Respiratory Flashcards
peculiar feature about newborn respiratory physiology
obligate nose breathers
RV vs. ERV
RV is the volume of air remaining after a maximal expiration. ERV is the volume remaining after normal expiration.
Characteristic of NRDS
Atelectasis. This is because without surfactant, the surface tension of the small alveoli collapse into the large aveoli.
- Lack of surfactant also decreases compliance.
When does surfactant appear?
Around week 24
Asthma physiology
Wheezing + tachypnea. Hypoxemia causes tachypnea, which drives PCO2 down.
What happens to intrapleural pressure with inspiration?
Becomes more negative than it is at rest or during expiration.
When airway pressure is equal to atmospheric pressure…
This is equilibrium and there is no airflow. ***Volume in the lungs = FRC.
What happens to alveolar PO2 with a PE?
Alveolar PO2 is equal to the PO2 in inspired air.
Blood flow in the systemic vs. pulmonary circulations…
Blood flow in the systemic and pulmonary circulations is nearly equal. Pulmonary flow is slightly less than the systemic flow because about 2% of systemic CO bypasses the lungs.
Resistance in pulmonary circulation
Resistance in the pulmonary circulation is lower than in the systemic circulation.
Compared with the apex of the lung, the base of the lung has…
a higher pulmonary capillary **PCO2
Mean arterial PO2 and PCO2 during exercise…
There is no change in mean arterial PO2 or PCO2. This is because ventilation rate increases to match the increased O2 consumption and CO2 production.
BUT venous pCO2 increases.
Central chemoreceptor location
Medulla. (medullary chemoreceptors).
Peripheral chemoreceptor location
Carotid and aortic bodies
If an area of the lung is not ventilated because of bronchial obstruction, the pulmonary capillary blood serving that area will have a PO2 that is…
Equal to mixed venous PO2. This is because pulmonary blood will NOT equilibriate with alveolar PO2 but will have a Po2 equal to that of mixed venous blood.
What happens with transporting CO2 from tissues to lungs?
CO2 is hydrated to form H+ and HCO3- in RBCs. H+ is buffered inside the RBCs by deoxyhemoglobin, which ACIDIFIES RBCs. HCO3- leaves RBCs in exchange for Cl- and is carried to the lungs in the plasma.
Carbonic anhydrase
Sits in RBCs and CO2 + H2O H2CO3.
What buffers H+ in RBCs?
Deoxyhemoglobin
hypoxemia
Decreased arterial PO2
Causes of hypoxemia
1) high altitude
2) hypoventilation
3) right to left cardiac shunt
Which cause of hypoxemia is associated with an increased AA gradient?
Right-to-left cardiac shunt. This is because the shunt “dilutes” the PO2 of the normally oxygenated blood thus decreasing the arterial O2.
Causes of hypoxemia with normal A-a gradient?
High altitude + hypoventilation
Causes of hypoxemia with increased A-a gradient?
1) V/Q mismatch
2) Diffusion limitation (fibrosis)
3) right-to-left shunt
Why is pH of venous blood only slightly more acidic than the pH of arterial blood?
H+ generated from CO2 and H2O is buffered by deoxyhemoglobin in venous blood.
Function of J (juxtacapillary) receptors
Receptors located in the alveolar walls, close to the capillaries. Engorgement of pulmonarry capillaries such as with left HF stimulates J receptors, which then cause rapid, shallow breathing.
How do you calculate dead space?
Tidal volume x ((arterial PCO2-expired PCO2)/arterial PCO2))
Initial development of lungs and when it happens
Lung bud buds off from distal end of respiratory diverticulum during week 4
embryonic stage events + timeframe
4-7 weeks
lung bud –> trachea –> mainstem bronchi –> secondary (lobar) bronchi –> tertiary (segmental) bronchi
what do errors in embryonic stage lead to?
TE fistula
pseudoglandular stage events + timeframe
5-16 weeks.
Endodermal tubules –> terminal bronchioles. Surrounded by modest capillary network.
Canalicular stage events + timeframe
16-26 weeks.
Terminal bronchioles –> respiratory bronchioles –> alveolar ducts. Surrounded by prominent capillary network.
*increase in airway diameter.
When is respiration possible?
