Lower Respiratory Disorders Flashcards

1
Q

Asthma pathophysiology

A

Presence of airway inflammation that causes hyper responsiveness of the airways(bronchoconstriction),
airway Edema, and production of thick mucous.

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2
Q

Status asthmaticus

A

Severe long continuous asthma attack.
Medical emergency.
Sx: labored breathing, prolonged exhalation, wheezing.
As it worsens, cyanosis and wheezing will disappear. Ominous sign!! Means air has stopped moving

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3
Q

COPD: 2 resp disorders classified as copd

A

Chronic bronchitis- mucous secreting glands secrete excess mucous due to chronic irritation (smoking). Small airways are blocked with mucous. Atelectasis.

Emphysema- cause unknown. Smoking.
Alveolar walls lose elasticity and enlarge and then are destroyed. Collapse of airways.

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4
Q

Cor pulmonale

A

Right sided ventricular heart failure.
Can be caused by increased pressure in right ventricle from increased pulmonary vascular resistance.
Can be caused by chronic bronchitis

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5
Q

2 types of emphysema

A

Centilobar emphysema (CLE) upper portion of lungs

Panlobar (PLE) usually in lower lungs. Tends to occur with AAT deficiency(genetic)

A patient can have both types

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6
Q

Pathophysiological changes in emphysema

A

Loss of elastic recoil, causing lungs to be overdistended.
Increased airway resistance due to collapse of small airways.
Air trapping, causing further overdistention and pressure to diaphragm.
Decreased diaphragm movement, becomes fixed.
Destruction of alveolar- capillary membrane surface.
Resp acidosis.

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7
Q

Symptoms of chronic bronchitis

A

Productive cough on waking.
Sputum is grayish white.
Increasing dyspnea, eventually using accessory muscles.
Difficulty walking due to DOE.
Cyanosis, dusky skin, bloated appearance, ankle edema.
Later stages: right side heart failure and respiratory failure.

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8
Q

Emphysema- clinical manifestations- sx

A

DOE, then constant dyspnea
Orthopnea
Thin with barrel chest
Little to no sputum. (Unlike chronic bronchitis)

Pursed lip breathing which helps decrease airway collapse and prolong expiration.
Accessory muscles

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9
Q

Huff coughing

A

Remove secretions and minimize bronchospasms.
Inhale through nose, lean forward, exhale through pursed lips.
Repeat several times.
Then take slow deep breath through nose -and exhale with short coughs.

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10
Q

What kind of bacteria causes tuberculosis?

A

Mycobacterium tuberculosis

Acid-fast aerobic rod that is inhaled.

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11
Q

Granulomas- as related to tuberculosis

A

Deposits of live and dead bacilli.

Granulomas are surrounded by macrophages.
Macrophages “wall off” granulomas to prevent further infection.

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12
Q

Caseation necrosis

A

In tuberculosis, a granuloma Is compressed by fibrotic tissue. A necrotic, cheesy mass develops at the center of the nodule.
The cheesy material can liquefy and be coughed up by the patient, leaving cavities and lung tissue

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13
Q

Ghon tubercle

A

Sometimes granulomas from tuberculosis calcifies in a scar forms.
When calcification develops, bacteria in the tubercle become dormant and the disease is no longer active.
this is called latent TB infection. the calcified tubercle is known as Ghon tubercle.

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14
Q

TB treatment drugs and side effects

A

Isoniazid (INH) -peripheral neuritis, hepatitis

Rifampin- hepatitis, N/V

Pyrazinamide- hepatomegaly, high uric acid levels

Streptomycin- nephrotoxicity, deafness

Ethambutol- skin rash, optic neuritis

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15
Q

Signs and symptoms of tuberculosis

A
Cough 
sputum production 
weight loss 
night sweats 
low-grade fever
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16
Q

Pneumothorax

A

Collapsed lung—-

develops when pleura of the lungs have been punctured, allowing atmospheric air to enter the plural space.

17
Q

Three types of pneumothorax

A

Closed
Open
Tension

18
Q

Closed pneumothorax

A

A.k.a. simple or spontaneous

Can be caused from chronic lung problems, Which can cause air blebs, or blisters, on the lungs that rupture and lead to pneumothorax.

Fractured ribs

19
Q

Open pneumothorax

A

A.k.a. traumatic pneumothorax.

Caused by laceration or puncture of the lung that allows air to leave the lung and enter the plural space.

Can lead to a shift in the heart, trachea (mediastinal shift) toward the uninjured side with each breath the patient takes.

Serious life-threatening problem

20
Q

Hemothorax

A

Development of blood in the plural space.
can be caused by major chest trauma.
if air and blood are both present, then it is referred to a hemopneumothorax.
If the wound is large enough, air will move freely in and out of the chest with each respiration and that is called a sucking chest wound.

21
Q

Tension pneumothorax

A

Air is drawn through a small puncture into the plural space but is unable to escape.
Each time the patient takes a breath, more air is drawn into the lungs and increases the intra-thoracic pressure. The lung collapses and the heart and trachea shift toward the unaffected side.
Medical emergency

22
Q

Medical management of pneumothorax

A

Dependent on size of pneumothorax.
Chest tube inserted into the second intercostal space with gentle suction. Supplemental oxygen.
If open sucking chest wound is present it must be immediately covered with Hair type dressing to prevent development of a tension pneumothorax.

23
Q

Symptoms of pulmonary embolus

A

Sometimes instant death.
Onset of symptoms is usually sudden. Depending on size of embolus, symptoms may be tachypnea, cough, pleuritic chest pain hemoptysis and low-grade fever. Elevated WBC due to inflammation. crackles may be heard and plural friction rub.

Dyspnea, Severe chest pain, diaphoretic anxious, hypotensive and develop shock.

24
Q

D-dimer

A

Diagnosis of PE can be excluded if D dimer level is less than 500.

D- dimer greater than 500, with clinical symptoms of PE should undergo CT pulmonary angiography.

CT is the final diagnostic tool.

25
Q

Adult respiratory distress syndrome (ARDS)

A

Occurs and critically ill adults. mortality rate up to 50%. Typically occurs with major trauma.

26
Q

Four phases of ARDS-

Adult respiratory distress syndrome

A

Phase 1- acute injury phase. Mild hypoxemia and dyspnea develop within 24 hours.
Phase 2- Latent phase/ can last up to 24 hours. hypoxemia that is refractory to supplemental oxygen. PEEP is started (Ventilation)
Phase 3-Exudative phase- onset of acute respiratory failure begins between 2 to 10 days after injury. other organs may be involved
Phase 4- fibroproliferative phase. Occurs about 10 days after injury. Multi system organ involvement in severe instability. Respiratory acidosis develops and PEEP is no longer effective

27
Q

PEEP Ventilation

A

Positive End expiratory pressure.

Prevents alveolar collapse and improves ventilation/ perfusion ratio.