Quiz 2 Flashcards
What is Pulmonary Embolism?
- an occlusion of a pulmonary vessel
- life threatening
- mortality rate as high as 30%
Etiology of pulmonary embolism
DVT - deep vein thrombosis
(Popliteal, femoral, iliac)
Other sources:
Air
Fat - from a broken bone
Amniotic fluid - during delivery
P. Embolism patho
DVT➡️embolus➡️thrombus in arterial bed➡️impaired perfusion
Ventilation: perf imbalance ➡️ hypoxemia
Platelet degranulation ➡️ bronchial and arterial constriction ➡️ hemodynamics instability
Neurally triggered bronchoconstriction
⬇️ CO
L/O surfactant ➡️ atelectasis
RHF
Mnfts of P. Embolism
- depend on size and sight
- usually: dyspnea, tachypnea, chest pain, tachycardia
Dx of P Embolism
- Hx, Px
- ABG
- LDH3 - a lung enzyme lactate dehydrogenase- indicative of cell damage
- D-dimer - a byproduct of breakdown of protein
- lung scan
- CT, MRI
- pulmonary angiogram
Tx of P Embolism
STAT! The larger the vessel, the more problematic
Maintain cardiopulmonary Fx
Thrombolytics, anticoagulants
Address DVT
Pulmonary HTN
Persistent elevation in pulmonary arterial pressure >25mmHg
Pulmonary Circuit Qualities
- Low pressure and resistance (makes the circuit compliant)
- If CO increases, there is minimal increase in pulmonary pressure
- Pulmonary vasoconstriction increases circuit pressure
Pulmonary HTN Etiology
Cardiac and pulmonary disorders
3 categories:
- Increase in pulmonary volume (cardiac septal defects)
- Hypoxemia
- Increase in pulmonary venous pressure (LV dysfx)
Pulmonary HTN Mnfts
- dyspnea
- chest pain on exertion
- syncope
- fatigue
- mnfts of RHF (right sd pumping against resistance)
- RV hypertrophy
- distended pulmonary arteries
Pulmonary HTN Tx
- treat underlying cause
- vasodilators —Calcium Channel Blockers
- —prostacyclin—
- a potent vasodilator
- prevents regurgitation
- anti-thrombolytic
Acute Respiratory Distress Syndrome ARDS
AKA wet lung
- severe progressive damage to alveoli and capillaries
- Rapid onset
- thick layer of impermeable fluid disallowing gas exchange into capillary bed
- up to 60% mortality
ARDS Etiology
Aspiration - near drowning - gastric contents Inhaled gases - NH3 Fat Embolism Severe Burns Drugs - free-base cocaine - heroin - radiation Infections - septicemia DIC (Disseminated Intravascular Coagulation)
ARDS Patho
- Pulmonary and systemic inflm
- lung trauma > neutrophil influx > free radicals, phospholipids and protease release > alveolar and cap damage > increase permb > proteins, cells and fluids enter IS and alveoli > decrease compliance and impaired gas exchange
- Diffuse consolidation
- Surfactant inactivation > atelectasis
- Thick exudate lines alveoli
- Impervious hyaline membrane lines alveoli > no gas exchange
- Profound hypoxemia
ARDS Mnfts
- Severe respiratory distress
- dyspnea
- tachypnea —- early sign
- marked hypoxemia
- early resp alkalosis
- late metb acidosis
- multi-organ failure
ARDS Tx
- Stat intervention—-provide O2
- respiratory support to maintain vital organs
- correct hypoxemia
- reverse underlying cause
- treat complx
(Stabalize pt, treat cause)
Lung Cancer
- Primary and Secondary
- aggressive, invasive, metastic
- leading cause of CA death
- mets to bone, liver, brain
4 major types of Lung CA
- Small cell carcinoma (~12%) SCLC
- Large cell carcinoma (~12%) NSCLC
- Squamous cell carcinoma (~27%) NSCLC
- Adenocarcinoma (~#)%) NSCLC
Lung Cancer Etiology
- Smoking
- genetic predisposition
- toxins (asbestos)
- marijuana
Lung CA Patho in SCLC
- aka oat cell carcinoma
- 99% in smokers
- aggressive, invasive, early mets (esp to brain)
- 70% mets at Dx
- tiny, oval cells (tumors too small to remove Sx)
- paraneoplastic syndromes (Cushing’s, SIADH)
Lung CA Patho in adenocarcinoma
- common form in women and non-smokers
Central > tracheal and bronchi
Peripheral > smaller airways - peripheral origin
Lung CA Patho in squamous cell carcinoma
- Central origin (intraluminal)—-in the bronchi
- impacts mediastinum
- spreads to hilar nodes—-only entrance/exit of lungs associated with structures
- More common in men
Lung CA Patho in large cell carcinoma
- Peripheral origin
- Large, undifferentiated cells
- Early mets
- Poor prognosis
Lung CA mnfts
- based on type, extent, mets, paraneoplastic syndromes
- if central > impact breathing»coughing, wheezing, dyspnea
> cardiac mnfts»tumor causes external pressure
> hemoptysis
> pain»r/t stimulation of nerves
Lung Cancer Dx
- Hx, Px
- CXR, US, CT, MRI
- bronchoscopy, needle biopsy
- sputum/bronchial wash cytology
Lunc CA Tx
- depends on type
- chemo and radiation SCLC
- Sx, radiation, chemo NSCLC
»»»»POOR PROGNOSIS»»»»»
Cystic Fibrosis
- defective chloride channel in cell membrane
- leads to fluid hypersecretion
- GI, resp and reproductive system
CF Etiology
- defective CFTR gene on Chr 7
»_space;»>Cystic Fibrosis Transmembrane Regulator»» - autosomal recessive
CF Patho
- CFTR gene codes chloride channel on cell membrane
- mutation > defective channel > alters CM CL permb
- impaired CL transport across CM
- impact is tissue specific
»»Chloride gets stuck in the secretory cells- making musous thick and sticky. Giving way for infecx and decreased a/w exchange»»
CF Respiratory
- thick, copius mucous > excessive decrease in mucocilliary Fx
- a/w obstructed > ventilation impaired
- bacterial infecx
- > 90% death from severe pulmonary disease