Resp Care 265 Pulmonary Pathology Quiz 1

Front 1

List the normal pulmonary defense mechanisms

Back 1

1-airway structure
2-reflex bronchospasm
3-airway clearance
4-phagocytosis
5-interstitial lymphatic system
6-lung conditions

Front 2

Describe the normal pulmonary defense mechanisms: airway structure:

Back 2

airway structure: inertial impact causes large particles to get stuck in the airway due to inertial impaction. Turbulent airflow enhances impaction along airway walls. Where does this happen? In nose, turbinates, ridges in sinus cavity.

Front 3

Describe the normal pulmonary defense mechanisms: reflex bronchospasm

Back 3

reflex bronchospasm: cough or tightening of muscle due to airway irritation

Front 4

Describe the normal pulmonary defense mechanisms: airway clearance

Back 4

AIRWAY CLEARANCE:
Ciliated: takes place in the trachea and small bronchioles. Can last for a few moments up to 5 hours
Nonciliated: takes place in 17-24 hours time up to 60-100 days.
Mucociliary escalator is a major factor and those things that affect it: secretions, viscosity, cilia damage, etc.

Front 5

Describe the normal pulmonary defense mechanisms: phagocytosis

Back 5

Phagocytosis: macrophages ingest or kill the invader

Front 6

Describe the normal pulmonary defense mechanisms: interstitial lymphatic system

Back 6

The lymph system is the drain of our lungs

Front 7

Describe the normal pulmonary defense mechanisms: lung conditions

Back 7

Lung Conditions:

1- Mucus is made of phospholipids with a pH 7.8 (alk…bacteria don’t like) phospholipids (soapy protein) effect viscosity of mucus

2-bronchospasm -tightening of muscle / cough in reaction to irritant

3- increased qty of secretions, increased viscosity and change in color

4-fibrosis irreversible: no turning back

Front 8

List the clinical symptoms of acute hypoxia

Back 8

increased WOB
increased SOB
increased secretions
chest wall movement
increased secretions

Front 9

List the clinical symptoms of chronic hypoxia

Back 9

clubbing

mental and physical fatigue, loss of ability to perform many physical tasks.

may increase pulmonary hypertension, enhanced right-heart load

Front 10

State how obstructive diseases differ from restrictive diseases

Back 10

Obstructive: increased resistance of airflow, inelastic or airway resistance. decreased expiratory flows and decreased expiratory volumes.

Examples: inflammation, increased mucus, bronchospasm, foreign body and growth (tumor)

Front 11

State how restrictive diseases differ from obstructive diseases

Back 11

Restrictive: chest limitations, elastic resistance, increased expiratory flow with decreased expiratory volumes

Examples:
interstitial: edema, fibrosis, hemorrhage, hyaline membrane,

loss of subambient pressure: pneumothorax, hemothorax, empyema, pleural effusion, loss of surfactant

External factors: scar tissue, splinting for pain, loss of thorax movement, kyphosis, scoliosis, lordosis,

Front 12

Obstructive versus Restrictive

Back 12

Restrictive: increased expiratory flow and decreased expiratory volumes

Obstructive: decreased expiratory flow sand decreased expiratory volumes

Front 13

How does Obstructive and Restrictive vary on the flow / volume curve?

Back 13

On the flow / volume curve an obstructive breath looks like an O and a restrictive breath is steep on the flow side (vertical) and then drops off below the obstructive breath

Front 14

Define pneumonia

Back 14

An inflammation of the lung parenchyma as a result of infection. There is a replacement of air by inflammatory cell exudate ** memorize this!! on test!!

Front 15

List the 5 steps of immune response:

Back 15

1- IgA
2- IgG
3- alveolar macrophage
4- leukocytes
5- antibodies

Front 16

State and describe the immune response to infection: 5 steps:

Back 16

1- secretion of IgA : histamine complex starts secretion response and mucus increases. This is the first response.

2-secretion of IgG: bonds to foreign invaders & acts as a marker for macrophages. It is found in human serum: blood, lung tissues, capillaries. more powerful than IgA.

