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Pathophysiology Exam 2 > Disorders of Respiratory Function Pt. 2 > Flashcards

Disorders of Respiratory Function Pt. 2 Flashcards

1
Q

Mr. K’s Girlfriend Stabbed Him with a Knitting Needle …Now he is having breathing problems, and his breath sounds are diminished on the side with the wound
His trachea seems to be slanting toward the other side of his chest, and his heart sounds are displaced away from the wound
He has an increased respiration rate and blood pressure, is pale and sweating with bluish nail beds, and has no bowel sounds
What is going on?

A

Tension Pneumothorax

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2
Q

Asthma

A

Chronic inflammatory disorder of the bronchial mucosa.
Causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible.
Big inflammatory response/Episodic attacks of bronchospasm, bronchial inflammation, mucosal edema, and increased mucous production

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3
Q

Early Asthmatic Response

A

Immunoglobulin E (IgE) causes the mast cells to degranulate, releasing a large number of inflammatory mediators.
Vasodilation
Increased capillary permeability
Mucosal edema
Bronchial smooth muscle contraction (bronchospasm)
Tenacious mucous secretion

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4
Q

FLU SHOT IS BEST FOR PATIENTS WITH ASTHMA BECAUSE OF HIGH RISK OF PNEUMONIA

A

True

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5
Q

Late asthmatic response

A

Begins 4 to 8 hours after the early response.
Chemotactic recruitment of lymphocytes, eosinophils, and neutrophils occurs.
Prolonged smooth muscle contraction
Airway scarring
Increased bronchial hyperresponsiveness
Impaired mucociliary function with accumulation of mucous and cellular debris, forming plugs in the airways
Remodels airways

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6
Q

S/S of Late Asthmatic Response

A

Air trapping
Hyperinflation distal to obstructions
Increased work of breathing
Hypoxemia

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7
Q

Clinical Manifestations of Asthma

A

Asymptomatic between attacks

Chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea

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8
Q

Pulsis Paradoxus

A

Drop in systolic BP in inspiratory phase

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9
Q

Status asthmaticus

A

Bronchospasm not reversed by usual measures (treatment)

Life threatening

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10
Q

Ominous signs of impending death in an Asthma patient

A

Silent Chest, and a PaCO2 greater than 70 mm Hg

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11
Q

Asthma Treatment

A

Immediate administration of oxygen and inhaled beta-agonist bronchodilators
Oral corticosteroids administration early in the course of management
Careful monitoring of gas exchange and airway obstruction in response to therapy

Antibiotics are not indicated for acute asthma unless a bacterial infection is documented

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12
Q

Status asthmaticus

A

Prolonged asthma attack that does not respond to typical drug therapy
May last several minutes to hours
Medical emergency

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13
Q

A child has asthma. Which pathophysiologic process occurs in this disease?

A

Chronic inflammatory disorder, causing mucosal edema and reversible airflow obstruction

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14
Q

COPD

A

COPD describes a group of conditions characterized by obstruction to airflow in the lungs

Emphysema and Chronic Bronchitis

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15
Q

Emphysema

A

Loss of lung elasticity, permanent enlargement of the air spaces, destruction of the alveolar walls & capillary beds, with hyperinflation of the lungs (The respiratory tissues)
Inflammation and fibrosis of bronchial wall
Hypertrophied mucus glands excess mucus
Obstructed airflow
Loss of alveolar tissue and elastin lung fibers
Effective respiration is impaired, Air spaces enlarge

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16
Q

Chronic Bronchitis

A

inflammation of major and small airways and excessive mucous production in the large airways (The conducting airways)

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17
Q

What’s one factor that differentiates COPD from Asthma?

A

Asthma is reversible, COPD is not

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18
Q

Risk Factors for COPD

A 
Exposure to particles
Tobacco smoke
Occupational dusts
Oxidative stress
Gender: Male (Bronchitis) Female (Emphysema)
Age
Nutrition
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19
Q

A genetic defect in alpha1-antitrypsin synthesis leads to alveolar damage

A

True. Neutrophils in alveoli secrete trypsin
can damage alveoli particularly elastic walls
Alpha1-antitrypsin inactivates the trypsin before it can damage the alveoli

20
Q

Bleb (complication of Emphysema)

A

Intrapleural airspace separated from alveoli by a thin pleural covering
Caused by structural changes in lung tissue
Can rupture and lead to pneumothorax.

21
Q

Bulla: (Large complication of Emphysema)

A

Subpleural airspace that results from the destruction of pulmonary tissue
Caused by structural changes in lung tissue
Can rupture and lead to pneumothorax.