Canalicular stage, at 25 weeks
Saccular stage events + timeframe
Weeks 26-birth.
Alveolar ducts –> terminal sacs. Terminal sacs separated by primary septa. Pneumocytes develop.
Alveolar stage events + timeframe
Weeks 32-8 years.
Terminal sacs–> adult alveoli (due to secondary separation)
of alveoli at birth and at 8 ye
At birth: 20-70 million
By 8 years: 300-400 million
How does breathing in utero work?
Aspiration and expulsion of amniotic fluid, which leads to increased vascular resistance.
Changes in pulmonary vascular resistance at birth.
At birth, fluid gets replaced with air, leading to decreased pulmonary vascular resistance.
Pulmonary hypoplasia
Poorly developed bronchial tree with abnormal histology.
Which lung does pulmonary hypoplasia usually involve?
Right lung
bronchogenic cysts
- Code: Jeep broncho in living room/bronchogenic cysts. Bronchi hanging overhead + guts hanging on top/caused by abnormal budding of the foregut (lung buds arise from the ventral foregut) and dilation of terminal or large bronchi. Metal railing around broncho + round cysts all over car + air tanks in back spraying air everywhere/discrete + round + sharply defined + air-filled densities on CXR. Chelsea on top with drains in her chest + bugs flying into mouth/Drain poorly and cause chronic infections.
- Location: Living room
Collapsing pressure equation
P = (2(surface tension))/radius
surfactant mechanism
decreases alveolar surface tension, preventing alveolar collapse, DECREASING lung recoil and increasing compliance.
Club cell histology
Conciliated; low-columnar/cuboidal with secretory granules.
Club cell function
1) Secrete component of surfactant.
2) Degrade toxins
3) Act as reserve cells
NRDS presentation on CXR
ground glass
L/S ratio predictive of NRDS
less than 1.5
Screening tests for fetal lung maturity
1) L/S ratio
2) Foam stability index test
3) surfactant-albumin ratio
Sequela of NRDS
1) PDA
2) metabolic acidosis
3) necrotizing enterocolitis
NRDS RF’s
1) prematurity
2) maternal diabetes (due to increased fetal insulin)
3) C-section delivery
Why is C-section a risk factor for NRDS?
Decreased release of fetal glucocorticoids.
NRDS management
Maternal steroids before birth; artificial surfactant for infant.
Therapeutic O2 can cause…
RIB
Retinopathy of prematurity
Intraventricular hemorrhage
Bronchopulmonary dysplasia
Large airways
Nose –> bronchi
Small airways
Bronchioles –> terminal bronchioles
Function of conducting zone
Warm, humidify and filter airs but no gas exchange (dead space).
Extent of cartilage and goblet cells
End of bronchi
Epithelium of bronchus
psuedostratified ciliated columnar cells
Extent of psuedostratified ciliated columnar cells
Extend to beginning of terminal bronchioles, then transition to cuboidal cells
Extent of airway smooth muscle cells
End of terminal bronchioles.
Respiratory zone components
Lung parenchyma; respiratory bronchioles + alveolar ducts + alveoli.
Histology of respiratory bronchioles
Mostly cuboidal
Histology after respiratory bronchioles up to alveoli
simple squamous
When do cilia terminate?
Respiratory bronchioles
Relation of pulmonary artery to bronchus at each lung hilum
RALS – Right Anterior; Left Superior
Lingula…
left lung
If you aspirate a peanut upright where will it end up?
Inferior segment of right inferior lobe.
If you aspirate a peanut while supine where will it end up?
superior segment of right inferior lobe
central tendon
big tendon in the diaphragm
Where does IVC perforate diaphragm?
T8
Where does vagus perforate diaphragm?
T10
Where does aorta perforate diaphragm?
T12
Where does esophagus perforate diaphragm?
T10
Where does thoracic duct perforate diaphragm?
T12
Where does azygos vein perforate diaphragm?
T12
Where does the trachea bifurcate?
T4 (bifourcate)
Where does the common carotid bifurcate?
C4 (bifourcate)
What innervates the diaphragm?
