The right branch, because it is straighter. The left one curves more because it has to go around the heart.
trachea-->main stem bronchi-->preterminal bronchiole-->terminal bronchiole-->respiratory bronchiole-->alveoli
What is the functional unit of the lung?
the acinus, which is a respiratory bronchiole and its associated alveolar ducts and alveoli
What are the two types of lung cells that line the alveoli?
Type I pneumocytes cover 90% and do gas exchange, Type II pneumocytes are rounded and granular and secrete surfactant, and undergo hyperplasia when type I cells are injured.
Macrophages and mast cells are also present.
What are the most common causes of congenital pulmonary hypoplasia?
SOL in the uterus, or impaired fetal respiratory movements dt diaphragmatic hernia and renal cystic dz
What is the most common cause of NRDS?
hyaline membrane disease of the newborn
(because of a lack of surfactant, dt born prematurely-before 28 weeks gestation)
What are some possible causes of NRDS?
over-sedation of mother, head injury during delivery, aspiration of blood/amniotic fluid, intra-uterine hypoxemia
What is the pathophysiology of NRDS?
Premature birth (before 28 weeks) means neonate is not producing surfactant, lack of surfactant causes the formation of hyaline membranes
What does NRDS stand for?
Neonatal Respiratory Distress Syndrome
What treatment of the mother can induce formation of surfactant in the neonate?
What's the most common cause of pulmonary edema?
heart failure, esp left ventricular failure in acute: increase in LV filling pressure moves plasma through pulmonary capillaries into alveoli
What are some other causes of pulmonary edema?
--fluid overload: renal failure, iatrogenic (doc gives too much IV fluid)
--hypoalbuminemia: liver dz,nephrotic syndrome, severe malnutrit
--lymphatic obstruction: cancer
--high altitude sickness
--injury to alveolar septal capillaries
--infection (mycoplasma-->atypical pneumo)
--gas inhalation (smoke)
What is a histological sign of longterm pulmonary edema?
alveolar walls lose elasticity-->fibrose & micro-hemorrhage-->iron deposition-->macrophages clean up and are loaded with hemosiderin, these called HEART FAILURE CELLS
What do you call a detached mass carried by the blood away from its site of origin?
Where do most emboli come from?
What are some other materials that form emboli?
air, fat, amniotic fluid, talc or other foreign material, cosmetics, drugs
What do bronchial arteries bring to the lungs?
Which arteries bring deoxygenated blood to the lungs?
Thrombi in the deep veins of the legs or pelvis are common sources of emboli in which arteries of the lung?
large and intermediate pulmonary arteries, most often (x4) in lower lobes
What effect does cancer have on clotting capacity?
What population in the US provides the most plastic surgery customers now?
How does DVT usually present?
not at all, or by history (Virchow's triad for predisposing factors)
S/Sx of a DVT:
--throbbing leg pain (1/3 rule)
--palpable calf cord
--pain w/ pressure to calf
--referred pain w/ dorsiflexion of foot
What are the three components of VIRCHOW'S TRIAD?
--vessel wall injury: trauma, infx, IV's, pressure
--blood stasis: sitting, imobilization, CHF, MI, cardiac valvular incompetence, peripheral venous incomp
--hypercoagulability: cancer (esp pancreatic), polycythemia vera, pneumo, pyelonephritis, OCP, HRT, estrogen, testosterone
What happens to lung tissue when the pulmonary artery is occluded?
--it is ventilated but not perfused-->pt breathes hard but isn't getting any O2 into blood
--tissue usually stays viable dt collateral circ from bronchial artery
--pts with pre-existing compromise to cardio-pulmonary status have high mort rate (~25%)
--otherwise healthy pts go into cardiogenic shock w/ 50-75% of lung parenchyma unperfused-->death in 1-2 hours
Name five things that can kill you in a moment:
--pulmonary embolism (a biggun, ex: a saddle embolus that blocks arterial supply to both lungs)
What part of lung circulation is blocked by fat and amniotic fluid emboli?
--microcirculation: arterioles and capillaries
What syndrome can emboli to the microcirculation initiate?
ARDS (adult resp distress syndrome)-->50-60% mortality, alveolar walls cover with hyaline, membrane of cytoplasmic and lipid remnants from necrotic epithelial cells and fibrin from intra-alveolar edema, not easily resolved.
Where do fat emboli come from?
broken long bones
How often is fat embolism clinically "silent"?
90% of the time
If there are going to be symptoms, how long after the long bone fracture do they appear?
1-3 days, Sx: tachypnea, dyspnea, tachycardia
What fraction of pulmonary emboli result in pulmonary infarction?
less than 10%, and mainly in pts with underlying lung/cardiac dz
What is a typical shape for a pulmonary infarct?
wedge or pie shaped
What are S/Sx of a PI?
--pleuritic chest pain, sound of a friction rub
--severe hypotension if cardiogenic shock
What do you call it when someone has acute alveolar injury, severe & sudden pulmonary edema (diffuse infiltrates in x-ray) and respiratory failure with rapid onset of severe cyanosis?
ARDS, adult/acute respiratory distress syndrome
After what challenges would one suspect ARDS could develop?
--pneumo (Mycoplasma, Pneumocystis, viral, bacterial)
--gastric fluid aspiration
--severel multi-organ damage
--less common: lung trauma, burns, inhaled gases/chems
--disseminated intravascular coagulation
--heroin or methadone OD
--paraquat (on marijuana crops-->birth defects)
What does PIH stand for?
pulmonary hypertension (don't ask me where the I comes from): arterial system becomes resistant to blood flow, increases pressure, primary (ideopathic smooth muscle thickening of medium and small pulm arts-->no lumen, reduced NO production) or secondary
What is the mechanism by which the arteries of the lungs become more resistant to blood flow?
Damaged endothelial cells release cytokines and growth factors that induce the migration of smooth muscles cells to the vessels which thickens the intima and reduces the diameter of the lumen. The endothelial damage also reduces nitric oxide production (EDRF=endothelium derived relaxation factor), and the loss of NO means that the lungs can no longer signal the smooth muscle in the arteries to relax, and the lumen does not dilate. Persistent elevated pressure causes enlargment of the right ventricle, which is called COR PULMONALE.
Who gets more primary pulmonary hypertension?
women 5x more than men
What is the mean age of onset?
What do you call right ventricular enlargement secondary to lung pathology?
What's the difference between primary and secondary pulmonary hypertension? NOT CLEAR ON THIS
--primary means it's due to pulmonary causes, emphysema, sleep apnea
--are cardiac causes primary or secondary??? congential or acquired heart dz can result in PIH dt resistance from the LEFT side of the heart->backup in lungs
--secondary means its due to external influences such as mucltiple recurrent thromboemboli, fen-phen, and the entire arterial system (incl veins & capillaries) may be thickened
What is the greatest single cause of pulmonary hypertension?
the anti-obesity drug combo fen-phen (fenfluramine-phentermine) causes mitral and aortic valve damage and resultant PH (Crotalaria aka bush tea is also implicated)
How do you treat PH?
--not very easily
--O2 and vasodilator drugs
--steroids don't work
--ilprost (like viagra) has shown moderate success (increases prostacycline-->increases NO and decreases inflam)