# Hypertension Nursing – Flashcards

## Unlock all answers in this set

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What is hemodynamics?
Hemodynamics is the study of the forces involved in circulating blood throughout the body
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What is arterial Blood Pressure?
Arterial blood pressure is the driving force that moves blood through the arterial side of systemic circulation.
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What is arterial pressure (AP)? How is it calculated?
Arterial pressure (AP) is a product of Cardiac Output (CO) and Systemic Vascular Resistance (SVR) or peripheral resistance (PR). To calculate Arterial pressure you use the equation: AP=CO x SVR/or PR
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What is cardiac output (CO)? How is it calculated?
Cardiac output is determined by Heart Rate (HR) x Stroke Volume (SV) for one minute. CO=HR x SV
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What is stroke volume (SV)?
Stroke volume (SV) is the amount of blood ejected from the heart with each contraction.
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What is systemic vascular resistance (SVR)?
Systemic vascular resistance (SVR) is the force opposing the movement of blood within the blood vessels (SVR or PR - Peripheral resistance)
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What are five factors that affect arterial blood pressure?
1. Cardiac Output (CO), 2. Elastic Recoil, 3. Peripheral Resistance (PR), Blood volume, Blood viscosity.
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If CO = HR x SV, what three factors heavily influence SV (stroke volume)
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Preload is the amount of blood volume in the ventricle at the end of diastole, just before the next contraction.
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What is LVED pressure? (in relation to stroke volume)
LVED pressure is: Left ventricular end diastolic pressure - the degree of stretch in the ventricle.
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Afterload is the amount of resistance that the heart must pump against.
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Stroke volume is affected by contractility, what is contractractility exactly?
Contractility in relation to stroke volume refers to the force and velocity of contraction.
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What does inotropic mean? Negative inotropic state? Positive inotropic state?
Inotropic refers to the state in which the heart muscle constractility is either increased (+ Positive inotropic state/inotrope) or decreased (- inotropic state/inotrope)
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What is a negative inotropic agent?
A negative inotropic agent is an agent which decreases (weaken) the force of muscular contractions in the heart.
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What is a positive inotropic agent?
A positive inotropic agent is an agent which increased (strengthens) the force of muscular contractions in the heart.
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Which 4 regulating systems in the body control and maintain blood pressure?
1. Autonomic nervous system, 2. Vascular endothelium, 3. Renal system (fluid volume regulating and RAAS, 4. Endocrine system
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The human renal system regulates/maintains/controls/affects blood pressure in the body through which two mechanisms?
The renal system can affect blood pressure in the body through two mechanisms. One is the Kidneys which regulate fluid volume in the body, Two is the Renin-Angiotensin-Aldosterone System.
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In which ways does the autonomic nervous system (ANS) regulate blood pressure in the body?
The autonomic nervous system (ANS) has baroreceptors (think barometric->weather->air pressure) and chemoreceptors in the heart that provide feedback. The ANS is made up of the sympathetic and parasympathetic branches
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In terms of vascular tone, what is "Steady State" referring to with regards to stimulation of the sympathetic nervous system?
If the sympathetic nervous system is stimulated, think fight or flight! You get sympathetic tone which is reflected by an increased HR and increased contractility. This results in increased cardiac output .
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Which ANS state is reflected by an increased HR and contractility? What does it result in?
The ANS state of sympathetic tone (sympathetic stimulation) is reflected by an increased HR and contractility. These increases raise cardiac output.
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In terms of vascular tone, what is "Steady State" referring to with regards to stimulation of the parasympathetic nervous system?
If the parasympathetic nervous system is stimulated, think rest and digest! You get parasympathetic tone which is reflected by an decreased HR and decreased CO cardiac output.
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Decreased HR and decreased CO are associated with stimulation of which branch of the ANS?
Decreased HR and decreased CO is indicative of parasympathetic nervous system stimulation
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Which branch of the ANS regulates blood vessels?
Blood vessels are regulated by the sympathetic branch of the ANS.
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What happens when Beta 1 (b1) receptors are stimulated?
In the heart, beta 1 (b1) stimulation results in increased HR, increased contractility, increased conduction. In the kidney b1 stimulation increases renin secretion.
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What two organs of the body does beta 1 effect?
Beta 1 (b1) receptors influence the Heart and the Kidneys
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What does beta 2 (b2) stimulation influence?
B2 stimulation influences the lungs (bronchodilation), and the arterioles (vasodilation)
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What do alpha receptors influence?
Alpha receptors influence peripheral arterioles and can cause vasoconstriction
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Describe the baroreceptor reflex (pressoceptors). In particular, where are they located, what do they do, and how do they respond to an increase/decrease in Arterial pressure (AP)?
The baroreceptor reflect is primarily located in the carotid sinus and the aortic arch. These receptors sense Arterial Pressure (AP) and relays that info the the medulla. When the AP drops, the baroreceptor reflex activates the Sympathethic Nervous System (SNS) which results in constriction of the blood vessels. This constriction increases systemic vascular resistance (SVR), increases venous return, and increases HR. When the arterial pressure (AP) is too high, the baroreceptor reflex dilates blood vessels and slows the heart rate.
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What does the baroreceptor reflex do when Arterial Pressure (AP) is too high?
The baroreceptor reflex dilates blood vessels and slows HR when arterial pressure (AP) is too high
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What does the baroreceptor reflex do when arterial pressure (AP) drops?
The baroreceptor reflex activates the sympathetic nervous system (SNS) when AP drops. This activation results in constriction of blood vessels which in turn causes an increase in systemic vascular resistance (SVR), an increase in venous return, and an increase in HR.
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Describe what vascular endothethelium is?
Vascular endothelium is exactly what is sounds like, it is a single layer of cells that lines the interior of blood vessels. It has the ability to produce vasoactive substances and growth factors.
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What functions do the vascular epithelium carry out?
Because the vascular epithelium line in interior of blood vessels and they can produce vasoactive substances and growth factors, the vascular endothelium maintain low arterial tone at rest, secrete growth factors that help the blood flow normally, and they inhibit platelet aggregation (blood clots)
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With regards the the kidneys, what happens when arterial pressure remains low?
When arterial pressure (AP) is low, the kidneys respond by retaining water. This happens by the release of renin and the activation of the renin angiotensin aldosterone system. Renal blood flow is also reduced, thereby reducing GFR (glomerular filtration rate) so you get less urine and more retained water and salt which increases blood pressure
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So, if you have arterial pressure that remains low, the kidneys release what? (which activates what?), and also what else happens to blood flow to the kidneys, which in turn causes?
AP that remains low = Renin release-> activation of RAAS. Blood flow reduced to kidneys -> decreased GFR ->more retained water and salt-> BP increase->less urine
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What is renin? Why is it released?
Renin is an enzyme produced by the kidney, duh. It is released when arterial pressure remains low and there is a decrease in renal perfusion
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What does renin do when it is released?
Renin takes this stuff called angiotensinogen (which is released by the liver), and converts it to angiotensin I.
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Great, so Renin is released, and it turns angiotensinogen into angiotensin I. Then what happens?
So renin is secreted, converts angiotensinogen to angiotensin I. Angiotensin I is the converted to Angiotensin II by what? ACE! (angiotensin converting enzyme).
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Where is angiontensin converting enzyme (ACE) found? What does it do?
Angiotensin converting enzyme (ACE) is found in the lungs primarily, but also in endothelial cells and the kidneys. It converts angiotensin I into angiotensin II.
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What does angiotensin II do in circulation?
Angiotensin II is a vasoconstrictor, it increases systemic vascular resistance and blood pressure
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Angiotensin III is actually degraded Angiotensin II (degraded by angiotensinases in the blood). It is also a vasoconstrictor - but not as strong as A II. A II and A III have very similar abilities in causing a release of aldosterone from the adrenal glands.
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What causes the release of aldosterone from the adrenal glands?
Angiotensin II & III.
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What happens as a result of aldosterone?
Aldosterone release causes sodium and fluid retention which effectively increases circulating volume. This results in an increase cardiac output and increases blood pressure.
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The endocrine system is also key in regulating blood pressure. It does this through which chemicals?
The endocrine system contains antiduretic hormone (ADH), aldosterone, and catecholamines (epinephrine and norepinephrine)
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What catecholamines that are released by the endocrine system from the adrenal medulla effect BP? What stimulates this release?
The catecholamines that are released from the adrenal medulla are epinephrine and norepinephrine. They are released as a result of sympathetic nervous system (SNS) stimulation.
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What are the effects of the release of these catecholamines?
The catecholamines (epinephrine and norepinephrine) when released activate alpha and beta receptors.
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There is another chemical besides catecholamines that is released by the adrenal gland, but instead of from the adrenal medulla this one is released from the adrenal cortex.
Aldosterone is released from the adrenal cortex as a result of angiotensin II/II stimulation
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Which hormone is released from the posterior pituitary that is also called vasopressin? What causes it to be released?
ADH (antidiuretic hormone) aka Vasopressin is released from the posterior pituitary gland. It release is stimulated when blood sodium osmolarity is increased. ADH increases extracellular volume which results in an increased blood pressure.
