NURS PRORTAGE PATHOPHYSIOLOGY ATI EXAM
QUESTIONS WITH CORRECT ANSWERS
2022/2023
ABG Arterial Blood Gas Normal Ranges: - pH=acid
or base 7.35-7.45
PCO2=partial pressure of carbon
dioxide 35-45 mm Hg
HCO3=bicarbon
ate 22-26 mEq/L
PO2=partial pressure of
oxygen 80-100 mmHg
Acute respiratory distress syndrome (ARDS - - can be caused by several
different conditions, all lead to similar pathologic lung changes.:
Aspiration:
- Near drowning, aspirating gastric contents
Drugs, Toxins, and Therapeutic Agents
- Free-base cocaine smoking, heroin,
inhaled gases (smoke, ammonia),
breathing high concentrations of
oxygen, radiation
Infection
- Septicemia
Trauma and Shock
- Burns, fat embolism, chest trauma
Disseminated intravascular coagulation
Multiple blood transfusions
affinity (of the hemoglobin molecule) - - the degree to which it is able to bind
oxygen.
Each hemoglobin molecule can bind up to four molecules of oxygen when
fully saturated. After the first oxygen is bound, it changes shape to make
each consecutive oxygen molecule easier to bind. Therefore, the affinity of
hemoglobin for oxygen increases with hemoglobin saturation. As
hemoglobin must not only bind but also release oxygen into the
,NURS PRORTAGE PATHOPHYSIOLOGY ATI EXAM
QUESTIONS WITH CORRECT ANSWERS
2022/2023
surrounding tissues, the affinity must decrease. Opposite to the binding
sequence, the affinity decreases with each passing release of oxygen.
,NURS PRORTAGE PATHOPHYSIOLOGY ATI EXAM
QUESTIONS WITH CORRECT ANSWERS
2022/2023
Airway inflammation - - caused by bronchial hyper-responsiveness to stimuli
and recurrent episodes of respiratory symptoms which are usually associated
with reversible airflow obstruction.
- three components:
1. Airway inflammation (primary event)
2. Airway hyperresponsiveness (secondary
event) 3. Airflow obstruction (secondary
event
Airway inflammation causes - - Inflammation results from complex
interactions among many inflammatory cells and mediators, including
eosinophil recruitment and airway edema. As such, inflammation is a direct
response of the immune system to a trigger.
At cellular level:
- caused by multiple inflammatory cells, including eosinophils,
lymphocytes, and mast cells. Secreted by many of these cell types,
cytokines also play a role in the chronic inflammatory response. Recent
studies further suggest the T-helper 2 (T2H) cell response is exaggerated
when children have frequent viral infections. When T2H cells are released,
more IgE is produced, further predisposing the airways for an allergic
reaction.
- Contact with a trigger stimulates the cascade of neutrophils, eosinophils,
lymphocytes, and mast cells which causes epithelial injury. This causes
airway inflammation, which further increases hyperresponsiveness and
decreased airflow. As mast cells release histamine and leukotrienes, this
causes major bronchoconstriction, inflammation, and mucus secretion. Mast
cells can trigger multiple cytokine release, which causes even more airway
inflammation. The contraction of the airways and subsequent swelling leads
to further airway obstruction.
Airway narrowing - - due to many factors.
- As the airway walls thicken due to these inflammatory reactions, the
amount of airway narrowing produced by a given amount of smooth muscle
contraction in asthma is much greater than it is in a normal airway. Thus,
even a small contraction of bronchial smooth muscle can lead to dramatic
increases in airway resistance when the bronchial walls are already
thickened from the actions of inflammatory cells and airway edema.
airway remodeling - - refers to the development of specific structural
changes in the airway wall in asthma accompanying long-standing and
severe airway inflammation. Airway remodeling and fibrosis may be the
, NURS PRORTAGE PATHOPHYSIOLOGY ATI EXAM
QUESTIONS WITH CORRECT ANSWERS
2022/2023
cause of "fixed" airflow obstruction in asthma that is not reversible with
steroids, bronchodilators, or both.
- Histologically, one will see hypertrophy of bronchial smooth muscle and
deposition of subepithelial collagen. There is a thickening of the basement
membrane of the bronchial epithelium. There is also edema and
inflammatory infiltrate in the bronchial walls, with a prominence of
eosinophils and mast cells.
Alveolar dead space - alveoli that are ventilated but not perfused (no blood
flow).
