NUR 226 Exam 2 Questions and Correct
Answers
RAAS regulates long-term BP and extracellular volume
1. Angiotemsionogen released by the liver in response to low BP and changes in blood
volume
2. Low fluid volume stimulates the kidney to release renin which causes the liver to
convert angiotensinogen to angiotensin I
3. Angiotensin I travels to the lung where it is converted by Angiotensin II by ACE
(angiotensin-converting enzyme)
4. Angiotensin II acts on the adrenal glands to cause the release of aldosterone, which
then causes fluid retention
5. Angiotensin II is a potent vasoconstrictor-- it also seems to cause inappropriate
remodeling of the heart after a heart attack
6. This ultimately causes the nephron to retain fluid and the BP goes up ✅Renin
Angiotensin Aldosterone System
- receptors in the carotid sinus, aorta, and left ventricle
- sense BP and can alter the BP by altering heart rate
- can also impact vasodilation and vasoconstriction ✅Arterial baroreceptors
- helps maintain consistent levels of tissue perfusion
- regulates based on mean arterial pressure
- alters the resistance (diameter) in arterioles
- helps keep consistent BP at the tissue levels despite changes that are occurring in
other mechanisms ✅Vascular autoregulation
Systolic— less than 120 AND Diastolic— less than 80 ✅Normal BP
Systolic— 120-129 AND
Diastolic— less than 80 ✅Elevated BP
Systolic— 130-139 OR
Diastolic— 80-89 ✅High BP Stage 1
Systolic— 140 or higher OR
Diastolic— 90 or higher ✅High BP Stage 2
Systolic— higher than 180 AND/OR
Diastolic— higher than 120 ✅Hypertensive crisis
- Occurs when there is NO KNOWN CAUSE of hypertension— usually because of an
absence of underlying disease process
, - Occurs due to complicated interactions of genetics and the environment, and involving
several neurohormonal effects (SNS, RAAS, Natriuretic peptides) ✅Primary/Essential
hypertension
- smoking
- excess sodium intake
- sedentary lifestyle
- hyperlipidemia
- stress
- family history and genetics
- obesity
- age >60
- African Americans
- high alcohol consumption ✅Risk factors for primary hypertension
- hypertension with a KNOWN cause
- usually related to underlying disease or disorder: health conditions, certain medicines,
pregnancy, hormonal therapy, renal disease, tumors, drugs such as corticosteroids,
antihistamines, cocaine, and amphetamines
- treatment is to treat the underlying cause ✅Secondary hypertension
NO! "silent killer"
- must look for signs of end-organ damage: chest pain (heart), headache (brain), visual
changes (eyes), weakness or pain in extremities (brain/stroke) ✅Are there signs and
symptoms of hypertension?
- increased left ventricular work
- hypertrophy— enlargement of LV
- accelerated progression of atherosclerosis
- increased risk for aortic aneurysm ✅Long term outcomes of hypertension— cardiac
Primary cause of end-stage renal disease ✅Long term outcomes of hypertension—
kidneys
Higher risk for stroke, aneurysm, or hemorrhage ✅Long term outcomes of
hypertension— brain
Retinopathy and blindness ✅Long term outcomes of hypertension— eyes
Gangrene and intermittent claudication ✅Long term outcomes of hypertension— lower
extremities
- uncontrolled BP that leads to end-organ damage (>180/120)
- symptoms: headache, blurry vision, stroke, brain hemorrhage, chest pain, acute
coronary syndrome, heart dysfunction
Answers
RAAS regulates long-term BP and extracellular volume
1. Angiotemsionogen released by the liver in response to low BP and changes in blood
volume
2. Low fluid volume stimulates the kidney to release renin which causes the liver to
convert angiotensinogen to angiotensin I
3. Angiotensin I travels to the lung where it is converted by Angiotensin II by ACE
(angiotensin-converting enzyme)
4. Angiotensin II acts on the adrenal glands to cause the release of aldosterone, which
then causes fluid retention
5. Angiotensin II is a potent vasoconstrictor-- it also seems to cause inappropriate
remodeling of the heart after a heart attack
6. This ultimately causes the nephron to retain fluid and the BP goes up ✅Renin
Angiotensin Aldosterone System
- receptors in the carotid sinus, aorta, and left ventricle
- sense BP and can alter the BP by altering heart rate
- can also impact vasodilation and vasoconstriction ✅Arterial baroreceptors
- helps maintain consistent levels of tissue perfusion
- regulates based on mean arterial pressure
- alters the resistance (diameter) in arterioles
- helps keep consistent BP at the tissue levels despite changes that are occurring in
other mechanisms ✅Vascular autoregulation
Systolic— less than 120 AND Diastolic— less than 80 ✅Normal BP
Systolic— 120-129 AND
Diastolic— less than 80 ✅Elevated BP
Systolic— 130-139 OR
Diastolic— 80-89 ✅High BP Stage 1
Systolic— 140 or higher OR
Diastolic— 90 or higher ✅High BP Stage 2
Systolic— higher than 180 AND/OR
Diastolic— higher than 120 ✅Hypertensive crisis
- Occurs when there is NO KNOWN CAUSE of hypertension— usually because of an
absence of underlying disease process
, - Occurs due to complicated interactions of genetics and the environment, and involving
several neurohormonal effects (SNS, RAAS, Natriuretic peptides) ✅Primary/Essential
hypertension
- smoking
- excess sodium intake
- sedentary lifestyle
- hyperlipidemia
- stress
- family history and genetics
- obesity
- age >60
- African Americans
- high alcohol consumption ✅Risk factors for primary hypertension
- hypertension with a KNOWN cause
- usually related to underlying disease or disorder: health conditions, certain medicines,
pregnancy, hormonal therapy, renal disease, tumors, drugs such as corticosteroids,
antihistamines, cocaine, and amphetamines
- treatment is to treat the underlying cause ✅Secondary hypertension
NO! "silent killer"
- must look for signs of end-organ damage: chest pain (heart), headache (brain), visual
changes (eyes), weakness or pain in extremities (brain/stroke) ✅Are there signs and
symptoms of hypertension?
- increased left ventricular work
- hypertrophy— enlargement of LV
- accelerated progression of atherosclerosis
- increased risk for aortic aneurysm ✅Long term outcomes of hypertension— cardiac
Primary cause of end-stage renal disease ✅Long term outcomes of hypertension—
kidneys
Higher risk for stroke, aneurysm, or hemorrhage ✅Long term outcomes of
hypertension— brain
Retinopathy and blindness ✅Long term outcomes of hypertension— eyes
Gangrene and intermittent claudication ✅Long term outcomes of hypertension— lower
extremities
- uncontrolled BP that leads to end-organ damage (>180/120)
- symptoms: headache, blurry vision, stroke, brain hemorrhage, chest pain, acute
coronary syndrome, heart dysfunction
