Pulm Flashcards
A-a gradient
Greater if you have primary lung disease. Ventilation defect, perfusion defect, diffusion defect.
Nasal polyps
Allergic is most common. In a KID, NEVER. Allergic polyps develop in adults that have chronic. In child, THINK CYSTIC FIBROSIS. Triad asthma - ASA or NSAID –> asthma + nasal polyps. Middle-aged woman with chronic pain syndrome develops asthma = NSAID. Mech - blockage of cyclooxygenase -> shunting to the lipoxygenase pathway LTC, D, E4 are BRONCHOconstrictors -> asthma. NOT a HS-1.
Laryngeal carcinoma
True - pseudo stratified columnar; False - squamous. Etios - smoking, alcohol. Synergistic RF’s. True for ANY squamous cancer (mouth, upper esophagus).
Epiglottitis
Inspiratory stridor. Haemophilus influenzae.
Croup
Parainfluenza. TRACHEAL inflammation.
Hyaline membrane disease = RDS
COLLAPSED alveoli. MASSIVE atelectasis. WHY? Surfactants (lecithins, phosphatidylcholine, phosphatidylglycerol) are deficient b/c collapsing pressure = Surface tension / radius. On expiration, airways get smaller, increased collapsing pressure -> atelectasis unless surfactants DECREASE surface tension. Etios = Prematurity (surfactant synthesis poor; tx = glucorticocoids to mom to stimulate synthesis; THYROXINE is another, Prolactin does too). Etios = Diabetes (mom) -> hyperglycemia -> baby increased insulin -> DEC. surfactant. Etios = C-Section -> stress is MISSING -> NO ACTH and cortisol -> LESS surfactant.
Why macrosomia in babies of gestational diabetics?
Baby’s insulin is increased. Insulin INCREASES fat storage (TG synthesis and deposition). Most adipose is central. Insulin leads to uptake of aa’s in muscle. Hypoglycemia when they’re born.
RDS commonly have PDA?
Hypoxemia
Hyaline membrane
Degeneration of type 2 pneumocytes. Leakage of fibrinogen.
ARDS
PEEP therapy in order to uncollapse the alveoli + surfactant.
Lamellar bodies
CONTAIN surfactant. EM picture. Type II pneumocytes.
ARDS
Same as RDS in pathophysiology. But usually a NEUTROPHIL-related injury. Etio = septic shock (most common is E. coli 2/2 indwelling). Neutrophils in the lung -> destroying type I/ii pneumocytes -> MASSIVE atelectasis. Leaky capillary syndrome 2/2 neutrophils -> protein and fibrinogen -> hyaline membranes in ARDS.
Spontaneous pneumothorax
Etio - most common is ruptured sub pleural bleb -> collapse of that part of the lung b/c lose negative intrapleural pressure. Trachea deviation toward side + up diaphragm
Tension pneumothorax
Most commonly due to knife injuries, gunshot wound. Tear of pleura that is a FLAP. Air goes in but can’t LEAVE out. Pushes lung and mediastinum to the other side. Compression atelectasis. Pushes on VC, RV -> compromised blood flow. Diaphragm pushed DOWN.
Pneumonia
Typical and atypical. Typical - sudden onset. Atypical - slow and insidious onset. Community acquired and nosocomial.