Pathophysiology

Front 1

tension pneumothorax

Back 1

1)clinical diagnoses
2)In a chronic condition, airways don't re-expand spontaneously because of scarring

Front 2

Underventilation lung due to pressure from mechanical ventilation

Back 2

1)susceptible to puncture
2)hypotensive
3)tachycardic
4)hypoxic
5)code

Front 3

PCO2 of 100 in a COPDer

Back 3

Patients can have PCO2's of up to 100, and, as long as they crept up slowly, can still be talking

Front 4

PaO2

Back 4

tension of oxygen in an arterial blood gas sample

Front 5

advantages to the shape of the O2 dissociation curve

Back 5

1)In the physiologic range of 70-100, significant changes in the arterial 02 do not affect the oxygen saturation

Front 6

PaO2 55-60

Back 6

1)indications of giving the pt. oxygen to prevent the complications of hypoxemia

Front 7

Factors affecting the Oxyhemoglobin dissociation curve

Back 7

1)Temperature
2)2,3 DPG
3)PCO2
4)ph

Front 8

Chronic hypoxemia and red blood cell production

Back 8

1) stimulus goes out the kindeys to put out erythropoeitin
2)Eth. stimulates production of RBC's

Front 9

Anemia and PO2 and O2

Back 9

Assuming the lungs are normal, the PO2 and O2 will be normal

Front 10

Partial Pressure of O2 in the lungs

Back 10

As the O2 gets to gas exchange, it encounters O2, and the partial pressure of O2 decreases

Front 11

Before O2 gets to the systemic arteries

Back 11

1) Some ventilation/perfusion inequalities
2)1-2% of the blood is shunted to the left side without going through the lung, causing alveolar and oxygen tensions to be different

Front 12

Alveolar air equation

Back 12

Allows us to estimate PO2 in the alveolus

Front 13

R in the aveolar air equation

Back 13

1)represents the respiratory exchange ratio
2)Ratio between the volume of CO2 added to the alveolus and the volume of O2 removed from the alveolus

Front 14

R=VCO2/VO2

Back 14

Used to correct for the fact that more O2 is taken up than CO2 is excreted back into the airways (0.8)

Front 15

As PCO2 increases

Back 15

Alveolar O2 decreases

Front 16

P(A-a)O2 over age

Back 16

normally increases with age, 2.5 +age/5

Front 17

PO2 for our altitude

Back 17

122

Front 18

PCO2 at our altitude

Back 18

36-39

Front 19

Normal values for PaO2

Back 19

65-75

Front 20

causes of hypoxemia

Back 20

1)hypoventilation
2)ventilation/perfusion mismatch
3)shunt

Front 21

V/Q mismatch

Back 21

Most common cause of hypoxemia in pts with COPD

Front 22

Hypoventilation

Back 22

There is no change in A-A difference

Front 23

v/q mismatch and A-a diff

Back 23

There will be a a-A difference of more than to 10, using the formula for age

Front 24

COPD PaO2

Back 24

1)There will be a PaO2 of 50-60

Front 25

Widened A-a gradient

Back 25

Both shunt and V/Q mismatch results in a widened A-a gradient

Front 26

Physiologic consequences of chronic hypoxemia

Back 26

1)pulmonary hypertension
2)erythrocythemia
3)CNS dysfunction
4)Decreased exercise tolerance
5)Cor pumonale
6)shortened survival rate

Front 27

Hypoxemia in lung vessels

Back 27

1)Causes vasoconstrictionb
2)remodeling

Front 28

Failure of R VENTRICLE

Back 28

Patients develop edema
neck veins distended

Front 29

Cor pulmonale

Back 29

Due to pulmonary hypertension

Front 30

Liquid Oxygen system

Back 30

1)High flow rates
2)Oxygen coming out is 100%

Front 31

COPD

Back 31

Leading cause of morbidity and mortality

Front 32

Natural History of COPD

Back 32

15-20% of smokers develop COPD

Front 33

definition of COPD

Back 33

A disease state characterized by airflow limitation that is not fully reversible

Front 34

Genetic predispositions to COPD

Back 34

linked to enzymatic deficiency

Front 35

Subcategories of COPD

Back 35

1)chronic bronchitis
2)emphysema
3)Asthma

Front 36

Chronic bronchitis is a _____

Back 36

Clinical Diagnoses (must have symptoms for 3 months out of the year for two consecutive years)

Front 37

Emphysema

Back 37

Pathological Diagnoses
Alveoli walls are destructed. Visible on CT scan

Front 38

Asthma

Back 38

1)Chronic inflammatory disease
2)Characterized by the increased responsiveness of trachea and bronchioles to different stimuli

Front 39

Pts who show complete responsiveness to a bronchodilator

Back 39

Do not have COPD

Front 40

Other causes of COPD

Back 40

1)tobacco
2)smoke inhalation
3)chemical inhalation
4)Childhood infections
5)deficiency of alpha one antitrypsin

Front 41

Areas of body affected by COPD

Back 41

1)central airways
2)peripheral airways
3)lung parenchyma
4)pulmonary vasculature

Front 42

Changes brought about by COPD

Back 42

1)ciliary dysfunction
2)increased sputum production
3)loss of airway elasticity
4)pulmonary hyperinflation
5)pulmonary hypertension

Front 43

Clinical Features of COPD

Back 43

20 cigarettes a day for 20 or more years

Front 44

Clinical symptoms of COPD continued

Back 44

-Acute bronchitis every winter
-upper respiratory depression that doesn't go away
-prescriptions don't help
-acute phase 50's, present with SOB in 60's
-weight loss
-muscle wasting
-headache/delirium
-right side heart failure/cor pulmonale

Front 45

Why do COPDers have right sided heart failure

Back 45

Because, when alveoli get destroyed, there is an increase in interstitum. Pulmonary pressures increase.

