Pulm Patho Flashcards
dyspnea
difficult of painful breathing
orthopena
easier breathing while up right, difficult lying down. (usually a sign of pulm edema or pulm effusion)
parxoysmal nocturnal dyspnea
attacks of SOB at night
kussmaul resp
rapid deep breaths (running to class); blowing out CO2, if doing this at rest- compensation for metabolic acidosis (often ketoacidosis)
Cheyne-Stokes resp
sign that patient is going to die; brain stem damage (NTS not working properly) O2 plummets during apnea, O2 detector sends alarm message to NTS resulting in fast, deep rapid breaths, alarm turns off, apnea, rapid respirations, apnea, etc. (alternating apnea and tachypnea)
hypoventilation
hypercapnia-high PaCO2–respiratory acidosis
hyperventilation
hypocapnia–low PaCO2–resp alkalosis
hypoxemia
low O2 tension
low O2 sat
Hypoxia
low O2 content one cause is hypoxemia, another is anemia
clubbing
enlargement of the distal ends of fingers due to chronic hypoxemia
hemoptysis
coughing up blood
pain with breathing
usually pleuritic causing rubbing of visceral and parietal pleura
acute resp failure
inadequate gas exchange
ex: dive into pool and can’t swim
pulm edema
most common, most acute
excess fluid in interstitium or alveoli
- most common: increased vascular pressure ex: 2nd to heart failure: Increased pulmonary venous pressure due to left-sided heart problem → edema
- most acute: increase permeablility ex: injury to capillary endothelia cells ex: ARDS: Injury to capillary endothelium → inflammation → increased vascular permeability → water gets into lumen of alveoli due to vascular permeability → Fluid (water) not good substitute for surfactant → some alveoli hyperventilate, some collapse
Atelectasis
collapse of lung tissue (failure to ventilate alveoli)
Compression-compression of alveoli but something heavy
Absorption-obstructed airway and gas absorption alveoli shrivel up.
Bronchiectasis
chronic abnormal dilation of bronchi
Bronchiolitis
inflamm obstruction of bronchioles
Pneumothorax 4
gas in the pleural space
- open pneumothorax: rib wants to go out, lungs want to go in; stick knife or syringe into patient so that gas can fill vacuum, chest will go up, lungs will go down and air will fill in the middle
- tension: as we are expanding lung, as we inhale more gas into area, exhalation can’t get it out: pneumothorax increases with each inhalation
- spontaneous: idiopathic
- secondary pneumothorax: caused by other lung problem
Pleural effusion 5 types
fluid in pleural space
1 Transudative – low protein content (usually systemic problem, e.g. heart failure) pressure problem
2 Exudative – high protein content (usually local inflammation) permeability problem ex: CA or infection
3. Hemothorax – blood in pleural space
4. Chylothorax – lymph in pleural space
5. Empyema – pus in pleural space: results in orthopnea; if standing, fluid accumulates at bottom
mechanical problems with chest wall
chest wall restriction- impairs breathing
flail chest- fractured ribs interfere with normal ventilation
Restrictive lung disease
Loss of compliance: difficulty opening up lungs → difficulty getting air IN
Decreased FVC
1Acute intrinsic: (pulm edema) ARDS
2Chronic intrinsic: (diseased lung parenchyma) pulm fibrosis
3Chronic extrinsic: 9chest wall, intra-bad and neuromuscular disease) spinal cord damage
4Disorders of Pleura and Mediastinum
PNA
Many!
Fibroblasts lay down collagen, thicker membrane impairs gas exchange and makes lung less compliant although maintains good recoil
Obstructive lung disease
Difficulty getting air OUT loss of recoil or obstruction of airways; decreased FRV1/FRC, decreased FEV1: amount of air getting out quickly is highly decreased Asthma COPD -dyspnea and wheezing
Resp tract infection
PNA-6th most common cause of death in US
bacterial (most common ex: strep) and viral
TB
Acute bronchitis
Abscess formation in cavitation- often result of PNA
Cystic fibrosis
genetic
pulm vascular disease
pulm embolism
pulm HTN
Cor pulmonale: right-sided heart failure due to lung problem
Lung CA
Non-small cell lung cancer: Squamous cell carcinoma, Adenocarcinoma, Large cell carcinoma,
Small cell carcinoma
Asthma
Triggered by allergen or irritant exposure → immune activation/mast cell degranulation
want to get irritant out of lung so you want conductive airways to get smaller to help, but in asthma, this is over-reactive,
*airways over-constrict → bronchoconstriction/spasm + immune mediated damage to airways → asthma
Tx: Epinephrine: vasodilator,
S/S: recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and in the early morning.
What is the strongest identifiable predisposing factor for developing asthma
Atopy- the genetic predisposition for the development of an IgE- mediated response to common aeroallergens.
COPD: simple answer
Chronic Obstructive Pulmonary Disease
Combination of chronic bronchitis and emphysema
Both cause obstructive pulmonary disease
Chronic Bronchitis
inflamed and mucus-filled bronchi
large airway: trachea, bronchi: have mucus hypersecretion, inflammation
sm airways: peribronchiolar fibrosis
airway obstruction
*chronic infection
chronic productive cough, last for at lease 3 months of the year for at least 2 years
mucus is thicker
Emphysema
walls between alveoli are damaged and alveoli blow up to big balloons instead of clusters of little balloons which causes loss of surface area for gas exchange,
lung loses recoil elasticity because elasticity came from septa between alveoli
lose recoil so can’t get air out, need to increase intrathoracic pressure to exhale
**Loss of Elastic Recoil
-centriacinar
-Panacinar
COPD risk factors
Cigarette smoking Passive smoking? Ambient air pollution? Hyper-responsive airways ? Occupational factors? Alpha1-antitrypsin deficiency: Only known genetic abnormality that leads to COPD < 1% of cases
Characteristic Changes in Restrictive Lung Disease
(Normal VC is >70ml/kg.)
All lung volumes have decreased (total lung capacity, RV, VC, RVC)
Lost compliance: Harder to get in air, but easy to get air out once you get it in
FEV1 decreased because lung is smaller
Normal:
Expiratory flow rates
ratio of FEV1/FVC is normal
Inherited a-1 antitrypsin deficiency
basically break down elastin too fast lose recoil
Antitrypsin -trypsin-elastate-elastin
elastase and elastin need to be the same amt., make and break down–want elastin to be fresh so constantly replace.
Trypisn breaks down elastase, if don’t have enough then elastase breaks down elastin too fast.
Antitrypsin breaks down trypsin so don’t have enough with this inherited deficiency then don’t break down trypsin…..rats i hate rats they drive me crazy…
Absorption Atelectasis
caused by lack of collateral ventilation through pores of Kohn
-plugged alveoli can be ventilated still with deep breathing…opens pores of Kohn
Restrictive disease
inspiration is limited-reduced compliance of lung or chest wall= stiff lungs
reduction in lung compliance= increased WOB, Dyspnea
Rapid, shallow breathing pattern= increased dead space ventilation
*normal gas exchange
until advanced disease-increased PaCO2, decreased PaO2 with pulm HTN and Cor pulmonale
Pulm edema
Fluid leakage from the intravascular space into the lung interstitium and alveoli caused by:
1 Increased capillary/hydrostatic pressure: (example: cardiogenic, valcular dysfunction, coronary artery disease, LV dysfunction– lead to increased L atrial press–increase pulm capillary hydrostatic press
2 Increased capillary permeability: endothelium–increased capillary permeability and disruption of surfactant production–mvmt of fluid and plasma proteins from capillary to interstitial space and alveoli
*both CXR will show bilateral symmetrical opacities
