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28 Cards in this Set

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  • Back
State the etiologies of emphysema
(5)
1- age- degenerative process
2- alpha 1 antitrypsin deficiency
3- chronic irritation
4- secondary to chronic bronchitis, asthma or other lung condition.
5- altered chest condition
Define the two pathological of emphysema
1 - centralobular - lesions occur around the small bronchioles in the upper airways

2 - panulobular - clusters of big air sacs or lesions involve the periphery of the acinus, middle lobe and lower lobe.
What agents are responsible for tissue breakdown?
alveoli fuses, less surface area, forms the following:

Cyst- small
Bleb- moderate
Bolus- large

causes air trapping
List the clinical features found in emphysema
look at Pink Puffer for symptoms
use of accessory muscles- tripod position
distended neck veins
barrel chest
dypsnea or SOB
tachypnea with prolonged exhalation

Also:
decreased blood return
decreased blood pressure
decreased cardiac output
cor pulmonale
List the lab results found in emphysema
chest xray- barrel chest, flattened diaphragm,

PFT- because of air trapping = increased RV, FRC and TLC
FVC and FEV1 decreased because of airflow obstruction

ABG resp alkalosis with moderate hypoxemia in mild to moderate emphysema and resp acidosis with more severe hypoxemia generally occurs during acute exacerbations and the terminal stages of the disease.
Pink Puffer vs Blue Bloater
Pink Puffer: dypsneic cachetic (SOB and underweight). leans toward emphysema, large or hyperexpanded lungs, less secretions, pursed lips, retraction or depressed notches in the clavicular or sternal notch, distended neck veins, use of accessory muscles, older patients, ABG: slightly lower PCO2 with a normal PO2
Blue Bloater vs Pink Puffer
Blue Bloater: cardiac polycythemic, leans toward, chronic bronchitis, overweight, cardiac issues: cardiomegaly, CHF, increased secretions, increased cough, ABG would show an increased CO2 with hypoxia and a decreased PaO2, more hb or blood cells, younger patients, no tripoding or notch depressed
cardiac polycythemic is what?
an increase in red cell mass caused by increased erythropoiesis, which may occur as a compensatory physiologic response to tissue hypoxia
What are two other types of emphysema
compensatory - lungs fill and overexpand to fill voids. lungs hyperexpand to fill chest cavity.

subcutaneous- leakage of air outside of lung into chest wall, face, shoulder, neck chest
Define emphysema
an anatomical alteration of the lung characterized by abnormal enlargement of the air spaces accompanied by destructive changes to the alveolar and airway walls.
what are the different types of alpha 1 antitrypsin deficiency?
m variant: normal - 250 mg/100 ml

s variant: intermediate - less than 50 mg/100 ml

z variant- true disease- less than 50 mg/ 100 ml
what is the treatment for alpha 1 deficiency?
tx- prolastin - plasma derived, given by IV every week or gene therapy
what is the pathophysiology of emphysema?
destruction of lung alveolar tissue. tears in the alveolar septa, loss of surface area and less recoil in lung tissue with an increase in lung size. Also damage to capillary bed will cause V/Q mismatch due to loss of surface area.
chest xray for emphysema will look like what?
flattened diaphragm
hyperexpanded lungs
barrel chest
increased AP diameter
narrow heart
chest xray for COPD chronic bronchitis Blue Bloater will look like what?
enlarged heart
What will breath sounds sound like in a chronic bronchitis or blue bloater patient?
increased secretions
crackles
what will breath sounds sound like in an emphysema patient
diminshed without adventitious (normal) breath sounds
PFT will be what in COPD?
decreased flow
FEV below predicted due to air trapping,
FVC, - normal to slightly increased
RV, TLC and FRC increased due ot air trapping
severe V/Q mismatch
Treatment for COPD
smoking cessation
ventilation
oxygen
hydration
meds
bronchial hygiene
rehab
family support
education
excercise
decreased allergens
surgical or laser resections or lobectomy
Complications for COPD
pneumothorax, bronchial infections, cor pulmonale (emphysema), pulmonary emboli, acute respiratory failure, chronic hypoxia which affects brain, kidneys liver, stomach
Describe the pathophysiology of extrinsic asthma
1- allergen exposure

2- water soluble proteins- broken down and absorbed by lymph tissue

3- IgE antibody formation in response to water soluble proteins

4- mast cell and basophil sensitization. Actual reaction: inflammation, swelling, bronchoconstriction.
Describe the pathophysiology of challenge reaction (all types of asthma)
1- re-exposure or internal response
2-degranulation -true mast cell degranulation
3- physiologic response: massive bronchospasm and broncho constriction, increased BP, hypersecretions, inflamatory response: edema, increased esinophil infiltration

substances released: histamines, leukotrienes, SRS-A, bradykinins, seratonin, prostaglandins
State the clinical features of all types of asthma
anxiety

cough - congested and rattling

increased white mucus

breath sounds- wheezing (broncho-constriction) severe- diminished

ABG-
early on: alkalotic, hypocapnia plus hypoxia because of hyperventilation
decreased CO2, decreased PaO2

later on: flip flop because patient is tired. acidotic, hypercapnea, increased CO2, decreased PH, hypoxia

labs- blood tests, look for esinophils

chest xray- usually it is normal initially but then hyperinflation, mucus plugging, air-trapping

PFT- severely decreased peak flow
FEV and FVC severely decreased
FEV severely dimished

RV increased
FRC increased
TLC increased

Can't get air out due to high airway resistance

tachypnea, tachycardia, increased BP, sweating profusely
Describe the treatment for asthma
- avoid trigger
- avoid stress
- prophylactic drugs- Intal (Cromolyn Sodium) prevents mast cell degranulation prior to an attack
- bronchodilators: inhaled or systemic (aminophylline) Theodur, theo-aire, theophylline
- steroids systemic: prednisone, hydrocortisone, inhaled: vasurel (beclomethasone), flovent
- O2
- bronchial hygiene: hydration, CPT, PD & P
- heliox 80% He and 20% O2
-psychological support
Define and state etiology for bronchiactasis
a disease characterized by permanent bronchial dilation due to weaknes and damage to the bronchial wall

etiology:
secondary effect due to a complication of some other pulmonary pathology

-repeated pneumonia
-childhood pneumonitis w/ pertussis
-bronchial obstruction: tumor, foreign body
-kartagener's syndrome: mucovicidosis w/dextrocardia and paranasal sinusits
- repeated bronchitis
describe the pathophysiology of bronchiactasis
destuctive changes to the airway wall structure. Destruction of smooth muscle tissue and bronchial wall cartiledge. squamous cell metaplasia. cartiledge rings breakdown and get floppy.

1- cylindrical- breaks down all around the cartiledge ring in the bronchi

2- fusiform- partial breakdown - area or patch affected

3- sacular- a sac forms. mucopurulent necrosis
list the tx for bronchiactasis
cant rebuild the cartiledge
but can...
treat infection
treat primary problem
Postural drainage
bronchial lavage
O2 therapy
hydration
surgical resection - remove sacular, patch stent
bronchidlators and steroids - limited affect


dont do percussion or IPPB
PFT for bronchiactasis
decreased flows (distended a/w)
decreased FVC
severe hypoxia due to v/q mismatch