C3,C4,C5 (Phrenic nerve, C3,C4C5 keeps the diaphragm alive). This explains why pain can be referred to shoulder (C5) and trapezius ridge (C3,4)
Typical tidal volume
500 mL
What can you not measure by spirometry
1) RV
2) FRC
3) *TLC
Dead space equation
FA 633
physiologic dead space
anatomic dead space + alveolar dead space
Largest contributor to alveolar dead space
Apex of lung
anatomic dead space
dead space of conducting airways
Pathologic dead space
ventilated but not perfused
Minute ventilation equation
Vt x RR
alveolar ventilation
VA = (Vt-Vd) x RR
Normal dead space volume
150 mL/breath
Why is system pressure atmospheric at FRC?
Inward pull of lung is balanced by outward pull of chest wall.
When is PVR at minimum?
FRC
When is alveolar pressure at FRC?
0
compliance expression
deltaV/deltaP. Change in lung volume for a change in pressure.
When is compliance increased?
1) emphysema
2) normal aging
* surfactant increases compliance.
Hysteresis
Concept that lung inflation curve follows a different curve than lung deflation curve due to need to overcome surface tension forces in inflation.
Taut form of hemoglobin
Deoxygenated; low affinity for O2, thus promoting release/unloading.
Relaxed form of hemoglobin
High affinity for O2 (300x). Hb exhibits positive cooperatively and negative allostery.
Cl affect of hemoglobin
Favors taut form over relaxed form.
Fetal Hb structure
2alpha and 2gamma
Why does fetal Hb have higher O2 affinity?
Decreased affinity of HbF for 2,3BPG
Oxidized Hb
decreased O2 affinity but increased cyanide affinity
What do you use to induce methemoglobinemia?
Nitrites, followed by thiosulfate.
Other things that can cause methemoglobin
benzocaine
carboxyhemoglobin
Hb bound to CO
left shift vs. right shift
Right shift = decreased affinity
Left shift = increased affinity
CO poisoning management
100% O2 + hyperbaric O2
O2 content of blood equation
= (1.34 x Hb x SaO2) + (0.003 x PaO2
normal Hb amount in blood
15 g/dL
normally 1 g Hb can bind…
1.34 mL O2
O2 binding capacity =
20.1 mL O2/dL blood
physiologic effects of decreased Hb on
1) arterial O2 content
2) O2 saturation
3) PaO2
1) decreased
2) no change
3) no change
Calculating O2 delivery to tissues
= CO x O2 content of blood
CO poisoning effect on total O2 content
Decreased
Anemia effect on…
1) Hb concentration
2) %O2 sat of Hb
3) dissolved O2 (PaO2)
4) total O2 content
1) decreased
2) normal
3) normal
4) decreased
Polycythemia effect on
1) Hb concentration
2) %O2 sat of Hb
3) dissolved O2 (PaO2)
4) total O2 content
1) increased
2) normal
3) normal
4) increased
V/Q mismatch
Either shunt physiology or dead space.
Examples of low V/Q
1) chronic bronchitis
2) asthma
3) hepatopulmonary syndrome
4) acute pulmonary edema
Perfusion limited gases
1) O2 (normal health)
2) CO2
3) N2O
Perfusion limited gas characteristics
1) Gas equilibrates early along the length of the capillary.
2) Diffusion can only be increased if blood flow increases.
Diffusion limited gases
1) O2 (emphysema, fibrosis)
2) CO
Diffusion limited gas graph + characteristic
Linear. Gas does not equilibrate by the time blood reaches the end of the capillary.
Diffusion equation
FA 613
What is the underlying diffusion problem with emphysema?
Decreased area for diffusion
DLCO
Extent to which oxygen passes from air sacs of lungs into blood.
Hypoxia
Decreased O2 delivery to tissue
Causes of hypoxia
1) decreased CO
2) hypoxemia
3) anemia
4) CO poisoning
Causes of ischemia
1) impeded arterial flow
2) decreased venous drainage
V/Q at apex of lung
3 (wasted ventilation), both perfusion and ventilation are reduced, but perfusion is reduced to a greater extent
Lung zones
Zone 1 is apex, 2 is middle lobe, 3 is base
V/Q at base of lung
0.6 (wasted perfusion)
When is ventilation greatest?
base of the lung
When is perfusion greatest?
base of the lung
Pa,PA,PV in Zone 1
PA greater than Pa greater than Pv
Pa,PA,PV in Zone 2
Pa greater than PA greater than PV
Pa,PA,PV in Zone 3
Pa greater than Pv greater than PA
What happens to V/Q with exercise?
