| ☉A-a gradient ↑ |
→shunting, V/Q mismatching, CHF
→High gradients result from impaired diffusion or, more commonly, by
ventilation-perfusion inequality of the "shunting" variety. A normal A-a
gradient is less than 10 torr. The age (years) / 4 + 4 is another
conservative estimate of a normal gradient.
→The calculations above assume 100% humidity at sea level and a
respiratory quotient of 0.8, using the alveolar gas equation to determine
PAO2:
PAO2 = ( FiO2 * (760 - 47)) - (PaCO2 / 0.8)
A-a gradient = PAO2 - PaO2 |
| ☉Asthma |
（ABS煞車） A: Anticholinergic: Atronvent(Ipratropium)
B: beta-2 agonist: Bricanyl(Terbutaline)
S: steroid
→pure TH2 response (elevated IL-4 and IL-5), IL-13
→inhibitory: IL-10 |
| ☉Flowmetry |
FEV1/FVC RV TLC
Obstructive: ↓ ↑ ↑
Restrictive: ↑ ↓ ↓
|
| ☉Aspiration pneumonia |
bil. upper lobe: post, sup segments
|
| ☉ARDS→criteria |
→criteria set forth by the American-European Consensus Conference:
Acute onset
Bilateral infiltrates
Pulmonary artery wedge pressure less than 19 mm Hg (or no clinical signs
of congestive heart failure)
PaO2/FIO2 ratio less than 200 (ARDS) or less than 300 (acute lung injury
[ALI]): ALI is a milder clinical expression of the injury of ARDS that may
or may not progress to ARDS.
|
| ☉ARDS→Causes: |
Infection - Pneumonia of any etiology (especially viral) and systemic
sepsis (especially gram negative)
Shock - Any type, particularly septic and traumatic shock
Aspiration - Gastric contents, near drowning, and toxic inhalation
Trauma - Pulmonary contusion, fat embolization, and multiple trauma
Other - Systemic inflammatory response syndrome, pancreatitis,
postcardiopulmonary bypass, massive blood transfusion, drug ingestion (eg,
heroin, methadone, barbiturates, salicylates) |
| ☉Paraneoplastic syndrome: |
SCLC: hypercalcemia, L-E MG→→化療為主：EP: etoposide(leukemia, BM supression),
cisplatin（腎耳神經毒）
NSCLC: SIADH, Cushing, Acromegaly→→手術為主，Iressa
|
| ☉Hamartoma |
→Echo: high intensity ←→CT: low density
→third most common cause of a solitary pulmonary nodule followed by
granuloma and neoplasm.
→composed of mesenchymal and epithelial tissues. Cartilage is generally
the dominant mesenchymal component and exhibits variable degrees of
calcification and ossification. Fat or myxomatous connective tissue may
also be a prominent tissue component. |
| ☉Pleural tail sign |
（魔鬼的尾巴）
desmoplastic reaction in the septa of the lung, producing a linear strand-
or bandlike density between a peripheral, subpleural pulmonary nodule and
the pleura. Causes include bronchogenic carcinoma, bronchioalveolar cell
carcinomatosis and granulomatous disease. The sign is not therefore useful
in differentiating benign and malignant processes. |
| ☉popcorn -like calcification |
（善良的玉米）
Hamartoma of the Lung:3rd common benign |
| ☉Oxygen |
Nasal canula: 5L/min=40%
simple mask: 60%
NRM: 100% |
| ☉TB Risk factors: |
1. primary infection include poverty and crowded, poorly ventilated living
conditions.
2. for reinfection include ★★gastrectomy, uncontrolled diabetes mellitus,
opportunistic infections, Hodgkin's disease, leukemia, corticosteroid
therapy, and immunosuppressant therapy.
|
| ☉Anti-TB drugs: |
H: INH→Peripheral neuritis, hepatitis→Pyridoxine(Vit B6) prophylaxis
E: EMB→Optic neuritis(red/green color, VA↓)→（EMB：EYE）
R: RIF→Hepatitis →Orange urine, secretions（RIF： RED）
Z: PZA→Hyperuricemia, hepatotoxicity →（尿酸結晶成金字塔）
Streptomycin:(Aminoglycoside) 腎耳毒性
→→E, Z: only bacteriostatic（一點都不EZ）
|
| ☉Allergic bronchopulmonary aspergillosis(ABPA) |
→common complication of cystic fibrosis (CF)
→pathogenesis is dependent upon impaired clearance and dense respiratory
epithelial exposure to A fumigatus (Af) spores with subsequent chemotactic
recruitment of CD4+ Th2 lymphocytes specific for Af to lung tissue.
→Susceptibility to ABPA appears to involve risk factors including atopy
and defined major histocompatibility complex-restricted alleles. Distinct
cytoplasmic Af molecules (Af2, 4, and 6), now available as recombinant
allergen reagents, appear to be associated with ABPA.
→Minimal criteria for diagnosis of ABPA in CF include clinical
deterioration(Asthma! wheezing, low-grade fever, and coughing up of
brown-flecked masses or mucus plugs), elevated total serum IgE, positive
immediate Af skin test or serum IgE antibodies, and Af serum
precipitins/IgG antibodies or radiographic changes(widened airways often
plugged with mucus)
→Annual screening of total serum IgE is recommended from age 6 yr.
Systemic glucocorticosteroids remain the mainstay of treatment.
Itraconazole has an established role as a steroid-sparing agent if the
patient has a slow or poor response to steroids, relapses, or is at risk
for or develops steroid toxicity. |
| ☉oxyhemoglobin dissociation curve |
shift to the right
CO2, H+, BT, 2,3-DPG(pregnancy: 30%)↑↑ |
| ☉Carbon monoxide intoxication |
→quickly binds with hemoglobin with an affinity 200 to 250 times greater
than that of oxygen to form COHb
→decrease in arterial oxygen content and shift of the ★oxyhemoglobin
dissociation curve to the left
→toxic effects of carbon monoxide cannot be explained by this process
alone. COHb levels do not correlate well with symptoms or outcome, and
this process cannot account for the phenomenon of delayed neurologic
sequelae
→intracellular uptake of carbon monoxide is a mechanism for neurologic
damage. When carbon monoxide binds to cytochrome oxidase, it causes
mitochondrial dysfunction that results in oxidative stress. The release of
nitric oxide from platelets and endothelial cells, which forms the free
radical peroxynitrite, can further inactivate mitochondrial enzymes and
damage the vascular endothelium of the brain. The end result is lipid
peroxidation of the brain, which starts during recovery from carbon
monoxide poisoning. With reperfusion of the brain, leukocyte adhesion and
the subsequent release of destructive enzymes and excitatory amino acids
all amplify the initial oxidative injury. |
| ☉Chylothorax: |
Chylothorax: TG ↑↑, chylomicron →→tumor, trauma
Pseudochylothorax: CHO ↑↑, cholesterol chrystal →→TB, nephrotic syndrome
|
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