QUESTIONS WITH CORRECT ANSWERS
2022/2023
ABG Arterial Blood Gas Normal Ranges: - pH=acid
or base 7.35-7.45
PCO2=partial pressure of carbon
dioxide 35-45 mm Hg
HCO3=bicarbon
ate 22-26 mEq/L
PO2=partial pressure of
oxygen 80-100 mmHg
Acute respiratory distress syndrome (ARDS - - can be caused by several
different conditions, all lead to similar pathologic lung changes.:
Aspiration:
- Near drowning, aspirating gastric contents
Drugs, Toxins, and Therapeutic Agents
- Free-base cocaine smoking, heroin,
inhaled gases (smoke, ammonia),
breathing high concentrations of
oxygen, radiation
Infection
- Septicemia
Trauma and Shock
- Burns, fat embolism, chest trauma
Disseminated intravascular coagulation
Multiple blood transfusions
affinity (of the hemoglobin molecule) - - the degree to which it is able to bind
oxygen.
Each hemoglobin molecule can bind up to four molecules of oxygen when
fully saturated. After the first oxygen is bound, it changes shape to make
each consecutive oxygen molecule easier to bind. Therefore, the affinity of
hemoglobin for oxygen increases with hemoglobin saturation. As
hemoglobin must not only bind but also release oxygen into the
,NURS PRORTAGE PATHOPHYSIOLOGY ATI EXAM
QUESTIONS WITH CORRECT ANSWERS
2022/2023
surrounding tissues, the affinity must decrease. Opposite to the binding
sequence, the affinity decreases with each passing release of oxygen.
,NURS PRORTAGE PATHOPHYSIOLOGY ATI EXAM
QUESTIONS WITH CORRECT ANSWERS
2022/2023
Airway inflammation - - caused by bronchial hyper-responsiveness to stimuli
and recurrent episodes of respiratory symptoms which are usually associated
with reversible airflow obstruction.
- three components:
1. Airway inflammation (primary event)
2. Airway hyperresponsiveness (secondary
event) 3. Airflow obstruction (secondary
event
Airway inflammation causes - - Inflammation results from complex
interactions among many inflammatory cells and mediators, including
eosinophil recruitment and airway edema. As such, inflammation is a direct
response of the immune system to a trigger.
At cellular level:
- caused by multiple inflammatory cells, including eosinophils,
lymphocytes, and mast cells. Secreted by many of these cell types,
cytokines also play a role in the chronic inflammatory response. Recent
studies further suggest the T-helper 2 (T2H) cell response is exaggerated
when children have frequent viral infections. When T2H cells are released,
more IgE is produced, further predisposing the airways for an allergic
reaction.
- Contact with a trigger stimulates the cascade of neutrophils, eosinophils,
lymphocytes, and mast cells which causes epithelial injury. This causes
airway inflammation, which further increases hyperresponsiveness and
decreased airflow. As mast cells release histamine and leukotrienes, this
causes major bronchoconstriction, inflammation, and mucus secretion. Mast
cells can trigger multiple cytokine release, which causes even more airway
inflammation. The contraction of the airways and subsequent swelling leads
to further airway obstruction.
Airway narrowing - - due to many factors.
- As the airway walls thicken due to these inflammatory reactions, the
amount of airway narrowing produced by a given amount of smooth muscle
contraction in asthma is much greater than it is in a normal airway. Thus,
even a small contraction of bronchial smooth muscle can lead to dramatic
increases in airway resistance when the bronchial walls are already
thickened from the actions of inflammatory cells and airway edema.
airway remodeling - - refers to the development of specific structural
changes in the airway wall in asthma accompanying long-standing and
severe airway inflammation. Airway remodeling and fibrosis may be the
, NURS PRORTAGE PATHOPHYSIOLOGY ATI EXAM
QUESTIONS WITH CORRECT ANSWERS
2022/2023
cause of "fixed" airflow obstruction in asthma that is not reversible with
steroids, bronchodilators, or both.
- Histologically, one will see hypertrophy of bronchial smooth muscle and
deposition of subepithelial collagen. There is a thickening of the basement
membrane of the bronchial epithelium. There is also edema and
inflammatory infiltrate in the bronchial walls, with a prominence of
eosinophils and mast cells.
Alveolar dead space - alveoli that are ventilated but not perfused (no blood
flow).