With increased CO, apical capillaries vasodilator, V/Q approaches 1.
Relative forms of CO2 transport
1) HCO3- (90%)
2) carbaminohemoglobin (HbCO2) (5%)
3) dissolved CO2 (5%)
carbaminohemoglobin
CO2 bound to Hb at N-terminus of globin (not heme)
Haldane effect
In lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO2 formation; therefore, CO2 is released from RBCs. (shifts equation to the left)
Bohr effect
In peripheral tissue, increased H+ from tissue metabolism shifts curve to right, unloading O2.
Pulmonary vasculature response to high altitude
Chronic hypoxic pulmonary vasoconstriction results in pulmonary HTN + RVH.
Renal response to high altitude
Increased renal excretion of HCO3- to compensate for respiratory alkalosis (this is why acetazolamide is also given for altitude sickness).
Rhinosinusitis pathophys
Obstruction of sinus drainage into the nasal cavity, leading to inflammation and pain over affected area
Sinuses typically affected in rhinosusitis and drainage
Maxillary sinuses, which drain into the middle meatus.
Common bacterial causes of rhinosinusits
S Pneumonia + H influenza + M cattarhalis
Most common area for epistaxis
Anterior segment of nostril (Kiesselach plexus)
Life-threatening hemorrhages location?
Posterior segment (sphenopalatine artery)
Sphenopalatine branches from…
Maxillary artery
Field cancerization
Carcinogen damages wide mucosal area leading to multiple tumors
Virchow triad
Stasis + hyper coagulability + endothelial damage
Endothelial damage and thrombosis mechanism
Exposed collagen triggers clotting cascade
D-dimer characteristics as a test
High sensitivity, low specificity
Homan sign
Sign of DVT. Dorsiflexion of foot –> calf pain.
Acute management of DVTs
unfractionated heparin or low-molecular weight heparins
DVT prophylaxis
unfractionated heparin or low-molecular weight heparins
DVT long-term prevention
warfarin + rivaroxaban
Imaging test of choice for DVTs
compression ultrasound
acid-base disturbance with PEs
Respiratory alkalosis (tachypnic)
What composes lines of Zahn?
areas of pink = platelets, fibrin
red = RBCs
Fat emboli triad
hypoxemia + neurologic abnormalities + petechial rash
amniotic fluid emboli association
DIC
Imaging test of choice for PE
CT pulmonary angiography
Cardiac sequela of obstructive lung disease
Chronic hypoxic pulmonary vasoconstriction can lead to cur pulmonale
Reid index
Thickness of mucosal gland layer to thickness of war between epithelium and cartilage. (NOT just surface area ratio)
Chronic bronchitis diagnosis
Productive cough for greater than 3 months (don’t need to consecutive) for over 2 consecutive years.
CXR in chronic bronchitis
Normal (mucus buildup is etiology)
Centriacinar vs. panacinar emphysema location
centriacinar usually in upper lobes, panacinar frequently in lower lobes.
emphysema pathophys
Increased elastase activity leads to loss of elastic fibers leading to increased lung compliance.
Breathing pattern in emphysema
Exhalation through pursed lips to increase airway pressure and prevent airway collapse.
recoil and compliance in emphysema
Increased compliance, decreased recoil
CXR finding in asthma
Peribronchial cuffing
Inspiratory/expiratory ratio in asthma
Decreased
Bronchiectasis pathophys + presentation
Chronic necrotizing infection of bronchi leading to permanently dilated airways + purulent sputum + recurrent infections + hemoptysis + digital clubbing
FEV1/FVC in restrictive lung disease
greater than or equal to 80%
ILD characteristics
Decreased diffusing capacity + increased A-a gradient
Pulmonary langerhans cell histiocytosis (eosinophilic granuloma)
…
Hypersensitivity pneumonitis hypersensitivity type
Mixed type III/IV
Hypersensitivity pneumonitis presentation
Dyspnea + cough + chest tightness + headache
Pneumoconioses cardiac sequela
Increased risk of cor pulmonale
asbestosis professional RF’s
Shipbuilding + roofing + plumbing
Pathognomonic finding of asbestosis
“Ivory white” calcified, supra diaphragmatic and pleural plaques.