22
Q

Chronic Bronchitis

A

Chronic irritation of airways
Increased number of mucus cells
Mucus hypersecretion
Productive cough

The mucus glands of the tracheobronchial tree become thickened and encroach on the diameter of the airway lumen.
Increased mucus production in the peripheral airways.
Prolonging the inhalation of toxic inhalants

23
Q

Blue Boater

A

Cannot increase respiration enough to maintain oxygen levels.
Hypoxemia, hypercapnia (excessive CO2) → Cyanosis, polycythemia (bone marrow increases RBC/hemoglobin)
Pulmonary HTN→ Rt. Heart failure → peripheral edema (“bloater”)

24
Q

Pink Puffers

A

(emphysema)
Increase respiration to maintain oxygen levels
Dyspnea; increased ventilatory effort
Use accessory muscles; pursed-lip breathing (“puffers”)

25
Q

Clinical Manifestations of Emphysema

A 
Accessory muscle use 
Pursed-lip breathing
Prolonged exhalation
Barrel chest 
Weight loss
26
Q

Clinical Manifestations of Chronic Bronchitis

A 
Dyspnea
↓exercise tolerance
Expiratory wheezes & crackles
Hypoxemia, hypercapnia
Cyanosis
Polycythemia
Peripheral edema
27
Q

Dx of COPD

A

Spirometry, Bronchodilator reversibility testing

History and Physical

28
Q

Treatment of COPD

A 
Reduce airflow limitations
Prevent secondary medical complications
Reduce Respiratory symptoms
Improve quality of life
Pharmacology
Avoiding risk factors
Pulmonary rehabilitation
Oxygen supplementation
29
Q

You Are Caring for a COPD Client … He has chronically high PCO2
He is being given low-flow oxygen and complains all the time that he “needs more air,” so you turn up his oxygen. As a result, he is unconscious and not breathing. What happened?

A

Hypoxic drive was eliminated (the need to take in oxygen based on the CO2 levels). Balance must exist between PCO2 and PO2

30
Q

Pulmonary Embolism

A

Obstruction of the pulmonary artery or one of its branches by a thrombus/clot
Originates somewhere in the venous system or in right side of heart
Due to a Blood clot: thrombis

31
Q

Risk Factors for Pulmonary Embolism

A

Virchow’s Triad!! Venous Stasis (Prolonged immobilization
Varicose veins), Hypercoagulability (Inherited coagulation disorders, Smoking, Malignancies, Hormone Therapy), and Venous Endothelial Disease (foreign bodies/trauma)

32
Q

Pulmonary Embolism Pathophysiology

A

Damaged endothelial wall
Thrombus completely or partially obstructs pulmonary artery or its branches
Alveolar dead space increased
Continues to be ventilated but receives little to no blood flow
Impaired gas exchange

33
Q

Ventilation-perfusion imbalance

Pulmonary Embolism

A

Increased pulmonary resistance→ increased right heart workload→ right ventricular failure→ decreased cardiac output→ SHOCK!!

34
Q

Clinical Manifestations of Pulmonary Embolism

A 
Dyspnea is most frequent symptom
Chest pain (Pleuritic in origin)
Sudden onset
May mimic MI (heart attack), angina, bronchopneumonia or heart failure
Apprehension
Cough
Diaphoresis
Hemoptysis
Syncope: passing out

Size of thrombus contributes to symptoms

35
Q

Pulmonary Hypertension (primary)

A

Blood vessel walls thicken and constrict

36
Q

Pulmonary Hypertension (secondary)

A 
Elevation of pulmonary venous pressure
MS, LV heart failure.
Increased pulmonary blood flow
L→R shunts septal defects
Pulmonary vascular obstruction (PE)
Hypoxemia (Stimulus for pulmonary vasoconstriction)
37
Q

Cor Pulmonale

A 
Right-sided heart failure secondary to respiratory disease
Decreased lung ventilation
Pulmonary vasoconstriction
Increased workload on right heart
Decreased oxygenation
Kidney releases erythropoietin  more RBCs made
Polycythemia makes blood more viscous
Increased workload on heart
38
Q

Pulmonary Edema

A

Excess water in the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure, or capillary permeability
Most common cause of pulmonary edema: Left-sided heart disease

39
Q

Clinical manifestations of Pulmonary Edema

A

Dyspnea, orthopnea, hypoxemia, and increased work of breathing, cough with pink/frothy sputum

40
Q

Pulmonary Edema Treatment

A

Increased hydrostatic pressure caused by heart failure
Improve cardiac output and volume status with diuretics, vasodilators, and drugs that improve the contraction of the heart muscle.
Increased capillary permeability resulting from injury
Remove offending agent and supportive therapy to maintain adequate oxygenation, ventilation, and circulation.
Oxygen/Mechanical Respiration

41
Q

Ventilation/perfusion mismatching occurs in

A

COPD and Atelectasis

42
Q

Impaired diffusion hypoxemia but not hypercapnia

occurs in

A

ARDS

Pulmonary edema

43
Q

What causes respiratory failure?

A

Hypoventilation: hypercapnia, hypoxia

44
Q

Hypoxemia

A

PO2 <60 mm Hg
Cyanosis
Activation of compensatory mechanisms (Sympathetic system activation)

45
Q

Hypercapnia

A

PCO2 >50 mm Hg
Respiratory acidosis
Decreased muscle contraction, increased respiration

Pathophysiology Exam 2 (4 decks)

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