Test I: Pumlonary Part I Flashcards
What factors are required in order to maintain adequate respiration?
Adequate intake of air
Rapid diffusion on alveolar ducts/walls
Adequate Perfusion
What is the functional unit of the lung?
Acinus: consists of the respiratory bronchiole, alveolar ducts and alveoli.
Where is the blood air interface?
The space between the endothelium and the type-1 pneumocyte.
Which lobes of the lungs hold the most air?
Upper
Spots found in the upper lung are thought to be……
TB or Cancer
When lungs begin to fill with fluid or blood what will be noticed on a chest xray?
Costo-phrenic angles will start to get blunted. Base of the lungs will be appear white on X-ray.
What are the classical classifications of pulmonary pathology? (4)
Degenerative
Inflammatory
Neoplastic
Pleural
This congenital defect involves defective development of one or both lungs and is found in 10% of neonate death autopsies.
Pulmonary Hypoplasia
What is the most common type of tracheo-esophageal fistula? (TE Fistula)
Esophageal Atresia and Distral TE Fistula (77%)
What is the primary defect of NRDS (Neonatal Respiratory Distress Syndrome)?
Lack of surfactant, which means lungs won’t open and wind up filling with fluid. AKA: Hyaline membrane disease.
Incidence of NRDS is ________ proportional to gestational age.
Incidence of NRDS is inversely proportional to gestational age.
Incomplete expansion or collapse of the lung is an anatomical/physiologic/geometric concept called….
Atalectasis (often due to failure to breathe deeply)
Atalectasis (incomplete expansion) can occur from…..(3)
Reabsorption (bronchial obstruction like tumor)
Compression (from pleural effusion)
Contraction (diffuse lung fibrotic process)
Accumulation of fluid in the lungs leading to impaired gas exchange
Pulmonary Edema
Pulmonary edema is generally due to either _______ or ________.
Pulmonary edema is generally due to either failure of the heart to remove fluid from lung circulation “cardiogenic pulmonary edema” or direct injury to the lung parenchyma “noncardiogenic pulmonary edema”.
Additional causes of PE include
Fluid overload (iatrogenic: IV fluids given too fast)
Lymphatic obstruction (cancer)
Injury to the capillaries of the alveolar septae
Infections agents
Liquid aspiration
Gas inhalation (too much oxygen, smoke)
Chemotherapeutic agents
What is HAPE
High Altitude Pulmonary Edema: damage to endothelium due to hypoxia from low oxygen in the air.
Why does hypoalbuminemia (liver disease, nephrotic syndrome) cause PE?
Oncotic pressure is necessary to hold plasma in the vascular space.
What is the worst thing about a lung transplant?
The first time you cough it’s not your phlem. hahahaha
What are the 4 main pathologic mechanisms of pulmonary edema?
Increased venous pressure
Increased oncotic pressure
Lymphatic obstruction
Alveolar injury
In PE gas exchange is compromised because _______breaks the structure of the ____________ cells and fluid entering the ________ spaces reduces or halts ____________.
In PE gas exchange is compromised because interstitial fluid breaks the structure of the alveolar epithelial cells and fluid entering the alveolar spaces reduces or halts gas exchange.
Acute PE is usually due to __________.
Acute PE is usually due to left ventricular failure.
In which form of PE may there be an absence of pain and sx?
Chronic PE
Acute PE s/sx:
Tachypnea (rapid breathing)
Extreme dyspnea (shortness of breath SOB)
Restlesness and anxiety (sense of suffocation)
Bronchospasm and wheezing (cardiac asthma)
Pronounced lung markings heading up towards the head =
Pronounced lung markings in the correct pattern, but exaggerated =
Pronounced lung markings heading up towards the head = ACUTE PE
Pronounced lung markings in the correct pattern, but exaggerated = CHRONIC PE
In chronic PE alveolar walls become _______
fibrotic (Alveolar walls lose their elasticity)
Alveolar fluid may act as a culture medium for bacterial growth: Acute or Chronic?
Chronic
Chronic PE is common with what other condition?
Congestive Heart Failure Chronic PE: micro-hemorrhages occur, macrophages phagocytize iron from micro hemorrhages - heart failure cells
What is a non-specific pattern of lung injury called?
ARDS: Acute Respiratory Distress Syndrome
ARDS results in exudate leaking into the alveoli: cardiogenic or non-cardiogenic?