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When blood sodium osmolarity is increased, the release of what is stimulated?
When blood sodium osmolality is increased, the release of ADH is stimulated in the posterior pituitary. ADH increases the retention and collection of water in the kidneys which increases extracellular volume, increasing BP
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What is the definition of hypertension? How is it qualified (BP levels)
Hypertension is the sustained elevation of blood pressure. 140/90 or greater without risk factors OR greater than 130/80 with risk factors means HYPERTENSION.
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Which risk factors indicate 130/80 as hypertensive?
Risk factors such as Diabetes (especially), renal issues, and previous history of MI all make a BP of 130/80 or greater indicative of hypertension.
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What is the optimal normal BP
The optimal BP as per the JNC is <120/80
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What qualifies as "Pre-hyptertension"?
Pre hypertension is characterized as BP between 121/81 and 139/89
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Statistically, how many americans are affected by hypertension?
1 in 4 (50 million), THIS IS INCORRECT BASED ON A 2012 CENSUS of 313.9 million
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Slightly increased blood pressure increases the risk of what?
Slightly increased blood pressure increases the risk for cardiac disease.
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Hyptertention contributed to approximately how many deaths in the year 2000 as a result of what?
Hypertension resulted in the deaths of over 250,000 people in the year 2000 as a result of end organ damage over time.
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Patients who have untreated or poorly treated hypertension are most prone to what?
Patients who have untreated or poorly treated hypertension are most prone to acute rises in blood pressure
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Classify these stages of blood pressure with numbers: Normal, Prehypertension, Stage 1, Stage 2
Normal = 120/80, Prehypertension=(121-139/81-89), Stage 1=HTN (140-159/90-99), Stage 2 HTN= (>159/ >99)
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What is important to do once hypertension has been identified in a patient? (think end results of htn)
It is important to specify the presence or absence of target organ disease and additional risk factors in a patient identified as having hypertension
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What is primary hypertension?
Primary hypertension is hypertension that is not secondary to any other comorbidity. The cause could be known (white coat effect).
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What is one manifestation of primary hypertension in terms of diastolic and systolic BP?
You could have a rise in solely the systolic blood pressure, with the diastolic WNL.
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What is considered hypertensive urgency in someone with primary hyptertension?
Hypertensive urgency is when you have a rise in BP without acute end-organ damage. The diastolic blood pressure is usually >120
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What is considered a hypertensive emergency in someone with primary hypertension?
Hypertensive emergency is when you have a rise in BP with acute end organ damage. The diastolic blood pressure is usually >120
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What is secondary hypertension?
Secondary hypertension is caused by another etiology
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What are (5) broad causes of secondary hypertension? (think systems)
Five causes of secondary hypertension are; Renal, structural, endocrine, medications, pregnancy
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If someone has secondary hypertension stemming from a renal cause, what could be going on (2)?
There are two main causes of renal hypertension. 1. Renal parenchymal disease: the most common cause of secondary hypertension. Damage occurs in the kidneys. 2. Renal artery disease/renal stenosis: narrowing of 1 or more arteries that carry blood to the kidneys.
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What is a structural secondary cause of hypertension?
A structural cause of secondary hypertension is Coarctation of the Aorta. Coarctation of the aorta is the congenital narrowing of the aorta
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What is the most common cause of secondary hypertension?
the most common cause of secondary hypertension is Renal parenchymal disease
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There are three major causes of secondary hypertension from an endocrine source, what are they?
1. Phaeochromocytoma is one of the endocrine causes of secondary hypertension. 2. Hyperaldosteronism causes secondary hypertension. 3. Cushing's disease is another endocrine cause of secondary hypertension
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What is Phaeochromocytoma?
Phaeochromocytoma is a benign tumor of the adrenal medulla with increased secretion of catecholamines (epinephrine) causing hypertension
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What is hyperaldosteronism?
Hyperaldosteronism involves an adenoma of the adrenal cortex, this increases aldosterone which results in hypertension.
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Which endocrine cause of secondary hypertension involves the adrenal medulla?
Phaeochromocytoma involves a benign tumor of the adrenal medulla.
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Which endocrine cause of secondary hypertension involves the adrenal cortex?
Hyperaldosteronism involves an adenoma of the adrenal cortex, this causes an increase in aldosterone which causes hypertension
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What is cushing's disease and why is it an endocrine source of secondary hypertension?
Cushing's disease involves a benign pituitary adenoma that excretes excess adrenocorticotropic (ACTH) hormone. This leads to higher amounts of cortisol being released from the adrenal cortex resulting in hypertension.
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Which endocrine source of secondary hypertension involves the pituitary gland?
Cushing's disease involves the pituitary gland and can result in hypertension.
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What are some medications that can be a cause of secondary hypertension? There are three of them.
1. NSAIDS cause fluid retention and decrease kidney function, therefore causing hypertension 2. Decongestants - especially pseudoephedrine increase the heart rate. Thereby increasing blood pressure. They can have a negative interaction with some blood pressure medications. Decongestants directly raise the BP. 3. Migraine headache meds work by constricting blood vessels in the head, but they also affect the body (raising bp)
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How do NSAIDS contribute to secondary hypertension?
NSAIDS like ibuprofen or naproxen contribute to secondary hypertension by causing fluid retention and decrease kidney function
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How do decongestants contribute to secondary hypertension? Which one in particular? Are their interactions with other drugs that are of particular interest to us?
Decongestants (like pseudoephedrine) increase HR, therefore increasing BP. They have a negative interaction with some BP meds where they directly raise BP.
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How do migraine headache medications contribute to secondary hypertension?
Some migraine headache medications work by constricting blood vessels in the head, but also systemically which raises blood pressure.
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What are two conditions relative to pregnancy that contribute to secondary hypertension?
1. Preeclampsia (toxemia) - related to kidney problems. This is dangerous to the mother and fetus. Women with known hypertension are more likely to develop preeclampsia 2. Eclampsia is high blood pressure with seizures.
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What are pregnant women with hypertension at risk for developing during their pregnancy?
Pregnant women with hypertension are at risk for developing preeclampsia
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What is "The silent killer"? Why
The "Silent Killer" is primary hypertension. It is called this because it usually has no symptoms and the causes are multifactorial.
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With regard to severe primary hypertension, when do you see the symptoms?
In severe hypertension you usually see the symptoms secondary to the effects the heightened blood pressure has on blood vessels, organs, and tissues. Or due to the increased work load on the heart.
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What are (6) secondary symptoms of primary hypertension?
Secondary symptoms of primary hypertension; 1. Fatigue, 2. Dyspnea, 3. Activity intolerance, 4. Dizziness, 5. Palpitations, 6. Angina
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What 5 target areas of the body are affected by primary hypertension?
These five target areas of the body are affected by primary hypertension; 1. The eyes, 2. The heart, 3. The Kidney, 4. The Brain, 5. Peripheral Blood vessels
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When we think about the affect primary hypertension has on the eyes, what kind of damage comes to mind? (4)
Primary tension has the following affects on the eyes; 1. Blood vessel changes in the eye, 2. Visual Disturbances (Blurred vision, potential blindness), 3. Fundoscopy (Staged retinal changes), 4. Nicking of arteries, retinal hemorrhages or exudates, and papilledema (optic disc swelling)
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When we think about the affect that primary hypertension has on the heart (CAD, LVH, HF), what comes to mind? (6)
Primary hypertension has the following effects on the heart; 1. Causes a change in lipid metabolism (atherosclerosis), 2. Increases the workload of the heart (resulting in hypertrophy), 3. Decreases coronary flow (results in chest pain and angina/MI), 4. CHF, 5. Tachycardia, 6. Distended neck veins
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When we think about the affect that primary hypertension has on the kidney (nephrosclerosis) , what comes to mind? (4)
Primary hypertension has the following effects on the kidney; 1. Nocturia, 2. Peripheral edema (H20/Na), 3. Urinary alterations (sediment, proteinuria, microalbuminuria), 4. Elevated serum creatinine
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What are some effects that primary hypertension has in the urine?
Primary hypertension can cause sediment in the urine as well as proteinuria, and microalbuminuria.
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What are some effects that primary hypertension has on the brain? (cerebrovascular disease)
Primary hypertension is often asymptomatic in the brain, however is can result in TIA, CVA, forgetfullness, dizziness, syncope, blackouts, anxiety, etc...
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Despite the effects of primary hypertension on the brain being asymptomatic, what symptoms might you see?
Primary hypertension's effect on the brain can result in the symptoms of headaches and migraines.
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What are (3) effects that primary hypertension can have on peripheral blood vessels (PVD)?
Primary hypertension can result in the following effects on the peripheral blood vessels; 1. Absence of major pulses, 2. Intermittent claudication, 3. Epistaxis
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What is intermittent claudication?
Intermittent claudication is pain that is experienced when walking or exercising that goes away when a person rests
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What are (4) non modifiable risk factors in primary hypertension?
Non-modifiable risk factors in primary hypertension; 1. Age, 2. Gender, 3. Family history, 4. Ethnic group
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What are five modifiable risk factors in primary hypertension?