asbestosis association
Increased risk of pleural effusions
Lung region affected in asbestosis
Lower lobes
Lung region affected in asbestosis in berylliosis
Upper lobes
Potential treatment for berylliosis
Occasionally responsive to steroids (granulomatous)
Coal workers’ pneumoconiosis findings
inflammation + fibrosis
Coal workers’ pneumoconiosis lung region affected
Upper lobes
Silicosis professional RF’s
Foundries + sandblasting + mines
Silicosis pathophys
Macrophages respond to silica and release fibrogenic factors, leading to fibrosis
Silicosis and increased TB risk pathophys
Silica disrupts phagolysosomes and impairs macrophages, thus increasing susceptibility to TB.
Silicosis lung region affected
Upper lobes
PaO2/FIO2 in ARDS
decreased
ARDS and fluid overload
no evidence of HF or fluid overload
ARDS associations
SPARTAS: Sepsis, Pancreatitis, Pneumonia, Aspiration, uRemia, Trauma, Amniotic fluid embolism, Shock
ARDS pathophys
endothelial damage leads to increased alveolar capillary permeability, leading to protein-rich leakage into alveoli, leading to diffuse alveolar damage and noncardiogenic pulmonary edema.
ARDS management
Mechanical ventilation with low tidal volumes, address underlying cause.
Initial ARDS damage pathophys
Release of neutrophilic substances toxic to alveolar wall –> activation of coagulation cascade –> oxygen derived free radicals
PaO2 in sleep apnea
Decreased at night, normal during day
Sleep apnea definition
Repeated cessation of breathing greater than 10 seconds during sleep.
Sudden death in sleep apnea pathophys
Nocturnal hypoxia –> systemic/pulmonary HTN –> arrhythmias (atrial fibrillation/fluter)
OSA etiology in adults and kids
Adults –> excess paraparyngeal tissue.
Kids –> adenotonsillar hypertrophy
Central sleep apnea
No respiratory effort due to CNS injury/toxicity, HF, opioids
Obesity hypoventilation syndrome labs
Decreased PaO2 and increased PaCO2 during sleep; increased PaCO2 during waking hours (retention).
Normal mean pulmonary artery pressure
10-14 mm Hg
Pulmonary HTN defined as..
greater than 35 mm Hg at rest
Arterial sequela of pulmonary HTN
Pulmonary arteries..
1) Arteriosclerosis
2) medial hypertrophy
3) intimal fibrosis
Heritable PAH genetics
Inactivating mutation in BMPR2 gene
BMPR2 gene function
normally inhibits vascular smooth muscle proliferation
Other causes of PAH
1) Amphetamines + cocaine
2) connective tissue disease
3) HIV infection
4) portal HTN
5) congenital heart disease
6) schistosomiasis
ID associated with PAH…
schistosomiasis
Microthrombi and pulmonary HTN mechanism
recurrent micro thrombi lead to decreased cross-sectional area of pulmonary vascular bed
fremitus
Vibratory sensation transmitted through the lungs.
Fremitus
1) Increased pathophys
2) decreased pathophys
1) Denser or inflamed lung tissue, eg pneumonia
2) air or fluid in pleural spaces, eg COPD or asthma
tracheal deviation with atelectasis (bronchial obstruction)
Toward side of lesion
Simple pneumo
1) breath sounds
2) percussion
3) fremitus
1) decreased
2) hyperresonant
3) decreased
tracheal deviation in simple pneumo
None
tracheal deviation in tension pneumo
Away from side of lesion
Simple pneumo
1) breath sounds
2) percussion
3) fremitus
1) decreased
2) hyper resonant
3) decreased
Consolidation (lobar pneumonia, pulmonary edema)
1) breath sounds
2) percussion
3) fremitus
1) bronchial breath sounds; late inspiratory crackles
2) dull
3) ***increased
typical organisms in lobar pneumonia
1) s pneumo most frequently
2) legionella
3) klebsiella
Lobar pneumonia characteristics
Intra-alveolar exudate leading to consolidation; may involve entire lobe or lung.