Non-cardiogenic, meaning much more than transudative fluid leaks into the alveoli: fibrin, protein and cells all leak in, resulting in exudate (protein rich)
ARDS results in severe acute lung injury (ALI). What is the process that leads to death of lung cells?
- low blood oxygen (due to microscopic clots: microthrombi)
- increased permeability of pulmonary blood vessels
- fluid accumulation in the lungs
- death of epithelial and endothelial cells
What are some common causes of ARDS?
Sepsis
Widespread lung infections (pneumonia, TB)
Gastric aspiration
Mechanical trauma (lung/head)
Multi-organ failure
Burns from inhaled gases/chemicals
In 20% of ARDS cases there are no identifying risk factors. This is called _______
Interstitial pneumonia
Damage to type 2 epithelial cells, resulting in decreased surfactant production is due to……..
Damage to type 2 epithelial cells, resulting in decreased surfactant production is due to……..hyaline membranes becomes covered with protein-rich fluid and dead alveolar epithelial cells.
Which cells are common in many lung pathologies, especially ARDS?
Neutrophils: produce pro-inflammatory products and eat elastin.
What is the mortality rate of ARDS?
30-70%
How does ARDS resolve?
- Resorption of the fluids and removal of debris by alveolar macrophages
- Replacement of epithelial cells with new functional cells
- Restoration of capillary endothelial cells
Losing elasticity of the lung = ________ = less gas transfer.
Xrays will look more or less opaque?
Losing elasticity of the lung = restriction = less gas transfer.
Xrays will look more opaque, with a ground glass appearance
_________ = air trapping and wheezing in the (large or small?) airways.
Obstruction = air trapping and wheezing in the small airways.
Is obstruction a problem of inspiration or expiration?
How will X-rays look?
Expiration
Hyper-expansion on X-ray (Lucency and density)
What appearance will restriction have on X-ray?
Ground glass (Opacity and density)
What is the main problem with restriction?
Reduced gas transfer.
Restrictive Airway Disease (decreased capacity, normal flow rate) has two major classes. What are they?
Chest wall disorders: poliomyelitis, severe obesity, pleural diseases and kyphoscoliosis
Acute or chronic interstitial and infiltrative diseases: ARDS, dust inhalation, interstitial fibrosis, pneumoconiosis
What is the difference between reactive airway disease and restrictive airway disease?
Reactive = sudden bronchial restriction and wheezing
Restrictive = diminished elasticity of the lung = reduced expansion and total lung capacity
What are the 3 main diseases of COPD (4th most common cause of morbidity and mortality in the US?
Chronic Bronchitis —> Emphysema
Asthma
Bronchiectasis
What does Asthma do to the airspaces in the lung?
Irreversible enlargement of the airspaces distal to the terminal bronchiole.
Is fibrosis seen in obstructive or restrictive lung diseases?
Restrictive
What are the characteristics of centrilobular emphysema?
Central acini affected but distal unharmed
More severe in upper lobes
Predominately in heavy smokers
What are the characteristics of panacinar emphysema?
Acini uniformly enlarged
More severe in lower lobes and anterior aspect of the lungs
Alpha 1 antitrypsin deficiency is present in Centrilobular or Panacinar emphysema?
Panacinar
Emphysema presents with increased numbers of what cells (3)?
Macrophages
T lymphocytes
Neutrophils
In emphysema activated inflammatory cells release……(3)
Leukotriene
IL-8
TNF
Alpha 1-antitrypsin normally presents in serum, tissue fluids and macrophages. What does it do?
Inhibits proteases (esp. elastase)
_______ and _______ inhibit Alpha 1-antitrypsin, allowing cellular proteases like elastase to cause tissue damage.
Oxidants and free radicals (found in smoke) inhibit Alpha 1-antitrypsin, allowing cellular proteases like elastase to cause tissue damage.
Nicotine and ROS in smoke activate ______
Nicotine and ROS in smoke activate NF-kB
NF-kB turns on genes that encode ______ and _____, which attracts and activates ________ (cell type), which release granules rich in ________ which damage lung tissue.
NF-kB turns on genes that encode TNF and IL-8, which attracts and activates neutrophils, which release granules rich in elastases which damage lung tissue.
Smoking also enhances elastase activity in _________(cell type).
Smoking also enhances elastase activity in macrophages.
_________ from macrophages and neutrophils also destroys lung tissue.
Metalloproteinase (MMP) from macrophages and neutrophils also destroys lung tissue.