3- Alveolar macrophage: primary defense with phagocytosis

4- leukocytes (WBC)

5- antibody protection - recognition for next time

Front 17

List and define the 3 zones of pneumonia

Back 17

Zone 1 - congestion, early consolidation:

vasoconstriction, vasodilation, bacterial growth, immune response, decreased gas exchange

Zone 2 - consolidation: red, pink, frothy,

Sx: increased temp, dehydration, SOB, hypoxia, nonproductive cough

red hepatization,exudate formation, increased waste, hemolysis (RBC breakdown)

Zone 3 Resolution: white/grey pus
Grey hepatization (complete RBC breakdown), exodate loosens, expectoration, alveolar clearance,

cough is productive here.

Front 18

Describe the etiology and organism of tuberculosis

Back 18

TB is a form of chronic pneumonia.
The organism is Mycobacterium tuberculosis: weak gram positive rod. true aerobe. high lipid coat that is unpenetrable (dormant in anaerobic condtitions)
Found only by acid fast bacillus test.

Front 19

What are the clinical features found in TB?

Back 19

• Fever
• Night sweats
• Fatigue, malaise
• Cough
• Weight loss (aneuria)
• Possible pleural effusion

which is a buildup of fluid between the layers of tissue that line the lungs and chest cavity. Symptoms: Chest pain, usually a sharp pain that is worse with cough or deep breaths;

Front 20

List the treatment and prevention measures used for TB

Back 20

Prevention: patient should be in isolation - negative pressure room
Dx -skin test, xray, sputum test, AFB test
Tx - O2 given for hypoxia, drug therapy: 4 drugs: Isoniazide (most effective), rifampin, ethambutol, streptomycin or pyrazinamide, for 2 months followed by 2 drugs for 4-7 months

Front 21

Define Chronic Bronchitis

Back 21

memorize this:
a clinical disorder characterized by excessive mucus secretion in the bronchial tree with chronic or recurent productive cough on most days for a minimum of 3 months a year for 2 years consecutive: back to back.

Front 22

List the etiologies for Chronic Bronchitis

Back 22

primary cause is smoking which is caused by heat, toxic fumes, chemicals, CO, Tar,
secondary causes are: environmental, chemical or foreign materials, recurrent infection, chronic asthma

Front 23

State the cellular changes in the airway related to chronic bronchitis

Back 23

Squamous Cell Metaplasia- tissue becomes fibrotic and lungs become stiffer. -conversion of tissue into a form that is not normal.

Replacement of PSCCE by more squamous cells.

Mucus Gland Hyperplasia increased number of goblet cells per area and Reid Index goes up. Increased number of mucus glands. Decreased number of serous tubules of submocosal glands: thinner secretions eliminated. Increased goblet cells, increased secretions, viscosity thicker

Front 24

List the clinical findings for chronic bronchitis

Back 24

cough - for 3 months in a year for 2 consecutive years.

dypsnea -

breath sounds- expiratory coarse crackles, fine crackles,

chest xray- air trapping,
Also: v/q mismatch, increased WOB, increased airway resistance, decreased elasticity, decreased PaO2,small airway collapse

PFT - increased residual volumes, decreased flow, decreased FEV1, decreased FVC

Front 25

Tx for chronic bronchitis

Back 25

smoking cessation
meds: bronchodilators, mucolytics, steroids, antiboltics
hydration, CPT, O2, bronchial lavage

Front 26

methods used to help treat smoking addiction

Back 26

education
medications
psychological
support groups

Front 27

diagnostic techniques used for determining pulmonary disease

Back 27

Chest x rays
broncography
pulmonary angiography
CT scans
MRI
PFT
V/Q scan
broncoscopy
Stethoscope
ABG

Front 28

Types of pneumonia

Back 28

•viral (most common)- Short, fast typically self-limiting - If not treated can turn into bacterial. Example of viral causing pneumonia: HEMOSYPHYLLIS INFLUENZA

Front 29

types of pneumonia

Back 29

Bacterial
Streptococcus pneumoniae (most common) Gram positive common in COPD

Staph aureus, common in flu outbreak

Strep pyrogenes, gram positive, most common if community outbreak

Kleibsiella pmneumonia (friedlanders), most common in diabetic or hospital patients
Legionella pneumoniae

Pepto streptococcus, secondary to aspiration in vent patients
nosocomial- E Coli, pseudoaeuregenosa,
Protozoa, pneumo cystitis carnii, candidas albicans,
opportunistic- herpes (viral)
opportunistic- aspergillus, candidda albicans (fungal)