typical organisms in bronchopneumonia
1) s pneumo
2) s aureus
3) H flu
4) klebsiella
bronchopneumonia characteristics
1) Acute inflammatory infiltrates from bronchioles into adjacent alveoli
2) patchy distribution involving more than 1 lobe
typical organisms in interstitial (atypical) pneumonia
1) mycoplasma
2) chlamydia
3) legionella
4) RSV
5) CMV
6) influenza
7) adenovirus
interstitial (atypical) pneumonia characteristics
Diffuse patchy inflammation localized to interstitial areas at alveolar walls; diffuse distribution involving one or more than one lobe.
lung abscess etiology
1) aspiration
2) bronchial obstruction (eg cancer)
lung abscess treatment
Clindamycin
Location of aspiration when upright
Basal segments of right lower lobe
Location of aspiration when supine
Posterior segments of right upper lobe or superior segment of right lower lobe
Sequela of mesothelioma
1) hemorrhagic pleural effusion (exudative)
2) pleural thickening
caveat about mesothelioma
Smoking is not a risk factor
mesothelioma markers
Cytokeratin + calretinin positive
area affected in Horner syndrome
Superior cervical ganglion
pan coast tumor associations
1) hoarseness
2) horner’s
3) SVC syndrome
4) sensorimotor deficit
Physical exam findings in SVC syndrome
1) facial plethora
2) blanching after fingertip pressure
3) JVD
4) upper extremity edema
SVC syndrome etiology
1) Pancoast tumor
2) thrombosis from indwelling catheter
SVC syndrome sequela pathophys
Raised ICP –> headaches, dizziness + increased risk of aneurysm/rupture of intracranial arteries.
Coin lesion on CXR…
lung cancer
non calcified nodule on CXR…
lung cancer
lung cancer mets
adrenals + brain + bone + liver
most common mets to lung
Breast, colon, prostate, bladder
lung cancer caveat
mets more common than primary neoplasms
small cell management
chemo +/- radiation
small cell origin
neoplasm of neuroendocrine Kulchitsky cells
adenocarcinoma genetics
Activating mutations in KRAS + EGFR + ALK.
adenocarcinoma association
Hypertrophic osteoarthropathy
CXR of adenocarcinoma in situ
hazy infiltrates similar to pneumonia.
adenocarcinoma in situ also known as…
bronchioloalveolar subtype
SCC location
hilar mass arising from bronchus
large cell carcinoma management
Less responsive to chemo; surgery.
large cell carcinoma marker
Can secrete beta-hCG
bronchial carcinoid tumor prognosis
Excellent; mets rare
bronchial carcinoid presentation
Symptoms due to mass effect or carcinoid syndrome (flushing, diarrhea, wheezing).
bronchial histology
Nests of neuroendocrine cells + chromogranin A positive.
First generation antihistamines
1) Diphenhydramine
2) dimenhydrinate
3) chlorpheniramine
Second generation antihistamines
1) Loratadine
2) fexofenadine
3) desloratadine
4) cetirizine
Guaifenesin caveat
just thins respiratory secretions; doesn’t suppress cough reflex.
N-acetylcysteine MOA
disrupts disulfide bonds
N-acetylcysteine use
Liquefying mucus in COPD
Dextromethorphan mechanism
1) antagonizes NMDA glutamate receptors
2) synthetic codeine analog
abuse potential of dextromethorphan?
Mild
pseudoephedrine mechanism
alpha-adrenergic agonist
pseudoephedrine SE’s
HTN + CNS stimulation/anxiety
Pulmonary HTN drugs
1) bosentan
2) sildenafil
3) epoprostenol, iloprost
Bosnian mechanism
Competitively antagonizes endothelin-e receptors
How can sildenafil be used for pulmonary HTN?