Modifiable risk factors in primary hypertension; 1. Stress, 2. Body weight, 3. Nutrients, 4. Health practices, 5. Secondary health problems
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What health practices in particular pose a risk factor for primary hypertension (4)?
Health practice risk factors in primary hypertension; 1. Smoking, 2. Elevated serum lipids, 3. Sedentary life style, 4. Excessive alcohol
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What is an example of a secondary health problem that is a modifiable risk factor in primary hypertension?
A secondary health problem that is a modifiable risk factor in primary hypertension is diabetes mellitus.
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When assessing a client with hypertension, what do we assess first?
We assess a clients history first. The history of present illness (HPI) is key.
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What are some signs and symptoms in a patient's history that point to hypertension? (5)
Signs and symptoms of hypertension; 1. Fatigue, 2. Early morning occipital and pulsing headache, 3. Dizziness or fainting, 4. Epistaxis, 5. Impotence
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At what point (BP level) does hypertension usually become symptomatic?
Hypertension is often not symptomatic until BP reaches 220/110
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What other components of a client's history are important in assessing for hypertension? (3)
The clients; 1. personal and family history, 2. Lifestyle, and 3. Medications all play an important role in assessing a client's history with hypertension.
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After getting a client's history, which assessment do we perform next?
After getting a client's history, we make a physical assessment next.
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After performing a physical assessment of a client with hypertension, what assessment do we conduct next?
Once the physical assessment is completed, a psychosocial assessment is done with the client.
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What are some important guidelines in performing the initial diagnostic bp assessment? (3)
During the initial diagnostic BP assessment; 1. The BP should be based on reproducible measurements 2-3 times (at least two minutes apart), 2. Refrain from smoking or caffeine (at least 30 minutes before), 3. Seated with feet on the floor, with back and arm supported and arm at heart level seated quietly for 5 minutes.
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How many readings should the initial diagnostic BP be based on? How far apart should they be spaced at least?
The initial diagnostic BP should be based on 2-3 readings at least 2 minutes apart
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How long before taking a blood pressure reading should a client refrain from caffeine or smoking?
A client should refrain from smoking or caffeine for at least 30 minutes before a reading is taken
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When measuring blood pressure, what part of the stethoscope should you use?
When assessing blood pressure, use the bell of the stethoscope
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How do you choose the correct BP cuff size for a patient?
The correct cuff size has the width of the bladder at 40 percent of arm circumference, and the length 80 percent of arm circumference
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Why take BP in both arms? What is the normal pressure difference between both arms of a client?
You should assess both arms and compare the two readings. The normal pressure difference between 2 arms is 5-10mmhg.
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What is the auscultatory gap?
The auscultory gap is the period between hearing Korotkoff sounds, then none, then hearing again. The mechanism is not clearly understood; but may be related to stiffening of the arteries in older hypertensive people.
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How do you avoid the auscultatory gap?
To avoid the auscultatory gap you should inflate the cuff 20-40mmhg more than needed to occlude the brachial pulse. Obtain BP by palpation before auscultating.
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What are some workups done prior to therapy in a patient with primary hypertension? (4)
Workups performed prior to therapy in a client with primary hypertension; 1. Urinalysis, 2. Blood chemistry, 3. 12-lead ECG, 4. Chest Xray (for LVH: left ventricular hypertrophy)
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When doing a urinalysis on a patient with primary hypertension, what are we looking at?
In a urinalysis for a patient with primary hypertension we look at protein, RBC, and casts to evaluate renal end organ effects.
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When we get a blood chemistry profile on a patient with primary hypertension, what are we looking at?
In a blood chemistry panel for a patient with primary hypertension we are looking at; Serum Electrolytes and Uric acid, BUN and Creat, Fasting blood glucose, Cholesterol: HDL & LDL & Triglycerides, and Hgb and HCT
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Why would we want to look at a 12 lead ECG of a patient with primary hypertension?
We would look at a 12 leak ECG because we want to assess cardiac involvement
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Why would we want to look at a chest xray in a patient with primary hypertension?
We would look at an xray in a patient with primary hypertension because we are assessing for left ventricular hypertrophy (LVH)
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Our primary goal in testing a patient with secondary hypertension is to what?
Our primary goal in testing a patient with secondary hypertension is to test for possible causative conditions.
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What 'venues' are we testing in a patient with secondary hypertension (think 5 causes of secondary htn)?
We are doing; 1: renal testing, 2. Structural, 3. Endocrine, 4. Medication, 5. Pregnancy
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What types of renal testing are we doing on patients with secondary hypertension? (5)
We are doing a renal arteriogram and digital subtraction test, captopril enhanced radiography to identify renal artery stenosis, Duplex ultrasonography, MRA (magnetic resonance angiography), 24 hr urine for 17-keto-steroids (to determine presence of abnormal androgens from the adrenal cortex)
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Why would we be doing a captopril enhanced radiography study on a patient with secondary hypertension?
We would do a captopril enhanced radiography study to identify renal artery stenosis
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Why would we want to conduct a digital subtraction test on a patient with secondary hypertension?
We use digital subtraction tests to visualize blood vessels in a bony or dense soft tissue environment
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What types of structural studies do we do on a patient with secondary hypertension? (3)
We conduct these structural studies on patients with secondary hypertension; 1. Aortogram, angiogram, BP in both arms (findings of a big difference)
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Why aren't beta blockers used in clients with diabetes and hypertension?
Beta Blockers are not used in patients with diabetes and hypertension because they mask hyperglycemia and alter the metabolism of glucose.
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What are the response when alpha receptor sites are blocked?
When alpha receptor sites are blocked the body effect is peripheral arterial vasodilation.
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What is something to keep in mind about the beta blocker, Corgard?
You should not stop taking Corgard QUICKLY if you plan on stopping.
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What should the nurse monitor for with a patient taking thiazide diuretics?
For a patient with taking thiazide diuretics the nurse should monitor for hypokalemia and hyperuricemia (low K high uric acid).
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What is a common side effect of prazosin (minipress), an alpha 1 blocker?
Orthostatic hypotension is a common side effect of prazosin (minipress).
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What are three physiological responses to beta blockers?
Beta blockers cause decreasd HR, decreased contractility, decreased renin release. It also reduces 02 consumption due to the lowered workload.
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What is propanolol (inderal)?
Propanolol is a non-selective beta blocker
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Which drug class is best used for angina and hypertension?
Calcium channel blockers work directly on the heart and are best used for angina and hypertension.
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Cough is a common side effect of which drug group?
Cough is a common side effect of ACE inhibitors. (ACE: ALWAYS COUGHING EXCESSIVELY). This is relevant because it bothers them so much they stop taking the meds.
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Which drug class is more effective with African Americans?
Thiazide diuretics are more effective with African Americans. (so are calcium channel blockers)
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Triamterne (Dyrnenium) is what kind of drug?
Triamterene (dyrenium) is a potassium sparing diuretic
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What is a sign and symptom of hyperkalemia?
Diarrhea is a sign and symptom of hyperkalemia.
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What is an adverse side effect of ARB's (angiotensin receptor blockers):
Angioedema is an adverse side effect of ARB's
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Which drug has the common side effects of constipation and CHF?
Diltiazem (cardizem) a calcium channel blocker can cause constipation and more importantly CHF.
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Which two drug classes can cause CHF if you get too much of them?
Beta blockers and calcium channel blockers can cause CHF if you get too much of them
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Which classes of drugs have a primary effect of decreasing preload?
Ace Inhibitors and diuretics, have the primary effect of decreasing preload. We want to decrease fluid volume to decrease preload so we know diuretics and angiotensin converting enzyme inhibitors are important.
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The nurse should monitor for which adverse side effect of a NEGATIVE INOTROPE?
You should be looking out for CHF because a negative inotrope makes the heart beat less intensely which can cause a backup.
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A patient on clonadine (catapress) therapy should be monitored for what?
The patient on clonadine should be monitored for rebound hypertension.
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Which drug should not be taken with grapefruit juice?
You don't want to take nifedipine (procardia) with grapefruit juice.
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What drug is recommended for pregnant women with hypertension?
Methyldopa is recommended for pregnant patients with hypertension.
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Which endocrine screenings are we giving patients with secondary hypertension? (5)
We are screening secondary hypertensive patients for; 1. Serum aldosterone, 2. Plasma Renin, 3. Metanephrines (urine or plasma), 4. Catecholamines (urine and plasma), 5. Scan for endocrine tumors.
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Where can we look for metanephrines, what do they indicate?
We can do a plasma or urine screening for metanephrines. Elevated metanephrines indicate adrenal issues.
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Where do we look for catecholamines? Which test is used more odten? What do they indicate?
We can do a plasma or urine screen for catecholamines. They can indicate the presence of a pheochromocytoma. Urine screens for vanillamandelic acid (VMA) is no longer commonly used.
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What are (5) non pharmacological methods to manage hypertension?
non pharmacological methods to manage hypertension; 1. Smoking cessation, 2. Diet, 3. Exercise, 4. Modification of ETOH ingestion, 5. Stress management.
