NUR 529 QUIZ 2 Exam Actual Exam 2026 || Most Recent Exam
2026|2027 Actual Complete Real Exam Questions And Correct
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Sympathetic outflow to the heart and blood vessels -ANSWER-arises
from neurons in the reticular formation of the brain stem. Axons of
these neurons exit the thoracic segments of the spinal cord to synapse
with the postganglionic neurons that innervate the heart. Cardiac
sympathetic fibers are widely distributed to SA and AV nodes and the
myocardium
Increased sympathetic activity -ANSWER-produces increased HR and
velocity and force of cardiac contraction.
Acute regulation of blood pressure -ANSWER-(seconds to minutes) is
necessary to correct temporary imbalances and during life-threatening
situations.
Acute blood pressure control -ANSWER-relies mainly on neural and
humoral mechanisms, with neural mechanisms producing the most
rapid response
Neural Control Centers -ANSWER-centers in the reticular formation of
the medulla and lower third of the pons, integrate and modulate with
the ANS to respond to changes in B/P
,reticular formation of the medulla and lower third of the pon -
ANSWER-This area of the brain contains the vasomotor and cardiac
control centers, and transmits parasympathetic impulses to the heart
through the vagus nerve and sympathetic impulses to the heart and
blood vessels through the spinal cord and peripheral sympathetic
nerves.
intrinsic circulatory reflexes (neural mechanism of acute arterial
pressure regulation) -ANSWER-baroreceptor and chemoreceptor
reflexes (regulation of arterial pressure)
extrinsic reflexes (neural mechanism of acute arterial pressure
regulation) -ANSWER-meaning found outside of circulation, i.e. pain,
cold (arterial pressure regulation)
neural control/pathways (neural mechanism of acute arterial pressure
regulation) -ANSWER-are channeled through the hypothalamus
(sympathetic response). (arterial pressure regulation)
Humoral Mechanisms of acute B/P regulation -ANSWER-include the
renin-angiotensin-aldosterone system, vasopressin (antidiuretic
hormone), and epinephrine/norepinephrine
Angiotensin II -ANSWER-powerful vasoconstrictor that causes BP to rise
(humoral mechanism)
,renin-angiotensin-aldosterone system (humoral mechanism) -ANSWER-
decrease BP>activation of juxtaglomerular cells in kidney>renin
production>renin to liver via circulation>renin encounters
angiotensinogen and forms angiotensin I>Angiotensin I to
lungs>encounters angiotensin-converting enzyme resulting in
conversion to Angiotensin II>stimulates secretion of aldosterone
Angiotensin II -ANSWER-stimulates the adrenal cortex to secrete
aldosterone.
Aldosterone -ANSWER-promotes sodium reabsorption by the kidney,
resulting in an increased vascular volume and an increased B/P.
Acute pericarditis -ANSWER-pericardial inflammation of less than 2
weeks, may occur as an isolated disease or the result of systemic
disease
Viral infections (e.g., with coxsackieviruses and echoviruses) -ANSWER-
are the most common cause of pericarditis
Pericarditis -ANSWER-Other causes include bacterial or mycobacterial
infections, connective tissue diseases (e.g., systemic lupus
erythematosus, rheumatoid arthritis), uremia, postcardiac surgery,
neoplastic invasion of the pericardium, radiation, trauma, drug toxicity,
and contiguous inflammatory processes of the myocardium or lung
, Acute pericarditis -ANSWER-manifestations include a triad of chest
pain, pericardial friction rub, and electrocardiographic (ECG) changes.
Nearly all people have chest pain, which is usually abrupt in onset and
sharp, occurring in the precordial area, and may radiate to the neck,
back, abdomen, or side. The pain is typically worse with deep
breathing, coughing, swallowing, and positional changes because of
changes in venous return and cardiac filling. The person often finds
relief by sitting up and leaning forward. It is important to differentiate
the chest pain from acute myocardial infarction (MI) or pulmonary
embolism (PE).
Acute pericarditis -ANSWER-diagnosis is based on clinical
manifestations.
ECG, chest radiography, and echocardiography
Friction rub
Rheumatic fever and rheumatic heart failure -ANSWER-complications of
the immune-mediated response to group A (beta-hemolytic)
streptococcal (GAS) throat infection
Rheumatic heart failure -ANSWER-can lead to the development of
chronic valvular disorders that produce permanent cardiac dysfunction
and sometimes fatal HF years later
2026|2027 Actual Complete Real Exam Questions And Correct
Answers (Verified Answers) Already Graded A+ | Guaranteed
Success!! Newest Exam | Just Released!!