Front 46

COPD lung morphology

Back 46

Increase in total lung capacity, and increase in functional residual capacity

Front 47

COPD CT scan

Back 47

shows bullae

Front 48

COPD FEV1 with bronchodilator

Back 48

1) at risk/mild--80 percent or less
2)moderate-50 to 80
3)Severe--less than 30

Front 49

Alpha-one antitrypsin disease

Back 49

1)Genetic disease
2)people diagnosed with COPD at a young age
3)runs in families

Front 50

Average rate of capacity loss in a smoker

Back 50

1)20-30 ml per year

Front 51

FVC

Back 51

Total volume of air that can be exhaled, from maximal inhalation to maximal exhalation

Front 52

Short acting bronchodilators

Back 52

increase exercise tolerance

Front 53

Long acting bronchdilators

Back 53

1)Improve health status
2)reduce symptoms

Front 54

Anticholinergics

Back 54

1)reduce exacerbations
2)reduce hospitalizations

Front 55

Steroids

Back 55

1)Act at multiple points in the inflammatory cascade
2)don't work as well in COPD as they do in asthma

Front 56

Pulmonary Rehabilitation

Back 56

1)Increases exercise tolerance
2)Improves dyspnea
3)Improves muscle tone

Front 57

Nutrition and COPD

Back 57

muscle wasting due to increased respiratory effort
--significant weight loss=pt. losses 5 percent of their weight in one month, or greater than 10 percent of their weight in six months

Front 58

Surgical options for COPD patients

Back 58

1)bullectomy
2)lung volume reduction sugery
3)lung transplant(less than 55 years old, have alpha-one antitrypin deficiency
4)must have 60% of FEV1 before surgery, to guarantee 40% after

Front 59

Exacerbations of COPD

Back 59

1)increased mucus production
2)dyspnea
3)fevers(pneumonia)

Front 60

Inpatient therapy for COPDers

Back 60

1)steriods
2)antibiotics
3)nebulizers
4)short acting bronchodilators(beta 2 agonist)
5)CXR
6)ABG gases (ph, oxygenation)

Front 61

BIPAP helps with

Back 61

1)hypercapnia
2)respiratory acidosis
3)CHF
4)COPD

Front 62

Contraindications for BIPAP

Back 62

1)facial fractures
2)excessive secretions
3)comatose,unconscious,unable to follow directions

Front 63

Pressure support increases

Back 63

1)Tidal volume
2)keeps airways open

Front 64

Prolastin augmentation therapy

Back 64

1)slows rate of decline in patients with alpha one antitrypsin deficiency
2)improves survival rate in patients with moderate airflow obstruction

Front 65

Causes of restrictive lung disease

Back 65

1)alteration in lung parenchyma
2)disease of the chest wall
3)disease of the pleura
4)disease of the neuromuscular apparatus

Front 66

Pathpophysiology of restriction

Back 66

1)Parenchymal destruction
2)Excessive elastic recoil of the lung
3)diease of the pleura
4)reduced FEV1
5)Arterial hypoxemia due to VQ mismatch
6)yperventilation at rest

Front 67

Definition of asthma

Back 67

chronic inflammatory disorder where many cells play a role

Front 68

cells that play a role in asthma

Back 68

1)mast cells
2)eosinophils
3)T lymphocytes

Front 69

Symptoms of asthma

Back 69

1)Wheezing
2)SOB
3)Chest tightness
4)Coughing at night, during morning

Front 70

Mediators in asthma

Back 70

1)Histamine
2)Activating Factors
3)Cytokines, such as interleukin three and five

Front 71

Bronchial hyperresponsivenes in asthma

Back 71

1)Exaggerated response to allergens, histamine, methylcholine, cold air, and environmental irritants

Front 72

Elements of airflow obstruction

Back 72

1)Acute bronchoconstriction
2)mucus plugging
3)bronchial wall edema

Front 73

Lung remodeling

Back 73

1)Smooth muscle hypertrophy
2)Lung loses recoil features

Front 74

Risk factors for asthma

Back 74

1)Genetics
2)Sex
3)Race
4)Envinronmental Factors

Front 75

Details of Genetic Risk Factors for asthma

Back 75

Short arm of chromosome five shows alterations. Pts. who have asthma have high IGE. Only in select groups of patients.

Front 76

Sex and asthma

Back 76

In childhood, more prevalent in males. In adolescence, more prevalent in females.

Front 77

Race and asthma

Back 77

More common in African Americans

Front 78

Environmental Factors

Back 78

Allergens, dust mites, cockroaches, pollen, industrialized cities, air pollution.

Front 79

Other respiratory infections associated with asthma

Back 79

1)Chylamidia
2)mycoplasma

Front 80

Miscellanous Asthma correlates

Back 80

1)weight
2)antioxidants

Front 81

Clinical Presentation of asthmatics

Back 81

1)wheezing
2)Hyper-resonant