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With regards to the non pharmacological approach to managing hypertension with Diet, list four components of this approach.
Diet management of hypertension involves; 1.Sodium restriction, 2. Electrolytes (K+, Ca, Mg), 3. Restrict cholesterol and saturated fats, 4. Reduce weight (if indicated)
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What are the goals of pharmacological therapy? (2)
The goals of pharmacological therapy are to; 1. Control blood pressure with minimum of side effects, 2. Maintain tissue perfusion during activity and rest.
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There are 8 types of antihypertensive medications that exist. These are the classes of medications. What are they?
Classifications of antihypertensive medications; 1. Diuretics, 2. Aldosterone Inhibitors, 3. Adrenergic inhibitors, 4. Angiotensin inhibiors, 5. Renin blockers, 6. Calcium channel blockers, 7. Vasodilators, 8. Combination drugs
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With regards to diuretics, there are three types. What are they and what are examples of each?
Three types of diuretics; 1. Thiazides (Hydrochlorothiazide, metolazone), 2. Loop (furosemide, bumetanide), 3. Potassium-sparing (spironolactone, triamterene)
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Hydrochlorothiazide (hydrodiuril) and metolazone (Zaroxolyn) are what type of antihypertensive medication?
Hydrochlorothiazide (hydrodiuril) and metolazone (Zaroxolyn) are thiazide diuretics.
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Furosemide (lasix) and bumetanide (bumex) are what types of antihypertensive medications?
Furosemide (lasix) and bumetanide (bumex) loop diuretics
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Spironolactone (aldactone) and triamterene are which type of antihypertensive medications?
Spironolactone (aldactone) and triamterene are potassium sparing diuretics.
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Spironolactone (aldactone) and eplenerone (inspra) are both effective at what? (a different antihypertensive class)
Spironolactone (aldactone) and eplenerone (inspra) are both effective at inhibiting aldosterone.
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There are 6 types of adrenergic inhibitors, what are they?
The six types of adrenergic inhibitors are; 1. Beta blockers, 2. Alpha 1 blockers (antagonists), 3. Alpha 2 agonists (central acting adrenergic antagonists), 4. Alpha-beta adrenergic blockers, 5. Ganglionic blocking agents, 6. Postganglionic agents (peripheral acting adrenergic antagonists)
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What are the two types of angiotensin inhibitors?
The two types of angiotensin inhibitors are; 1. ACE inhibitors, Angiotensin II receptor blockers (ARBS)
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What is an example of a Renin blocker (this is a new med)?
Aliskarin (tekturna) is an example of a renin blocker.
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With regards to calcium channel blockers, what three drugs are in this class?
Three calcium channel blocker drugs; 1. Dihydropyridine (nifedipine, amlodapine), 2. Phenylalkylamine (verapamil), 3. Benzothiazepine (diltazem)
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What does the drug Dihydropyridine (nifedipine, amlodapine) do? What is important to know about this drug? What kind of drug is it?
The drug Dihydropyridine (nifedipine, amlodapine) reduces SVR (systemic vascular resistance) and AP (arterial pressure). This drug is only for STABLE angina. This is a calcium channel blocker.
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What kind of drug is phenylalkylamine (verapamil), what does it do?
Phenylalkylamine (verapamil) is a calcium channel blocker. It is selective for the myocardium and reverses cardiovasospasm.
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What kind of drug is benzothiazapine (diltazem)? What does it do?
benzothiazapine (diltazem) is a calcium channel blocker. It is a cardiac depressant and has vasodilatory effects.
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With regards to the antihypertensive drug class of Vasodilators, what two types are they and what are examples of each?
Vasodilators; 1. Arterial vasodilators (Hydralazine/apresoline, Diazoxide/hyperstat, Minoxidil/minodyl), 2. Venous/Arterial vasodilators (Nitroprusside/nipride, prazosin/minipres)
question
What kind class and effect are the following drugs; Hydralazine (apresoline), Diazoxide (hyperstat), Minoxidil (minodyl)?
Hydralazine (apresoline), Diazoxide (hyperstat), Minoxidil (minodyl) are all ARTERIAL vasodilators
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What kind class and effect are the following drugs; Nitroprusside (nipride), Prazosin (Minipres)?
Nitroprusside (nipride), Prazosin (Minipres) are VENOUS/ARTERIAL vasodilators
question
What is the combination drug aldactazide?
Aldactazide is a comination of two diuretic medications; spironolactone ( a potassium sparing diuretic with aldosterone inhibiting activity) and hydrochlorothiazide (a thiazide diuretic)
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What is the comination drug combipres?
Combipres is clonidine and chlorthalidone.
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What is the combination drug dyazide?
Dyazide is diuretic combination; hydrochlorothiazide (a thiazide diuretic) and triamterene (a potassium sparing diuretic)
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What is the combination drug inderide?
Inderide is propanolol (inderal - a beta blocker) and Hydrochlorothiazide (a thiazide diuretic)
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What do diuretics do in the body?
Diuretics increase NA and H20 excretion. They initially reduce fluid volume (decrease preload through excretion of H20 and electrolytes) and decrease systemic vascular resistance (afterload)
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If you are taking a diuretic and are losing H20 and Na, what adverse side effects would you expect? (2)
If you are taking a diuretic and losing H20 and Na, you would expect to see; Hypovolemia/dehydration, Hyponatremia.
question
What are three examples of thiazide diuretics? What nursing considerations are important for thiazides?
Thiazide diuretics; Hydrodiuril, Zaroxolyn, Diuril. It is important to know that NSAIDS+Thiazides=nephrotoxicity, Thiazides+digoxin/digitalis=toxicity/hypercalcemia/hypokalemia, we must advise the client to eat K+ rich foods
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What is the action of thiazide diuretics?
Thiazide diuretics inhibit Na reabsorption in the distal convoluted tubule. It INCREASES Na and H20 excretion
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What is the bodies response to the action of thiazide diuretics?
Thiazide diuretics cause a decrease in SVR (PR), Decreased afterload, decreased preload
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Thiazide diuretics are best used in which populaions? They are good for what kind of therapy?
Thiazide diuretics are best used for African Americans and the Elderly. They are best suited for long term therapy.
question
Some side effects of thiazide diuretics are (7)?
Thiazide diuretics can cause; Hypovolemia, Hyponatremia, Hypokalemia, Hyperuricemia, Hyperglycemia (glucose intolerance), Hypercalcemia, and ARRYTHMIAS
question
We should use caution when giving thiazide diuretics to patients who have...(4)
Thiaizide diuretics should be used cautiously in patients with; 1. Diabetes, 2. Gout, 3. Severely impaired renal function, 4. On digoxin/digitalis
question
We should be checking what periodically throughout thiazide therapy? (2)
We should be checking orthostatic vital signs and monitoring lab values (Na, K BUN, Creat) periodically.
question
What are three examples of loop diuretics?
Loop diuretics; 1. Lasix, 2. Bumex, 3. Demadex
question
What is the action of loop diuretics?
Loop diuretics (Lasix, Bumex, Demadex) inhibit reabsorption of NaCl in the loop of henle. Na, Cl, K, and H20 excretion is increased
question
What is the physiological response to the action of loop diuretics?
Loop diuretics cause a decrease in SVR (PR), decrease in afterload, and decreased preload.
question
Loop diuretics are best used with which type of patients?
Loop diuretics are best used in patient's with impaired renal function and congestive heart failure.
question
What are some adverse effects of loop diuretics?
Loop diuretics have similar adverse affects as thiazides; hypovolemia, hyponatremia, hypokalemia, hyperuricemia, hyperglycemia, arrythmias, but NO HYPERCALCEMIA
question
We should use loop diuretics cautiously in..
Loop diuretics should not be used in patients with; Anuria and used cautiously in patients on Lithium (reduced renal function, lithium tox), Digoxin (K loss, dig toxicity), amino glycosides (antibiotics; streptomycin, neo, genta, tobra)
question
In general, we should use diuretics cautiosly in patients taking corticosteroids. Why is this?
Diuretics and corticosteroids can result in hypokalemia, and reduced effect of the diuretic.
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In general, we should use diuretics cautiously in patients taking sulfanylureas (diabetic -ides drugs). Why is this?
Because concurrent usage of diuretics and sulfonylureas can cause hyperglycemia.
question
What are two examples of potassium sparing diuretics?
Potassium sparing diuretics; 1. Aldactone (spironolactone), 2. Dyrenium (triamterene)
question
What is the action that potassium sparing diuretics take in the body?
Potassium sparing diuretics inhibit action of aldosterone on the sodium-potassium pump (Na-K pump) in the distal convoluted tubule, they exchange K+ for Na.
question
What is the physiological response to potassium sparing diuretics action in the body?
Potassium sparing diuretics cause decreasd SVR (systemic vascular resistance (PR), decreased afterload, decreased preload
question
Potassium sparing diuretics are best used.....
Potassium sparing diuretics are best used in patients who need to have K+ conserved, and together with a loop diuretic.
question
What are some adverse side effects of potassium sparing diuretics?
