
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
What are lines of Zahn (PE)?
Interdigiting areas of pink (platelets and fibrin) and red RBC found only in thrombi, formed after death
87
Types of PE?
```
Fat
Air
Thrombus
Bacterial
Amniotic fluid
Tumor
```
88
Characteristics of fat emboli?
Long bone fractures and liposuction
| Classic triad of hypozemia, neuro abnormal, and petechial rash
89
Amniotic fluid emboli?
Can lead to DIC in the post partum
90
Air emboli?
Nitrogen bubbles in divers as they ascend
Leads to decompression sickness
treat with hyperbaric
Can also be due to invasive procedure * central line)
91
What happens to air volumes in obstructive lung disease?
Increase in RV and FRC
Increase in TLC
Decrease in FeV1
Decrease in FVC
Decrease in FEV1/FVC ratio is the hallmark
92
Pathology and symptoms of chronic bronchitis>
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
Emphysema (pink puffer)
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
Asthma?
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
What is bronchiectasis?
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
Characteristics of restrictive lung disease?
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
Flow volume loops?
Obstructive shifts the loops to the left
| Restrictive shifts to the right.
98
Hypersensitivity penumonitis?
Mixed type III/IV hypersensitivity (reaction to enviromental antigen)
Dyspnea, cough, chest tightness, headache
Often seen in farmers exposed to birds.
99
Pneumoconioses?
Coal workers penumoconisosis
Risk of cor pulmonale
Cancer
Caplan syndrome (rheumatoid arthritis, penumoconiosis with intrapulmonary nodules
100
Asbestosis?
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
Berylliosis?
Exposure to beryllium in aerospace and manufacturing industries
Granulomatosis on histology and therefore occasionlly responsive to steroids
Affects the upper lobes
102
Coal worker's pneumoconisosi?
Prolonged coal dust exposure
Macrophafes with carbon
Known as black lung disease
Affects upper lobes
103
Anthracosis?
Asymptomatic condition found in many urban dwellers exposed to sooty air
104
Silicosis?
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
Where are common chemical pathogens to lungs found?
Asbestos: Roof (common within insulation)
| Silica and Coal: from the earth, but tend to affect the upper lobes of the lungs
106
Acute respiratory distress syndrome?
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
Sleep apnea?
```
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
Obstructive sleep apnea?
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
Central sleep apnea?
No respiratory effort due to CNS injury and toxicity
110
Obesity hypoventilation syndrome?
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
Pulmonary hypertension?
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
Etiology of pulmonary arterial hypertension?
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
Physical findings of pleural effusion?
Decrease in breath sounds
Dull percssion
Decrease fremitus
Tracheal deviation can occur (or away from the side of the lesion)
114
Physical findings of atelectasis (bronchial obstruction)
Decrease in breath sounds
Dull percussion
Decrease in fremitus
Toward side of the lesion
115
Simple pneumothorax?
Decrease in breath sounds
Hyperresonant
Decrease in fremitus
116
Tension pneumothorax?
Decrease in breath sounds
Hyperresonant
Decrease in fremitys
Moves away from the side of the leision
117
Findings for lobar pneumonia?
Decrease bronchial breath sounds
Late inspiratory crackles
Dull percussion
Increase in fremitus
118
Pleural effusion (transudate)?
Decrease in protein content
Due to increase hydrostatic pressure or decrease in oncotic pressure
Can occur in nephrotic syndrome
Cirrhosis
119
Pleural effusion (exudate)
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
Pleural effusion (lymphatic)
Chylothorax
Due to thoracic duct injury from trauma or malignanc
Milky appearing fluid
Increased triglycerides
121
Characteristics of pneumothorax?
```
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
Primary spontaneous pneumothorax?
Rupture of apical subpleural bleb or cysts
| Occurs within tall, thin, young males
123
Secondary spontaneous pneumothorax?
Due to diseased lung *bullae in epmphysemea)
Mechanical ventilation (with use of high pressures)
Barotrauma
124
Traumatic pneumothorax?
Blunt (rib fractre)
| Penetrating trauma
125
Tension pneumothoraz?
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
Lobar pneumonia?
S penumonia
Legionella
Klebsiella
Will have intre-alveolar exudate (consolidation) ma involve the entirelobe or lung
127
Bronchopenumonaia?
S. Penumonia
S aureus
H. Influenzae
Klebsielle
Acute inflammatory infiltrates from bronchioles with adjacent alveoli (patchy distribution involving more then 1 lobe)
128
Interstitial pneumonia?
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
Characteristics of lung abcess?
What is seen on the CXR?
Where abcess found depending on the position?
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
Mesothelioma?
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
Pancost tumor?
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
Superior vena cava syndrome?
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
What are the presentation of lung cancer?
Cough
Hemoptysis, bronchial obstruction
Wheezing
Pneumonic coin lesion on CXR
134
what are common sites of metastasis from lung CA?
Adrenals
Brain
Bone (pathological fracture)
Liver (jaunedice, heptomegaly)
135
What are possible complications?
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
Characteristics of small cell carcinoma?
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
Characteristics of adenocarcinoma of the lungs?
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
Squamous cell carcinoma
Central
Hilar mass arising from bronchus
Cavitation
Cigarette, hypercalcemia (produces PTHrP)
139
Large cell carcinoma?
```
Peripheral (highly anaplastic) undifferentiated tumor
Poor prognosis
Less responsive to chemotherpay
Removed surgically
Pleomorphic giant cell
Secrete BHCG
```
140
Bronchial carcinoid tumor?
Excellent prognosis
Mets are rare
Symptoms due to mass effect or carcinoid syndrome (flushing
141
Characteristics of antihistamines?
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
Second generation of antihistamines?
| Clinical uses?
Loratadine
Feofenadine
Desloratadine
Cetirizine
Clinical uses are allergt
Adverse effects:
Far less sedating then first generation because of decrease entry into the CNS
143
Expectorants?
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
What is dextromethorphan?
```
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
Pseudoephedrine, phenyllephrine?
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
What are drugs that can be used for pulmonary HTN?
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
Epoprostenol, iloprost?
PGI2 with direct vasodilatory effects on pulmonary and systemic arterial vascular beds
Inhibits platelet aggregation
Side effects include: flushing and jaw pain
148
Clinical use of B agonists?
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
Inhaled corticosteroids?
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
Muscarinic antagonists?
Ipratropium: competitively blocks muscarinic receptors
Prevents bronchoconstriction
Used for COPD
Tiotropim is long acting
151
Anti-leukotrienes?
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
Anti-IgE monoclonal therapy?
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
Methylxanthines
Theophylline (causes bronchodilatation by inhibiting phophodieseterase
Narrow therapeutic index (cardiotoxicity and neurotoxicity)
Metabolized by cytochrome
154
Methacholine?
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Muscarinic receptor (M3) agonist
Used in bronchial challene to diagnose asthma
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