Respiratory Flashcards
(37 cards)
rhinitis
associated with asthma and eczema
allergic polyps develop in adults - long term allergy
acute epiglottitis
H. flu
inspiratory stridor
scenario - 3 mo old kid dies
- tracheal inflammation - parainfluenza virus
mesothelioma
Psammoma bodies
COPDs
chronic bronchitis
emphysema (for a1-antitrypsin - cirrhosis will develop first and kill the patient, globules will be PAS pos and diastase resistant, diastase breaks down glycogen)
asthma
bronchiectasis
you will see a ventilation/perfusion mismatch
TH2 cells release
IL4 - class switching to IgE IL5 - calls in eos IL10 - inhibits TH1 phenotype, promotes TH2 phenotype
asthma
TH2 cells
restrictive lung diseases
aka interstitial lung diseases
idiopathic pulmonary fibrosis pneumoconioses sarcoidosis hypersensitivity pneumonitis drugs etc.
lobar pneumonia
S pneumo - middle-aged adults and elderly
- treat with penicillin G
Kleb
Legionella
nosocomial - E coli, Pseudomonas, S. aureus
lung consolidation - decreased percussion, increased tactile fremitus, E –> A
(v.s. pleural effusion - decreased percussion ONLY)
bronchopneumonia
S. aureus
H. flu
Pseudomonas aeruginosa - water-loving bacteria, will see this in pt on a respirator in the ICU
Moraxella
Legionella - water-loving bacteria, hyponatremia, knocks out JC apparatus, interstitial nephritis, liver disease
- treat with erythromycin
S pneumo
Kleb - alcoholic, mucoid appearing sputum (Kleb capsule), will cavitate in upper lobes
atypical pneumonia
aka walking pneumonia
Mycoplasma
Chlamydia (- if in newborns, staccato cough)
RSV
CMV - transplant pts
Influenza (+ increased risk for post bac pneumonia)
Coxiella
inflammation of interstitium
sarcoidosis
involves lungs
- uveitis, skin (cutaneous nodules or erythema nodosum)
- salivary and lacrimal glands - mimics sjogrens
pulmonary HTN
familial form - BMPR2 mutations –> increased proliferation of vascular smooth muscle
small cell carcinoma
arises from NE Kulchitsky cells
LABAs
salmeterol, formoterol - used in prophylaxis
ARDS - tremor, arrhythmia
inhaled corticosteroids
fluticasone/budesonide - 1st line therapy for chronic asthma
inhibit synthesis of all cytokines, inactivates NF-kB (which produces TNF-a, etc.)
may cause oral thrush
anti-LTs
-lukast
block LT receptors intracellularly
good for ASA-induced and exercise intolerant asthma
methylxanthines
theophylline
causes bronchodilation by inhibiting PDE —> increased cAMP, blocks actions of adenosine
narrow therapeutic index (cardiotox, neurotox)
metabolized by CYP450
ventilation/perfusion
both perfusion and ventilation are greater at the bases
- perfusion > ventilation in lower lobes - infarcts occur in the lower lobes
- why is ventilation greater at the bases? - at the end of expiration, alveoli are filled with air (and less compliant)
- during inspiration - additional air is directed to the lung apex, alveoli there are more compliant - V/Q ratio decreases as you go down the lung - perfusion increases more than ventilation
ventilation greater at apex (? goljan)
- Tb reactivates in the apex - aerobe
zone are formed because of gravity’s effects on blood flow (all zone 3 when supine)
zone 1: alveolar pressure > arterial pressure > venous pressure
- zone 1 forms during hemorrhage, high alveolar pressure (pos-P ventilation)
zone 2: arterial pressure > alveolar pressure > venous pressure
- blood flows in a pulsatile fashion - arterial pressure rises during systole so capillary (..venous) pressure can overcome alveolar pressure
zone 3: arterial pressure > venous pressure > alveolar pressure
A-a gradient
normal = 5-15
> 30 = something is wrong in the lungs
- high specificity
depression of respiratory center will NOT increase A-a gradient
- ALS, Guillan-Barre, barbiturates
- but you will have hypoxemia
PAO2 = PO2,inspired - PCO2/0.8
triad asthma
scenario: 35 yo woman with chronic headaches or fibromyalgia - point is she has pain
pt develops occasional bouts of asthma - mechanism is LTC,D,E4 are still formed
- non-type1 HSR asthma
triad = ASA + asthma + nasal polyps
anabolic steroids
produce benign liver cell adenomas - tendency to rupture
- well-built male who presents with liver/intraparenchymal hemorrhage
vocal cords
1) false vocal cords - squamous epithelium
2) commisure
3) true vocal cords - ciliated pseudostratified columnar epithelium
laryngeal carcinoma - 1 smoking, 2 alcohol (synergism - do both, develop carcinoma faster)
- hoarseness of throat
hyaline membrane disease
aka RDS
massive atelectasis
causes - prematurity (surfactant production peaks at 32-35 week)
corticosteroids, thyroxine, and prolactin all increase surfactant production
C-section produces respiratory distress syndrome - absence of stress - ACTH and cortisol are not increased –> surfactant is not being made
NRDS - often will have PDA (because of hypoxemia, machine-like murmurs)
- ventilation defect - lungs wont open
- shunt problem
- treat with PEEP therapy
hyaline membranes are due to degeneration of type 2 pneumocytes - fibrinogen leaks through membrane
ARDS - neutrophil related injury
- neutrophils destroy type 2 pneumocytes and capillaries
- most common cause is septic shock ( E coli)
(- side note - septic shock is the most common cause of DIC)
type 2 pneumocytes
contain lamellar bodies - pump out surfactant