Potassium sparing diuretics can cause hyperkalemia and orthostatic hypotension.
question
Potassium sparing diuretics should be used cautiously in patients with... (4)
Potassium sparing diuretics should be used cautiously in patients with; 1. Renal insufficiency, 2. Diabetics, 3. Usually not given with ACE inhibitors (excessive K, has an additive effect), 4. Usually not given with ARBS (angiotensin II receptor blockers)
question
Beta blockers are of what class of antihypertensive medications?
Beta blockers are adrenergic inhibitors (antagonists)
question
What receptors do the antihypertensive adrenergic inhibitor drugs known as beta blockers act on?
Beta blockers block beta-adrenergic receptors. There are 2 receptors; Beta 1 (Heart and Kidney), and Beta 2 (Bronchial and vascular smooth muscles)
question
What is the action of a drug that blocks beta 1 receptors?
Beta blockers that block; BETA 1 receptor blockers decrease HR, decrease contractility (aka inotropic), and decrease conduction. BETA 1 receptor blockers also decrease renin secretion in the kidney
question
Drugs that decrease contractility are called what?
Negative inotropes
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So, BETA 1 receptor blockers act on which target organs?
Beta 1 receptor blockers act on the Heart and the Kidneys
question
Beta 2 receptor blockers act on which target tissues? What do they do?
Beta 2 receptor blockers (antagonists) act on bronchial and vascular smooth muscles causing bronchocontriction.
question
There are two types of beta blockers, what are they and what makes them different from each other?
NON-CARDIOSELECTIVE beta blockers block both Beta 1 (Heart-decrease contractility & HR & Conduction, Kidneys-decrease renin secretion) and Beta 2 receptors (bronchial and vasular smooth muscle). CARDIOSELECTIVE beta blockers only block beta 1 receptors and have no effect on the lungs
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What is the primary physiological response that beta blockers have in the body? (7)
beta blockers primarily; Decrease SVR, decrease afterload, decrease contractility, decrease HR, decrease Renin, decrease myocardial O2 demand, cause bronchoconstriction.
question
Beta blockers are best used in which types of patients? Cardioselective beta blockers are preferred for who?
Beta blockers are best used in Caucasians, Patients post MI, patients with peripheral vascular disorders, and angina. CARDIOSELECTIVE beta blockers produce fewer side effects and are preferred for patients with Asthma/COPD and diabetics
question
What are some adverse side effects of beta blockers (4)? What are some that are specifically non-selective?
Beta blockers can cause; Bradycardia, CHF, fatigue, Hypertriglyceridemia. Specifically non-selective side effect is bronchospasm.
question
What happens if beta blockers are discontinued abruptly?
When beta blockers are discontinued abruptly the patient is at risk of reflex tachycardia
question
What drugs when abruptly discharged put the patient at risk for reflex tachycardia?
When beta blockers are abruptly withdrawn a patient is at risk for reflex tachycardia.
question
What should we watch for with a patient taking beta blockers? why?
With a patient taking beta blockers we should watch for S/S of heart failure. This is because decreased HR can lead to bradycardia and decreased contractility can lead to heart failure and fatigue.
question
What are some examples of cardioselective beta blockers?
Lopressor (metoprolol), Tenormin (atenolol), Brevibloc (esmolol) are all cardioselective (beta 1) beta blockers.
question
What are some examples of non-cardioselective beta blockers?
Inderal (propanolol) and corgard (nadolol) are all non-cardioselective (beta 1 and 2) blockers
question
We should use beta blockers cautiously in patients that... Specifically with non-cardioselective drugs we need to be careful with patients that..
We should use beta blockers cautiously in patients that have CHF, Heart Block (conduction issues). Specifically, non-cardioselective drugs should be used cautiously in patients with COPD (bronchospasm), Asthma (bronchospasm), and diabetics (masks S&S of hypoglycemia)
question
What are some other nursing considerations that we should have for patients taking beta blockers? (6)
Patients taking beta blockers should; 1. Have BP and HR monitored, 2. Be monitored for signs of HF, 3. Understand a decreased tolerance for exercise, 4. That beta blockers mask hypoglycemic signs (non-selective), 5. That caution must be taken with asthma (non-selective), 6. That they shouldn't be stopped abruptly (rebound hypertension, reflex tachycardia, and can exacerbate ichemic heart disease).
question
What do angiotensin inhibitors do? What three types are there?
Angiotensin inhibitors are drugs that act on the RAAS (Renin-Angiotensin-Aldosterone System). There are three types of Angiotensin inhibitors; 1. ACE inhibitors (ACEI's), 2. Angiotensin II receptor blockers (ARBs), 3. Renin blockers
question
There a 5 ACE inhibitors, how can they be identified (suffix), and what are they?
Ace inhibitors can be identified with the suffix "-pril". 1. Captopril (capoten), 2. Enalapril (vasotec), 3. Lisinopril (prinivil, zestril), 4. Benazapril (lotensin), 5. Quinapril (Accupril)
question
What is the action of ACE (angiotensin converting enzyme) inhibitors?
ACE inhibitors interfere with the conversion of angiotensin I to angiotensin II (II is a potent vasoconstrictor) and this results in vasodilation. They increases sodium and H20 excretion as well.
question
ACE inhibitors increase the excretion of what? (2)
ACE inhibitors increase the excretion of sodium and H20.
question
What physiological response do ACE inhibitors have on the body? (6)
ACE inhibitors cause; decreased SVR (PR), Decreased afterload, Decreased preload, decreased proteinuria, decreased nephropathy progress, decreaesed endothelial dysfunction.
question
ACE inhibitors are best used in patients with...
ACE inhibitors are best used in patients with; Myocardial infarction (MI), CHF, Diabetics, Young caucasians.
question
What are some adverse side effects of ACE inhibitors? (11)
Some adverse side effects of ACE inhibitors are; 1. Persistent dry cough, 2. Dizziness, 3. Headache, 4. Dizziness, 5. Diarrhea, 6. Rash, 7. Hyperkalemia, 8. "1st dose" HYPOtension, 9. Hypotension (NA/volume depletion), 10. Neutropenia, 11. Angioedema (rare)
question
What is a rare but serious adverse side effect of ACE inhibitors?
A rare but serious side effect of ACE inhibitors is Angioedema
question
What cautions should we take in a hypertensive patient taking an ACE inhibitor? (3)
Caution is advised in hypertensive patients taking an ACE inhibitor that are; 1. African American (may need to take a diuretic along with ACEI), 2. ASA/NSAIDS may reduce drug effectiveness, 3. NEVER used in pregnant women (teratogen)
question
What might African Americans require if they are taking an ACE inhibitor?
African Americans taking an ACE inhibitor may require a diuretic
question
Why should ACE inhibitors never be used in a pregnant woman?
ACE inhibitors should never be used in a pregnant woman because they are teratogenic
question
What other drugs can reduce the effectiveness of ACE inhibitors?
ASA/NSAIDS can reduce the efficacy of ACE inhibitors
question
What is a nursing consideration regarding the ACE inhibitor Captopril?
Captopril should be taken 1 hr before meals because food decreases it's absorption.
question
ACE inhibitors, ARB's, and Renin blockers are all considered...
Angiotensin inhibitors; ACEI's, ARB's, Renin blockers
question
Why do we want to monitor BP, especially on the first dose of an angiotensin inhibitor?
We want to monitor BP, especially on the first dose of an angiotensin inhibitor because of "1st dose" hypotension.
question
What are the most frequent adverse side effects of ARB's (angiotensin receptor blockers)? (3)
The most frequent side effects of ARB's (angiotensin receptor blockers) are; 1. Upper respiratory infection, 2. dizziness, 3. Diarrhea
question
What other nursing considerations (other than monitoring BP) are important in a patient taking angiotensin inhibitors? (4)
Nursing considerations for patients taking angiotensin inhibitors include; 1. Monitor I and O's, 2. Monitor WBC's (for agranulocytosis, neutropenia), 3. Monitor for hyperkalemia, 4. Monitor for side effects (cough, rash, loss of taste, angioedema <- swelling involves face, neck ,lips, larynx, hands, etc.)
question
Where should we assess for angioedema in a patient recieving angiotensin inhibitors?
In a patient receiving angiotensin inhibitors we want to look for angioedema (swelling) in the face, neck, lips, larynx, and hands)
question
What should we keep in mind when teaching about losartan (an angiotensin receptor blocker- ARB) to a patient?
When teaching about losartan to a patient we want to tell them that they should change positions slowly (orthostatic hypotension)
question
Why do we need to have caution with ASA/NSAIDS in patients taking angiotensin inhibitors? Who is particularly at risk?
Patients taking angiotensin inhibitors are at greater risk for nephrotoxicity if they take ASA/NSAIDS. Particularly the elderly and those patients taking a diuretic.
question
What is the action of ARB's (angiotensin receptor blockers)?
Angiotensin Receptor Blockers (ARBs) Directly block the effects of vasoconstrictor angiotensin II. They relax vascular smooth muscle tone, and increase excretion of Na and H20
question
What is the suffix associated with Angiotensin Receptor Blockers (ARBs)?