By inhibiting cGMP, prolongs vasodilatory effect of NO.
epoprostenol, iloprost SE’s
flushing + jaw pain
epoprostenol, iloprost MOA
PGI2 (prostacyclin)
formoterol
like salmeterol
salmeterol, formoterol AE’s
tremor + arrhythmia
1st line for chronic asthma
fluticasone, budesonide (inhaled corticosteroids0
fluticasone, budesonide MOA
1) inhibit synthesis of virtually all cytokines
2) inactivate NF-kappaB
NF-kappaB
TF that induces production of TNF-alpha and other proinflammatory agents
tiotropium vs. ipratropium
tiotropium is long acting
methacoline receptor
M3 agonist
best treatment for aspirin-induced asthma
Montelukast, zafirlukast
Montelukast, zafirlukast mechanism
block leukotriene receptors (CysLT1)
Zileuton SE
hepatotoxic
Zileuton MOA
5-lipoxygenase inhibitor
Omalizumab clinical use
allergic asthma with increased IgE levels resistant to inhaled steroids and LABAs
theophylline MOA
bronchodilator via phosphodiesterase inhibition, leading to increased cAMP levels due to decreased cAMP hydrolysis
theophylline caveats
1) limited usage due to narrow therapeutic index (cardiotoxic + neurotoxic)
2) adenosine
Phosphodiesterase (PDE)
cAMP –> AMP
cAMP respiratory mechanism
bronchodilator
molecules that cause bronchoconstriction
1) ACh
2) adenosine
Phospholipase A2 in arachidonic acid pathway
Converts membrane phospholipids to arachidonic acids
What activates COX-2?
NF-kB
5-lipoxygenase
Arachidonic acid –> 5-HPETE (eicosanoid)
COX-1 action in arachidonic acid pathway
arachidonic acid –> cyclic endoperoxides
arachidonic acid pathway
1) membrane phospholipids –> arachidonic acid –> 5-HPETE –> Leukotrienes
2) membrane phospholipids –> arachidonic acid –> cyclic endoperoxides –> prostacyclin + PGs + thromboxane
Leukotrienes that increase bronchial tone
1) LTC4
2) LTD4
3) LTE4
Dinoprostone
PGE2
Alprostadil
PGE1
Carboprost
PGF2alpha
thromboxane actions
1) increase platelet aggregation
2) increase vascular tone
PGE1 actions
Decreases vascular tone
PGE2 actions
Increases uterine tone
PGF2alpha actions
Increases uterine tone
Prostacyclin (PGI2) action
1) decreases platelet aggregation
2) decreases vascular tone
Pulmonary hypertension characteristic finding
Coronary sinus dilation is a characteristic finding (coronary sinus contains venous blood and communicates freely with the RA and therefore may become dilated secondary to any factor that causes right atrial dilatation).
Causes of transudate
1) increased hydrostatic pressure
2) decreased oncotic pressure
examples of transudate
1) nephrotic syndrome
2) cirrhosis
Conditions that cause exudate
1) malignancy
2) pneumonia
3) collagen vascular disease
4) trauma
* states of increased vascular permeability.
chylothorax
AKA lymphatic effusion
Cause of lymphatic effusion
thoracic duct injury from trauma or malignancy
lymphatic effusion presentation
1) Milky-appearing fluid
2) increased TGs
Pneumothorax
1) breath sounds
2) percussion
3) fremitus
1) diminished
2) hyperresonant
3) decreased
Cause of secondary spontaneous pneumo
1) Diseased lung (eg bullae in emphysema, infections).
2) mechanical ventilation with use of high pressures leading to barotrauma.
Tension pneumothorax
Can be any of other types. Air enters pleural space but cannot exit. Increased trapped air leads to tension pneumothorax.
tension pneumo management
Immediate needle decompression + chest tube placement.
tracheal deviation in tension pneumo
Trachea deviates away from affected lung.
Phases of lobar pneumonia
Hippo with cold in lawn chair/congestion. Red lungs + covered in blood vessels + francis’s climbing all over it/1) congestion (first 24 hrs): red, heavy and boggy lobe + vascular dilation + alveolar exudate contains mostly bacteria.
red hippo in lawn chair/red hepatization. Red lungs + newts crawling around everywhere + big RBCs on the ground + lawn chair covered in fibrin/2) red hepatization (2-3 days): red, firm lobe (liver-like consistency + alveolar exudate contains erythrocytes + neutrophils + fibrin.
Grey hippo in lawn chair/grey hepatization. Grey lobe + disintegrating RBCs on ground + lawn chair covered in fibrin + newts crawling around/3) grey hepatization (4-6 days): gray-brown firm lobe + RBCs disintegrate + alveolar exudate contains neutrophils and fibrin.