Sympathetic outflow to the heart and blood vessels -ANSWER-arises
from neurons in the reticular formation of the brain stem. Axons of
these neurons exit the thoracic segments of the spinal cord to synapse
with the postganglionic neurons that innervate the heart. Cardiac
sympathetic fibers are widely distributed to SA and AV nodes and the
myocardium
Increased sympathetic activity -ANSWER-produces increased HR and
velocity and force of cardiac contraction.
Acute regulation of blood pressure -ANSWER-(seconds to minutes) is
necessary to correct temporary imbalances and during life-threatening
situations.
Acute blood pressure control -ANSWER-relies mainly on neural and
humoral mechanisms, with neural mechanisms producing the most
rapid response
Neural Control Centers -ANSWER-centers in the reticular formation of
the medulla and lower third of the pons, integrate and modulate with
the ANS to respond to changes in B/P
,reticular formation of the medulla and lower third of the pon -
ANSWER-This area of the brain contains the vasomotor and cardiac
control centers, and transmits parasympathetic impulses to the heart
through the vagus nerve and sympathetic impulses to the heart and
blood vessels through the spinal cord and peripheral sympathetic
nerves.
intrinsic circulatory reflexes (neural mechanism of acute arterial
pressure regulation) -ANSWER-baroreceptor and chemoreceptor
reflexes (regulation of arterial pressure)
extrinsic reflexes (neural mechanism of acute arterial pressure
regulation) -ANSWER-meaning found outside of circulation, i.e. pain,
cold (arterial pressure regulation)
neural control/pathways (neural mechanism of acute arterial pressure
regulation) -ANSWER-are channeled through the hypothalamus
(sympathetic response). (arterial pressure regulation)
Humoral Mechanisms of acute B/P regulation -ANSWER-include the
renin-angiotensin-aldosterone system, vasopressin (antidiuretic
hormone), and epinephrine/norepinephrine
Angiotensin II -ANSWER-powerful vasoconstrictor that causes BP to rise
(humoral mechanism)
,renin-angiotensin-aldosterone system (humoral mechanism) -ANSWER-
decrease BP>activation of juxtaglomerular cells in kidney>renin
production>renin to liver via circulation>renin encounters
angiotensinogen and forms angiotensin I>Angiotensin I to
lungs>encounters angiotensin-converting enzyme resulting in
conversion to Angiotensin II>stimulates secretion of aldosterone
Angiotensin II -ANSWER-stimulates the adrenal cortex to secrete
aldosterone.
Aldosterone -ANSWER-promotes sodium reabsorption by the kidney,
resulting in an increased vascular volume and an increased B/P.
Acute pericarditis -ANSWER-pericardial inflammation of less than 2
weeks, may occur as an isolated disease or the result of systemic
disease
Viral infections (e.g., with coxsackieviruses and echoviruses) -ANSWER-
are the most common cause of pericarditis
Pericarditis -ANSWER-Other causes include bacterial or mycobacterial
infections, connective tissue diseases (e.g., systemic lupus
erythematosus, rheumatoid arthritis), uremia, postcardiac surgery,
neoplastic invasion of the pericardium, radiation, trauma, drug toxicity,
and contiguous inflammatory processes of the myocardium or lung
, Acute pericarditis -ANSWER-manifestations include a triad of chest
pain, pericardial friction rub, and electrocardiographic (ECG) changes.
Nearly all people have chest pain, which is usually abrupt in onset and
sharp, occurring in the precordial area, and may radiate to the neck,
back, abdomen, or side. The pain is typically worse with deep
breathing, coughing, swallowing, and positional changes because of
changes in venous return and cardiac filling. The person often finds
relief by sitting up and leaning forward. It is important to differentiate
the chest pain from acute myocardial infarction (MI) or pulmonary
embolism (PE).
Acute pericarditis -ANSWER-diagnosis is based on clinical
manifestations.
ECG, chest radiography, and echocardiography
Friction rub
Rheumatic fever and rheumatic heart failure -ANSWER-complications of
the immune-mediated response to group A (beta-hemolytic)
streptococcal (GAS) throat infection
Rheumatic heart failure -ANSWER-can lead to the development of
chronic valvular disorders that produce permanent cardiac dysfunction
and sometimes fatal HF years later