Angiotensin receptor blockers (ARB's) have the suffix "-sartan"
question
Which antihypertensive drugs have the suffix "-sartan"?
The angiotensin inhibitors ARBs (angiotensin receptor blockers) have the suffice "-sartan".
question
What are the names of two ARB's (angiotensin receptor blockers)?
Losartan (cozaar), and Valsartan (diovan) are both ARB's
question
What is the physiological response that the body has to ARBs?
ARBs have the following effects on the body; decreased SVR (PR), decreased afterload, decreased preload, decreased endothelial dysfunction
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What are some adverse side effects of ARB's? What are the serious side effects?
Adverse effects of of ARB's are upper respiratory infection, headache, dizziness, diarrhea. SERIOUS side effects are Angioedema, hyperkalemia.
question
What patients are ARB's best used in?
ARB's (angiotensin II receptor blockers) are best used in the same patients that ACE inhibitors are best used in; MI, CHF, Diabetics, Young Caucasians. We give them to avoid side effects of ACEI's (cough). We also give ARB's to reduce afterload.
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Why would we want to give ARB's instead of ACEI's?
We would give ARB's instead of ACEI's to someone who was experiencing the adverse side effect of cough from ACEI's.
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Why would we use caution in using ARB's?
We would use caution in elderly and renal patients due to increased sensitivity and an increase in adverse effects.
question
What is the only FDA approved Renin-blocker (an angiotensin inhibitor)
The only FDA approved Renin blocker is aliskirin (tekturna)
question
What is the action of the angiotensin inhibitor Aliskirin (tekturna)?
Renin blockers inhibit action of renin in the kidney which prevents the initiation of the RAAS
question
What is the primary physiological response to Renin blockers?
Renin Blocker Aliskirin (tekturna) decreases; SVR (PR), Afterload, Proteinuria, nephropathy progress, endothelial dysfunction
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In which patients is the Renin blocker Aliskirin (tekturna) best used?
Aliskirin (tekturna) is best used in patients with MI, CHF, Diabetics, and Young caucasians
question
What are some adverse side effects of the renin blocker Aliskirin (Tekturna)
Some adverse effects of Aliskirin (tekturna) are; Stomach upset, diarrhea, angioedema, cough, headache, increased blood potassium (rare), decreases action of lasix
question
Aliskirin (tekturna) causes a decrease in the action of what drug?
Aliskirin (tekturna) decreases the action of Furosemide (Lasix)
question
We should use caution when giving the renin blocker Aliskirin (tekturna) in which patients?
We do not give the renin blocker Aliskirin (tekturna) to pregnant women.
question
What is the action of Calcium channel blockers?
Calcium channel blockers interfere with the influx of calcium ions into heart and smooth muscle, causing vasodilation. Affects contraction and conduction.
question
What is the primary physiological response the body has to calcium channel blockers?
Calcium channel blockers have the following effects on the body; Decreased SVR (PR), Afterload, Contractility (neg inotropic), HR, Atrialventricular Conduction (AVCond), and decreased myocardial demand for O2.
question
Calcium channel blockers are best used in these patients... (6)
Calcium channel blockers are are best used in African Americans, Diabetics, Angina, Gout, Hyperlipidemia, COPD
question
What are some adverse side effects of Calcium channel blockers? (8)
Some adverse effects of calcium channel blockers are Abdominal discomfort, constipation, GI Bleed, Bradycardia, AV block, headache, peripheral edema
question
What is a unique adverse side effect of Calcium channel blockers?
A unique adverse side effect of calcium channel blockers is Atrial ventricular block.
question
We should use caution in giving calcium channel blockers to which patients?
When giving calcium channel blockers we should use caution in; Short acting CCB's like nifedipine (procardia) can cause reflex tachycardia and risk for first cardiac event. Verapamil and diltiazem decrease contactility (neg inotrope) and can cause HF. We also need to be ware of Digoxin toxicity if taking Digoxin concurrently.
question
Short acting CCB's like nifedipine (procardia) can cause reflext tachycardia. It can also worsen proteinuria in patients with nephropathy.
question
What suffix is used in short acting CCB's?
The suffix "-dipine" indicates that the drug is a short acting CCB
question
Which CCB's cause Bradycardia, constipation, and peripheral edema? What should you monitor with these drugs?
The CCB's Diltiazem (cardizem) and Verapamil (calan) cause bradycardia, constipation, and peripheral edema. We need to monitor for CHF with these drugs b/c they decrease contractility.
question
Which short acting CCB causes hypotension, and reflex tachycardia?
The short acting CCB Nifedipine (procardia) causes hypotension and reflex tachycardia. You also should not have grapefruit while you are eating it.
question
Which short acting CCB requires no grapefruit or grapferuit juice intake prior to administration or high fat diet?
The short acting CCB nisoldipine requires you do not eat or drink grapefruit prior or have a high fat diet.
question
What are five common CCB's?
Common CCBs; Diltazem (cardizem), Nifedipine (procardia) - short acting, Amlodipine (Norvasc) - short acting, Verapamil (calan, isoptin), Nicardipine (cardene) - short acting.
question
What drug must we monitor the levels of if a patient is taking it and CCB's?
Digoxin and CCB's concurrently necessitate getting digoxin levels because of an increased risk of digoxin toxicity.
question
What are some nursing considerations for the less common antihypertensive drugs "Vasodilators"?
When giving vasodilators we need to be mindful of; Orthostatic Hypotension, reflex tachycardia, and fluid retention (Na and H2O).
question
What is the action of vasodilators? What about selective vasodilators?
Vasodilators directly relax the smooth muscle. Selective vasodilators directly relax arterioles and/or veins.
question
What is the physiological response to vasodilators?
Vasodilators cause; decreased SVR (PR), Arterial dilators cause decreased afterload. Venous dilators cause decreased preload.
question
What kinds of vasodilators are there? (3)
There are three types of vasodilators; Arterial dilators, arterial and venous dilators, and dopamine da-1 receptor agonists (effect peripheral/renal)
question
Vasodilators are best used in patients with...
Vasodilators are best used in patients with severe hypertension and patients in a hypertensive crisis.
question
What are some adverse side effects of vasodilators?
Vasodilators can cause postural hypotension, reflex tachrycardia, expansion of blood volume (through Na/H2O retention)
question
We should use caution in giving selective specific vasodilators because...
Selective specific vasodilators are better tolerated when used in combination with other drugs such as beta blockers and diuretics.
question
What are some examples of arterial vasodilators? (3)
Some examples of arterial vasodilators are; Hydralazine (apresoline), Diazoxide (Hyperstat), Minoxidil (Minodyl)
question
What are some examples of arterial and venous vasodilators? (2)
Some examples of arterial and venous vasodilators are; Nitroprusside (nipride) and Prazosin (minipres)
question
What is the name of the dopamine da-1 receptor agonist vasodilator?
The dopamine da-1 receptor agonist is called Fenoldopam. Fenoldopam has similar side effects as nitroprusside, but without toxicity.
question
Which arterial vasodilator can cause lupus-like symptoms?
The arterial vasodilator Hydralazine can cause lupus-like symptoms (Myalgia-muscle pain, athralgia-athritis like pain w/o inflammation)
question
Which arterial and venous Vasodilator has these side effects; CNS disturbances (disorientaction, headache, psychotic behavior), and requires an opaque covering. We want to avoid cyanide thiocyanate toxicity with this drug as well.
The vasodilator Nitroprusside (nipride) can have CNS side effects such as disoreintation, headache, and psychotic behavior). It does require an opaque covering so it does not degrade. Cyanide thiocynate toxicity is possible as nitroprusside breaks down.
question
Which dopamine da-1 receptor agonist has similar side effects to nitroprusside (nipride) but does not have the toxiicty?
Fenoldopam (corlopam) is the da-1 dopamine receptor that has similar effects to nitroprusside (nipride) except for the cyanide toxicity.
question
What are the side effects of the arterial vasodilator diazoxide (hyperstat)?
The arterial vasodilator diazoxide (hyperstat) has the following side effects; hyperglycemia, hyperuricemia
question
Which arterial and venous vasodilator has the side effect of hursutism (hair)?
Minoxidil (minodyl) has the side effect of hursutism
question
What are two examples of Alpha 1 blocking agents?
Two alpha-1 blocking agents are; Prazosin (minipres), Doxazosin (cardura)
question
What is the action of alpha 1 adrenergic blockers (antagonists)?
Alpha 1 blockers block the effect of norepinephrine on alpha 1 adrenergic receptors in vascular smooth muscle. Alpha 1 blockers stop the work of norepinephrine on arterioles and veins. This opposes constriction and causes vasodilation.
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Alpha 1 blockers (antagonists) block the activity of which which chemical? Where do they do this?
Alpha 1 blockers (antagonists) block the activity of norepinephrine (which typically constricts) in the arterioles and veins. Administering alpha 1's stop this and result in vasodilation
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What is the physiological response to alpha 1 blockers (antagonists)?
The effect that alpha 1 blockers (antagonists) have on the body are; decreased SVR (PR), decreased afterload
question
What types of patients are alpha blockers (antagonists) best used in?