Hippo dancing around/4) resolution: restoration of normal architecture + enzymatic digestion of the exudate.
methemoglobinemia presentation
dizziness + dyspnea + confusion + seizures + coma
Complication of nitric oxide administered for pulmonary HTN disease of newborn
methemoglobinemia
Systemic mastocytosis
o Code: Scott Massed: huge cat spewing acid from its mouth behind him/mast cell proliferation in the bone marrow and in other organs, resulting in increased histamine secretion gastric acid hypersecretion. Scott looking like below + flushed face + itching himself intensely + booting everywhere/presentation = pruritis + rash + flushing + GI symptoms (abdominal cramps, nausea, vomiting). Huge nests at top of all the sail boat masts + intestines in the nests/small bowel biopsy = nests of mast cells within the mucosa.
o Location: Boat yard, end of dock near exit from Royal River
Worsening SOB + malaise + continued respiratory symptoms in a patient with pneumonia
pulmonary effusion
CXR of pulmonary effusion
blunting of costophrenic angle + air fluid level.
Physical exam findings of pleural effusion
pleural friction rub on auscultation.
Characteristic finding in severe PAH
Lesions can progress to form plexiform lesions (interlacing tufts os mall vascular channels)
presentation of IPF
insidious onset of dyspnea on exertion + dry cough present for more than 3 months + bibasilar rales clubbing + diffuse reticular opacities.
inflammatory mediators of chronic bronchitis
monocytes + CD8+ T cells + neutrophil infiltration
cough productive of yellow sputum…
chronic bronchitis
common pathogen in smokers with chronic bronchitis
H flu
sputum findings in bronchial asthma
Luke in corner and it’s hailing on him + eoss goddesses wrapped around all the hanging spiral/sputum findings = **eosinophils, which are recruited and activated by IL-5 secreted by TH2 type helper T-cells.
bronchiectasis association
hypertrophic osteoarthropathy (HOA)
leukocoria
White reflex
leukocoria associations
1) retinoblastoma
2) congenital cataracts
ARDS on CXR
bilateral radiographic opacities
Brain abscess RF’s
endocarditis + bronchiectasis + IV drug use
lung abscess presentato
indolent + fever + night sweats + weight loss + cough productive of foul-smelling sputum (indicative of anaerobes).
How do enteric bacteria (e coli + klebsiella + enterococci) cause hepatic abscesses?
Ascend biliary tract
other route of infection to hepatic abscess
portal vein pyemia
How does staph aureus cause hepatic abscesses?
Francis with a blow dart gun shooting seeds at liver/another route of infection = hematogenous seeding of the liver with staph aureus.
pneumoconiosis associated with insulation…
asbestosis/mesothelioma
Mesothelioma histology
tumor cells with long, slender microvilli + abundant tonofilaments
typical pneumonia
♣ Code: Margaret Lawrence: she’s sweating profusely + coughing up sputum all over her chest/presentation = high fever + lobar consolidation + productive sputum. Newts crawling around floor everywhere/these symptoms result from the primary responding immune cell, the neutrophil, which enters area, releases pyrogenic products (fever), causes innocent bystander damage to lung, and creates abscesses (lobar consolidation). /usually EXTRACELLULAR organisms, gram-negatives (1) s. pneumo + 2) H. influ + 3) M. cattarhalis + 4) S. aureus). /lobar infiltrate. Steph in a track suit flashing her tits + prostitutes sitting at table/treatment = empirical ceftriaxone + azithromycine.
♣ Location: Conference room in library first floor
typical pneumonia treatment
ceftriaxone + azithromycine
neonatal atypical pneumonia presentation
crackles + wheeze
cold agglutinins
antibodies (usually IgM) produced in response to certain kinds of infection such as m. pneumoniae.
Relation between lung volume and pulmonary vascular resistance
o Code: huge massive U/graph is U shaped. /This is because high lung volumes (eg following inspiration) increase PVR due to the longitudinal stretching of alveolar capillaries by the expanding alveoli. Decreased lung volumes also increase PVR due to decreased radial traction from adjacent tissues on the large extra-alveolar vessels. /thus, PVR is lowest at the FRC.
o Location: Above DIA
What can you use to measure FRC and RV?
helium dilution technique
Lamellar body or granule
Phospholipids are stored in lamellar bodies and serve as pulmonary surfactant.