What are the antioxidants normally found in the lung that are depleted by tobacco smoke? (2)
Superoxide dismutase
Glutathione
Emphysema manifests after at least _____ of functioning of the lung has been lost.
Emphysema manifests after at least 1/3 of functioning of the lung has been lost.
What, shown here, is a hallmark of COPD that can often lead to a pneumothorax?
Blebs or bullae whose walls are paper thin and easily rupture, forming a pneumothorax.
What are symptoms commonly found in emphysema patients who don’t have a history of chronic bronchitis?
Weight loss
Barrel-chested (hunched over)
Limited expiratory airflow
Pulse ox normal
Pts. over ventilate PINK PUFFER
Develop cor pulmonale and CHF
- Cor pulmonale is failure of the right side of the heart brought on by long-term high blood pressure in the pulmonary arteries and right ventricle of the heart.
Death often due to
Respiratory acidosis and coma
R sided heart failure (collapse of lungs due to pneumothorax)
Chronic Bronchitis is defined clinically by persistent cough with sputum production for at least ____ months in at least ____ consecutive years in the absence of any other identifiable cause.
Chronic Bronchitis is defined clinically by persistent cough with sputum production for at least 3 months in at least 2 consecutive years in the absence of any other identifiable cause.
Etiology of chronic bronchitis is due to:
tobacco smoke
breathing smog dust from grains, cotton and silica
What is the major morphology of chronic bronchitis?
Hyper-secretion of mucus.
Cigarette smoke predisposes to infection b/c of loss of ciliary function of the epithelium = mucus production = inhibition of bronchial and alveolar macrophages.
In chronic bronchitis, there is increased mucus production because of increased number of ______ cells; proteases _____ and _____ released from _________ (cell type) stimulate hyper-secretion.
In chronic bronchitis, there is increased mucus production because of increased number of goblet cells; proteases MMP and Elastase released from neutrophils stimulate hyper-secretion.
Can you see acute bronchitis on Xray?
No. In acute bronchitis you hear honks and wheezes which clear with coughing.
What are the 4 classical histological findings in bronchial asthma?
1) Inflammation
2) Bronchial (luminal) narrowing
3) Increased mucous (looks like chronic bronchitis)
4) Smooth muscle hyperplasia
If the asthma etiology is from allergy what other histological finding will there be?
Eosinophils.
Chronic bronchitis has sputum production, where Asthma has ______.
Chronic bronchitis has sputum production, where Asthma has wheezing and no sputum.
A hallmark of asthma is increased or decreased airway responsiveness to a variety of stimuli?
A hallmark of asthma is increased airway responsiveness to a variety of stimuli. This leads to bronchoconstriction/spasm, inflammation and increased mucus production.
What is status asthmaticus?
Unremitting asthma attacks
What is asthma hygiene theory?
Incidence of asthma is lower in populations exposed to an abundance of microbes.
Which type of asthma is most common, atopic of non-atopic?
Atopic: Type I IgE mediated, often begins in childhood
What is Sampter’s triad? (Hint: involves aspirin)
Asthma
Rhinitis and nasal polyps
Hives
Exposures to caustic agents from fumes, dusts , gases or chemicals are triggers for ___________ asthma.
Occupational
Exercise induced asthma may be due to extreme sensitivity to changes in _________ and ________ of air entering the lungs.
Exercise induced asthma may be due to extreme sensitivity to changes in humidity and temperature of air entering the lungs. (exercise induced asthma lacks inflammatory changes)
What are the early phase characteristics of asthma (3)?
Bronchoconstriction
Increased mucus production
Vasodilation/increased vascular permeability
In the late phase of asthma secretions of _____ cells, _______ cells and T cells recruit _________, _________ and T cells, causing inflammation.
In the late phase of asthma secretions of mast cells, epithelial cells and T cells recruit eosinophils, neutrophils and T cells, causing inflammation.
What chemo-attractant and activator of eosinophils is produced by airway epithelium?
Eotaxin
Over time, asthma changes the structure of the bronchial wall by hypertrophy and hyperplasia of both the ______ layer and the ______ glands.
Over time, asthma changes the structure of the bronchial wall by hypertrophy and hyperplasia of both the muscle layer and the mucus glands.
Does asthma cause increased or decreased airway vascularity over time?
Increased
What are triggers of asthma?
Irritants
Cold air
Stress
Exercise
Infections
What are the gross morphologies of asthma? (3)
Mucus plugs: occlude bronchi and bronchioles
Hyperinflation of the lungs
Bronchoconstriction