Alpha 1 blockers are best used in Hypertensive clients with BPH. This medication relaxes the prostrate muscle.
question
Which type of adrenergic inhibitor medications are best used in hypertensive patients with BPH? Why?
Alpha 1 blockers are best used in Hypertensive clients with BPH. It helps because the medication relaxes the prostrate muscle
question
What are some adverse side effects of alpha 1 adrenergic blockers (antagonists)
Alpha-1 adrenergic blockers can have the following side effect; Orthostatic hypotension
question
Why should we use caution when giving alpha 1 adrenergic blockers (antagonists)?
We should use caution when giving alpha 1 blockers with what is called the "first dose phenomenon". To remedy this we want to take the first dose just before bedtime (or lying down). This lessens the risk of orthostatic hypertension.
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Which adrenergic inhibitor do we have to use caution in regarding the "First dose" effect? How can we remedy this issue?
When we use the alpha 1 blockers we face a possible "first dose" effect. We can remedy this by giving the med before bedtime (or lying down) to lessen the risk of orthostatic hypertension.
question
About how many hours after administration of an alpha 1 blocker would we see the "first dose" phenomenon?
We would see the effects of the "first dose" phenomenon approximately 1-3 hours after administration of an alpha 1 blocker.
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What are some nursing considerations beyond the "first dose" phenomenon that we want to keep in mind when giving alpha 1 blockers?
Some nursing considerations for alpha-1 blockers are; That they are often used in combination with other drugs, they can cause orthostatic hypotension, and that they increase retention of Na and H2O
question
What are some examples of Alpha 2 agonist agents (centrally acting adrenergic antagonists)?
Some alpha 2 agonist agents (centrally acting adrenergic antagonists) are; Clonidine (Catapres), Methyldopa (aldomet)
question
What is the action of alpha 2 agonistic agents (centrally acting adrenergic antagonists) in the body?
Alpha 2 agonists (centrally acting adrenergic blockers/antagonists) inhibit the sympathetic nervous system (SNS) through stimulation of central alpha 2 receptors. As a result the release of NE is inhibited causing vasodilation.
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Which type of antihypertensive medication inhibits the release of NE through stimulation of central alpha 2 receptors?
Alpha 2 agonists (centrally acting adrenergic blockers/antagonists) inhibits the release of NE, therefore causing vasodilation.
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What is the physiological response the body has to alpha 2 agonists (central acting adrenergic blockers)?
The physiological response form alpha 2 agonists are; decreased SVR, decreased afterload, decreased HR
question
What is the difference in physiological response between alpha 1 blockers and alpha 2 agonists?
Alpha 1 and 2's both decrease SVR and afterload, but alpha 2's also decrease HR
question
Alpha 2 agonists (central-acting adrenergic blockers) are best used in which patients?
Alpha 2 agonists (central acting adrenergic blockers) are best used as a second line drug. This drug is also best used in pregnant women.
question
What are some adverse side effects of alpha 2 agonists (central acting adrenergic blockers)?
Alpha 2 agonists (central acting adrenergic blockers) have the following adverse side effects; dry mouth, drowsiness that lessens with time, Na/H20 retention over time which increases BP so a diuretic is required.
question
Which drug over time causes NA/H20 retention and necessitates the use of a diuretic? Why?
Alpha 2 agonists (central acting adrenergic blcokers) have the effect over time of NA/H20 retention which increases BP. A diuretic is needed is reduce fluid volume.
question
We should use caution when giving patients alpha 2 agonists (central-acting adrenergic blockers) because...
If alpha 2 agonists are discontinued abruptly the patient will experience rebound hypertension.
question
What are some specific nursing considerations for the alpha 2 agonist clonidine (catapres)?
Withdrawl from the alpha 2 agonist Clonidine (catapres) can cause tachycardia, headache, and sweating. It can also be given transdermally.
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What are some specific nursing considerations for the alpha -2 agonist Methyldopa (aldomet)?
Methyldopa can be used in pregnant women. A bedtime dose can minimize the sedative effect that methyldopa has.
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What is an example of an alpha-beta blocker?
Labetalol (transdate) is an example of an alpha-beta blocker.
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What is the action of the alpha-beta blocker labetalol (transdate)?
The alpha-beta blocker labetalol (transdate) blocks alpha as well as beta receptors.
question
What is the physiological response to labetalol (transdate)?
When the alpha-beta blocker labetalol (transdate) is given is causes; vasodilation, decreases HR and contractility (neg inotrope), decreases renin release, decrease SVR (PR), decreased afterload
question
What is the best use of labetalol (transdate)?
The best use of lebatelol is in hypertensive crisis. It can be given IV in hypertensive crisis.
question
What are some adverse side effects of labetalol (transdate) the alpha-beta blocker?
Labetalol (transdate) the alpha -beta blocker can have the following adverse side effects; Dizziness, fatigue, N & V, severe postural hypotension (esp after exercise), bronchospasm
question
We should use caution in giving labetalol (transdate) the alpha beta blocker to patients that...
We should use caution when giving labetalol to clients with; CHF
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What are some important nursing considerations in a patient who is taking labetalol?
Labetalol can cause hepatotoxicity. Patients who take labetalol also need to get periodic eye exams because long term use of labetalol can effect the eyes. We also want to monitor orthostatic BP especially after exercise.
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Which drug should we monitor orthostatic BP especially after exercise with.. why?
We should monitor orthostatic BP after exercise in clients taking labetalol because they are at risk for severe postural hypotension.
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Which drug requires the patient to seek periodic eye exams? why?
Labetalol (transdate) requires the patient to seek out periodic eye exams because long term use can effect the eyes.
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What is an example of a ganglionic blocker?
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What is the action of the ganglionic blocker arfonad?
The ganglionic blocker arfonad blocks transmission of impulses at the ganglia, causing vasodilation.
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What is the physiological response to the ganglionic blocker arfonad?
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What is the best use of the ganglionic blocker arfonad?
The best use for arfonad is for SEVERE hypertension.
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The ganglionic blocker arfonad can use; visual disturbances, dry mouth, h20 retention.
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What are some nursing considerations to take with a patient who is using arfonad?
With a patient taking arfonad we want to monitor for urinary output b/c it can cause retention. We also want to monitor for visual disturbances and dry mouth.
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What is an example of a post-ganglionic antihypertensive medication (peripheral-acting adrenergic antagonist)?
A post ganglionic antihypertensive medication is Reserpine (serpasil) as well as Ismelin
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What is the action of the post-ganglionic antihypertensive Reserpine (serpasil)?
The post-ganglionic antihypertensive medication Reserpine (serpasil) inhibits NE (the neurotransmitter of the SNS) thus inhibiting vasoconstriction. It has no central nervos system effect and no sedation.
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What is the physiological response to a post-ganglionic antihypertensive agent?
Post-ganglionic antihypertensive agents such as Reserpine and ismelin decrease SVR (PR) and decrease afterload.
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What is the best use for post-ganglionic antihypertensive agents?
Post ganglionic antihypertensive agents such as reserpine and ismelin are best used when other antihypertensive medications are ineffective.
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What are some adverse side effects of the post-ganglionic antihypertensive agents?
Adverse side effects of post-ganglionic antihypertensives are; Severe postural hypotension, post exercise hypotension, mental depression (at high doses), nasal stuffiness.
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What are some nursing considerations in particular for the post-ganglionic antihypertensive ismelin?
the post ganglionic antihypertensive medication ismelin can cause severe postural hypotension and post exercise hypotension. Monitor for this.
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What are some nursing considerations in particular for the post-ganglionic antihypertensive reserpine (serpasil)
The post-ganglionic antihypertensive Reserpine (serpasil) can cause depression at high doses so we must monitor for mental depression, suicidal tendencies, and AVOID CNS depressants
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Which antihypertensive drug should we avoid using CNS depressants with?
We should avoid using CNS depressants in patients that are taking REserpine (serpasil) the post ganglionic antihypertensive agent.
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What constitutes HYPERTENSIVE CRISIS?
Hypertensive crisis is when diastolic BP is greater than 120mmhg
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What (2) important things do we need to do with a patients that has severe hypertension?
In a patient with severe hypertension we need to 1. rule out causes (such as renovascular htn) , and 2. Evaluate signs of encephalopathy and target organ damage.
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With severe hypertension, we can give several antihypertensives IV, which ones?
We can give the following antihypertensives via IV; 1. Labetalol (transdate)- alpha beta blocker, 2. Nicardipine (Cardene)-CCB, 3. Nitroprusside (nipride)-vasodilator, 4. Fenoldapam (corlopam)-vasodilator
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What are some nursing considerations when giving labetalol (transdate) IV in a patient with severe hypertension?
In a patient with severe hypertension receiving the alpha-beta blocker labetalol (transdate) IV we need to instruct them to get periodic eye exams.
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What are some nursing considerations when giving Nicardipine (Cardene) IV in a patient with severe hypertension?
