NUR 502 Advanced Pathophysiology – Dissertation Consulting Company

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Terms in this set (56)

The inner epithelial lining of the uterus is the:

A) myometrium.
B) perimetrium.
C) endometrium.
D) epimetrium.

C) endometrium.

Which female organ produces and releases the ovum?

A) Ovary
B) Uterus
C) Fornix
D) Vestibule

A) Ovary

The duct that carries the ovum to the uterus is called the:

A) ductus deferens.
B) fundus.
C) endocervical canal.
D) fallopian tube.

D) fallopian tube.

The portion of the uterus that descends into the vagina is the:

A) fundus.
B) cervix.
C) fornix.
D) isthmus.

B) cervix.

The release of a matured ovum from the follicle is a process called:

A) reproduction.
B) ejaculation.
C) menarche.
D) ovulation.

D) ovulation.

The most potent and abundant of the estrogens is:

A) estriol.
B) estradiol.
C) estrone.
D) estrase.

B) estradiol.

Estrogen and progesterone are primarily produced and secreted by the:

A) ovaries.
B) uterus.
C) anterior pituitary.
D) posterior pituitary.

A) ovaries.

Which of the following are functions of progesterone?

A) Development of secondary sex characteristics
B) Stimulating uterine smooth muscle contraction
C) Maintaining the endometrium during pregnancy
D) All of the above

C) Maintaining the endometrium during pregnancy

The first ovarian phase of the menstrual cycle is the:

A) lunar phase.
B) follicular phase.
C) adrenarche phase.
D) luteal phase.

B) follicular phase.

Ovulation occurs immediately after which of the following uterine phases in the endometrial cycle?

A) Ischemic
B) Secretory
C) Proliferative
D) Menstrual

C) Proliferative

Terms in this set (54)

Discuss the role of inflammation in asthma

Early asthmatic response: bronchospasm (immediate peaks 30-60 min, lasts 1-2 hours)
Exposure to antigen, triggers IgE -> inflammatory response

Compare and contrast the clinical symptoms and underlying mechanisms of bacterial pneumonia, viral pneumonia.

– Inflammatory reaction in the alveoli and interstitium caused by an infectious agent
– Causative microorganism influences symptoms and signs, treatment and prognosis

– Aspiration of oropharyngeal secretions composed of normal bacterial flora or gastric contents (25%-35%)
– Inhalation of contaminants
– Virus
– Mycoplasma
– Contamination from the systemic circulation
– Bacteremia from infections in the body or IV drug abuse

– Acquired when normal pulmonary defense mechanisms are compromised
– Aspiration of oropharyngeal secretion is the most common route of lower respiratory tract infection.
– Inhalation of microorganisms.
– Bacteria from bacteremia.
Organism enters lung, multiply, and trigger pulmonary inflammation
– Inflammatory response to organism
– Alveolar spaces fill with fluid and inflammatory cells invade the site
– Acute bacterial pneumonia can be associated with significant V/Q mismatch and hypoxia d/t fluid
– Viral pneumonia does not produce exudative fluids

Presentation varies due to pathogen, age of pt, and severity of disease
– Some just have fever, others have rales (crackles) and bronchial breath sounds over affected lung.
– Pleuritic chest pain, myalgia, headache, chills, fever, productive cough, chest splinting, tachycardia, dyspnea, tachypnea
– Viral pneumonia can present with fever, cough, hoarseness with wheezing and/or rales
– Mycoplasma pneumonia is common in older children and adults. Fever cough, headache and malaise
On auscultation: crackles, wheezing, bronchial breath sounds, breath sounds may be decreased or absent, tactile fremitus, dullness on percussion

Differentiate between hypoxia and hypoxemia.


Reduced oxygenation of cells in tissues
– Difficult to measure (assume when blood flow or PaO2 is low)
– Can be hypoxemia
– Low cardiac output
– Shock


Reduced oxygenation of arterial blood
– Measured by ABG or pulse oximetry (O2 saturation)
Caused by
– Decreased available O2 at alveoli
– Altered diffusion of O2 into the blood (V/Q mismatch)
– Altered perfusion of pulmonary capillaries

Define acute respiratory failure and identify risk factors.

Impaired Gas Exchange resulting in abnormal ABGs
– PaO2 ≤ 60 mmHg; PaCO2 ≥ 50mmHg; pH ≤ 7.3 on room air

Caused by direct or indirect injury to lungs, airways, or chest wall (physical injury, or disease processes)
– A potential complication of any major surgical procedure
– Common complications include atelectasis, pneumonia, pulmonary edema, pulmonary emboli

Symptoms vary with the cause (hypoxemia or hypercapnia)
– Headache, dyspnea, confusion, restlessness, hypertension followed by hypotension and tachycardia…

Treatment depends on primary cause – often both
– hypercapnia (↑CO2)-inadequate arteriolar ventilation
-Requires ventilatory support

– hypoxemic – inadequate O2 exchange between alveoli and capillaries
– Requires supplemental O2

Describe the pathophysiology associated with pulmonary edema and acute respiratory distress syndrome.

– Acute injury and inflammation to the alveolocapillary membrane

Pulmonary inflammation
Increased capillary permeability
Severe pulmonary edema*
V/Q mismatch

Discuss the risk factors and pathologic changes associated with pulmonary hypertension.

Risk Factors:
Classified into several groups based on cause
– No known cause
– Heart disease
– Chronic lung disease or hypoxia (COPD common)
– Multifactorial mechanisms (blood, metabolic and systemic diseases)
Hypoxemia causes vasoconstriction of pulmonary arteries

Pathologic changes:
– Endothelial dysfunction – ↑ vasoconstrictors, ↓ vasodilators
– Hypertrophy of smooth muscles in the pulmonary artery wall, narrowing the small pulmonary artery (arterioles)
– Remodeling: Fibrosis and thickening of vessel walls increasing vascular resistance
– ↑ pressures in the lung, ↑pressures in right ventricle

Describe similarities, clinical manifestations, underlying mechanisms, and consequences of obstructive pulmonary diseases.

– Progressive loss of lung tissue
– “Pink puffer”
– Weight loss
– Mild hypoxemia, no hypercapnia initially
– Hypoventilation and hypercapnia noted in later stages
– Few secretions

Chronic Bronchitis
– Chronic airway inflammation
– “Blue bloater”
– Obese
– Hypoxemia and hypercapnia
– Increased hematocrit
– Cor pulmonale
– Lots of secretions

Chronic Bronchitis

– Hyper secretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years.

Inflammation d/t inspired irritants or an upper respiratory infection
– Infiltration of neutrophils, macrophages, and lymphocytes into bronchial wall
– Continued inflammation leads to chronic bronchitis

Increased mucus production – ↑number of goblet cells resulting in ↑ mucus

– Edema and spasms – chronic inflammation
-Chronic cough – Impaired movement and eradication of cilia
– Airways collapse early in expiration trapping air in distal portion of lung

– V/Q abnormalities
– Hypoventilation and hypercapnia

– Overweight, smoker, shortness of breath upon exertion, excessive sputum, chronic cough
– Copious amounts of sputum as disease progresses with frequent pulmonary infections.
– ABGs: Hypoxemia, hypercapnia, respiratory acidosis
– Evidence of airway obstruction
-Spirometry: Decreased FEV1; decreased FEV1/FCV (<70%)
– ↑ residual volume as airway obstruction and air trapping become more pronounced

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