review Flashcards
what happens to the airways in bronchiectasis?
they are permanently dilated and instead of seeing tapering of them we actually see them get bigger
mecocium ileus
clinical feature of CF
laboratory CF
- sweat chloride
- genetic testing for CTFR
- nasal trnasepithelial potential difference
CF tx.
- chest physical therapy
- antibiotics
- nebulized DNase
- Nebulized 7% saline
- bronchodilators but not an anti-cholinergic which causes slowing of the gut
no benefit for CF tx.
- inhaled steroids
prednisone in CF
benefit but risk outweighs as well as nsaids
hallmarks of asthma a
- airway inflammation
- airway hyperresponsiveness
- airflow obstruction
early asthma phase
mast cell driven in releasing histamine resulting in bronchospams
late asthma phase
cytokine and eosinophil driven leading to not onyl bronchospasm but also edema and inflammation
classic triad of asthma
- intermittent wheeze
- cough
- dyspnea
nocturnal asthma
lung function declines early morning driven to to decrease in catecholamines and increase in leukotriens and inflammatory cells
EIB
maybe there is water loss inducing an increases in tonicity
EIB treatment
- Beta-2 agonist before exercise
- exercise a little before to get warmed up
ILD can bypass inflammatory pathway?
yep
ground glass opacities show ______ and can be treated with
acute and can be treated with steroids
honecombing show _______ and it is usually treated with
chronic but it is hard to treat… too late
reticular nodules are
infection
Exaggerate immune response to unidentified Ag (increase CD4)
sarcoidosis
Type 1 RADS
hypoxemic due usually to either a V/Q or shunt
acute RADS what do we see
increase catecholamines
- carotid body detects and increases respiratory rate and thus ventilation
chronic RADS
increases in erythropoetin leading to icnrease in gemoglobi n and thus increase in o2 concentration
Type II RADS
hypercapcnic
acute Type II rads
decrease in Ph leading to high CO2 narcosis
chronic type II rads
increase in renal bicarb. leading to increase in Ph
how much do you extract O2
about 25%
what happens if you can no longer compensate and extract the O2?
consumption drops and leads to acute organ failure
when do we thinking of dead space
hypercapnia
hypercapnia respiratory failure
- increase in dead space
- increase in VCO2
- decrease in resp. drive
decrease in resp. pump - increase in work of breathing
HFNC is used for
hypoxemia not a ton of ventilation but will help increase WOB
what happens with too much O2
acute lung injury leading to increased dead space, abnromal resp. drive and haldane effect
what can happen with supplemental O2 with atelectasis
washout of N2 from alv and venous blood accelerates resorption of air leading to resorption atelectasis
when should give non-invasive ventilation
- acute resp failure with COPD
- acute cardiogenic pulm. edema, pneumonia
Refractory Hypoxemic Respiratory Failure
shunt
Ventilatory (Hypercapnic) Respiratory Failure
Elevated Work of Breathing
Respiratory Muscle Weakness/Endurance
Insufficient Respiratory Drive
all what must be present in ARDS
- Acute Onset: respiratory symptoms within one week of known clinical insult
- Abnormal CXR or CT: bilateral opacities c/w pulmonary edema, not fully explained by other processes
- Respiratory Failure: not fully explained by fluid overload or CHF
- Hypoxemia:
PaO2/FiO2 <300
what happens in ARDS
acute lung injury leads to increase permeability that then causes increased lung water in the interstitial and alveoli now we have two issues: 1. reduced compliance
2. shunting (no ventilation but perfusion is present) leading to hypoxemia
wheen to administer PEEP?
when volume is low
ventilator induced lung injury:
- volutrauma
- barotrauma
- biotrauma
- atelectrauma
repetitive opening
and closing of alveoli can injury
alveoli
Atelectrauma:
injury to lung
releases harmful cytokines
further lung injury and injury
to other organs
Biotrauma:
rupture of alveoli
with gas escaping into pleural
space (pneumothorax)
Barotrauma
injury to lung
indistinguishable from ARDS
Volutrauma:
PEEP keeps
alveoli open at end expiration
what does cAMP does?
increase smooth muscle relaxation and thus bronchodilate
Beta receptor for the lungs
Beta-2
Beta-1 will do what?
increase heart rate and contractility
who converts ATP to cAMP?
adenylate cyclase
Tachycardia will be caused
Beta-1 stimulation due to some oral absorption or swallowing
tremors with Beta-agonist?
Beta-2 fault
albuterol
fast/ short acting
slameterol
long acting
black box warning for the long-acting beta agonist
regular use may increase risk of severe asthma episodes
preferred asthma medications
inhaled corticosteroids
cortisol has an efffect on
glucose metabolism due to the overlap in aldosterone thus there might be some problems with fat deposition
breaks down muscle; catabolic effect
prednisone
dexamethasone has only what type of activity
glutocorticoid leading to higher anti-inflammatory effects
Acetylcholine will bind to muscarinic receptors leading to
bronchoconstriction
ipratropium is a
muscarininc antagonist that prevents the release in cGMP thus reduced bronchoconstriction
COPD does the best with which pharmacological tx.
muscarininc antagonistic long actign
side-eefects of muscarinic antagonist
dry mouth, gut issues
cromolyn
mast cell stabilizers
theophylline
both a bronchodilator and an antgonist for bronchoconstriction
Ipratropium
is short or long acting
short acting
Tiotropium
short or long acting
long
Indication for chronic O2 therapy:
PaO2 < 55 mmHg (<60 mmHg if Pulm HTN)
a consequence of expiratory flow limitation
hyperinflation
why is hyperinlfation bad for inspiration?
good expiration?
-Bad: diaphragm flat and fibers are shortened; elastic WOB increased
Good: higher lung volume maximizes elastic recoil; airways are wider at higher lung volumes
Serum to pleural fluid albumin gradient < 1.2 g/dL
exudate
hypoalbuminemia
nephrotic syndrome
hemothorax treatment
- requires chest tube drainage
tension pneumothorax depends on
Degree of collapse depends on size of PTX and elasticity of lung.
treatment for Pneumothorax
big pneumothorax gets a chest tube
small/minimal- 100%O2
If PCWP > 15 mmHg
Pulm. venous HTN
PCWP < 15 mmHg
PAH
PH mean PA should be
more than 25 mmHg at rest
General measure of PH tx.
oxygen and diuretics
WHO group 1 tx for PH
- calcium channel blockers
- prostacyclins
- endothelian antagonist
- PD5-% antagonist
PDE-5
blocks the production of cGMP
Prostanglandins
promote adenylate cyclase
PE can cause Pulm HT
true there is a release of mediators- seotonin
V/Q perfusion is good for those that
had recurrent PE
people dying of a PE
give a thrombolyisis
How long to treat PE therapy?
depends on underlying cause
Central, cavitates, obstructs airways
Hypercalcemia from ectopic PTH-like (Paraneoplastic)
Local spread is a big problem
squamous cells
Most cases from tobacco
When lung cancer occurs in a patient without tobacco exposure it is usually Adenocarcinoma
Usu peripheral, generally don’t cavitate, can be slow growing
Metastases a big problem
Targeted therapy (EGFR, ALK, ROS-a)
adenocarcinoma
slow-growing; mimics pneumonia
adenocarcinoma in situ
ptosis, miosis, anhydoris, endophtalmus
horner’s syndrom
ulnar radiation
pancoast/superior sulcus tumor
facial and upper chest edema, suffusion of mucous membranes, plethora (vascular obstruction of SVC
SVC syndrome
which cancer molecular analysis of tumor can result in targeted therapy that will improve response rate
adenocarcinoma