In a patient with severe hypertension receiving the CCB Nicardipine (cardene) IV, we need to keep in mind it can cause hepatotixicty in patients with impaired hepatic function
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What are some nursing considerations when giving Nitroprusside (nipride) IV in a patient with severe hypertension?
In a patient with severe hypertension receiving the vasoldilator Nitroprusside (Nipride) IV, We should know that it can cause CNS disturbances (disorientation, HA, psychotic beavior). We should also know it needs opaque covering to prevent degredation and to avoid cyanide thiocyanate toxicity.
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What are some nursing considerations when giving Fenoldopam (corlopam) IV in a patient with severe hypertension?
In a patient with severe hypertesion receiving the vasodilator Fenoldom (corlopam) IV, we should know that it causes similar side effects as nitroprusside (CNS disturbances) but does not have toxicity
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What should we know about African-Americans with hypertension when it comes to selecting an antihypertensive for them? (4)
In African Americans; 1. They produce less renin, so not as receptive to ACEI's, ARB'S or Renin blockers. We wouldn't use these on their own., 2. African Americans respond better to CCB's and Thiazide diuretics, 3. We can give combination therapy Thiazide/ACEI's with or without kidney disease, 4. African americans do well on a LOW SALT diet
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What are some important things to consider with Diabetics when it comes to antihypertensive medication? (4)
Diabetics; 1. ACEI's decrease proteinuria and slow nephropathy in diabetics, 2. CCB's instead of beta blockers, 3. Avoid nonselective beta blockers beucase they effect glucose metabolism and cause cause prolonged and severe hypoglycemia., 4. Beta 1 blockers can cause bradycardia and mask symptoms of hypoglycemia.
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Why should we not give beta blockers to diabetics?
non selective beta blockers effect glucose metabolism and can cause prolonged and severe hypoglycemia. Beta 1 blockers can cause bradycardia and mask symptoms of hypoglycemia.
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What is the first choice antihypertensive for elderly adults?
The first choice antihypertensive for elderly adults are THIAZIDE DIURETICS. Elderly adults can also use CCB's
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Elderly adults often have either systolic HTN (SBP>140 but DBP140 and DBP>90)
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Why might ACEI's and ARB's be less effective in elderly adults?
Elderly adults produce less renin, so are more resistant to ACEI's and ARB's. They need higher doses BUT have a slower metabolism. They key is to start low and GO SLOW.
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In elderly adults, what can happen is systolic blood pressure is reduced below 120mmhg?
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What are (4) important considerations in pregnant women with hypertension regarding medications?
Pregnant women with hypertension; 1. Can take alpha receptor agonists (central acting) such as Aldomet (methyldopa), 2. Can take vasodilators such as Hydralazine (apresoline), 3. Beta blockers are an option BUT MUST BE D/C'd BEFORE DELIVERY, CAUSES FETAL BRADYCARDIA, 4. ACEI's are teratogenic!
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What antihypertensive drug can be given to pregnant women but must be D/C'd before delivery? Why?
Pregant women can take beta blockers, but they must be d/c'd before delivery because they cause fetal bradycardia
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Which antihypertensive medication is teratogenic?
ACEI's are teratogenic.
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What is a good drug choice for post-menapausal women? why?
Thiazide diuretics are a good choice for post menepausal women because they promote Ca reabsorption (this slows osteoporosis)
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What antihypertensive medications are not a good choice for patients with renal issues?
Patients with renal issues should not really be taking ACEI's, ARB's, or renin blockers because they work on and through the kidneys.
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What is the best choice of antihypertensive medication for patients with renal issues?
The best choice for medication in a patient with renal issues is a loop diuretic (furosemide/lasix). They may need a large dose. Thiazide diuretics are not that effective.
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In a patient with renal failure, which medications can be used?
A patient with renal failure can take CCB's (diltiazem, verapamil) and ARB's because they are metabolized through the liver.
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When do we need to do a routine BP screening on children?
When they are overweight and have a family history of hypertension.
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What are three main causes of secondary HTN in children?
Causes of secondary HTN in children; 1. Renovascular disease, 2. Coarctation of aorta, 3. birth control pills in girls.
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What is the preferred antihypertensive med for HTN and migraine in children? What do we need to be cautious of?
Beta blockers are the preffered med for HTN and migraine in children. We want to avoid HR<60
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Do thiazide diuretics have more or less side effects in children vs adults?
Thiazide diuretics have LESS side effects in children than adults.
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In children with Diabetes (microalbuminuria, proteinuric renal disease) and HTN, what is the preffered drug?
Children that have diabetes (microalbuminuria, proteinuric renal disease) and HTN are usually given ACEI's.
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Why shouldn't sexually active girls take ACEI's or ARB's?
Sexually active girls should not take ACEI's because ACEI's are teratogenic. They should not take ARB's because they can harm the fetus as well.
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What do we give to children over 6 who do not tolerate ACEI's?
Children over 6 who do not tolerate ACEI's are given ARB's.
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Can calcium channel blockers (CCB's) be used in children with HTN?
Yes, CCB's can be used in acute and chronic HTN in children. Typically Norvasc (amlodipine) is used in child dosing.
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Which CCB is typically given to children with acute and chronic HTN?
The CCB Norvasc (amlodipine) is used in children with acute and chronic htn.
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What are some reasons that therapy fails in patients with hypertension? (5)
Therapy fails in patients frequently due to; 1. Asymptomatic nature of disease (people dont take it seriously), 2. Difficult life style changes (hard to motivate), 3. Annoying side effects of meds (dry cough from zestril), 4. The high cost of meds (especially newer ones), 5. Inconvenience of taking meds
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How many BP readings should you take in a patient when monitoring and evaluating for hypertension?
When monitoring and evaluating for hypertension, 2 or more readings should be taken supine or seated, and 2 or more readings should be taken standing.
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What should we assess in the environment when taking a BP reading?
When taking a BP reading, we should assess environmental effects such as: quiet, stress, food, tobacco, and caffiene.
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How do we determine if the BP cuff is the correct size?
The bladder width should be 40 percent of the circumfrence of the arm at midpoint. The bladder length should be 2x the recommended circumfrence width
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How can we best measure the diastolic reading?
We can best measure the diastolic reading by using the dissappearence of korotkoff sound
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When assessing risk with patients, what is important? (3)
Assessing patient risk factors; 1. Assess risk factors of patient, 2. Evaluate and rank from most serious to least, 3. Work with patient to make plan to address each factor in order.
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When assessing patient compliance, what should we keep in mind? (4)
Patient compliance considerations; 1. Patient preconceptions, 2. incorrect information about drug, disease, therapies, 3. Finances, 4. Support system
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What are some nursing dx's for a patient with hypertension? (8)
Hypertension nursing dx's; Decreased CO, ineffective tissue perfusion, knowledge deficit, ineffective health maintenance, ineffective therepeutic regimen management, fatigue, sexual dysfunction, noncompliance.
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What is the single most important predictor of cardiovascular risk?
Hypertension is the single most important predictor of cardiovascular risk.
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What are some symptoms of Hypokalemia? (THINK A SIC WALT)
Symptoms of Hypokalemia; Alkalosis, Shallow respirations, Irritability, Confusion, Weakness, Arrythmias, Lethargy, Thready pulse, also Decreased motility
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What are some symptoms of Hyperkalemia?
Some symptoms of hyperkalemia; Muscle cramps/Weakness/Paralysis, Drowsiness, Low BP, ECG changes, Dysrhthmias, Abdominal cramping, diarrhea, oliguria.
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Do children have a higher or lower prevalence of secondary HTN than adults?
Children have a higher prevalence of secondary HTN than adults.
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Which special population has greater effects from beta blockers than caucasians?
Asians experience greater effects from Beta blockers than caucasians
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Which poplulations may need lower doses due to slower metabolization of antihypertensive medications?
Asians, Arab Americans, Egyptian Americans, and German americans may need lower doses due to possibly slower metabolization of antihypertensive medications.
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Which race has the highest rate of hypertension in the world?
African Americans
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Which percentage of african americans in the US have hypertension? How many deaths dose HTN account for in the african american population? How does this relate to the white population?
35 percent of african americans in the US have hypertension. 20 percent of african american deaths in the US are a result of hypertension. This is twice the rate of whites.
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Compared to whites, african americans develop hypertension when, and with what severity?
Comapred to whites, african americans develop hypertension earlier in life and BP is much higher.
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What percentage higher chance do african americans with high blood pressure have of dying from a stroke than the general population?
African americans have an 80 percent higher chance of dying from a stroke than the general population
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What end stage disease are african americans with high blood pressure at 4 times greater risk of developing than the general population?
African americans with high blood pressure are at 4 times greater a risk of developing end stage renal disease than the general population?
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Are CCB's, Alpha 1 receptor blockers, and labetalol more effective, less effective or have similar efficacy in whites vs african americans?
CCB's, alpha 1 receptor blockers, and labetol (alpha beta blocker) have similar efficacy in whites vs african americans.
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When are beta blockers used in african americans?
Beta blockers are used in african americans as part of a multidrug regimen. Higher doses are needed.
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What are some downsides of thiazide diuretics in elderly adults?